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Biology Somatotypes Genetics Nutrition Personality Lifestyle
Choices
Environment Mindfulness Social Support Quality
of Life
Social Support
Relationships
As social beings, humans benefit from positive, meaningful, healthy, and productive relationships. Positive relationships encourage personal growth, provide help and support, increase feelings of happiness, life satisfaction and purpose, and are ultimately related to health and longevity.
Family
Whether it's the immediate, extended or adopted family, those we include in our definition of family can be quite different. What matters most is the way family provides support, education, sustenance, protection, affection or any other need for a healthy life.
Friends
Friendships can have a major impact on health, happiness and wellbeing and it is therefore important to understand their role as well as how to cultivate and nurture them.
Quality of Life
Stress
The physical, mental and emotional burden of acute and chronic stress is very different for each of us. Some people are more sensitive to certain stressors than others and the body's reaction to stress can vary greatly.
Life Satisfaction
Life satisfaction is a concept in positive psychology that encompasses many factors and may include feelings of happiness and positive feelings, social integration, quality of life, perceptions of success, among others.
Environment
Exposomics
The biochemical effects of environmental pollutants, toxins, radiation, frequencies and pharmaceuticals provide a more holistic view of human health and disease so it's important to consider these for improved strategies to prevent and treat related illnesses.
Geomedicine
Based on the principles of exposomics in which environmental pollutants affect our health, geomedicine looks at the specific impacts in a geographical area. Modern technology allows complex geographically referenced information to be captured, analyzed and distributed in more comprehensive ways.
Mindfulness
Meditation
Whether it's through the practice of yoga, guided imagery, deep relaxation of repetitive prayer and mantras, there are many ways to meditate and switch off the brain to allow the body to release tension completely and fully relax providing psychological and physical benefits.
Mindful Eating
One could choose to eat mindfully, being aware of what to eat, or get used to healthy habits to the point that they become so second nature that they're not even thought of.
Biology
Anthropometry
The combination of your genes and environment creates who you are today, so measurements of the various parts of the body have been associated with certain physical conditions, personal experiences and behavioral traits.
Endocrinology
The endocrine system is composed of the hypothalamus, the adrenal, pituitary, thyroid and thymus glands, the reproductive system and the interaction with several major organs. It is a complex system of hormones that affect both the body and the mind.
Embryology
Although embryology is mainly focused on the study of fertilization, and the development of embryos and fetuses, it's research into diseases and physical conditions that occur before birth has shed a lot of light on inherent conditions we have in the adult body and from where they stem.
Phenotype
The phenotype is the combination of the genotype, the expression of the genes that determine the type of body you would have (including skin color, hair texture, eye color, etc), and the environment (such as with diet, pollution, family influences, etc).
Molecular
When you take biochemistry and combine it with genetics, you get molecular biology and the study of how molecular mechanisms affect cellular replication, transcription, translation and function.
Genetics
DNA
The more we uncover the mysteries lying in the depths of our genetic makeup, the more we can revolutionize our ability to prevent, cure and manage disease.
Epigenetics
Unlike DNA mutations, epigenetic variations are potentially reversible, so understanding the epigenetic markers of common chronic diseases is like retracing the steps taken along a path and finding a better route to health in a personalized therapy.
Somatotypology
Chronobiology
The circadian rhythm is the body's inner clock that tells us when to eat and sleep, as well as how organs function, hormones are secreted, the brain works, etc. This natural pacemaker keeps us in sync with the 24 hours of the day and plays an important role in health, wellbeing and longevity.
Ayurveda
Ayurveda is a 5,000 year old system of medicine that originates in the Vedic culture of India, using the means of Prakriti to explain the functions of an individual often based on general categorizations of body shape, composition, function, need, nutrition, behavior and personality.
TCM
Traditional Chinese Medicine dates back thousands of years. Using a holistic approach to understanding normal function of the body and mind and their relevant disease processes, this type of medicine focuses as much on the prevention of illnesses as it does on their treatment.
Psychology
Personality
The study of personality is about understanding your character traits and behaviors based by studying the neural mechanisms and connections of the brain, the hormonal and neurotransmitteral trends, or structured observational approaches.
Neurobiology
Understanding the brain and the nervous system is key to uncovering the complexity with which the cells and tissues generate our thoughts, feelings, senses, perceptions, movements, and even the underlying structure with which we learn.
Lifestyle
Exercise
Exercise can help strengthen muscles and bones, improve cardiovascular activity, control body weight and shape, perfect a physical skill or sport and relieve the body of some forms of stress. The effects exercise can have on the body vary, based on the type, duration and intensity of the exercise.
Sleep
Considering there are important physiological activities associated with digestion, cell repair, and growth that occur during sleep, it is no surprise that there are severe health effects that can occur from sleep deprivation.
Nutrition
Nutriceutics
Nutraceutics is the study of food substances and how they can be used in the treatment, prevention?and?reduction of a disease risk?or that provide health benefits to the body and mind.
Nutrigenomics
Individual genetic differences can affect the way we respond to nutrients and the foods we eat just like certain foods can affect our genes. This understanding is crucial in the development of personalized nutrition that can prevent, mitigate or cure?chronic disease.
Relationships
Marriage or being in a couple can have a positive influence on wellbeing.
People in positive couple relationships are happier, live longer, drink less, and even have few doctor's appointments than unmarried folks.
Feeling useful slows aging.
It is important to feel useful to family and friends as we age, even if our physical abilities decline, because this renders us less likely to suffer from chronic illness and have lower mortality rates.
Positive relationships can increase longevity.
There is a large body of epidemiological evidence that points to both the quantity and the quality of relationships is directly and indirectly related to longevity, with positive relationships being related to lower risks of disease and particular evidence with a reduced rate of cardiovascular and cancer mortalities.
Social isolation is linked to depression.
Depression is a psychiatric disorder that can be highly debilitating and has been correlated with several physical health outcomes and other psychiatric disorders. But depressive symptoms can be reduced through social support.
Family
Knowing yourself and knowing others improves family relationships.
Better understanding who you are as a person (your likes, your preferences, your needs, your habits) as well as of those of your family can greatly help improve or strengthen family bonds through positive communiation, proactive problem solving and conflict resolution, and providing the needed support to help each other grow.
Worrying about the health and wellbeing of family members can put a strain on you.
There is a physical and emotional stress that family members feel when they worry a lot about the health and wellbeing of their loved ones, which is why encouraging health and wellbeing within the family can have a very positive effects on your own condition.
Being a caregiver for young children can be a physical and mental burden.
Any new parent will admit that the physical and psychological burden of young children can be heavy. Whether it's sleep deprivation, lack of personal time, lack of social support, time management or overall stress, there are many factors that can contribute to the fatigue and strain of parents with young children.
A good family can make your happier.
Although economic conditions and work play a large role in happiness, a very big contributor comes from positive family circumstances.
Friends
Feeling rejected can have a huge psychological and physical impact.
The neural mechanisms in the brain that deal with emotional pain and physical pain overlap. As research continues to delve into the connected mechanisms of the brain and body, they regularly discover the effects emotions can have.
A variety of friendships can be better than a narrow group.
Having multiple roles in your network increases social connection and integration.
Friendships are highly related to your personality type.
Your personality, as measured by things like extraversion, neuroticism, agreeableness, and openness, are important predictrs of friendship quality and style.
Your friendship style may even be rooted in your genes.
There are several aspects of your peronality that may be influenced by the environment, while others come from the genes. This is the typical nature versus nurture debate in relation to human behavior and psychology. When looking at the nature side of the coin, researchers have found that there are innate traits, preferences and behaviors that can determine much about who you would naturally get along with or not.
Meditation
Meditation has a direct and indirect effect on the body and the brain.
The meditative effects of yoga can have great benefits on your mental and physical health and the reasons behind this mechanism are only partially understood yet continuously researched. The more science comes to understand this, the better we can harness the effects of this state of mind in health and wellbeing.
Mediative relaxation can activate disease-fighting mechanisms in the body.
Researchers at the Harvard Medical School examined the known benefits of meditative practice from a genetic perspective and discovered that those who practiced meditation over a long period of time had more active disease-fighting genes than the control group.
Sleep and vigilence are improved with meditation.
Vipassana meditation is a type of mindfulness meditation that has been shown to improve sleep, wakefulness and cognitive states. Other types of meditative practice have also been shown to improve the stability of the mind, which has enhanced the quality of sleep and therefore provided sleep-related health benefits.
Mindful Eating
Portion sizes can make a difference.
Not only do large portion sizes increase the amount of calories consumed, ultimately leading to unwanted weight gain and difficult weight management, but reducing portion sizes has been shown to be an easy way to be mindful of how much should be eaten.
People raised on junk food may not be able to trust their body.
The body has a natural wisdom related to food, knowing what's good, what's needed and what's enough. But people who have been raised on junk food and bad eating habits have most likely altered the epigenetic, hormonal and neuronal circuit enough that the body's sibtle signs can't be blundly trusted. Foods found most rewarding and the body's reaction to sugar, salt, and fat may have changed significantly.
Learning about environmental triggers for food craving may be essential for healthy eating habits.
Environmental triggers can include things like watching TV and being triggered into a food craving through commercials, or having the habit of finishing a meal with something sweet, or associating events (like Christmas or Birthdays) with certain foods. Knowing when you're most likely going to be tempted, recognizing tempation and having methods available to resist temptation may prove to be essential for people who struggle most with healthy eating.
Anthropometry
The size of your waistline can tell a lot about your state of health.
There is an abundance of evidence that supports the link between the one's waist circumference and various health factors such as cardiovascular disease and diabetes. Keeping the waistline down plays a role in health and longevity.
Your life is written in your bone structure.
Your bones can tell a lot about who your are and what you did in your life. Though it would be quite intrusive to take a direct look at the bones inside your body, measuring the size of bony sturctures like height or wrist circumference can tell a lot about your phenotype.
Your body's shape may predict some health risks.
Many studies have shown that your physique or physical constitution is interlinked to health and disease.
Your biotrend can change during childhood and adolescence.
There are many factors that contribute to the shape, size and overall physical constitution of the adult body. Genetics can play a large roll, but so can the type of physical activity we have, our nutrition, our athletic engagement or even natural hormonal shifts. As studies in human development examine the natural changes our body goes through before, during and after puberty, it has been bringing further enlightment into somatotype changes that seem to stabilize in adulthood when the physical maturity of the body has been reached and we can consider the body fully developed.
Personality
Some of your personality is rooted in childhood.
Is it true that some people never change? Although life events will always influence a person's behaviors, there is also an underlying power of personality that can predict future behavior. Though we may be tought to act in a certain way, researchers are finding that there are personality traits that are truly our own and forcing them to change may not be in a person's best interest.
Being in an environment that fits your personality is healthy.
Though we may naturally tend to seek environments, jobs, social circles and hobbies that suit our personality style, there are many situations in which we may feel obligated to partake. When the environment you're in doesn't fit your natural personality, it can cause feelings of neuroticism, lower self-esteem, depression and frustration which are all psychological and emotional conditions that can even have a physical effect on the body.
Your personality can be directly linked to your health.
The way you think and feel has been shown to be directly related to your body's functions and your overall health. Just like meditation and relaxation can lower blood pressure by relaxing the mind, mental agitation, frustration, hostility can increase blood pressure.
Neurobiology
The fat content of your body is largely regulated by the brain.
The neurocircuits of your brain regulates much of the body's desire for food intake, including how much, when, how often and what kinds of foods. Using a combination of hormones, neurotransmitters and neural connections, the brain tends to regulate the way the body reacts to food.
Your brain's sense of pleasure is a double-edged sword.
Your brain's pleasure sensors can help you with imrpoved cognition, productivity, and overall health, but it can also lead to negative outcomes like addiction.
Your personality may be related to oxytocin levels.
Are you a naturally trusting, optimistic, cheerful, empathic and sociable? Then you may be influenced by all that oxytocin in your body.
Serotonin activity may be related to inherent personality traits.
The serotonergic activity in the brain, for instance, is related to one's more aggressive proactive approach to coping versus more passive or reactive styles of coping.
Endocrinology
Your body's shape can tell a lot about what hormones are predominant.
Hormones influence chemical reactions in the body, assist in transporting substances through membranes, and ultimately control cellular function. Hormones manage development, growth, reproduction, and behavior and their influence on the muscular-skeletal system, respiratory and cardiovascular systems, nervous, immune, and digestive systems are evident on the body.
Thyroid conditions can be improved with lifestyle changes.
Whether it's avoiding cruciferous vegetables, increasing iodine-riche foods, reducing phytoestrogens, regulating the intake of fats and sugars, or stabilzing energy levels and hunger throughout the day, a personalized approach to diet regulation can improve thyroid function.
Smoking can negatively affect the entire endocrine system.
Smoking involves the consumption of nicotine and many harmful chemicals that affect the pituitary, thyroid, adrenal, and genital functions. The management of various health risk factors and endocrine dysfunction due to smoking is therefore considered in a PH360 profile.
Embryology
Your body's constitution is largely formed during embryonic development.
Programmed in the DNA are nuclear receptors that regulate genetic expression, which control embryonic development and ultimately the physiological, physical, and psychological traits of the adult human body. This is why reverse engineering the adult body's development back down to the embryonic influences can determine the genetic factors that are more or less active in an individual.
Ectomorphs are more sensitive people.
Heightened activity in the central nervous system renders ectomorphs more sensitive to stimulti, which not only makes them more sensitive people but also often portraying an array of related traits like attention to detail, creativity, and deep thought.
Endomorphs or Kapha types are more conscientious people.
Studies have shown that there is an underlying tendency for inherent metabolic and growth factors that are controlled by the nervous system to affect the body and mind in a patterned way. Hence, the Kapha type (as defined in Ayurvedic medicine) is characterized by a slow and steady metabolic system resulting in a rounder yet sturdier type of body, will have a matching steady yet methodical type of thought and action.
DNA
Much of your personality may be genetically influenced.
Whether it be twin studies, genome expression, or biochemical correlates, science has examined one's inherent personality from various angles and continues to unravel the mystery behind how much of our personal thought and behavior are we born with. Turns out, it's about half!
A genetic susceptibility to a disease doesn't guarantee its activation.
The oldest human alleles originated in Africa, in parallel with the development of our species, millions of years before people first migrated out of Africa 50,000 to 60,000 years ago and they are shared by all human populations and account for approximately 90% of human variation. Yet there are new alleles appearing every day that generate an immense degree of genetic variation. This is why, though most human variation is ancient and shared, looking at recent and rare alleles can tell us a lot about inherent diseases. But genetics alone can only explain a piece of the puzzle.
The TCF7L2 gene is a significant type 2 diabetes susceptibility gene.
Studies on human genetics have made it possible to identify genetic loci that underlie diseases like type 2 diabetes and this is why knowing the family's prevelance of the disease can provide a clue about one's current risk factor for diabetes and glucose metabolism.
There are genes that may make some people inherently fat.
Various genes have been identified to be contributors to the the shape of body we have as adults. Just like some people tend to be more apple shaped (gaining fat mass around the waist), while others are more pear-shaped (tending to put their fat stores around the glutes), there are genes that contribute to bone thickness, metabolic tendencies and the way insulin is used, and other factors that contribute to an overall genetic tendency towards obesity.
Being taller than average increases the risk of cancer.
Science has long been interested in making the connection between height and health and the cumulative evidence has been showing that there are pros and cons to being taller than average. The benefit is a reduced risk of cardiovascular issues, but the downside is the increased risk of all types of cancer.
Short people have a higher risk of cardiovascular issues.
Being shorter than average, especially in the legs, increases the risk for metabolic issues, like glucose and lipid processing, that affect the circulatory system. The reasons behind this isn?t yet clear, but this understanding helps guide preventative medicine in the right direction.
Ayurveda
The Activator's and Connector's cardiovascular issues may be related to the Pitta body type.
It is a complex link with various factors involved, but essentially there are genetic triggers that affect mood, metabolism and the ciruclatory system. These influence the body's shape and size (including muscle tone and bone structure), while being associated with personality and mental function. Both the body's function and the personality under certain conditions has been associated with stress reaction patterns and ultimatey cardiovascular predispositions.
The Kapha body type has a clear genetic pattern.
Modern genetic examination of Ayurvedic body types has been able to uncover some of the mysteries of this ancient medicine and directly linked genetic predispositions to body types. The Kapha type, characterized by larger bones, a sturdier and founder figure with a stronger and resilient body has always been associated with higher parasympathetic activity, a slow and steady predisposition and a tendency to retain mass. Even the associated health conditions Ayurvedic medicine always associated with the Kapha type (including issues in the lungs, health problems related to obesity, stronger immune system but a tendency to accumulate toxins is being linked on a genetic level.
Scientists are continuously unravelling the correlation between DNA and Prakriti.
At the time of conception and during embryological development, the Ayruvedic system of medicine believes that there is a predominance of Dosha or fundamental body humors (Vata, Pitta and Kapha) that governs all functions of the body at the physical, mental and emotional levels. Similarly, research in genetics has found that many of our physical traits, behavioral tendencies, and risk for certain diseases has a genetic component to it. Connecting these two approaches has been a more recent development in personalized medicine with small puzzle pieces coming together to show a larger pictures that connects ancient and modern medicine.
TCM
The genetic link to TCM constitutions is becoming ever clearer.
There are a number of constitutions in traditional chinese medicine, including Qi Deficient, Yang Deficient, Yin Deficient, Blood Stasis, Phlegm-Dampness, Damp-Heat, and Qi-Stagnation, which regularly need balancing protocols to keep them healthy. Based on the notion that one's constitution is an indicator of health risks and therefore modifyable pathways to health and well-being, researchers have begun using modern science to build on an uphold this theory of preventative medicine.
TCM constitutions can be linked to mood and behavior.
Modern science has found that the way your body works is linked to and a reflection of the way your mind works and vice versa. Similarly, traditional chinese medicine has always looks at physical constitutions and syndroms being linked to certain types of behavioral trends.
TCM syndroms may be related to a specific type of cancer risk.
By looking at the constitution of people who suffer from certain types of cancers, it is possible to figure out what constitutions pose the greatest risks for certain types and trends. This has allowed researchers to better understand ways to prevent the disease as well as better, more personalized methods of treating it.
Korean constitutions are also being scientifically related to DNA.
Korean Constitutional Medicine is rooted in Traditional Chinese Medicine but was transformed into a new medical system by Lee Jee-ma in the 1800's. Known as the Sasang Constitutional Medicine (SCM), it is a medical principle that classifies humans into four constitutions and offers holstic treatments accordingly. These are Taeyangin, Soyangin, Taeumin and Soumin.
Phenotype
It's not just about whether or not you have a gene, but if it's being expressed.
Genome-wide studies in the associations between an existing gene, its expression, prevelance of disease and its progression has become increasingly popular in recent years as researchers race to better understand the gene-environment interaction and how it influences human health.
Air pollution can greatly affect your immune system from early on.
A fetus' T-lymphocyte and B-lymphocyte fractions can change enough to alter the immunophenotypes of the baby when the mother is exposed to inhaled particulate matter, polycyclic aromatic hydrocarbons and other air pollutants.
Though obesity is related to many health issues, it's also related to asthma.
Studies have noticed that the increase in worldwide obesity as well as asthma may be related and further investigation into this hypothesis confirms it. Though these are non-obese and even thin people with asthma, there are phenotype conditions that may create bronchopulmonary constriction or aggravate existing asthma. In accordance with other philosophies (including TCM, Ayurveda, Embryology, etc), there seems to be a distinct phenotype that has a heightened risk of pulmonary conditions.
Molecular
Stress can unleash molecular signalling pathways leading to chronic inflammation and cancer.
ADP-ribosylation of chromatin can help cells deal with stress-induced damages and help maintain the health of chromosomes that carry genetic information. In this process, enzymes place small molecules onto specific parts of a protein or remove them, thereby activating or deactivating the protein. Understanding the molecular signaling pathways that play a central role in cellular stress responses allows us to understand the disease-making processes which in turn enable us to prevent them.
Obstructive sleep apnoea is a risk factor for cardiovascular disease.
The risk of endothelial dysfunction and atherosclerosis is greatly increased with oxidative stress and inflammation which can be worsened by factors like obesity, metabolic syndrome and even sleep apnea.
Proper digestion means getting the right nutrients without the excess.
There are many components to the metabolic pathway, and looking at protein metabolism we already see that proper pH levels, enzymatic function, organ activity and removal of excesses are important factors in preventing unwanted conditions like gout, inflammation, hypercholesterolemia, etc.
Epigenetics
A mother's health can change a child's genetic predisposition to disease.
Though there are many examples of how a mother's health, nutrition, gestational wellbeing and birthing process can influence the health of her child, studies on specific genetic expressions have begun to shed light on epigenetic effects of intrauterine life. Intrauterine exposure to poor maternal nutrition or maternal obesity has consistently been demonstrated to contribute to a particular epigenotype that has a higher risk of obesity and metabolic syndrome.
About 70% of what causes aging can be modulated during the lifespan.
Evidence suggests that the aging process can be genetically modulated and although about 30% are genetic inputs, what's left are non-genetic factors and environmental stimuli like diet, exercise, stress, and other factors. Researchers have found that although much of who we are is relatively stable throughout life, some remodelling is still possible later through regulated factors that cause stable changes in healthspan and longevity.
Epigenetic markers are often used to assess the rate of aging.
Biomarkers commonly used in the study aging include expression levels of the cell cycle inhibitor CDKN2A?(also known as p16INK4A), telomere length attrition rate, and CpG DNA methylation.
Chronobiology
Metabolic and sleep disorders can affect your epigenome.
Metabolic pathways and the sleep-wake cycle are controlled by the circadian rhythm. Disturbing this cycle can have negative effects on metabolic disorders like obesity and diabetes, but effects can be reverted with strict times for eating. This may be because the circadian rhythm determines when certain amino acids and metabolites are released.
The body wants to run like a swiss watch.
The body has a natural 24 hour internal clock that resets itself with sunlight. This regulates our behaviors and body functions and needs to be kept relatively unchaging for the health benefits of the body. Studies on major changes to sleep and wake cycles have shown how this can put a strain on the biological clock and the effects this can ultimately have on the body.
There is no perfect time to exercise.
The human body benefits greatly from regular movement and intentional exercise to keep the blood flowing, the joints moving, the muscles active and the brain functioning well. Studies on endurance, resistance, and interval training have different theories about the best times to exercise, with most of the consensus being around mid-day, though variations in study results exist based on the type of exercise being performed, the intensity and duration of the exercise, and the physiological conditions of the person. Nonetheless, there are certain worst times to exercise, which include the middle of the night when the body should be in its resting state.
Exercise
Exercise can keep the brain from aging poorly.
Exercise may prevent cognitive decline in humans and regular physical activity is associated with longevity, a 30% reduction in all-cause mortality and a dose-response improvement in overall health in humans.
The epigenetic effect of exercise can be a life saver.
Exercise isn't just healthy for you in the way it builds muscles, encourages proper blood flow and reduces the health risks associated with being overweight, but researchers have found that regular exercise can have an epigenetic effect on the body by improving AMPK activity which improved the body's metabolism and protection against cellular weakness.
Women should lift weights.
Weight training is a great way to improve muscle mass and build strength, but women tend to spend more time are cardiovascular training and avoid the weights. But strength training can have several benefits to women, including building strength that can make chores and daily tasks easier to manage, increasing metabolism that helps burn more calories during rest, increase bone mineral density and reducing injury.
Sleep
You can fight wrinkles with sleep.
Sleeping allows the body to undergo some important mechanisms, among which are recuperative and healing processes. Though studies may not yet have fully examined the mechanisms behind sleep-deprivation causing facial wrinkles, we believe there is a link and use this as an example of how assumptions can be drawn by connecting various pieces of research.
Lack of sleep can create metabolic dysfunction.
There are two factors to consider for sleep problems and the effect on metabolism: the first is sleep-disordered breathing, which can range from snoring to sleep apnea and generally involves disrupted sleep due to breathing conditions, and the second is insufficient sleep due to shift work, being woken up at night, being uncomfortable, or just not giving yourself enough time to sleep. Both of these affect the required hours of quality sleep the body needs to recouperate from daily stresses and the effects can be detrimental on the digestive system.
Sleep function is related to the brain's health.
During sleep, the brain uses the glymphatic pathway, a?waste-clearing process that provides the brain cleansing cerebrospinal fluids (CSF) and interstitial fluid (ISF), to flush out toxins from the brain, including amyloid β and tau proteins that are unhealthy in the brain if they build up and can lead to neural disorders like Alzheimer's.
Exposomics
The air you breathe could be killing you.
Depending on where you live, there could be a huge amount of air pollution filled with dangerous ultrafine particles that penetrate deep into the lungs and enter the circulatory system carrying harmful chemicals and toxins. People with existing respiratory problems like asthma and emphysema are at greater risk of their effects, but further investigation has found that even healthy people can suffer.
Reducing exposure to pesticides can prevent many health problems.
Pesticides used in the agricultural industry are intended to kill, repel or sterilize a pest so that the product being cultivated can grow to maturity unharmed or undamaged. Toxicological and epidemiological research has found numerous exposures to these chemicals to be extremely harmful to human (and animal) health.
Reducing the risk for dementia is possible through exposomics research.
Whether is be environmental factors like pollution, exposure to toxins and other contaminants, or toxic effects of and unhealthy body like inflammation, thyroid conditions, kidney disease or any other condition, there are various components exposomics research has been able to highlight in relation to maintaining neural health.
Geomedicine
Depending on where you live, you may be exposed to toxic arsenic.
A recent American study has found that more than 50% of Americans will experience a moderate kidney disease in their lifetime, a risk that increases with age to the point that it is higher than diabetes, coronary heart disease and invasive cancer. Not only does the risk increase a lot with age, with most cases being in late life, but the study showed it is higher in women than men and racial discrepancies also exist.
One important risk factor for kidney conditions is chronic stress. Chronic stress can increase sympathetic nervous system activity, increase glucocorticoid secretion, and increase levels of inflammatory cytokines. All of these factors also play a role in higher risks for hypertension, diabetes, and cardiovascular disease, which have also been found to be major risk factors for chronic kidney disease (CKD).
People with CKD seem to have lower levels of the hormone, renalase which is responsible for metabolizing products of the sympathetic nervous system. It is therefore believed that chronic stressors that cause an increased sympathetic nervous system activity can exhaust the body to the points than renalase is no longer adequately produced, which sets in motion a vicious cycle.
The air you breathe at home could be contaminated.
Exposure to rocks high in uranium, such as uraniferous granites, marine black shales, and phosphate rock can cause people to inhale larger than safe amounts of radon gas. Soils and rocks beneath the building and building materials can release the gas into indoor air. People who use ground water may have an additional exposure source.
Knowing air conditions contributes to health risk estimates.
There are many factors that contribute to health risks that include genetics, epigenetics, lifestyle choices and environmental exposures. Among these, one of the most frustrating ones is air pollution because of the amount is affects us and the little control we as individuals have over it. Living in large cities already exposes us to more air pollution from exhaust fumes than would country life, but even non-urban dwellers have their exposures from the use of pesticides in fields or their vicinity to refineries.
Stress
Chronic stress can cause chronic pain.
Chronic stress can be exhausting on the hypothalamus, the pituitary glands and the adrenal glands, resulting in what is commonly known as burnout. But researchers have found that chronic pain may also arise. Beta-endorphins are usually released with stress as a pain suppression, allowing us to face adverse situations, but if the body is exhausted, this morphine-like hormone no longer gets release and we can become very sensitive to pain.
Stress can make you lose a kidney.
Hypertension, diabetes, and obesity are well known risk factors for chronic kidney disease, but chronic stress may also be an important contributing factor and the risk for kidney conditions has been increasing dramatically due to our modern lifestyle. "To lose a kidney" is part of an Italian expression to express extreme stress and science is beginning to prove the link.
How you handle stress may be an epigenetic factor.
Environmental conditions can affect epigenetic mechanisms and stress is a major player. Studies have been piecing together a bigger picture of the influence on stress and the vicious cycle it can have on the body. The body's chronic reaction to stress can alter genetic expression which in turn can affect the response to stress.
Nutrigenomics
Increasing good cholestorol may not lower cardiovascular risk in everyone.
It was once believed that cholesterol was bad and a major risk factor for heart disease. It was later discovered that there's a difference between LDL (bad) and HDL (good) types of cholesterol. But unlike conventional belief today, having high HDL cholesterol does not necessarily protect someone from cardiovascular complications. HDL should always be higher that LDL, which needs to be kept low. But even too much of a good thing isn't good.
Iron for some biotrends can be a double-edged sword.
A typical Western diet contains approximately 15 mg of daily iron, of which less than 10% is absorbed. But for some people, iron absorption and stores are considered more seriously. Whereas some are prone to iron deficiency anemia, iron overload can be a real issue leading to inflammation, neurological diseases, cardiovascular issues, among others. This can stem from genetic disorders, malfunctioning liver, candida infections, or other conditions but tends to be more common in specific biotrends.
Short intestines require different nutrition protocols.
In humans, the small intestine varies from about 275 cm (9 feet) to 850 cm (almost 28 feet), and tends to be shorter in women. Longer intestines tended to be related to weight, not height or other factors). It is then to no surprise that Sensors, the lightest biotrend, tend to have the shortest intestines and therefore particular nutritional needs to accommodate for the effects of a shorter bowel. These include the consideration of adequate electrolytes, increased carbohydrates, insuring there is an adequate mineral absorption, proper hydration, etc.
Nutriceutics
Antioxidants are beneficial in preventing neurodegenerative diseases.
Many neurodegenerative diseases and age-related degenerative processes have been associated with oxidative stress as a common factor. Whether it be Parkinson's, Alzheimer's, lateral sclerosis, multiple sclerosis, or age-related senility, neuronal oxidative stress have been linked and the use of antioxidants has been shown to help prevent or delay such degenerative conditions.
Turmeric is great for cardiovascular health, but not for everyone.
Turmeric has great anti-inflammatory and antioxidant properties that are excellent for protecting the body against cardiovascular disease, including atherosclerosis, vascular dysfunction, cardiac hypertrophy and heart failure. But the same benefits it can have for increasing blood flow through decreased platelet aggregation, for instance, can be a negative effect for someone who already has thin blood or who is taking blood thinners like aspirin, coumadin, warfarin or heparin. What is good for one, may not be good for the other.
IBD can be treated through diet, but the diet is different for many.
Inflammatory bowel disease (IBD) is a chronic or recurring immuno-inflammatory illness that can cause chronic and progressive inflammation of the gastrointestinal tract as well as ulcerative colitis. A diet for IBD may consider an increase in soluble fiber from beans and oats, the inclusion of healthy omega 3 fatty acids from olive oils and avocado, lots of anti-inflammatory foods like green leafy vegetables while avoiding pro-inflammatory foods like nuts, etc. But IBD is not a clear-cut condition that is the same in everyone and it often someone with IBD may have other conditions as well.
Life Satisfaction
Wellbeing can add 4 to 10 years to your life.
Various meta-analyses have repeatedly looked at the various studies and research methods behind happiness, social wellbeing, life satisfaction and optimism in relation to health and found that there are direct and indirect correlates to longevity.
Depression and anxiety can literally break your heart.
Cardiovascular issues have repeatedly been linked to anxiety and depression in various types of studies. The underlying mechanism behind this phenomenon is complex and continues to be understood, but the end message is pretty clear.
Happiness can lead to success.
Life satisfaction is composed of many factors, with happiness and success both being important components. Reviews of cross-sectional studies have found that happiness can lead to success in many areas of life, including work life, social relationships, and health.
Evidence Behind Marriage or being in a couple can have a positive influence on wellbeing.
Although it would be farfetched to create a causal relationship between marriage and health, there are two possibilities that support the established link between marriage and longevity. The first is that people who are more likely to get married and remain married are healthier to begin with. This could be based on the notion that certain attributes such as physical traits, intellect, mental well-being, self-sufficiency, and overall health render a person a more desirable marriage candidate.
But there is the other side to this coin that also points to marriage having real benefits to health and wellbeing. Though there is the potential of a married couple to have an indirect improvement in health through economic and social advantages like being in a dual income household and economic stability and thus increasing access to health care or lowering stress, there is a deeper link between married couples that shouldn't be ignored. For one, married couples can monitor and encourage healthy behaviors while discouraging unhealthy ones. But a happy couple also provides intimacy, emotional fulfillment, social connections and shared experiences that are positive for both physical and mental health.
References
  • Wood, Robert G., Brian Goesling, and Sarah Avellar. "The effects of marriage on health: a synthesis of recent research evidence." Washington DC: Mathematica Policy Research (2007).
  • Kaplan, Robert M., and Richard G. Kronick. "Marital status and longevity in the United States population." Journal of epidemiology and community health 60.9 (2006): 760-765.
  • Van den Berg, Gerard J., and Sumedha Gupta. "The role of marriage in the causal pathway from economic conditions early in life to mortality." Journal of health economics 40 (2015): 141-158.
  • Wilson, Chris M., and Andrew J. Oswald. "How does marriage affect physical and psychological health? A survey of the longitudinal evidence." (2005).
  • Holt-Lunstad, Julianne, Wendy Birmingham, and Brandon Q. Jones. "Is there something unique about marriage? The relative impact of marital status, relationship quality, and network social support on ambulatory blood pressure and mental health." Annals of behavioral medicine 35.2 (2008): 239-244.
  • Poulain, Michel, and Anne Herm. "Centenarians' Marital History and Living Arrangements: Pathways to Extreme Longevity." The Journals of Gerontology Series B: Psychological Sciences and Social Sciences (2015): gbv082.
  • van Jaarsveld, Cornelia HM, et al. "Marriage and cancer prevention: does marital status and inviting both spouses together influence colorectal cancer screening participation?." Journal of Medical Screening 13.4 (2006): 172-176.
  • Schulz-Aellen, M-F. Aging and human longevity. Springer Science & Business Media, 2012.
Evidence Behind Feeling useful slows aging.
Not only does a sense of ability and usefulness increase self-esteem and reduce the risk of depression, but there is a broad underlying construct of general social well-being when someone can feel like they have an integral role in a group. Feeling useful has been found to increase the sense of social connectedness which is ultimately related to many effects on positive health.
One example of a health benefit includes the engagement of healthy behaviors, like the avoidance of smoking or reducing the time being seated. Another is improved physiological resilience, such as better muscle tone and ability to heal due to an increase in physical activity. There is also the benefit of emotional stability, with positive coping mechanisms and stress management being worked on when one feels they have a role to play in a social context. A last example could be longer maintenance of mental acuity because mental engagement, memory and cognitive functions are continuously active when one has something to do.
References
  • Williams, Keith L., and Renee V. Galliher. "Predicting depression and self-esteem from social connectedness, support, and competence." Journal of Social and Clinical Psychology 25.8 (2006): 855.
  • Hazan, Cindy, and Mary I. Campa, eds. Human bonding: The science of affectional ties. Guilford Press, 2013.
  • Gruenewald, Tara L., et al. "Feelings of usefulness to others, disability, and mortality in older adults: The MacArthur study of successful aging." The Journals of Gerontology Series B: Psychological Sciences and Social Sciences 62.1 (2007): P28-P37.
  • Charles, Susan, and Laura L. Carstensen. "Social and emotional aging." Annual review of psychology 61 (2010): 383.
  • Mendes de Leon, Carlos F. "Social engagement and successful aging." European Journal of aging 2.1 (2005): 64-66.
  • L?vd?n, Martin, Paolo Ghisletta, and Ulman Lindenberger. "Social participation attenuates decline in perceptual speed in old and very old age." Psychology and aging 20.3 (2005): 423.
  • Hsu, H. C. "Does social participation by the elderly reduce mortality and cognitive impairment?." Aging & mental health 11.6 (2007): 699-707.
  • Brown, Stephanie L., et al. "Providing social support may be more beneficial than receiving it results from a prospective study of mortality." Psychological Science 14.4 (2003): 320-327.
Evidence Behind Positive relationships can increase longevity.
Whether it's about positive relationships being related to positive behaviors and actions that lead to good health, or that health and happiness is related to seeking and properly managing positive relationship, the overwhelming evidence points to a clear relationship between health and ultimately longevity and having a good marriage, supportive friends, a loving family or caring neighbors.
The evidence regularly supports the association between having a positive social circle and the behavioral factors that alter genetic risks associated with cardiovascular disease, diabetes/metabolic syndrome, obesity, and hypertension. Combining the research on positive wellbeing and mortality, it has been found that positive moods such as joy and happiness, life satisfaction, hopefulness, optimism, and sense of humor are all associated with reduced risk of mortality and even predict longevity.
Not only can social wellbeing help you live longer, but it may also increase the change of overcoming illness. Studies on patients with cancer or HIV have found that positive mood helps survival rates. PH360 therefore emphasizes the need to promote healthy positive relationships as part of a holistic approach to health, wellbeing and longevity.
References
  • Uchino, Bert N., et al. "The social neuroscience of relationships." Social neuroscience: Integrating biological and psychological explanations of social behavior (2007): 474.
  • Henderson, Gregor. "Public health approaches to social isolation and loneliness: a health and wellbeing directorate seminar." London: Public Health England (2013).
  • Harmon-Jones, Eddie, and Piotr Winkielman, eds. Social neuroscience: Integrating biological and psychological explanations of social behavior. Guilford Press, 2007.
  • Diener, Ed, and Micaela Y. Chan. "Happy people live longer: Subjective well?being contributes to health and longevity." Applied Psychology: Health and Well?Being 3.1 (2011): 1-43.
  • Holt-Lunstad, Julianne, Wendy Birmingham, and Brandon Q. Jones. "Is there something unique about marriage? The relative impact of marital status, relationship quality, and network social support on ambulatory blood pressure and mental health." Annals of behavioral medicine 35.2 (2008): 239-244.
  • Schulz-Aellen, M-F. Aging and human longevity. Springer Science & Business Media, 2012.
  • Ford, Earl S., Indu B. Ahluwalia, and Deborah A. Galuska. "Social relationships and cardiovascular disease risk factors: findings from the third national health and nutrition examination survey." Preventive Medicine 30.2 (2000): 83-92.
  • Joseph, Philip G., Guillaume Pare, and Sonia S. Anand. "Exploring gene-environment relationships in cardiovascular disease." Canadian Journal of Cardiology 29.1 (2013): 37-45.
  • Shumaker, Sally A., and Susan M. Czajkowski, eds. Social support and cardiovascular disease. Springer Science & Business Media, 2013.
  • Uchino, Bert N. "Social support and health: a review of physiological processes potentially underlying links to disease outcomes." Journal of behavioral medicine 29.4 (2006): 377-387.
  • Kroenke, Candyce H., et al. "Social networks, social support mechanisms, and quality of life after breast cancer diagnosis." Breast cancer research and treatment 139.2 (2013): 515-527.
  • Cohen, Sheldon. "Social relationships and health." American psychologist 59.8 (2004): 676.
Evidence Behind Social isolation is linked to depression.
There are many studies that have used the National Survey of Families and Households (NSFH), a nationally representative sample with two waves of data collection (1988-1989 and 1992-1994) to demonstrate how getting married, for instance, can reduce the prevalence of depressive symptoms whereas divorce or remaining unmarried can increase it. But the evidence is also highly supportive of friendships, neighbors and even with several degrees of separation (the friends' friends' friends).
In a meta-analysis of 286 studies, the quantity and quality of contacts with friends was a strong predictor of well-being, even stronger than that of contacts with family members. Not surprisingly, loneliness is negatively correlated with happiness, especially in older adults. It has even been found to be related to pain, fatigue, and an array of physical health problems that can affect someone at any stage in life.
One study found that ruminating thoughts can be an important mediator between the feelings of loneliness and depression, especially for peer-related loneliness among college students. Both cross-sectional and longitudinal examinations confirm that loneliness, measured by social isolation and dissatisfaction with social interactions, is a risk factor for depression and that both loneliness and depression have a synergistic effect on wellbeing.
References
  • Alpass, Fiona M., and Stephen Neville. "Loneliness, health and depression in older males." Aging & mental health 7.3 (2003): 212-216.
  • Cornwell, Erin York, and Linda J. Waite. "Social disconnectedness, perceived isolation, and health among older adults." Journal of health and social behavior 50.1 (2009): 31-48.
  • Kim, Hyoun K., and Patrick C. McKenry. "The relationship between marriage and psychological well-being a longitudinal analysis." Journal of Family Issues 23.8 (2002): 885-911.
  • Rosenquist, J. Niels, James H. Fowler, and Nicholas A. Christakis. "Social network determinants of depression." Molecular psychiatry 16.3 (2011): 273-281.
  • Kawachi, Ichiro, and Lisa F. Berkman. "Social ties and mental health." Journal of Urban health 78.3 (2001): 458-467.
  • Steptoe, Andrew, et al. "Social isolation, loneliness, and all-cause mortality in older men and women." Proceedings of the National Academy of Sciences 110.15 (2013): 5797-5801.
  • Cacioppo, John T., and Louise C. Hawkley. "Social isolation and health, with an emphasis on underlying mechanisms." Perspectives in biology and medicine 46.3 (2003): S39-S52.
  • Seeman, Teresa E. "Health promoting effects of friends and family on health outcomes in older adults." American Journal of Health Promotion 14.6 (2000): 362-370.
  • House, James S. "Social isolation kills, but how and why?." Psychosomatic medicine 63.2 (2001): 273-274.
  • Hawton, Annie, et al. "The impact of social isolation on the health status and health-related quality of life of older people." Quality of Life Research 20.1 (2011): 57-67.
  • Eisenberger, Naomi I., et al. "Inflammation and social experience: an inflammatory challenge induces feelings of social disconnection in addition to depressed mood." Brain, behavior, and immunity 24.4 (2010): 558-563.
  • Pinquart, M., & S?rensen, S. (2000). Influences of socioeconomic status, social network, and competence on subjective well-being in later life: A meta-analysis. Psychology and Aging, 15, 187?224.
  • Cattan, Mima, et al. "Preventing social isolation and loneliness among older people: a systematic review of health promotion interventions."?Ageing and society?25.01 (2005): 41-67.
  • Rokach, Ami.?Loneliness updated: Recent research on loneliness and how it affects our lives. Routledge, 2013.
  • Vanhalst, Janne, et al. "Loneliness and depressive symptoms: The mediating and moderating role of uncontrollable ruminative thoughts."?The Journal of psychology?146.1-2 (2012): 259-276.
  • Cacioppo, J. T., Hughes, M. E., Waite, L. J., Hawkley, L. C., & Thisted, R. A. (2006). Loneliness as a specific risk factor for depressive symptoms: Cross-sectional and longitudinal analyses. Psychology and Aging, 21, 140?151.
Evidence Behind Knowing yourself and knowing others improves family relationships.
Although there is a great amount of research that points to positive family circumstances being related to health because of socioeconomic status (generally a combination of education, income, and occupation) it is the physiological and psychological benefits of positive family relationships provided through support and care that PH360 focuses on. By understanding your personal social and emotional needs, as well as those within the family, positive relationships can be built and maintained to obtain the social support from loved ones. A lot of the research focuses on work-family issues, conflict resolution, time constraints and emotional support within the family, all of which can be positively influenced through the knowledge and understanding of each others personality and needs. In contrast, lack of partner support and unmanaged family strain can lower one's perceived quality of life and negatively influence physical and psychological wellbeing, especially for women.
References
  • Ross, Catherine E., John Mirowsky, and Karen Goldsteen. "The impact of the family on health: The decade in review." Journal of Marriage and the Family 52.4 (1990): 1059-1078.
  • Seeman, Teresa E. "Health promoting effects of friends and family on health outcomes in older adults." American Journal of Health Promotion 14.6 (2000): 362-370.
  • Bruck, Carly S., and Tammy D. Allen. "The relationship between big five personality traits, negative affectivity, type A behavior, and work-family conflict." Journal of Vocational Behavior 63.3 (2003): 457-472.
  • Austin, Elizabeth J., Donald H. Saklofske, and Vincent Egan. "Personality, well-being and health correlates of trait emotional intelligence." Personality and Individual differences 38.3 (2005): 547-558.
  • Cunningham, Christopher JL, and Gabriel M. De La Rosa. "The interactive effects of proactive personality and work-family interference on well-being." Journal of Occupational Health Psychology 13.3 (2008): 271.
  • Portes, Alejandro, and Lingxin Hao. "The price of uniformity: Language, family and personality adjustment in the immigrant second generation." Ethnic and Racial Studies 25.6 (2002): 889-912.
  • Klonsky, E. David, et al. "Recollections of conflict with parents and family support in the personality disorders." Journal of personality disorders 14.4 (2000): 327.
  • Walen, Heather R., and Margie E. Lachman. "Social support and strain from partner, family, and friends: Costs and benefits for men and women in adulthood." Journal of Social and Personal Relationships 17.1 (2000): 5-30.
  • Walen, Heather R., and Margie E. Lachman. "Social support and strain from partner, family, and friends: Costs and benefits for men and women in adulthood." Journal of Social and Personal Relationships 17.1 (2000): 5-30.
  • Millikan, Emily, Marianne Z. Wamboldt, and Joan T. Bihun. "Perceptions of the family, personality characteristics, and adolescent internalizing symptoms." Journal of the American Academy of Child & Adolescent Psychiatry 41.12 (2002): 1486-1494.
  • Luszczynska, Aleksandra, and Roman Cieslak. "Protective, promotive, and buffering effects of perceived social support in managerial stress: The moderating role of personality." Anxiety, Stress, and Coping 18.3 (2005): 227-244.
  • Armstrong, Mary I., Shelly Birnie-Lefcovitch, and Michael T. Ungar. "Pathways between social support, family well being, quality of parenting, and child resilience: What we know." Journal of child and family studies 14.2 (2005): 269-281.
Evidence Behind Worrying about the health and wellbeing of family members can put a strain on you.
Studies have shown that knowing that loved ones are healthy, have positive social integration, and are established in life (have some money, a home, food to eat and other basic needs met) results in higher perceived quality of life. On the other hand, drastic worries such as a severe health condition in the family, major changes in financial stability or family structure can create major physical and emotional effects like sleep disturbances, stress and anxiety, blood pressure problems, and even cancer. This is one of the reasons PH360 promotes healthy and positive relationships within the family and among loved ones.
References
  • Jokinen, N. S., and R. I. Brown. "Family quality of life from the perspective of older parents." Journal of Intellectual Disability Research 49.10 (2005): 789-793.
  • Shek, Daniel TL. "Economic disadvantage, perceived family life quality, and emotional well-being in Chinese adolescents: A longitudinal study." Social Indicators Research 85.2 (2008): 169-189.
  • Cruice, Madeline, et al. "Measuring quality of life: Comparing family members' and friends' ratings with those of their aphasic partners." Aphasiology 19.2 (2005): 111-129.
  • Kim, Ik Ki, and Cheong-Seok Kim. "Patterns of family support and the quality of life of the elderly." Social Indicators Research 62.1-3 (2003): 437-454.
  • Johnson, H. Durell, Joseph C. Lavoie, and Molly Mahoney. "Interparental conflict and family cohesion predictors of loneliness, social anxiety, and social avoidance in late adolescence." Journal of Adolescent Research 16.3 (2001): 304-318.
  • Li, Hong. "Hospitalized elders and family caregivers: a typology of family worry." Journal of Clinical Nursing 14.1 (2005): 3-8.
  • DiLorenzo, Terry A., et al. "A model of disease-specific worry in heritable disease: the influence of family history, perceived risk and worry about other illnesses." Journal of Behavioral Medicine 29.1 (2006): 37-49.
  • Bowen, Deborah J., et al. "The relationship between perceived risk, affect, and health behaviors." Cancer Detection and Prevention 28.6 (2004): 409-417.
  • Brosschot, Jos F., Eduard Van Dijk, and Julian F. Thayer. "Daily worry is related to low heart rate variability during waking and the subsequent nocturnal sleep period." International Journal of Psychophysiology 63.1 (2007): 39-47.
  • Brosschot, Jos F., William Gerin, and Julian F. Thayer. "The perseverative cognition hypothesis: A review of worry, prolonged stress-related physiological activation, and health." Journal of psychosomatic research 60.2 (2006): 113-124.
  • Hoehn-Saric, Rudolf, et al. "Effect of worry on regional cerebral blood flow in nonanxious subjects." Psychiatry Research: Neuroimaging 140.3 (2005): 259-269.
  • Salovey, Peter, et al. "Emotional states and physical health." American psychologist 55.1 (2000): 110.
Evidence Behind Being a caregiver for young children can be a physical and mental burden.
Though this burden can be heavy on men, especially when the intimate relationship takes a back seat to caring for the young one(s), mothers can feel particularly drained. One of the main factors that impacts the health of caregivers is chronic stress, which is associated with depression and negative mood, sleep problems and deprivation, poor health habits (bad diet, sedentary life), and even the increased risk of health problems or worsening of existing illnesses. Even the increase of stress hormones can lead to health conditions like hyperglycemia, hyperinsulinemia, high blood pressure, poor immune function and poor digestion.
References
  • Vitaliano, Peter P., Heather M. Young, and Jianping Zhang. "Is caregiving a risk factor for illness?." Current Directions in Psychological Science 13.1 (2004): 13-16.
  • McEwen, Bruce S. "Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators." European journal of pharmacology 583.2 (2008): 174-185.
  • Selye, Hans. Stress in health and disease. Butterworth-Heinemann, 2013.
  • Meltzer, Lisa J., and Jodi A. Mindell. "Relationship between child sleep disturbances and maternal sleep, mood, and parenting stress: a pilot study." Journal of Family Psychology 21.1 (2007): 67.
  • Luecken, Linda J., and Kathryn S. Lemery. "Early caregiving and physiological stress responses." Clinical psychology review 24.2 (2004): 171-191.
  • Vitaliano, Peter P., et al. "A path model of chronic stress, the metabolic syndrome, and coronary heart disease." Psychosomatic medicine 64.3 (2002): 418-435.
  • Vitaliano, Peter P., et al. "A path model of chronic stress, the metabolic syndrome, and coronary heart disease." Psychosomatic medicine 64.3 (2002): 418-435.
  • McBride, Brent A., Sarah J. Schoppe, and Thomas R. Rane. "Child characteristics, parenting stress, and parental involvement: Fathers versus mothers." Journal of Marriage and Family 64.4 (2002): 998-1011.
  • Gay, Caryl L., Kathryn A. Lee, and Shih-Yu Lee. "Sleep patterns and fatigue in new mothers and fathers." Biological Research for Nursing 5.4 (2004): 311-318.
  • Nystr?m, Kerstin, and Kerstin ?hrling. "Parenthood experiences during the child's first year: literature review." Journal of advanced nursing 46.3 (2004): 319-330.
  • Hung, Chich?Hsiu, and Hsin?Hsin Chung. "The effects of postpartum stress and social support on postpartum women's health status." Journal of advanced nursing 36.5 (2001): 676-684.
  • Beydoun, Hind, and Audrey F. Saftlas. "Physical and mental health outcomes of prenatal maternal stress in human and animal studies: a review of recent evidence." Paediatric and perinatal epidemiology 22.5 (2008): 438-466.
  • Goodman, Janice H. "Paternal postpartum depression, its relationship to maternal postpartum depression, and implications for family health." Journal of advanced nursing 45.1 (2004): 26-35.
Evidence Behind A good family can make your happier.
The is a large body of evidence that supports the notion that socio-economic status is positively related to family happiness because of access to resources, a reduction of stress for obtaining basic needs, the greater likelihood to engage in healthy behaviors and the cognitive ability to solve problems within the family or manage conflicts positively. But there is a growing evidence that shows that despite this, there is a more powerful underlying mechanism that truly determines what makes a happy family and that's emotional satisfaction, having a positive and optimistic state of mind, altruism within the family and interpersonal coordination and harmony amoung family members. So when you combine family cohesion with personal satisfaction and health, there is a great increase in overall life satisfaction and perceived quality of life. As wisely stated in Diener and Oishi's (2005) paper: "Although laypeopleprobably understand that close friends and family arecorrelated with happiness, they may not realize thatthey are necessary for happiness, as well as for healthand optimal cognitive functioning."
References
  • Easterlin, Richard A. "Life cycle happiness and its sources: Intersections of psychology, economics, and demography." Journal of Economic Psychology 27.4 (2006): 463-482.
  • Bruhin, Adrian, and Rainer Winkelmann. "Happiness functions with preference interdependence and heterogeneity: The case of altruism within the family." Journal of Population Economics 22.4 (2009): 1063-1080.
  • Anqi, Xu. "A Preliminary Analysis of the Effect Mechanism of Economic Factors on Family Happiness [J]." Jiangsu Social Sciences 2 (2012): 018.
  • Louis, Vincent V., and Shanyang Zhao. "Effects of family structure, family SES, and adulthood experiences on life satisfaction." Journal of Family Issues 23.8 (2002): 986-1005.
  • Benjamin, Daniel J., et al. "Beyond Happiness and Satisfaction: Toward Well-Being Indices Based on Stated Preference." The American economic review 104.9 (2014): 2698-2735.
  • Diener, Ed, and Shigehiro Oishi. "The nonobvious social psychology of happiness." Psychological Inquiry 16.4 (2005): 162-167.
Evidence Behind Feeling rejected can have a huge psychological and physical impact.
Though scientists may argue about exactly where this is located (whether it's specifically in the anterior cingulate cortex or in the broader sympathetic nervous system) many have personally experienced such emotional-physical connections (such as being sick with worry or being so angry you can hardly breathe). So on that same postulate, researchers have found that people with insecure relationships are more likely to suffer from cardiovascular and other health problems than those who have more secure and supportive friendships. With the understanding that friendship quality is important to health and wellbeing, combined with the notion of an existing interplay between personality types and friendship styles, it is possible that social rejection can be reduced by better understanding the self and the social groups that would be more accepting of that innate and natural self.
References
  • Eisenberger, Naomi I., and Matthew D. Lieberman. "Why rejection hurts: a common neural alarm system for physical and social pain." Trends in cognitive sciences 8.7 (2004): 294-300.
  • Keyes, Corey LM, and Mary Beth Waterman. "Dimensions of well-being and mental health in adulthood." (2003).
  • Barlow, Fiona Kate, Winnifred R. Louis, and Miles Hewstone. "Rejected! Cognitions of rejection and intergroup anxiety as mediators of the impact of cross?group friendships on prejudice." British Journal of Social Psychology48.3 (2009): 389-405.
  • Ford, M?ire B., and Nancy L. Collins. "Self-esteem moderates the effects of daily rejection on health and well-being." Self and Identity 12.1 (2013): 16-38.
  • Mendes, Wendy Berry, et al. "How attributional ambiguity shapes physiological and emotional responses to social rejection and acceptance."Journal of personality and social psychology 94.2 (2008): 278.
  • Slavich, George M., et al. "Neural sensitivity to social rejection is associated with inflammatory responses to social stress." Proceedings of the national academy of sciences 107.33 (2010): 14817-14822.
  • Gruenewald, Tara L., et al. "Acute threat to the social self: Shame, social self-esteem, and cortisol activity." Psychosomatic medicine 66.6 (2004): 915-924.
  • Maunder, Robert G., et al. "The relationship of attachment insecurity to subjective stress and autonomic function during standardized acute stress in healthy adults." Journal of psychosomatic research 60.3 (2006): 283-290.
  • Berscheid, Ellen S., and Pamela C. Regan. Psychology of Interpersonal Relationships. Psychology Press, 2016.
Evidence Behind A variety of friendships can be better than a narrow group.
Theories related to role enhancement and convoy models of social relations have found that people, especially women, who are well integrated in a diverse network of friends are more likely to have better mental health outcomes than those who hold a more restricted network. Psychological health can be improved through the reduction of a sense of isolation, depression and inadequacy, and also enhanced through an increase of social support in a wider variety of areas. Since different relationships can provide different functions and support roles, it is to no surprize that PH360 promotes social cohesiveness as well as personal and emotional understanding, to help maintain positive morale and overall psychological health.
References
  • Fiori, Katherine L., Toni C. Antonucci, and Kai S. Cortina. "Social network typologies and mental health among older adults." The Journals of Gerontology Series B: Psychological Sciences and Social Sciences 61.1 (2006): P25-P32.
  • Moen, P. (2001). The gendered life course. In R. H. Binstock (Ed.), Handbook of aging and the social sciences (5th ed., pp. 179-196). San Diego, CA: Academic Press.
  • Litwin, H. (2001). Social network type and morale in old age. The Gerontologist, 41,516-524.
  • Umberson, Debra, Robert Crosnoe, and Corinne Reczek. "Social relationships and health behavior across life course." Annual review of sociology 36 (2010): 139.
  • DuPertuis, Leslee L., Carolyn M. Aldwin, and Raymond Boss?. "Does the source of support matter for different health outcomes? Findings from the Normative Aging Study." Journal of Aging and Health 13.4 (2001): 494-510.
  • Bagwell, Catherine L., et al. "Friendship quality and perceived relationship changes predict psychosocial adjustment in early adulthood." Journal of Social and Personal Relationships 22.2 (2005): 235-254.
Evidence Behind Friendships are highly related to your personality type.
There are numerous studies that support the notion that quality friendships promote psychological and physical health, but perhaps there's something to be said about who we select as friends. Examining personality types, emotional intelligence, affect and social behavior, researchers have found that there are certain traits that seek and/or attract certain types of friends. In other words, it may not just be that the quality of the friendships affects wellbeing, but that our own state of mind affects the quality of those relationships. There have even been relationships found between the neurological function of the brain (such as hormones and neurotransmitters) and the relationships we hold.
References
  • Berry, Diane S., Julie K. Willingham, and Christine A. Thayer. "Affect and personality as predictors of conflict and closeness in young adults' friendships." Journal of Research in Personality 34.1 (2000): 84-107.
  • Markiewicz, Dorothy, Anna Beth Doyle, and Mara Brendgen. "The quality of adolescents' friendships: Associations with mothers' interpersonal relationships, attachments to parents and friends, and prosocial behaviors."Journal of Adolescence 24.4 (2001): 429-445.
  • Settle, Jaime E., et al. "Friendships moderate an association between a dopamine gene variant and political ideology." The Journal of Politics 72.04 (2010): 1189-1198.
  • Selfhout, Maarten, et al. "Emerging late adolescent friendship networks and Big Five personality traits: A social network approach." Journal of personality78.2 (2010): 509-538.
  • Sprecher, Susan, and Pamela C. Regan. "Liking some things (in some people) more than others: Partner preferences in romantic relationships and friendships." Journal of Social and Personal Relationships 19.4 (2002): 463-481.
  • Lopes, Paulo N., Peter Salovey, and Rebecca Straus. "Emotional intelligence, personality, and the perceived quality of social relationships."Personality and individual Differences 35.3 (2003): 641-658.
  • Soares, Marta C., et al. "Hormonal mechanisms of cooperative behavior."Philosophical Transactions of the Royal Society of London B: Biological Sciences 365.1553 (2010): 2737-2750.
  • LeMarquand, David, et al. "Biochemical Factors in Aggression and Violence."Encyclopedia of Violence, Peace, & Conflict: AF 1 (2008): 174.
  • Hruschka, Daniel J. Friendship: Development, ecology, and evolution of a relationship. Vol. 5. Univ of California Press, 2010.
  • Lopes, Paulo N., et al. "Emotion regulation abilities and the quality of social interaction." Emotion 5.1 (2005): 113.
Evidence Behind Your friendship style may even be rooted in your genes.
Scientisis have been uncovering more and more of the connection between genetic expression and social behavior, including traits like altruism, egoism, depression, generosity, extraversion, neurotisism and so many more. Though genetic expression is not the sole explanation for human behavior or social dynamics in life, it can play a significant role in many social theories of attachment, group behavior and psycho-emotional traits. Understanding the phenotypic structure of personality is what allows predictive elements to be utilized in the assessment of harmoneous or non-cohesive human relationships. The ultimate purpose is to allow for a self-understanding and acceptance of the self to the fullest for healthy and positive social inclusion into quality relationships.
References
  • Fraley, R. Chris, et al. "Interpersonal and genetic origins of adult attachment styles: A longitudinal study from infancy to early adulthood." Journal of Personality and Social Psychology 104.5 (2013): 817.
  • Blum, Kenneth, et al. "Neuropsychiatric genetics of happiness, friendships, and politics: hypothesizing homophily ("birds of a feather flock together") as a function of reward gene polymorphisms." Journal of genetic syndrome & gene therapy 3.112 (2012).
  • Segal, Nancy L., and Kevin B. MacDonald. "Behavioral Genetics and Evolutionary Psychology: Unified Perspective on Personality Research."Human Biology 70.2 (2013): 2.
  • Bearman, Peter. "Exploring Genetics and Social Structure." American Journal of Sociology 114.S1 (2008).
  • Viken, Richard J., et al. "A developmental genetic analysis of adult personality: extraversion and neuroticism from 18 to 59 years of age."Journal of personality and social psychology 66.4 (1994): 722.
  • Krueger, Robert F., and Wendy Johnson. "Behavioral genetics and personality." Handbook of personality: Theory and research (2008): 287-310.
  • Brendgen, Mara. "Genetics and peer relations: A review." Journal of Research on Adolescence 22.3 (2012): 419-437.
  • Holden, Constance. "The Sociable Brain." Science 321.5888 (2008): 487-487.
  • Juhasz, Gabriella, et al. "CNR1 gene is associated with high neuroticism and low agreeableness and interacts with recent negative life events to predict current depressive symptoms." Neuropsychopharmacology 34.8 (2009): 2019-2027.
  • Ebstein, Richard P., et al. "Genetics of human social behavior." Neuron 65.6 (2010): 831-844.
Evidence Behind Meditation has a direct and indirect effect on the body and the brain.
Whether it's the quality of breathing, the calmness of emotions, the harmony within the neural network, the improvements in cardiovascular function, or the many other effects regularly revealed by research, what we know for certain is that regular meditation can have a great benefit on one's mental and physical wellbeing. Various studies on the cognitive effects have shown increase in grey matter, enhanced mental speed and attention, and improved coordination. Studies on the physical effects have shown improved glucose metabolism, enhanced cellular rejeuvenation and immune systems, better pulmonary functions and digestive processes, reduced blood pressure and improved weight management. Research into the quality of life has also revealed higher perceived life satisfaction and overall happiness in relation to meditation.
References
  • Luders E, Toga AW, Lepore N, Gaser C. The underlying anatomical correlates of long-term meditation: Larger hippocampal and frontal volumes of gray matter. Neuroimage 2009;45:672-8. Back to cited text no. 16
  • Sharma VK, Das S, Mondal S, Goswami U, Gandhi A. Comparative effect of sahaj yoga on EEG in patients of major depression and healthy subjects. Biomedicine Journal 2007;27:95-9
  • Lazar SW, Kerr CE, Wasserman RH, Gray JR, Greve DN, Treadway MT, et al. Meditation experience is associated with increased cortical thickness. Neuroreport 2005;16:1893-7
  • Mody BS. Acute effects of Surya Namaskar on the cardiovascular & metabolic system. J Bodyw Mov Ther 2011;15:343-7.
  • Ankad RB, Herur A, Patil S, Shashikala GV, Chinagudi S. Effect of Short-Term Pranayama and Meditation on Cardiovascular Functions in Healthy Individuals. Heart Views 2011;12:58-62
  • Paul-Labrador M, Polk D, Dwyer JH, Velasquez I, Nidich S, Rainforth M, et al. Effects of a randomized controlled trial of transcendental meditation on components of the metabolic syndrome in subjects with coronary heart disease. Arch Intern Med 2006;166:1218-24.
  • Chung, Sheng-Chia, et al. "Effect of sahaja yoga meditation on quality of life, anxiety, and blood pressure control." The Journal of Alternative and Complementary Medicine 18.6 (2012): 589-596.
  • Brown, Kirk Warren, and Richard M. Ryan. "The benefits of being present: mindfulness and its role in psychological well-being." Journal of personality and social psychology 84.4 (2003): 822.
  • Pace, Thaddeus WW, et al. "Effect of compassion meditation on neuroendocrine, innate immune and behavioral responses to psychosocial stress." Psychoneuroendocrinology 34.1 (2009): 87-98.
  • Gard, Tim, et al. "Effects of a yoga-based intervention for young adults on quality of life and perceived stress: the potential mediating roles of mindfulness and self-compassion." The Journal of Positive Psychology 7.3 (2012): 165-175.
  • Sharma, R, Gupta, and R. L. Bijlani. "Effect of yoga based lifestyle intervention on subjective well-being." Indian J Physiol Pharmacol 52.2 (2008): 123-131.
Evidence Behind Mediative relaxation can activate disease-fighting mechanisms in the body.
As we now know, genes can switch on and off based on our environment, behavior, mood, nutrition or any other external factor. Well it turns out that proper meditation of a given period of time can intentionally activate speicifc genes related to the immune system, lowering inflammation, regulating blood pressure and balancing hormone levels.
Also, the longer one practices, the better the effects of relaxation are on the body. One of the theories behind this is that the stress-hormones adrenalin and cortisol, which ultimately raise the heart rate and blood pressure while weakening immunity, are reduced through relaxation. In contrast, serotonin and alpha brain waves can increase tissue and cellular repair while activating the parasympathetic nervous system (the one that tells us to relax the body, lower stress levels, etc). When the mind completely switches off, the body can release all tension and ultimately improve our mental and physical health and wellbeing in many ways.
References
  • Benson, Herbert, and William Proctor. Relaxation revolution: The science and genetics of mind body healing. Simon and Schuster, 2010.
  • Dusek, Jeffery A., et al. "Genomic counter-stress changes induced by the relaxation response." PloS one 3.7 (2008): e2576.
  • Saatcioglu, Fahri. "Regulation of gene expression by yoga, meditation and related practices: a review of recent studies." Asian journal of psychiatry 6.1 (2013): 74-77.
  • Bhasin, Manoj K., et al. "Relaxation response induces temporal transcriptome changes in energy metabolism, insulin secretion and inflammatory pathways." PLoS One 8.5 (2013): e62817.
  • Kaliman, Perla, et al. "Rapid changes in histone deacetylases and inflammatory gene expression in expert meditators."Psychoneuroendocrinology 40 (2014): 96-107.
  • Coghlan, Andy. "Meditation boosts genes that promote good health." New Scientist 218.2916 (2013): 12.
Evidence Behind Sleep and vigilence are improved with meditation.
Studies have shown that advanced practitionners of meditation have improved slow wave sleep (SWS) and deep sleep with rapid eye movement (REM) than control groups, indicating an improved quality of sleep. Since aging can reduce the activity of SWS because of a loss of neural pathways, reduced activation of pathways and sleep spindle generation. But even novice meditators can improve parasympathetic activity needed for proper sleep, so much so that meditation has been successfully used to help with conditions of insomnia.
Not only does it provide improved sleep, this then has an effect on wakefulness and the ability to be alert and concentrated during the day, especially in long-term meditators. Various mediation practices, intensities and duration have found improvements in alertness and vigilance, and neuroimaging studies have found a reduced reliance on the default mode network (the auto-pilot mechanism that allows us to function without paying attention) and can even increase cortical thickness.
References
  • Mourtazaev, M. S., Kemp, B., Zwinderman, A. H., and Kamphuisen, H. A. (1995). Age and gender affect different characteristics of slow waves in the sleep EEG. Sleep 18, 557-564.
  • Nicolas, A., Petit, D., Rompre, S., and Montplaisir, J. (2001). Sleep spindle characteristics in healthy subjects of different age groups. Clin Neurophysiol 112, 521-527.
  • Wu, S. D., and Lo, P. C. (2008). Inwardattention meditation increases parasympathetic activity: a study based on heart rate variability. Biomed. Res. 29, 245-250
  • Nagendra, Ravindra P., Nirmala Maruthai, and Bindu M. Kutty. "Meditation and its regulatory role on sleep."?Frontiers in neurology?3.54 (2012): 1-4.
  • Ong, J. C., Shapiro, S. L., and Manber, R. (2008). Combining mindfulness meditation with cognitive-behavior therapy for insomnia: a treatmentdevelopment study. Behav. Ther. 39, 171-182.
  • Britton, Willoughby B., et al. "Awakening is not a metaphor: the effects of Buddhist meditation practices on basic wakefulness."?Annals of the New York Academy of Sciences?1307.1 (2014): 64-81.
  • Olbrich S, Mulert C, Karch S, et al. EEG-vigilance and BOLD effect during simultaneous EEG/fMRI measurement.?NeuroImage.?2009;45:319
  • Lazar SW, Kerr CE, Wasserman RH, et al. Meditation experience is associated with increased cortical thickness.?Neuroreport.?2005;16:1893-7
Evidence Behind Portion sizes can make a difference.
There is a huge discrepancy in what is considered a standard portion size and many food frequency questionnaires have had different results in their studies about how much of various food types people eat because of this. Nonetheless, the overall consensus remains that portion sizes have been increasing and this has been found to be related to obesity.
An examination of portion sizes from Danish recipes over the past 100 years has shown that the caloric intake in homemade meals increased by 77%, calories from meat increased 27%, calories from starchy products by 148% and vegetables by 37%. Similarly, a recent study on Australian portion sizes found that the quantities eaten are generally much larger than recommended serving sizes.
Large portion sizes were found to be related to taking larger bites and eating faster. A meta analysis on the effects of portion sizes also found that doubling a portion size increases consumption by 35%, which undoubtedly leads to unwanted weight gain.
Thankfully, long-term studies have found that reduced portion sizes effectively reduces consumption. Though lack of knowledge of recommended portion sizes and health benefits?of foods was found to be a big barrier to adherence to healthy eating habits in Americans, providing awareness is one of the main efforts in which PH360 engages. By increasing awareness of what foods are healthier than others in a giver time, how much of these foods to eat, and how much food overall, it is believed that health improvements through proper dietary practices can be achieved.
References
  • Koster-Rasmussen, Rasmus, et al. "Missing portion sizes in FFQ?alternatives to use of standard portions."?Public Health Nutr?18.11 (2015): 1914-21.
  • Zheng, Miaobing, et al. "Typical food portion sizes consumed by Australian adults: results from the 2011?12 Australian National Nutrition and Physical Activity Survey."?Scientific reports?6 (2016): 19596.
  • Eidner, Maj Bloch, et al. "Calories and portion sizes in recipes throughout 100 years: An overlooked factor in the development of overweight and obesity?."?Scandinavian journal of public health?41.8 (2013): 839-845.
  • Almiron-Roig, Eva, et al. "Large portion sizes increase bite size and eating rate in overweight women."?Physiology & behavior?139 (2015): 297-302.
  • Jeffery, Robert W., Sarah Rydell, Caroline L. Dunn, Lisa J. Harnack, Allen S. Levine, Paul R. Pentel, et al. (2007), "Effects of Portion Size on Chronic Energy Intake," International Journal of Behavioral Nutrition and Physical Activity, 4 (1), 27?32.
  • Freedman, Marjorie R. and Carolina Brochado (2010), "Reducing Portion Size Reduces Food Intake and Plate Waste," Obesity, 18 (9), 1864?66.
  • Nicklas, Theresa A., et al. "Barriers and facilitators for consumer adherence to the dietary guidelines for Americans: the HEALTH study."?Journal of the Academy of Nutrition and Dietetics?113.10 (2013): 1317-1331.
Evidence Behind People raised on junk food may not be able to trust their body.
Research on the endocrine system has found that the brain can be tricked into overeating and choosing fattening foods over healthier choices. It has been repeatedly shown that when people are really hungry, they will be more inclined to seek foods with the highest amount of energy (especially high fat and high calorie choices). In contrast, if they're not very hungry, they are more likely to make healthier choices.
One main culprit for this is the hormone called Ghrelin that stimulates appetite and plays a big role in the body's signals of hunger and cravings by acting on the hypothalamus, hindbrain, and mesolimbic reward system. The removal of ghrelin or the ghrelin-receptor gene results in a reduced food intake and consequently body weight, but extensive reviews of the genetic influence of abnormal eating behaviors have been unable to find specific candidate genes or ghrelin secretion and processing.
This suggests that rather than being a genetic factor, it's most likely a sum of habits and lifestyle choices that increases the amount of ghrelin-related eating. Factors include sleep deprivation, eating foods high in fructose, skipping meals, fetal exposure to smoke, altered metabolism of ghrelin in childhood, parental influences during childhood, and many others.
References
  • Goldstone, Anthony P., et al. "Ghrelin mimics fasting to enhance human hedonic, orbitofrontal cortex, and hippocampal responses to food."?The American journal of clinical nutrition?99.6 (2014): 1319-1330.
  • Cummings, David E. "Ghrelin and the short-and long-term regulation of appetite and body weight."Physiology & behavior?89.1 (2006): 71-84.
  • Bittel, Douglas C., and Merlin G. Butler. "Prader-Willi syndrome: clinical genetics, cytogenetics and molecular biology."?Expert Reviews in Molecular Medicine?7.14 (2005): 1-20.
  • Yi, Chun-Xia, Kristy Heppner, and Matthias H. Tsch?p. "Ghrelin in eating disorders."?Molecular and cellular endocrinology?340.1 (2011): 29-34.
  • Hudson, James I., et al. "Binge-eating disorder as a distinct familial phenotype in obese individuals."Archives of General Psychiatry?63.3 (2006): 313-319.
  • Garaulet, Marta, et al. "Ghrelin, sleep reduction and evening preference: relationships to CLOCK 3111 T/C SNP and weight loss."?PloS one?6.2 (2011): e17435.
  • Teff, Karen L., et al. "Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women."?The Journal of Clinical Endocrinology & Metabolism?89.6 (2004): 2963-2972.
  • Paslakis, Georgios, et al. "Intrauterine exposure to cigarette smoke is associated with increased ghrelin concentrations in adulthood."Neuroendocrinology?99.2 (2014): 123-129.
  • Solomon, Thomas PJ, et al. "The effect of feeding frequency on insulin and ghrelin responses in human subjects."?British journal of nutrition?100.04 (2008): 810-819.
  • Butte, Nancy F., et al. "Metabolic and behavioral predictors of weight gain in Hispanic children: the Viva la Familia Study."?The American journal of clinical nutrition?85.6 (2007): 1478-1485.
  • Fisher, Jennifer O., et al. "Heritability of Hyperphagic Eating Behavior and Appetite?Related Hormones among Hispanic Children."?Obesity?15.6 (2007): 1484-1495.
Evidence Behind Learning about environmental triggers for food craving may be essential for healthy eating habits.
Emotional triggers (like feeling bored, depressed, anxious, tense, or sad) and physiological triggers (like social events or being around others who are eating) can both promote a sense of feeling hungry or an urge to eat something in particular, despite not being physically in need of food. This seems to be especially strong in what scientists call "restrained eaters", meaning people who limit the amount or types of foods to eat.
Dietary restrictions can be difficult to follow for some, and various strategies can be applied to make it easier to follow healthy food choices. Whether it be smaller portion sizes or plate sizes, setting clear and measureable goals, making restricted foods less readily available, being aware of the impact from advertisements, or some other strategy, the most successful approaches are ones that are personally meaningful and effective based on one's physical condition and personality traits.
References
  • Vanderlinden, Johan, et al. "Which factors do provoke binge-eating? An exploratory study in female students."?Eating Behaviors?2.1 (2001): 79-83.
  • Lattimore P, Caswell N. Differential effects of active and passive stress on food intake in restrained and unrestrained eaters.?Appetite.?2004;42(2):167-173.
  • Tanofsky-Kraff, Marian, et al. "Psychometric properties of a new questionnaire to assess eating in the absence of hunger in children and adolescents."?Appetite?51.1 (2008): 148-155.
  • Polivy, J., and C. P. Herman. "Eating in response to external cues. "Managing and Preventing Obesity: Behavioural Factors and Dietary Interventions?(2014): 181.
  • Papies, Esther, Wolfgang Stroebe, and Henk Aarts. "Pleasure in the mind: Restrained eating and spontaneous hedonic thoughts about food."?Journal of Experimental Social Psychology?43.5 (2007): 810-817.
  • Ouwehand, Carolijn, and Esther K. Papies. "Eat it or beat it. The differential effects of food temptations on overweight and normal-weight restrained eaters."?Appetite?55.1 (2010): 56-60.
  • Scott, Maura L., et al. "The effects of reduced food size and package size on the consumption behavior of restrained and unrestrained eaters."?Journal of Consumer Research?35.3 (2008): 391-405.
  • Papies, Esther K., and Petra Hamstra. "Goal priming and eating behavior: enhancing self-regulation by environmental cues."?Health Psychology?29.4 (2010): 384.
  • Blechert, Jens, et al. "To eat or not to eat? Availability of food modulates the electrocortical response to food pictures in restrained eaters."?Appetite?54.2 (2010): 262-268.
  • Harris, Jennifer L., John A. Bargh, and Kelly D. Brownell. "Priming effects of television food advertising on eating behavior."?Health psychology?28.4 (2009): 404.
Evidence Behind The size of your waistline can tell a lot about your state of health.
There are three main markers that have been repeatedly linked to health risks (waist circumference, waist-height ratio, waist-hip ratio) and all of them clearly point to certain health risks including, but not limited to, cardiovascular disease, metabolic syndrome and diabetes. It is a measure that works well for both men and women, across all ethnicities and age groups.
The reason behind this is that visceral fat (fat deposited around the belly area, or more scientifically excess intra-abdominal adipose tissue accumulation) is a type of fat that is deep in the body and that wraps around important organs like the pancreas, liver and kidneys. Inflammatory reactions in the body, hormonal interference and even altered brain function have been associated with excess visceral fat. Nonetheless, being larger than average around the waistline does not necessarily mean that there are distinct metabolic issues. It's all about whether it's an excess for your own personal body type or not.
References
  • Kissebah, Ahmed H., et al. "Quantitative trait loci on chromosomes 3 and 17 influence phenotypes of the metabolic syndrome." Proceedings of the National Academy of Sciences 97.26 (2000): 14478-14483.
  • Ashwell, Margaret, and Shiun Dong Hsieh. "Six reasons why the waist-to-height ratio is a rapid and effective global indicator for health risks of obesity and how its use could simplify the international public health message on obesity." International journal of food sciences and nutrition 56.5 (2005): 303-307.
  • Janssen, Ian, et al. "Body mass index and waist circumference independently contribute to the prediction of nonabdominal, abdominal subcutaneous, and visceral fat." The American journal of clinical nutrition 75.4 (2002): 683-688.
  • Janssen, Ian, et al. "Body mass index and waist circumference independently contribute to the prediction of nonabdominal, abdominal subcutaneous, and visceral fat." The American journal of clinical nutrition 75.4 (2002): 683-688.
  • Kuk, Jennifer L., et al. "Visceral fat is an independent predictor of all?cause mortality in men." Obesity 14.2 (2006): 336-341.
  • Fontana, Luigi, et al. "Visceral fat adipokine secretion is associated with systemic inflammation in obese humans." Diabetes 56.4 (2007): 1010-1013.
  • Carroll, Joan F., et al. "Visceral fat, waist circumference, and BMI: impact of race/ethnicity." Obesity 16.3 (2008): 600-607.
  • Despr?s, Jean-Pierre. "Health consequences of visceral obesity." Annals of medicine 33.8 (2001): 534-541.
  • Wimalawansa, Sunil J. "Visceral adiposity and cardiometabolic risks: epidemic of abdominal obesity in North America." Res Rep Endocr Disord 3 (2013): 17-30.
  • Sims, Ethan AH. "Are there persons who are obese, but metabolically healthy?." Metabolism 50.12 (2001): 1499-1504.
  • Bl?her, Matthias. "The distinction of metabolically 'healthy' from 'unhealthy' obese individuals." Current opinion in lipidology 21.1 (2010): 38-43.
  • Kramer, Caroline K., Bernard Zinman, and Ravi Retnakaran. "Are metabolically healthy overweight and obesity benign conditions?: A systematic review and meta-analysis." Annals of internal medicine 159.11 (2013): 758-769.
Evidence Behind Your life is written in your bone structure.
There are many studies that have used the National Survey of Families and Households (NSFH), a nationally representative sample with two waves of data collection (1988-1989 and 1992-1994) to demonstrate how getting married, for instance, can reduce the prevalence of depressive symptoms whereas divorce or remaining unmarried can increase it. But the evidence is also highly supportive of friendships, neighbors and even with several degrees of separation (the friends' friends' friends).
One of the underlying mechanisms behind this is the increase in proinflammatory cytokines in response to perceived isolation. One study on older adults found that increased activity of the nuclear factor (NF) pathway in response to activation of inflammatory response genes. Proinflammatory cytokines, like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), can cause fatigue, anorexia, social withdrawal and depressed mood.
References
  • Deng, Hong-Wen, et al. "Determination of bone size of hip, spine, and wrist in human pedigrees by genetic and lifestyle factors." Journal of Clinical Densitometry 5.1 (2002): 45-56.
  • Silventoinen, Karri. "Determinants of variation in adult body height." Journal of biosocial science 35.02 (2003): 263-285.
  • Deng, Hong?Wen, et al. "Several genomic regions potentially containing QTLs for bone size variation were identified in a whole?genome linkage scan." American Journal of Medical Genetics Part A 119.2 (2003): 121-131.
  • Livshits, Gregory, et al. "Genetic variation of circulating leptin is involved in genetic variation of hand bone size and geometry." Osteoporosis international 14.6 (2003): 476-483.
  • Riggs, B. Lawrence, et al. "Population?based study of age and sex differences in bone volumetric density, size, geometry, and structure at different skeletal sites." Journal of Bone and Mineral Research 19.12 (2004): 1945-1954.
  • Claessens, Albrecht L., et al. "Maturity-associated variation in the body size and proportions of elite female gymnasts 14-17 years of age." European journal of pediatrics 165.3 (2006): 186-192.
  • Haapasalo, H., et al. "Exercise-induced bone gain is due to enlargement in bone size without a change in volumetric bone density: a peripheral quantitative computed tomography study of the upper arms of male tennis players." Bone 27.3 (2000): 351-357.
  • Sundberg, M., et al. "Physical activity increases bone size in prepubertal boys and bone mass in prepubertal girls: a combined cross-sectional and 3-year longitudinal study." Calcified tissue international 71.5 (2002): 406-415.
Evidence Behind Your body's shape may predict some health risks.
Though the subject is quite complex, one simple way of looking at the body's shape in relation to disease is to look at the somatotype (endomorphy, mesomorphy and ectomorphy). Endomorphy is typical of soft rounded features of the body that had a predominance of energy put into the inner organs and digestive viscera during embryonic development. Mesomorphy is a term used to describe the bodies who had more energy placed on the mesoderm during embryonic development, meaning mostly muscles and connective tissues. And ectomorphy reflects the outer layer of the ectoderm that forms the skin, nails and sensory organs.
This is a very oversimplified explanation of the science of somatotypes and how to identify one's constitution, but the matter to consider is the scientific evidence that shows a link between physical traits and health conditions. Cluster analyses of arterial hypertension and liver disease, for instance, tend to be higher in people with endomorphic and mesomorphic traits. Young ectomorphs rarely have high blood pressure, but this can change significantly as they get older and throughout their life they have a higher risk of injury to the bones.
Though there may not ever be a clear-cut relationship between your somatotype and risks of disease, there is a strong enough scientific link that it's worth taking it into consideration as a component of a broader complex matrix of health predictors in more holistic models.
References
  • Williams, Simon RP, et al. "Somatotype and angiographically determined atherosclerotic coronary artery disease in men." American Journal of Human Biology 12.1 (2000): 128-138.
  • Koleva, M., A. Nacheva, and M. Boev. "Somatotype and disease prevalence in adults." Reviews on environmental health 17.1 (2002): 65-84.
  • Katzmarzyk, P. T., and R. M. Malina. "Familial resemblance for physique: heritabilities for somatotype components." Annals of human biology 27.5 (2000): 467-477.
  • Peeters, M. W., et al. "Heritability of somatotype components: a multivariate analysis." International journal of obesity 31.8 (2007): 1295-1301.
  • Singh, S. P. "Somatotype and disease-A review." The Anthropologist: International Journal of Contemporary and Applied Studies of Man 3.Special Issue (2007): 251-261.
Evidence Behind Your biotrend can change during childhood and adolescence.
It is well known that hormones play a huge role in child and adolescent growth and development. Fine tuning our understanding of exactly how they do can shed a lot of light on what hormones were more or less active, what life factors influences our development, and what natural genetic mutations and activities took place and at what stage of development based on our body's current physique. Estradiol, for instance, can play a role in bone thickness in girls. Testosterone can have an influence in bone length, especially in the legs. Androgen hormones can affect overall height and bone mineral content. GH (growth hormone), of which there are various types, also plays a role in bone growth and body mass.
Physical activity during early adolescence has an influence on bone mineral density. The size of the elbow can even reflect muscle strength. There are so many factors that contribute to the overall picture that pinpointing an exact biotrend too early in development is quite difficult to do. Factors that influence hormonal release (such as physical activity, nutrition, stress, disease and other factors) can greatly change the way the adult body will become.
References
  • ?zener, B., and I. Duyar. "The effect of labour on somatotype of males during the adolescent growth period." HOMO-Journal of Comparative Human Biology 59.2 (2008): 161-172.
  • Arce, P. Lizana, et al. "Changes of somatotype in high school students, V region, Chile: 1985-2010." Nutr Hosp 27.1 (2012): 270-275.
  • Izaak, S. I., T. V. Panasyuk, and R. V. Tambovtseva. "The Constitutional Factor of a Child's Growth and Maturation." Human Physiology 27.6 (2001): 671-679.
  • Prokopec, Miroslav. "What happens to children when they grow up? How does the human body change after the age of 18." Collegium antropologicum27.1 (2003): 3-10.
  • Wang, Qingju. "Bone growth in pubertal girls: cross-sectional and longitudinal investigation of the association of sex hormones, physical activity, body composition, and muscle strength with bone mass and geometry." (2005).
  • Veldhuis, Johannes D., et al. "Endocrine control of body composition in infancy, childhood, and puberty." Endocrine Reviews 26.1 (2005): 114-146.
Evidence Behind Some of your personality is rooted in childhood.
Whether you are adaptable, impulsive, love to talk, or tend to minimize your self-worth, there are many traits that seem to be rather intrinsic and part of our personal nature. Your level of cheerfulness, intellectual curiosity, sense of security, humility, autonomy, congruence or depressiveness may a trait you have within you and not one that has been nurtured. So although there are behaviors and traits that may manifest in different ways throughout life, there is a type of personality that remains relatively congruent throughout the lifespan. This is why the child that has a particular character at a young age develops into an adult but always remains that same person with characteristics that were always identifyable early on.
References
  • Shiner, Rebecca L., Ann S. Masten, and Jennifer M. Roberts. "Childhood personality foreshadows adult personality and life outcomes two decades later." Journal of personality 71.6 (2003): 1145-1170.
  • Diener, Ed, Shigehiro Oishi, and Richard E. Lucas. "Personality, culture, and subjective well-being: Emotional and cognitive evaluations of life." Annual review of psychology 54.1 (2003): 403-425.
  • Nave, Christopher S., et al. "On the contextual independence of personality: Teachers' assessments predict directly observed behavior after four decades." Social psychological and personality science (2010).
  • Roberts, Brent W., Kate E. Walton, and Wolfgang Viechtbauer. "Patterns of mean-level change in personality traits across the life course: a meta-analysis of longitudinal studies." Psychological bulletin 132.1 (2006): 1.
  • Chamorro-Premuzic, Tomas, and Adrian Furnham. "Personality predicts academic performance: Evidence from two longitudinal university samples."Journal of Research in Personality 37.4 (2003): 319-338.
Evidence Behind Being in an environment that fits your personality is healthy.
Your satisfaction in life is more greatly determined by depression or positive emotions than by personality itself. That means that we may be born with a cheerful disposition or a proactive approach to problem solving, but that doesn't mean we are born satisfied and happy. What truly makes us happy in life is feeling accepted as who we are naturally. When we are in an environment that makes us feel good, positively reinforces our natural ways, and where we feel we like we are successful using our natural talents and abilities, things flow more easily and we are showered by positive emotions.
The contrary can also happen. Feeling a mismatch with the environment, where our natural ways, behaviors, thoughts and talents are not appreciated or even worse, rejected, can cause depression. It is therefore important to find an environment (be it social, vocational or other) that matches who we truly are, rather than trying to fit into a role we don't feel we belong.
References
  • Roberts, Brent W., and Richard W. Robins. "Person?Environment fit and its implications for personality development: A longitudinal study." Journal of personality 72.1 (2004): 89-110.
  • Rauthmann, John F., et al. "Personality-driven situation experience, contact, and construal: How people's personality traits predict characteristics of their situations in daily life." Journal of Research in Personality 55 (2015): 98-111.
  • Kristof-Brown, Amy, and Russell P. Guay. "Person-environment fit." (2011). Zedeck, Sheldon (Ed), APA handbook of industrial and organizational psychology, Vol 3: Maintaining, expanding, and contracting the organization. Washington, DC, US: American Psychological Association, viii
  • Schimmack, Ulrich, et al. "Personality and life satisfaction: A facet-level analysis." Personality and social psychology bulletin 30.8 (2004): 1062-1075.
  • Eisenberger, Naomi I., and Matthew D. Lieberman. "Why rejection hurts: a common neural alarm system for physical and social pain." Trends in cognitive sciences 8.7 (2004): 294-300.
  • Mendes, Wendy Berry, et al. "How attributional ambiguity shapes physiological and emotional responses to social rejection and acceptance."Journal of personality and social psychology 94.2 (2008): 278.
Evidence Behind Your personality can be directly linked to your health.
There are many bodily functions that have been shown to directly change based on how we're thinking and feeling in the moment. This is how lie-detectors work, for instance, by measuring the body's reaction to what's being said with the theory that a lie can be associated with stress and therefore the body's reactions to stress. Personality is how we think, feel and behave on a regular basis throughout life and this can have a continuous effect on the body. People with naturally relaxed states of mind can have lower blood pressure than people who have a more hostile disposition.
Type A personalities (generally characterized by excessive ambition, aggression, competitiveness, drive, impatience, and a need for contro) tend to have a higher risk of coronary heart conditions than Type B personalities (characterized by relaxed, laissez-faire and even-tempered tendencies). Similarly, the Type D personality (characterized by distress, worry, irritability, depression and social inhibition) tends to have higher cortisol levels that also affect cardiovascular health. There's also the Type C personality (characterized by detail-orientedness, perfectionism, and over-agreeableness) tend to bottle things up more than other types, resulting in a higher risk of infectious diseases and cancer.
But overall, there is no perfect personality type and the A, B, C and D types mentioned here are just skimming the surface of a much more complex understanding of personality. The biggest thing to consider is the understanding of one's unique personal style and having stress and coping mechanisms that suit you best to consequentially be and stay as healthy as possible.
References
  • Smith, Timothy W., et al. "Hostility, anger, aggressiveness, and coronary heart disease: An interpersonal perspective on personality, emotion, and health." Journal of personality 72.6 (2004): 1217-1270.
  • Myrtek, Michael. "Meta-analyses of prospective studies on coronary heart disease, type A personality, and hostility." International journal of cardiology79.2 (2001): 245-251.
  • Denollet, Johan, Ang?lique A. Schiffer, and Viola Spek. "A general propensity to psychological distress affects cardiovascular outcomes evidence from research on the Type D (distressed) personality profile." Circulation: cardiovascular quality and outcomes 3.5 (2010): 546-557.
  • Sher, L. "Type D personality: the heart, stress, and cortisol." Qjm 98.5 (2005): 323-329.
  • Matthews, Gerald, et al. "Personality variable differences between disease clusters." European journal of personality 17.2 (2003): 157-177.
  • Zozulya, Andrey A., et al. "Personality, coping style, and constitutional neuroimmunology." Journal of Immunotoxicology 5.2 (2008): 221-225.
  • Nakaya, Naoki, et al. "Personality and the risk of cancer." Journal of the National Cancer Institute 95.11 (2003): 799-805.
  • Saklofske, Donald H., et al. "Individual difference correlates of health-related behaviors: Preliminary evidence for links between emotional intelligence and coping." Personality and Individual Differences 42.3 (2007): 491-502.
  • Connor-Smith, Jennifer K., and Celeste Flachsbart. "Relations between personality and coping: a meta-analysis." Journal of personality and social psychology 93.6 (2007): 1080.
  • Strober, L., et al. "It's all about personality: its impact on health, coping, psychological well-being and quality of life." MULTIPLE SCLEROSIS JOURNAL. Vol. 21. 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND: SAGE PUBLICATIONS LTD, 2015.
Evidence Behind The fat content of your body is largely regulated by the brain.
The brain contains a biological process called energy homeostasis, which essentially increases or decreases food desires based on what it thinks the body needs. This is the epicenter of hunger regulation, cravings for sweet, salty or creamy foods, the desire for midnight snacks, or even much of how the body digests food, replenishes its energy from food, and preserves energy stores for later. Stress, trauma, illness and disease can shift this natural homeostasis, ultimately causing other health problems.
Food addiction, eating disorders, and other behaviors related to eating habits have also been linked to these neural mechanisms. Researchers are still mapping out this complex relationship but have included factors like the effects of leptin receptors on dopaminergic neurons, ghrelin's effect on the neurons that secrete neuropeptides, the activation of opioid pathways in relation to eating pleasures, how serotonin and melatonin can affect appetite, the neurological response to food cues, and so many more factors.
References
  • Morton, Gregory J., Thomas H. Meek, and Michael W. Schwartz. "Neurobiology of food intake in health and disease." Nature reviews. Neuroscience 15.6 (2014): 367.
  • Hausswolff?Juhlin, Y., S. J. Brooks, and M. Larsson. "The neurobiology of eating disorders?a clinical perspective." Acta Psychiatrica Scandinavica131.4 (2015): 244-255.
  • Kaye, Walter H., Ursula F. Bailer, and Megan Klabunde. "Is Anorexia Nervosa an Eating Disorder? How neurobiology can help us understand the puzzling eating symptoms of anorexia nervosa." (2014).
  • Carter, Adrian, et al. "The Neurobiology of" Food Addiction" and Its Implications for Obesity Treatment and Policy." Annual Review of Nutrition36.1 (2016).
  • Murray, Susan, et al. "Hormonal and neural mechanisms of food reward, eating behavior and obesity." Nature Reviews Endocrinology 10.9 (2014): 540-552.
  • Smith, Dana G., and Trevor W. Robbins. "The neurobiological underpinnings of obesity and binge eating: a rationale for adopting the food addiction model." Biological psychiatry 73.9 (2013): 804-810.
  • Zigman, Jeffrey M., and Joel K. Elmquist. "Minireview: from anorexia to obesity?the yin and yang of body weight control." Endocrinology 144.9 (2003): 3749-3756.
  • Sainsbury, Amanda, Gregory J. Cooney, and Herbert Herzog. "Hypothalamic regulation of energy homeostasis." Best Practice & Research Clinical Endocrinology & Metabolism 16.4 (2002): 623-637.
Evidence Behind Your brain's sense of pleasure is a double-edged sword.
The brain's opioid and dopamine systems perform important functions in both pain and pleasure. The endogenous opioids (which include endorphins, enkephalins, and dynorphin) modulate how we react to pain, hunger, thirst, mood, immune triggers and other processes. Initiating this release of natural opioids is dopamine, a neurotransmitter that plays a key role in the reward mechanism while also being essential for motricity, attentiveness, motivation, learning, and memorization.
The details of the relationship between dopamine and the endogenous opioids is still being studied, but researchers do know that dopamine is more involved in our desire to have a reward while opioids are released when there is actual enjoyment of something. This trigger-response mechanism has revealed a lot about drive and motivation versus lethargy and depression or cravings and addictions versus satisfaction and gratification. In this way, pain and pleasure are seen as mechanisms that steer us into certain behaviors and can be closely linked to personality types.
Whether we are the type that needs lots of stimili and is always looking for the next adventure, or one who is easily overstimulated and seeks calm and balance, researchers are finding that it could be greatly related to your individual sensitivity to reward and punishment which may have been developed in childhood.
References
  • Esch, Tobias, and George B. Stefano. "The neurobiology of pleasure, reward processes, addiction and their health implications." Neuroendocrinology Letters 25.4 (2004): 235-251.
  • Kringelbach, Morten L., and Kent C. Berridge. Pleasures of the brain. Oxford University Press, USA, 2010.
  • Fosha, Diana, Daniel J. Siegel, and Marion Solomon, eds. The Healing Power of Emotion: Affective Neuroscience, Development & Clinical Practice (Norton Series on Interpersonal Neurobiology). WW Norton & Company, 2009.
  • Kringelbach, Morten L., and Kent C. Berridge. "Towards a functional neuroanatomy of pleasure and happiness." Trends in cognitive sciences13.11 (2009): 479-487.
  • Depue, Richard A., and Paul F. Collins. "Neurobiology of the structure of personality: Dopamine, facilitation of incentive motivation, and extraversion."Behavioral and Brain Sciences 22.03 (1999): 491-517.
  • Leknes, Siri, and Irene Tracey. "Pain and pleasure: masters of mankind."Pleasures of the brain (2010): 320-335.
  • Peci?a, Marta, et al. "Personality trait predictors of placebo analgesia and neurobiological correlates." Neuropsychopharmacology 38.4 (2013): 639-646.
  • Ribeiro, Saulo C., et al. "Interface of physical and emotional stress regulation through the endogenous opioid system and μ-opioid receptors." Progress in Neuro-Psychopharmacology and Biological Psychiatry 29.8 (2005): 1264-1280.
Evidence Behind Your personality may be related to oxytocin levels.
Oxytocin is a feel-good hormone produced in the brain. It can increase the ability to read social cues, which can ultimately improve social-cognitive performance resulting in positive social interactions. In fact, it's even used clinically in some cases of autism where identifying the emotions of others is difficult and social interactions are hindered. These positive effects of oxytocin have also been linked to lowered effects of stress, such as a reduction of blood pressure and cortisol levels. In contrast, oxytocin levels are generally low in people who suffer from depression, anxiety or stress-related disorders, and chronic pain.
Extending current knowledge of oxytocin onto personality and genetics, researchers are beginning to uncover an important link. The oxytocin-related genes may be related to characteristics like trust, agreeableness, extroversion, cheerfulness and positive social behavior.
References
  • Mikolajczak, Mo?ra, et al. "Oxytocin makes people trusting, not gullible." Psychological Science 21.8 (2010): 1072-1074.
  • Montag, Christian, et al. "Interaction of 5-HTTLPR and a variation on the oxytocin receptor gene influences negative emotionality." Biological psychiatry 69.6 (2011): 601-603.
  • Bartz, Jennifer A., et al. "Oxytocin selectively improves empathic accuracy."Psychological Science 21.10 (2010): 1426-1428.
  • Donaldson, Zoe R., and Larry J. Young. "Oxytocin, vasopressin, and the neurogenetics of sociality." Science 322.5903 (2008): 900-904.
  • Kim, Heejung S., et al. "Gene-culture interaction oxytocin receptor polymorphism (OXTR) and emotion regulation." Social Psychological and Personality Science 2.6 (2011): 665-672.
  • Uvnas-Moberg, Kerstin, and Maria Petersson. "Oxytocin, a mediator of anti-stress, well-being, social interaction, growth and healing." Z Psychosom Med Psychother 51.1 (2005): 57-80.
  • Guastella, Adam J., et al. "Intranasal oxytocin improves emotion recognition for youth with autism spectrum disorders." Biological psychiatry 67.7 (2010): 692-694.
  • Andari, Elissar, et al. "Promoting social behavior with oxytocin in high-functioning autism spectrum disorders." Proceedings of the National Academy of Sciences 107.9 (2010): 4389-4394.
  • Haram, Marit, et al. "An attempt to identify single nucleotide polymorphisms contributing to possible relationships between personality traits and oxytocin-related genes." Neuropsychobiology 69.1 (2014): 25-30.
  • Darragh, Margot, Roger J. Booth, and Nathan S. Consedine. "?Oxytocin'for the outwardly oriented: Evidence for interactive effects in placebo responding." Journal of Psychosomatic Research 83 (2016): 10-15.
  • Kogan, Aleksandr, et al. "Thin-slicing study of the oxytocin receptor (OXTR) gene and the evaluation and expression of the prosocial disposition."Proceedings of the National Academy of Sciences 108.48 (2011): 19189-19192.
  • Moons, Wesley G., Baldwin M. Way, and Shelley E. Taylor. "Oxytocin and vasopressin receptor polymorphisms interact with circulating neuropeptides to predict human emotional reactions to stress." Emotion 14.3 (2014): 562.
Evidence Behind Serotonin activity may be related to inherent personality traits.
One study showed that men with a rather inhibitory control of the 5-HT neuron (meaning less serotonin associated with feelings of well-being and happiness) have a more aggressive and proactive approach to coping with challenges. In contract, men that have a more passive way of coping with stress tend to have more serotonin. Another study found that serotonin can affect one's reaction to stress by diminishing or preventing anxiety and panic.
Another way to study the effects of serotonin on the brain is to alter 5-HT levels through acute tryptophan depletion (ATD). In this way, researchers have found that lowered serotonin/ADT can render a person more impulsive and faster as decision-making. Even cognitive flexibility and focused attention are influenced by 5-HT turnover.
A genetic look at the serotonin transporter gene suggests that personality traits associated with lower anxiety and neuroticism but increased harm avoidance and passive coping could be inherent. It is strongly possible that this may be related to a variability in the CYP2D6 gene that tends to reduce serotonin levels in poor metabolizers.
References
  • Koolhaas, J. M. et al. (2010) Neuroendocrinology of coping styles: towards understanding the biology of individual variation. Frontiers of Neuroendocrinology, 31, pp. 307-321.
  • Lowry, Christopher A., and Matthew W. Hale. "Chapter 3.6-Serotonin and the Neurobiology of Anxious States." Handbook of Behavioral Neuroscience 21 (2010): 379-397.
  • Crean J., Richards J. B., de Wit H. 2002 Effect of tryptophan depletion on impulsive behavior in men with or without a family history of alcoholism. Behav. Brain Res. 136, 349-357. doi:10.1016/S0166-4328(02)00132-8
  • Talbot, Peter S., et al. "Rapid tryptophan depletion improves decision-making cognition in healthy humans without affecting reversal learning or set shifting." Neuropsychopharmacology 31.7 (2006): 1519-1525.
  • Evers, Elisabeth Anna Theresia, et al. "Serotonin and cognitive flexibility: neuroimaging studies into the effect of acute tryptophan depletion in healthy volunteers." Current medicinal chemistry 14.28 (2007): 2989-2995.
  • Schmitt, J. A. J., et al. "Serotonin and human cognitive performance." Current pharmaceutical design 12.20 (2006): 2473-2486.
  • Munafo, M. R., T. Clark, and J. Flint. "Does measurement instrument moderate the association between the serotonin transporter gene and anxiety-related personality traits? A meta-analysis." Molecular psychiatry 10.4 (2005): 415-419.
  • Gonz?lez, Idilio, et al. "Relation between CYP2D6 phenotype and genotype and personality in healthy volunteers." (2008): 833-840.
Evidence Behind Your body's shape can tell a lot about what hormones are predominant.
Hormones a key to how the body functions. Every second of the day, the body is flooded with particular hormones that determine how the body functions. It's not just about sexual reproduction, but there's a huge hormonal influence on mood, organ function, skin and tissue health, blood pressure, electrolyte balance, metabolism and so much more.
For instance, the amount of testosterone and cortisol running through a man's body has been shown to be related to age, waist circumference and body mass (with younger, leaner and more muscular bodies having a higher testosterone to cortisol ratio). Similarly, estrogen plays an important role in regulating the female metabolic system whereby the location of fat deposits change in relation to declining estrogen to testosterone ratios (with younger, more pear-shapes bodies having more estrogen than those with more visceral fat).
Stepping away from sex hormones, we can look at serotonin. This is another neurotransmitter that is primarily found in the nervous system, blood and gastrointestinal tract and has been linked to particular patterns of adiposity, especially abdominal fat. The metabolism is also influenced by Insulin. The bodies that tend to use up a lot of their energy, have more insulin sensitivity (therefore tend to be more tonic with less fat deposits) but tend to have higher HDL-cholesterol levels probably have higher levels of epinephrine running through their body.
There are complex interplays between hormones, neurotransmitters and body shape and function, but these are examples of how a program like PH360 can use body measurements and ratios as indicators of the neuroendocrine profile.
References
  • Chan, J., et al. "Measurement of cortisol and testosterone in hair of obese and non-obese human subjects." Experimental and clinical endocrinology & diabetes: official journal, German Society of Endocrinology [and] German Diabetes Association 122.6 (2014): 356-362.
  • Rettberg, Jamaica R., Jia Yao, and Roberta Diaz Brinton. "Estrogen: a master regulator of bioenergetic systems in the brain and body." Frontiers in neuroendocrinology 35.1 (2014): 8-30.
  • Mondrag?n-Ceballos, Ricardo, et al. "Waist-to-Hip Ratio, but Not Body Mass Index, Is Associated with Testosterone and Estradiol Concentrations in Young Women." International journal of endocrinology 2015 (2015).
  • Hodge, Stephanie, et al. "Obesity, whole blood serotonin and sex differences in healthy volunteers." Obesity facts 5.3 (2012): 399-407.
  • Yosmao?lu, Ahmet, et al. "Correlation of selective serotonin re-uptake inhibitor use with weight gain and metabolic parameters." Anatolian Journal of Psychiatry 14.3 (2013): 245-251.
Evidence Behind Thyroid conditions can be improved with lifestyle changes.
What we eat can have a significant effect on the body's various functions and numerous studies have examined this effect on thyroid function from various angles. The endocrine system is very complex but there are many choices we can make to support its healthy function.
Whether it's the effect of high-fat diets on hormone secretions that in turn impact thyroid-stimulating hormones, the effect that iodine imbalance can have on thyroid activity and goiter production, the effects of selenium, iron and zinc on thyroid metabolism, the effect phytoestrogens inhibitory effect on thyroid peroxidase, or several other factors that contribute to proper thyroid function, the endocrine system is quite multifaceted yet research is becoming increasingly clearer on how dietary alterations can significantly improve thyroid dysfunction.
References
  • Cano, Pilar, et al. "Effect of a high-fat diet on 24-h pattern of circulating levels of prolactin, luteinizing hormone, testosterone, corticosterone, thyroid-stimulating hormone and glucose, and pineal melatonin content, in rats."Endocrine 33.2 (2008): 118-125.
  • Kunisue, Tatsuya, Jeffrey W. Fisher, and Kurunthachalam Kannan. "Modulation of thyroid hormone concentrations in serum of rats coadministered with perchlorate and iodide-deficient diet." Archives of environmental contamination and toxicology 61.1 (2011): 151-158.
  • Leung, Angela M., and Lewis E. Braverman. "Iodine-induced thyroid dysfunction." Current Opinion in Endocrinology, Diabetes and Obesity 19.5 (2012): 414-419.
  • Eftekhari, Mohammad Hassan, et al. "The relationship between iron status and thyroid hormone concentration in iron-deficient adolescent Iranian girls."Asia Pacific journal of clinical nutrition 15.1 (2006): 50.
  • Maxwell, Christy, and Stella Lucia Volpe. "Effect of zinc supplementation on thyroid hormone function." Annals of Nutrition and Metabolism 51.2 (2007): 188-194.
  • Hampl, R., et al. "Short-term effect of soy consumption on thyroid hormone levels and correlation with phytoestrogen level in healthy subjects."Endocrine regulations 42.2-3 (2008): 53-61.
  • Waring, R. H., and R. M. Harris. "Endocrine disrupters: a human risk?."Molecular and cellular endocrinology 244.1 (2005): 2-9.
  • Truong, Th?r?se, et al. "Role of dietary iodine and cruciferous vegetables in thyroid cancer: a countrywide case-control study in New Caledonia." Cancer Causes & Control 21.8 (2010): 1183-1192.
Evidence Behind Smoking can negatively affect the entire endocrine system.
The endocrine system is very multifaceted and complex, yet also very sensitive to changes, toxins and lifestyle choices. Smoking is a great example of and avoidable action that greatly impacts endocrine health.
Smoking is believed to reduce thyroid secretion, have an anti-estrogenic effect, and impact other hormones like SHGB, testosterone, steroids and androgens, essentially affecting the overall endocrine system. Research has found that a large factor related to this is the nicotine content of cigarettes, which stimulates catecholamine release, thus affecting adrenaline and noradrenaline levels. Other researchers suppose it's the nicotine-stimulated plasma renin activity that raises aldosterone levels while others are looking at nicotine's effect on neurotransmitters that affect the anterior pituitary or hypothalamus. Perhaps it's also related to other chemicals in commercial cigarettes, like an endocrine-damaging chemical called thiocyanate, a potential goitrogen.
There are many theories behind the effects of nicotine and smoking with ongoing research continuously highlighting new discoveries in the effect smoking can have on the endocrine system, but the conclusion is clear: it's not a good one.
References
  • Vestergaard P. Smoking and thyroid disorders. European Journal of Endocrinology 2002 146 153-161.
  • Tanko LB & Christiansen C. An update on the antiestrogenic effect of smoking: a literature review with implications for researchers and practitioners. Menopause2004 11 104-109
  • Trummer H, Habermann H, Haas J & Pummer K. The impact of cigarette smoking on human semen parameters and hormones. Human Reproduction2002 17 1554-1559
  • Tansavatdi K, McClain B & Herrington DM. The effects of smoking on estradiol metabolism. Minerva Ginecologica 2004 56 105-114.
  • English KM, Pugh P, Parry H, Scutt N, Channer K & Jones TH. Effect of cigarette smoking on levels of bioavailable testosterone in healthy men. Clinical Science 2001 100 661-665
  • Jorde R, Saleh F, Figenschau Y, Kamycheva E, Haug E & Sundsfjord J. Serum parathyroid hormone levels in smokers and nonsmokers. The fifth Tromso study.European Journal of Endocrinology 2004 152 1-8
  • Friedman AJ, Ravnikar VA & Barbieri RL. Serum steroid hormone profiles in smokers and nonsmokers. Fertility and Sterility 1987 47 398-401.
Evidence Behind Your body's constitution is largely formed during embryonic development.
Ancient traditions right through to modern science have seen patterns in human constitutions and classified them in various ways. Whether it's Sheldon's ectomorph, mesomorph and endomorph types, Hippocrates blood, yellow bile, black bile, and phlegm humor types, Ayurdevic Pitta, Khapa and Vata classifications, or many others that have been used throughout history, the common thread is that patterns of body shape, function, health tendencies and personality have been greatly studied.
For instance, heightened development of the endoderm of the embryo would affect the internal organs of the body, whereas mesodermic activity would influence muscles and connective tissues. Finally, changes in skin and sensory organs would have been influenced by the activity of the ectoderm. This embryonic activity has been shown to influence what will later be the shape and function of the adult body.
Recent research into the genetic influence of this has been able to shed a lot of light into how body types come to be, and it is believed that nuclear receptors are triggering specific gene expressions which initiate a chain of events : embryonic development, child growth, behavioral tendencies, hormone development and influence of body functions, and so on.
Studies on transgenerational changes in DNA expression (phenotypes) have found that the reprogramming of the germ-line epigenome is highly involved. Environmental compounds that affect a first generation can also affect a second and third generation, what is called an epigenetic transgenerational phenotype.
Though we are currently unable to perfectly outline the mechanisms between embryonic development and adult constitution, reverse analysis of development and trends in cellular development as well as genetic and epigenetic influences on the body's adult form has been able to substantiate many of the ancient constitutional beliefs and practices.
References
  • Rizzo-Sierra, Carlos V. "Ayurvedic genomics, constitutional psychology, and endocrinology: the missing connection." The Journal of Alternative and Complementary Medicine 17.5 (2011): 465-468.
  • Singh, S. P. "Somatotype and disease?A review."?The Anthropologist: International Journal of Contemporary and Applied Studies of Man?3.Special Issue (2007): 251-261.
  • Metri, Kashinath G., Hemant Bhargav, and Nagendra Hongasandra Ramarao. "OA01. 25. The first direct experimental evidence correlating ayurveda based tridosha prakriti, with western constitutional psychology somatotypes." Ancient Science of Life 32.Suppl 1 (2012): S25.
  • Skinner, Michael K. "What is an epigenetic transgenerational phenotype?: F3 or F2." Reproductive toxicology 25.1 (2008): 2-6.
Evidence Behind Ectomorphs are more sensitive people.
The ectoderm of the embryo plays an important role in the development of the central nervous system and heightened activity during this time may be the reason why 20% of adults have particularly amplified sensitivity due to a more active nervous system.
Having a more responsive arousal system in the brain can render a person more detail-oriented, sensitive to cues and stimuli, more tuned to information processing and deeper mental reflections. It is believed that this group of people will therefore also reflect traits such as perfectionism, inventiveness, imagination, creativity, higher perception and an aptitude for theory and abstract reasoning. Sound like someone you may know?
It is examples like these that provide the scientific background to ancient beliefs and practices based on constitution and behavioral generalizations. Whether it be a Vata dosha in Ayurvedic medical principles, a Soumin in Korean constitutional medicine, or an ectomorph in Sheldon's somatotypes, there are many approaches that have intuitively known about constitutions and modern science is beginning to confirm them.
References
  • Aron, Elaine N., and Arthur Aron. "Sensory-processing sensitivity and its relation to introversion and emotionality." Journal of personality and social psychology 73.2 (1997): 345.
  • Rizzo-Sierra, Carlos V. (2013) The Human Sensory Processing Sensitivity: Biological Implications for Introversion, Submission and Creativity. Neuronikas Research Group, Advanced Biomedical Research Center,Bogota, Colombia.
  • Aggarwal, S. et al. (2010). EGLN1 involvement in high-altitude adaptation revealed through genetic analysis of extreme constitution types defined in Ayurveda. Proceedings of the National Academy of Sciences of the United States of America, 107, pp. 18961-18966.
  • Aron, A. et al. (2010) Temperament trait of sensory processing sensitivity moderates cultural differences in neural response. Social, Cognitive and Affective Neuroscience, 5, pp. 219-226.
  • Rizzo-Sierra, Carlos V., Martha E. Leon-S, and Fidias E. Leon-Sarmiento. "Higher sensory processing sensitivity, introversion and ectomorphism: New biomarkers for human creativity in developing rural areas." Journal of neurosciences in rural practice 3.2 (2012): 159.
Evidence Behind Endomorphs or Kapha types are more conscientious people.
According to Ayurvedic medical practice, the Kapha dosha plays an important role in anabolism, growth and maintenance of structure, storage and stability. This is said to render a person to have thicker bones with a solid frame and ultimately also a tendency to have higher triglycerides and cholesterol levels but better immune systems.
Modern genome studies on body types and specific genetic expressions related to physical conditions like metabolism have confirmed these tendencies. This includes CYP2C19 gene polymorphism, but potentially also the GAD2 gene and the ENPP1 gene.
As a result of this innately sturdier body, the mind tends to be steady and strong as well, with a cognitive function that is not easily perturbed and not overly excitable. This seems to be associated with lower stimulation of the reticular activation, the amygdala, and the sympathetic nervous system, leading to less impulsivity and sensation-seeking and more of a methodical, stable and conscientious type of mental processing.
Thanks to this type of research, we are beginning to put the pieces together and build a stable bridge between ancient medicine and modern science, with embryology being a keystone.
References
  • Mahalle NP, Kulkarni MV, Pendse NM, Naik SS. Association of constitutional type of Ayurveda with cardiovascular risk factors, inflammatory markers and insulin resistance. J Ayurveda Integr Med 2012;3:150-7.
  • Prasher B, Negi S, Aggarwal S, Mandal AK, Sethi TP, Deshmukh SR, et al. Whole genome expression and biochemical correlates of extreme constitutional types defined in Ayurveda. J Transl Med 2008;6:48
  • Dey S, Pahwa P. Prakriti and its associations with metabolism, chronic diseases, and genotypes: Possibilities of new born screening and a lifetime of personalized prevention. J Ayurveda Integr Med 2014;5:15-24.
  • Ghodke Y, Joshi K, Patwardhan B. Traditional medicine to modern pharmacogenomics: Ayurveda Prakriti type and CYP2C19 gene polymorphism associated with the metabolic variability. Evid Based Complement Alternat Med 2011;2011:249528.
  • Kurup RK, Kurup PA. Hypothalamic digoxin, hemispheric chemical dominance, and the tridosha theory. Int J Neurosci 2003;113:657-81.
  • Sharma, Urvashi, and Ravindra Kumar. "Ectomorphic and Endomorphic Personality: A Study of Emotional Quotient among Women." (2014).
  • Travis, Frederick T., and Robert Keith Wallace. "Dosha brain-types: A neural model of individual differences." Journal of Ayurveda and Integrative Medicine 6.4 (2015): 280.
Evidence Behind Much of your personality may be genetically influenced.
Studying twins, Eysenk showed that 55% of the personality traits of identical twins was similar, in comparison to 13% in dizygotic twins, indicating a large portion of personality influence stemming from genetics. This was then confirmed by many other researchers. Other genetic links to personality have been made in relation to social aversion or attraction, impulsivity, criminal tendencies, openness, intellect, and many other personality traits.
For instance, one study found that the dopamine D4 receptor played a large role in externalizing behavior in young children. Another twin study on self-esteem, life satisfaction and optimism found significant genetic influences for these traits, especially self-esteem. Even depression has been found to have a genetic association to the Serotonin Transporter Gene (5-HTTLPR) and aggression with the Monoamine oxidase A gene (MAOA).
There are many examples of genetic influences on behavor to date, and many more will be revealed in the years to come. As research into the genetic link continues to unfold, so does our understanding of the nature versus nurture debate in relation to innate versus acquired personality.
References
  • Markiewicz, Renata, et al. "Biological determinants of social maladjustment." (2012).
  • Hamer D, Copeland P: Genes and character. Warsaw, Jacek Santorski & Co., 1998
  • Hansell NK, Wright MJ, Medland SE, Davenport TA, Wray NR, Martin NG, Hickie IB. Genetic co-morbidity between neuroticism, anxiety/de-pression and somatic distress in a population sample of adolescent and young adult twins. Psychol Med. 2012;42(6): 1249-60
  • Cuartas Arias JM, Palacio Acosta CA, Valencia JG et al: Exploring epis-tasis in candidate genes for antisocial personality disorder. Psychiatr Genet, 2011; 21(3): 115-24
  • Niv S, Tuvblad C, Raine A et al: Heritability and longitudinal stability of impulsivity in adolescence. Behav Genet, 2012; 42(3): 378-92
  • Wojew?dzka J, Ilnicki P, Tworus R: Biological correlates of personality disorders. Post Psychiatr Neurol, 2000; 9: 259-62
  • Deyoung CG, Cicchetti D, Rogosch FA et al: Sources of Cognitive Exploration: Genetic Variation in the Prefrontal Dopamine System Predicts Openness/Intellect. J Res Pers, 2011; 45(4): 364-71
  • Caprara, Gian Vittorio, et al. "Human optimal functioning: The genetics of positive orientation towards self, life, and the future." Behavior genetics 39.3 (2009): 277-284.
  • Risch, Neil, et al. "Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: a meta-analysis." Jama 301.23 (2009): 2462-2471
  • McDermott, Rose, et al. "Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation." Proceedings of the National Academy of Sciences 106.7 (2009): 2118-2123.
Evidence Behind A genetic susceptibility to a disease doesn't guarantee its activation.
Whole-genome sequencing efforts have revealed millions of previously unreported variants in healthy individuals, including single base pair substitutions, small insertions and deletions, and larger copy number mutations. Examining the mutations that cause disease and disability revealed that mutations associated with early-onset disease are relatively rare.
For instance, a cancer gene causes errors of DNA repair and ultimately to tumor development, but cancer results from any one of thousands of different mutations in any one of multiple different genes. This is why researchers who compare allele frequencies at hundreds of thousands of polymorphic sites (SNPs) in thousands of cases of common diseases label their findings as "risk variants". Though genome-wide association studies (GWAS) have published hundreds of common variants whose allele frequencies are statistically correlated with various illnesses and traits, they are not sufficient to claim a cause-effect relationship. In other words, just because you have a gene for a specific disease, doesn't mean you get it but it does increase your risk for it.
For example, a recently published 12 year follow-up study of cardiovascular disease (CVD) in more than 19,000 women found that the 101 SNPs identified by GWAS as risk variants for CVD did not predict cardiovascular outcomes. Of course, there are many conditions in which the presence of a gene does practically guarantee the passing on of a condition and studies on genetic homogeneity continue to make these links, but epigenetic research has been revealing the added influence of environmental factors as gene triggers or activators to play a crucial role in this genetic mechanism.
References
  • McKernan, Kevin Judd, et al. "Sequence and structural variation in a human genome uncovered by short-read, massively parallel ligation sequencing using two-base encoding." Genome research 19.9 (2009): 1527-1541.
  • Cavalli-Sforza, L. L., P. Menozzi, and A. Piazza. "The History and Geography of Human Genes. Princeton, NJ (Princeton University Press) 1994." (1994).
  • Tishkoff, Sarah A., and Brian C. Verrelli. "Patterns of human genetic diversity: implications for human evolutionary history and disease." Annual review of genomics and human genetics 4.1 (2003): 293-340.
  • Ramachandran, Sohini, et al. "Support from the relationship of genetic and geographic distance in human populations for a serial founder effect originating in Africa." Proceedings of the National Academy of Sciences of the United States of America 102.44 (2005): 15942-15947.
  • Walsh, Tom, and Mary-Claire King. "Ten genes for inherited breast cancer." Cancer cell 11.2 (2007): 103-105.
  • Paynter, Nina P., et al. "Association between a literature-based genetic risk score and cardiovascular events in women." Jama 303.7 (2010): 631-637.
  • Jaenisch, Rudolf, and Adrian Bird. "Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals." Nature genetics 33 (2003): 245-254.
Evidence Behind The TCF7L2 gene is a significant type 2 diabetes susceptibility gene.
Type 2 diabetes (T2DM) is generally the result environmental factors interacting with a hereditary component. Obesity, sedentary lifestyle, nutrition and stress are common environmental factors that contribute to the development of diabetes but don't seem to impact everyone in the same way. What makes some people more susceptible to T2DM seems to be a genetic factor. Having one parent with T2DM increases the risk of developing diabetes by 40%, and it goes up to 70% if both parents are affected.
Genome wide association studies (GWAS) have identified TCF7L2 as a locus conveying an increased risk for developing T2DM, but T2DM (unline Type 1 diabetes) seems to be a polygenic disorder that involves an interaction of interaction of multiple genes throughout the genome. CAPN10 are likely to be associated with glucose metabolism, IRS-1 and IRS-2 genes encode peptides that play an important role in insulin signal transduction, the KCNJ11 gene plays an important role in the decreased insulin secretion by beta cells, the SLC30A8 gene is involved in the storage and secretion of insulin granules in the pancreas, and several others may also be involved. So far, over 60 variants have been found thanks to GWAS studies but TCF7L2 has been shown to be the single most significantly associated diabetes risk gene in the world.
It is obvious that genes influence the risk of diabetes by altering insulin action or secretion and glucose metabolism, but also by altering how an individual's body reacts to environmental factors and unhealthy lifestyles.
References
  • Grant, Struan FA, et al. "Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetes." Nature genetics 38.3 (2006): 320-323.
  • Tillil H, K?bberling J. Age-corrected empirical genetic risk estimates for first-degree relatives of IDDM patients. Diabetes. 1987;36:93-99.
  • Song Y, Niu T, Manson JE, Kwiatkowski DJ, Liu S. Are variants in the CAPN10 gene related to risk of type 2 diabetes? A quantitative assessment of population and family-based association studies. Am J Hum Genet. 2004;74:208-222.
  • Le Fur S, Le Stunff C, Bougn?res P. Increased insulin resistance in obese children who have both 972 IRS-1 and 1057 IRS-2 polymorphisms. Diabetes. 2002;51 Suppl 3:S304-S307.
  • Gloyn AL, Weedon MN, Owen KR, Turner MJ, Knight BA, Hitman G, Walker M, Levy JC, Sampson M, Halford S, et al. Large-scale association studies of variants in genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) confirm that the KCNJ11 E23K variant is associated with type 2 diabetes. Diabetes. 2003;52:568-572.
  • Lefebvre B, Vandewalle B, Balavoine AS, Queniat G, Moerman E, Vantyghem MC, Le Bacquer O, Gmyr V, Pawlowski V, Kerr-Conte J, et al. Regulation and functional effects of ZNT8 in human pancreatic islets. J Endocrinol. 2012;214:225-232.
  • Gaulton KJ, Willer CJ, Li Y, Scott LJ, Conneely KN, Jackson AU, Duren WL, Chines PS, Narisu N, Bonnycastle LL, et al. Comprehensive association study of type 2 diabetes and related quantitative traits with 222 candidate genes. Diabetes. 2008;57:3136-3144.
Evidence Behind There are genes that may make some people inherently fat.
There are several specific genes that have been found to be related to an inherent endomorphic body type and many more continue to be found. For instance, chromosome 22q12.1 contains the KREMEN1 gene that functions as a receptor for the DKK1 gene which forms a complex with low-density lipoprotein receptor-related protein 6 (LRP6). Double null KREMEN 1/ KREMEN 2 mice show increased bone volume (something that may prove the link between endomorphy's increased risk for T2DM).
Another example lies in chromosome 2q24.3 that contains the GRB14 gene, a growth factor receptor, that binds directly to the insulin receptor. Mice that didn't have the GRB14 gene had enhanced body weight, mainly explained by increased lean mass on normal diet, improved glucose homeostasis despite lower circulating insulin levels, and enhanced insulin signaling in liver and skeletal muscle. Grb14 expression is increased in adipose tissue of insulin-resistant animal models and type 2 diabetic human patients, suggesting that Grb14 may modulate insulin sensitivity.
Chromosome 1p12 contains the TBX15 gene that is related to subcutaneous fat, variations in fat distribution, as well as overall obesity as measured by the BMI. There is also chromosome 1q41 that contains the LYPLAL1 gene that encodes the lysophospholipase-like 1 protein, which is thought to act as a triglyceride lipase and tends to be overactive in obese patients.
Many such scientific discoveries have helped clarify the genetic tendency for some people to gain mass more easily than others, or have great difficulties in losing it. Even the contrary has been found in chromosome 12p11.23 that contains the ITPR2 gene, an intracellular calcium release channel. Mice lacking both ITPR2 and ITPR3 exhibited impaired calcium signaling, secretion defects, hypoglycemia and lean body type (all typical of ectomorphy).
References
  • Ellwanger, K. et al. Targeted disruption of the Wnt regulator Kremen induces limb defects and high bone density. Mol Cell Biol 28, 4875-82 (2008).
  • Mao, B. et al. Kremen proteins are Dickkopf receptors that regulate Wnt/beta-catenin signalling. Nature 417, 664-7 (2002).
  • Holt, L.J. & Siddle, K. Grb10 and Grb14: enigmatic regulators of insulin action?and more? Biochem J 388, 393-406 (2005).
  • Cooney, G.J. et al. Improved glucose homeostasis and enhanced insulin signalling in Grb14-deficient mice. EMBO J 23, 582-93 (2004).
  • Cariou, B. et al. Increased adipose tissue expression of Grb14 in several models of insulin resistance. FASEB J 18, 965-7 (2004).
  • Conrad, D.F. et al. Origins and functional impact of copy number variation in the human genome. Nature (2009).
  • Gesta, S. et al. Evidence for a role of developmental genes in the origin of obesity and body fat distribution. Proc Natl Acad Sci U S A 103, 6676-81 (2006).
  • Steinberg, G.R., Kemp, B.E. & Watt, M.J. Adipocyte triglyceride lipase expression in human obesity. Am J Physiol Endocrinol Metab 293, E958-64 (2007).
  • Futatsugi, A. et al. IP3 receptor types 2 and 3 mediate exocrine secretion underlying energy metabolism. Science 309, 2232-4 (2005).
Evidence Behind Being taller than average increases the risk of cancer.
One study on 10,304 Han Chinese participantsexamined the relationship between sitting height (allowing them to distinguish also the influence of leg-length) on various health factors. They found that people with with longer legs had a lower pulse as well as lower LDL and HDL cholesterol levels (both good and bad types of cholesterol). However, people with greater sitting height tend to have higher triglyceride levels and a greater risk of diabetes and dyslipidemia, despite adjustments for obesity, ethnicity, gender or age. Taller people, however, had an increase in cancer mortality with the risk of cancer increasing by 5% in men and 9% in women for every 6cm that they were taller than average (averaging 169 cm for and 157 cm for women). Smoking and systolic blood pressure did not have an effect on the results. The finding that cancer risk increases with height has been found in many previous studies.
Genetic factors may also play a role in height and health and future genome-wide association studies may eventually make the link between the two. But what remains clear is that healthy lifestyle choices can have a great impact when they?re done early on and preventative medicine isn?t the same for everyone. For example, the taller than average group may need to consider managing their stress levels, limiting their exposure to heavy metals and toxins in food and water by eating fresh organic foods, and consume cancer-fighting antioxidants in fruits and vegetables to protect themselves from their greater health risk. The hypothalamic-pituitary-adrenal (HPA) axis is the body?s internal stress regulator and controls cortisol and stress hormone levels. Protecting the neuroendocrine and immune systems would be an important focus for this group, with psychological stressors playing a big role in this.
But keep in mind that just because someone is tall, doesn?t mean they will get cancer nor that they are protected from metabolic issues. Risk factors, genetic factors and lifestyle choices are all clues to a bigger puzzle of understanding the complex domain of health and disease.
References
  • Schooling?CM,?Jiang?C,?Lam?TH,?et al. Height, its components, and cardiovascular risk among older Chinese: a cross-sectional analysis of the Guangzhou Biobank Cohort Study.Am J Public Health?2007;97:1834?41.
  • Lee, Crystal Man Ying, et al. "Adult height and the risks of cardiovascular disease and major causes of death in the Asia-Pacific region: 21 000 deaths in 510 000 men and women."?International Journal of Epidemiology?(2009): dyp150.
  • Albanes, Demetrius, et al. "Adult stature and risk of cancer."?Cancer research48.6 (1988): 1658-1662.
  • Rodriguez, Carmen, et al. "Body mass index, height, and prostate cancer mortality in two large cohorts of adult men in the United States."?Cancer Epidemiology Biomarkers & Prevention?10.4 (2001): 345-353.
  • Hebert, Patricia R., et al. "Adult height and incidence of cancer in male physicians (United States)."?Cancer Causes & Control?8.6 (1997): 591-597.
  • Batty, G. D., et al. "Adult height in relation to mortality from 14 cancer sites in men in London (UK): evidence from the original Whitehall study."?Annals of Oncology?17.1 (2006): 157-166.
  • Kabat, Geoffrey C., et al. "Adult stature and risk of cancer at different anatomic sites in a cohort of postmenopausal women."?Cancer Epidemiology Biomarkers & Prevention?22.8 (2013): 1353-1363.
  • Allen, Hana Lango, et al. "Hundreds of variants clustered in genomic loci and biological pathways affect human height."?Nature?467.7317 (2010): 832-838.
  • Visscher, Peter M. "Sizing up human height variation."?Nature genetics?40.5 (2008): 489-490.
  • Kurian, Allison W., et al. "Clinical evaluation of a multiple-gene sequencing panel for hereditary cancer risk assessment."?Journal of Clinical Oncology32.19 (2014): 2001-2009.
  • Srivastava, Kshitij, and Anvesha Srivastava. "Comprehensive review of genetic association studies and meta-analyses on miRNA polymorphisms and cancer risk."?PLoS One?7.11 (2012): e50966.
  • Gunnell, D., et al. "Height, leg length, and cancer risk: a systematic review."Epidemiologic reviews?23.2 (2001): 313-342.
Evidence Behind Short people have a higher risk of cardiovascular issues.
A NHANES III?study on a total of 5,944 US citizens between 1988 through 1994 found that shorter men and women had greater insulin resistance and impaired glucose tolerance, even when adjusting for age, body fat, gender and ethnicity. Another Chinese study 510,800 participants found that shorter height in men was related to an increased risk of coronary heart disease, stroke, cardiovascular disease, injury and a shorter life span. For?women, shorter height was found to be associated with an increased risk for coronary heart disease, haemorrhagic stroke and cardiovascular disease.
The mechanisms behind why short stature increases the risk for metabolic issues, like glucose and lipid processing, that affect the circulatory system are still being researched because there are complex interplays to consider. For instance, malnutrition and disease during childhood can cause shorter leg length. Genetic factors may also play a role in height and health and future genome-wide association studies may eventually make the link between the two.
While research continues to attempt to answer the question as to why there may be a link, it becomes increasingly obvious that lifestyle choices and health practices early on are important to consider. For example, those who are short in stature, especially in the legs, may need to pay more attention to the effects sugars have on the body because of their greater risk for glucose intolerance. Maintaining a healthy weight, engaging in regular exercise, getting good doses of plant-based foods and whole grains, including legumes, nuts and lean protein in the diet, and even considering specific foods like fish oil, cinnamon, tea and vinegar for their beneficial effects on the metabolism should be considered. This group would also have to avoid artificial sweeteners that alter the gut microbiota and can worsen glucose intolerance, while maintaining a healthy cardiovascular system with monitored cholesterol levels.
But keep in mind that just because someone is short, does not mean they will get diabetes and cardiovascular disease, nor that they are protected from cancer. Similarly, just because someone is tall, doesn?t mean they will get cancer nor that they are protected from metabolic issues. Height is just a piece of a very large and complex puzzle.
References
  • Asao?K,?Kao?WH,?Baptiste-Roberts?K,?et al.?Short stature and the risk of adiposity, insulin resistance, and type 2 diabetes in middle age: the Third National Health and Nutrition Examination Survey (NHANES III), 1988?1994.?Diabetes Care?2006;29:1632?7.
  • Lee, Crystal Man Ying, et al. "Adult height and the risks of cardiovascular disease and major causes of death in the Asia-Pacific region: 21 000 deaths in 510 000 men and women."?International Journal of Epidemiology?(2009): dyp150.
  • Wadsworth, M. E. J., et al. "Leg and trunk length at 43 years in relation to childhood health, diet and family circumstances; evidence from the 1946 national birth cohort."?International Journal of Epidemiology?31.2 (2002): 383-390.
  • Allen, Hana Lango, et al. "Hundreds of variants clustered in genomic loci and biological pathways affect human height."?Nature?467.7317 (2010): 832-838.
  • Visscher, Peter M. "Sizing up human height variation."?Nature genetics?40.5 (2008): 489-490.
  • Wheeler, Jeremy G., et al. "Four paraoxonase gene polymorphisms in 11 212 cases of coronary heart disease and 12 786 controls: meta-analysis of 43 studies."?The Lancet?363.9410 (2004): 689-695.
  • Lettre, Guillaume, et al. "Genome-wide association study of coronary heart disease and its risk factors in 8,090 African Americans: the NHLBI CARe Project."?PLoS Genet?7.2 (2011): e1001300.
  • Frayling, Timothy M. "Genome?wide association studies provide new insights into type 2 diabetes aetiology."?Nature Reviews Genetics?8.9 (2007): 657-662.
  • Grarup, Niels, et al. "Genetic susceptibility to type 2 diabetes and obesity: from genome-wide association studies to rare variants and beyond."Diabetologia?57.8 (2014): 1528-1541.
  • O?Keefe, James H., Neil M. Gheewala, and Joan O. O?Keefe. "Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health."?Journal of the American College of Cardiology?51.3 (2008): 249-255.
  • Suez, Jotham, et al. "Artificial sweeteners induce glucose intolerance by altering the gut microbiota."?Nature?514.7521 (2014): 181-186
  • Carr, Molly C., and John D. Brunzell. "Abdominal obesity and dyslipidemia in the metabolic syndrome: importance of type 2 diabetes and familial combined hyperlipidemia in coronary artery disease risk."?The Journal of Clinical Endocrinology & Metabolism?89.6 (2004): 2601-2607.
Evidence Behind The Activator's and Connector's cardiovascular issues may be related to the Pitta body type.
A genetic examination of patterns in Ayurvedic body types revealed that Pitta types (associated with mesomorphy) have high hemoglobin and red blood counts. It also revealed that there was an increased immune response and more active oxydative stress pathways but higher metabolism, which could lead to a higher risk of auto-immune conditions and arthritis, later confirmed by a study that found the HLA DRB1*02 and HLA DRB1*13 to be more present in the Pitta type than the others. It seems to be a type of body that is also associated with increased heart rate, anxiety and stress reaction due to a more emotional and sensation-seeking neurotype. In association with a faster activation of the reticula of the brain that increases arousal, activation of the amygdala that triggers the sympathetic nervous system, and activation of the anterior cingulate gyrus that stimulates attention, is a neural pattern of a type of personality scientists have linked to increased stress, blood pressure and cardiovascular issues.
References
  • Prasher B, Negi S, Aggarwal S, Mandal AK, Sethi TP, Deshmukh SR, et al. Whole genome expression and biochemical correlates of extreme constitutional types defined in Ayurveda. J Transl Med 2008;6:48.
  • Juyal RC, Negi S, Wakhode P, Bhat S, Bhat B, Thelma BK. Potential of ayurgenomics approach in complex trait research: Leads from a pilot study on rheumatoid arthritis.
  • Dishman RK, Nakamura Y, Garcia ME, Thompson RW, Dunn AL, Blair SN. Heart rate variability, trait anxiety, and perceived stress among physically fit men and women. Int J Psychophysiol 2000
  • Randy Larsen, David Buss (2013). Personality Psychology: Domains of Knowledge About Human Nature. McGraw-Hill Education
  • Stoops, William W., et al. "The reinforcing, subject-rated, performance, and cardiovascular effects of d-amphetamine: influence of sensation-seeking status." Addictive behaviors 32.6 (2007): 1177-1188.
Evidence Behind The Kapha body type has a clear genetic pattern.
One study examined the link between common variations rs479200 (C/T) and rs480902 (T/C) in the EGLN1 gene associated with Kapha body types as defined by Ayurvedic type medicine, indicating this type of body to have a higher risk of high-altitude pulmonary problems. Another study examined the genome expression and biochemical correlates of Ayurvedic body types, showing poorer detoxification and metabolism mechanisms than in other types. Further examination of the biochemical dominance of this body type revealed higher digoxin levels, increased free radical production with a reduced radical scavenging function, increased tryptophan catabolites but reduced tyrosine catabolites, increased glycoconjugate levels, and increased cholesterol levels in the blood. The stronger immune system, however, seems to be related to an increased level of CD25 (activated B cells) and CD56 (Natural killer cells) in this type of body.
References
  • AggarvalsNegi S, Jha P, Singh PK, Stobdan T, Pasha MA, Ghosh S, Agrawal A; Indian Genome Variation Consortium, Prasher B, Mukerji MEGLN1 involvement in high-altitude adaptation revealed through genetic analysis of extreme constitution types defined in Ayurveda. "ProcNatlAcadSci U S A."[jour] 2010 Nov 2;107(44):18961-6.
  • Shilpiagaval, sapnanegi, Bhavana Prasher genomics and molecular medicine, institute of genomics and integrative Biology, CSIR, Newdelhi;Whole genome expression and biochemical correlates of extreme constitutional types defined in AyurvedaJtrans Medicine.2008
  • Bhushan, Patwardhan, Joshi Kalpana, and Chopra Arvind. "Classification of human population based on HLA gene polymorphism and the concept of Prakriti in Ayurveda." Journal of Alternative & Complementary Medicine 11.2 (2005): 349-353.
  • Kurup RK, Kurup PA. Hypothalamic digoxin, hemispheric chemical dominance, and the tridosha theory. Int J Neurosci 2003;113:657-81
  • Rapolu SB, Kumar M, Singh G, Patwardhan K. Physiological variations in the autonomic responses may be related to the constitutional types defined in Ayurveda. J Humanitas Med 2015
  • Rotti H, Guruprasad KP, Nayak J, Kabekkodu SP, Kukreja H, Mallya S, Nayak J, Bhradwaj RC, Gangadharan GG, Prasanna BV, Raval R, Kamath A, Gopinath PM, Kondaiah P, Satyamoorthy K. Immunophenotyping of normal individuals classified on the basis of human dosha prakriti. J Ayurveda Integr Med. 2014 Jan;5(1):43-9.
Evidence Behind Scientists are continuously unravelling the correlation between DNA and Prakriti.
The are an increasing number of genetic correlates being found that match Ayurvedic principles thanks to genome wide studies being conducted in the past decades. For instance, Ayurveda claims that individuals with Pitta Prakriti are fast metabolizers while the Kapha are slow metabolizers and this seems to be related to the CYP2C19 enzymes involved in metabolism. Another example is found in the alterations in the EGLN1 gene typical of the Kapha body supports their tendency for a higher risk of lung issues. Or how about the HLA genetic patterns that revealed a higher predisposition for rheumatoid arthritis (RA) in the Pitta body type, followed by the Kapha and much less in the Vata type.
Looking deeper into RA, it seems that the rare cases in the Vata type are related to the CD40 gene, and the Pitta type is associated with PON1 and SOD3 (rs699473). This may be indicating that the risk for RA in the Vata body type could be mediated by inflammatory genes, whereas oxidative stress genes may be the key determinants for the Pitta body type.
An examination of androgen (An), T-cells (Tc) and thyroxine (Th) nuclear receptor behaviors also showed a distinct pattern in the embryonic development of mesomorphic or andrus (Pitta), endomorphic or thymus (Kapha), and ectomorphic or thyrus (Vata) body types. This has lead to a study on the genetic link between EGLN1 (important gene for red blood cells and cellular oxygen) and VWF (gene provides instructions for making a blood clotting protein) in relation to a variation in rs1063856 that modulates thrombosis/bleeding susceptibility and outcomes of hypoxia in Kapha body types.
These are just some examples of the genetic link between Ayurvedic constitutions and genetic medicine that provides a strong link between ancient and modern approaches to health and healing.
References
  • Lurie, Diana. "Ayurveda and pharmacogenomics." Ann Ayurvedic Med 1 (2012): 126-8.
  • Rastogi S. Building bridges between Ayurveda and modern science. Int J Ayurveda Res 2010;1:1-6
  • Patwardhan B, Bodeker G. Ayurvedic genomics: Establishing a genetic basis for mind-body typologies. J Altern Complement Med 2008;14:571-6
  • Ghodke, Yogita, Kalpana Joshi, and Bhushan Patwardhan. "Traditional medicine to modern pharmacogenomics: Ayurveda Prakriti type and CYP2C19 gene polymorphism associated with the metabolic variability." Evidence-Based Complementary and Alternative Medicine 2011 (2011).
  • AggarvalsNegi S, Jha P, Singh PK, Stobdan T, Pasha MA, Ghosh S, Agrawal A; Indian Genome Variation Consortium, Prasher B, Mukerji MEGLN1 involvement in high-altitude adaptation revealed through genetic analysis of extreme constitution types defined in Ayurveda. "ProcNatlAcadSci U S A."[jour] 2010 Nov 2;107(44):18961-6.
  • Bhushan, Patwardhan, Joshi Kalpana, and Chopra Arvind. "Classification of human population based on HLA gene polymorphism and the concept of Prakriti in Ayurveda." Journal of Alternative & Complementary Medicine 11.2 (2005): 349-353.
  • Juyal, Ramesh C., et al. "Potential of ayurgenomics approach in complex trait research: Leads from a pilot study on rheumatoid arthritis." PloS one 7.9 (2012): e45752.
  • Frazer, Kelly A., et al. "Human genetic variation and its contribution to complex traits." Nature Reviews Genetics 10.4 (2009): 241-251.
  • Rizzo-Sierra CV. Ayurvedic genomics, constitutional psychology, and endocrinology: the missing connection. J Altern Complement Med. 2011 May;17(5):465-8.
  • Aggarwal S, Gheware A, Agrawal A, Ghosh S, Prasher B, Mukerji M; Indian Genome Variation Consortium. Combined genetic effects of EGLN1 and VWF modulate thrombotic outcome in hypoxia revealed by Ayurgenomics approach. J Transl Med. 2015 Jun 6;13:184.
Evidence Behind The genetic link to TCM constitutions is becoming ever clearer.
Recent research into the genetic link between TCM constitutions, diseases and biological trends have regularly highlighted the evidence that supports this ancient wisdom. For instance, DRB1*09012 in the Phlegm-wetness group (the Guardiand-Connector area) and DPB1*0501 in the Yin-deficiency group (the Crusaders closest to the Activators) are related to immune response and cell cycles. Significant genetic differences in these two groups as well as the Yin-deficiency group were found in the polymorphisms of PPARD, PPARG and APM1 further supporting the significant differences in metabolic features.
A closer look at the phlegmatic constitution (endomorphic) shows upregulated genes (COPS8, GNPDA1, CD52 and ARPC3) and downregulated genes (GSPT2, CACNB2, FLJ20584, UXS1, IL21R and TNPO) that are consistent with their higher risk of obesity, metabolic syndrome, hypertension and diabetes. In contract, the genetic expression of people with cold syndrom, especially kidney deficiency (generally in the Sensor area or ectomorphs) has been found to be significantly different in the protein and energy metabolisms.
But regardless of how many genetic associations can be made, PH360 will regularly apply a macroscopic systems approach on genetics, rather than the single genes association approach, to look at trends from a more holistic perspective.
References
  • Chen, Shangwu, et al. "HLA class II polymorphisms associated with the physiologic characteristics defined by traditional Chinese medicine: linking modern genetics with an ancient medicine." The Journal of Alternative and Complementary Medicine 13.2 (2007): 231-240.
  • Wu, Yanrui, et al. "Polymorphisms in PPARD, PPARG and APM1 associated with four types of Traditional Chinese Medicine constitutions." Journal of Genetics and Genomics 37.6 (2010): 371-379.
  • Wang, Ji, et al. "Phlegm-dampness constitution: genomics, susceptibility, adjustment and treatment with traditional Chinese medicine." The American journal of Chinese medicine 41.02 (2013): 253-262.
  • Yang, L. P., et al. "Effects of warming-needle therapy on gene expression pathways in the patient with knee osteoarthritis of deficiency-cold syndrome." Zhongguo zhen jiu Chinese acupuncture & moxibustion 27.9 (2007): 677-680.
  • Wang, J. G., et al. "Familial characteristics of kidney-yang deficiency and cold syndrome." Journal of Toxicology and Environmental Health, Part A 69.21 (2006): 1939-1950.
Evidence Behind TCM constitutions can be linked to mood and behavior.
New developments in the personality theory of traditional chinese medicine and the psychology behind its elemental constitutions are revealing strong links to what we know and practice in modern western medicine.
The blood stasis constitution has been found to be related to anxiety, whereas qi and blood deficiency types were associated with depression. Another study found that heat-phlegm and blood stasis constitutions were more related to Type A personalities, especially in relation to athymia and anxiety, whereas the qi and yin deficiency types were more related to Type B personalities. A study on post traumatic stress disorder found a higher prevalence in constitutions with qi deficiencies as well as phlegm and blood types. Using the Eysenck personality questionnaire, qi stagnation was associatied with neuroticism.
There have been many approaches to linking the ancient perspective of syndroms and constitutions used in TCM to the modern psychological assessments of personality types, all of which reveal significant links that could be related to the way the body and mind are functioning from birth.
References
  • Liu, Jia-qiang, et al. "The Development of TCM Psychology: Personality Theory of TCM." Chinese Archives of Traditional Chinese Medicine 9 (2011): 023.
  • Geng, Dong, and Rong-juan Guo. "Clinical investigation on TCM symptoms and syndrome factors of generalized anxiety disorder [J]." Journal of Beijing University of Traditional Chinese Medicine 6 (2013): 015.
  • Guo, Rong-juan, Jia-lin Wand, and Yun-ling Zhang. "Analysis on the Relevance of Elements of TCM Syndromes in Depression Patients [J]." Journal of Traditional Chinese Medicine 9 (2008): 035.
  • Zheng, Kai-mei, Lei Zheng, and Hong-gen Zhen. "Personality of five types of people with five kinds of constitution in patients with depression [J]." Journal of Tianjin University of Traditional Chinese Medicine 2 (2007): 003.
  • Qiu-li, Y., and T. Chong-cheng. "The Personality Theory of Medicopsychology of TCM and the Five-Pattern Personality Inventory." Chinese Journal of Basic Medicine in Traditional Chinese Medicine 10 (2006): 026.
  • Yang, Jun-hua, Guo-jing Yang, and Ru Liu. "The Relationship between A-type Character with Different Classification of TCM and Emotional Disturbance in Coronary Artery Disease Patients [J]." Chinese Journal of Information on Traditional Chinese Medicine 8 (2009): 013.
  • Sinclair-Lian, Nityamo, et al. "Developing a traditional chinese medicine diagnostic structure for post-traumatic stress disorder." Journal of Alternative & Complementary Medicine 12.1 (2006): 45-57.
  • Shi-lin, Y. A. O. "Study on Personality Characteristics of Qi-stagnation Constitution." Journal of Anhui Traditional Chinese Medical College 1 (2008): 009.
Evidence Behind TCM syndroms may be related to a specific type of cancer risk.
Studies on the most common types of cancer found that blood stasis is most associated with liver, lung, and pancreatic cancers, with therapies that should promote blood circulation and remove blood stasis since they tend to have problems with microcirculation and hypercoagulation.
The dampness-heat type seems to be mostly related to gastrointestinal disturbances that lead to inflammatory conditions, including eczema, psoriasis, cystitis, urethritis, gastroenteritis, vaginitis, cervicitis, meningitis, conjunctivitis, rheumatoid arthritis, and allergic reactions, possibly due to changes in expression of inflammation cytokines. This could be the reason why the dampness-heat type is associated with an increased risk of liver, colorectal, and pancreatic types of cancers.
Symptoms of yin deficiency seem to be more common in cancers of the liver, lung, breast, stomach, and colon, possibly due to dysfunction of the vegetative nervous system of the GI tract, immune pathways, and endocrine processes.
Knowing the specific conditions a person tends to have, in combination with many other factors that can be determined about the body, risks for one type of ailment over another can be estimated with confidence.
References
  • Chen, Zhen, and Peng Wang. "Clinical distribution and molecular basis of traditional Chinese medicine ZHENG in cancer." Evidence-Based Complementary and Alternative Medicine 2012 (2012).
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  • N. J. Cui, L. Hu, and S. X. Lao, "Relationship between Pi-Wei damp-heat syndrome with expressions of nuclear factor kappaBmRNA and heat shock protein 70 mRNA in patients with chronic gastritis," Zhongguo Zhong Xi Yi Jie He Za Zhi, vol. 30, no. 1, pp. 18-21, 2010.
  • X. H. Li and G. Q. Xie, "The correlation study between damp-heat syndrome and pro-inflammatory cytokines in primary nephrotic syndrome," Liaoning Journal of Traditional Chinese Medicine, vol. 38, no. 6, pp. 1096-1098, 2011.
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Evidence Behind Korean constitutions are also being scientifically related to DNA.
Genetic analysis of the Korean Constitutional Medicine found that the obesity-risk variant in intron 1 of the fat mass and obesity-associated (FTO) gene on chromosome 16 played a significant role in the Taeumin (endomorphic) body type, yet was inversely related to the Soumin (ectomorph) body type. The Taeumin body type also had a significant genetic loci on rs10937331 (located on chromosome 3) as well as a significant relationship with the GPM6A, SYT4, and GRIK1 genes, the Soumin on rs7180547 (located on chromosome 15) with specific relationships to the DRGX and AKAP11 genes, and the Soyangin (meso-ecto) on rs12431592 (located on chromosome 14) with correlations to the ZFP42, CDH22, ALDH1A2, OTX2, and EN2 genes.
In Taeumin body types, the near apolipoprotein and the near endothelial lipase genes were significantly related, providing another support of their higher risk of increased triglycerides and cholesterol. Another study showed that Taeumins (Guardians and Diplomats or endormophs) have a higher risk of cerebral infarction than other constitutions due to their ACE/DD genotype (Angiotensin I converting enzyme in relation to hypertension), with Soeumins (Crusaders or ecto-mesomorphs) who seem to have a protective factor against it.
The issues with pathological processes that disturb the arterial wall integrity and influence the development of thrombotic brain infarction seems to be a condition with a higher predisposition in Asian populations, but the overall increased risk of hypertension, hypercholesterolemia and obesity-related diseses of the Taeumin body type remains a genetic influence that has an even greater risk when associated with poor lifestyle choices (like diet and lethargy).
References
  • Yin, Chang Shik, et al. "Genome-wide association study of the four-constitution medicine." The Journal of Alternative and Complementary Medicine 15.12 (2009): 1327-1333.
  • Cha, Seongwon, et al. "The obesity-risk variant of FTO is inversely related with the So-Eum constitutional type: genome-wide association and replication analyses." BMC complementary and alternative medicine 15.1 (2015): 1.
  • Kim, Bu-Yeo, Hee-Jeong Jin, and Jong Yeol Kim. "Genome-wide association analysis of Sasang constitution in the Korean population." The Journal of Alternative and Complementary Medicine 18.3 (2012): 262-269.
  • Chung, Sun-Ku, et al. "Genetic loci associated with changes in lipid levels leading to constitution-based discrepancy in Koreans." BMC complementary and alternative medicine 14.1 (2014): 1.
  • Ishigami T., Iwamoto T., Tamura K. et al., (1995). Angiotensin I converting enzyme (ACE) gene polymorphism and essential hypertension in Japan. Ethnic difference of ACE genotype. Am. J. Hypertens. 8: 95-97
Evidence Behind It's not just about whether or not you have a gene, but if it's being expressed.
Research is beginning to improve methodologies to better understand the genotype-phenotype associations, since this field of science is relatively new. However, reliable associations have been found in factors like peroxisome proliferator-activated receptor-γ (PPARG) 13 and the transcription factor TCF7L2 that seem to be related to a risk of diabetes, or the nucleotide-binding oligomerization domain containing 2 (NOD2) and its relationship to Crohn's disease, or the complement factor H (CFH) that's associated with age-related macular degeneration, or even the risk of prostate cancer that's associated with chromosome region 8q24.
Other research has found genome-wide association studies have found 2q35 and 16q12 chromosomal variants to be associated with breast cancer and the 9p21 chromosomal allele to be related to a higher risk of coronary heart disease. Because this can get very complex, a public data archive called the Database of Genotypes and Phenotypes (dbGaP) has been established so that research in genome-wide associations together with aggregated genotype and phenotype data can be researched with new hypotheses and methods to expand our knowledge in this growing field.
References
  • Altshuler, D. et al. The common PPARγ Pro12Ala polymorphism is associated with decreased risk of type 2 diabetes. Nature Genet. 26, 76-80 (2000).
  • Helgason, A. et al. Refining the impact of TCF7L2 gene variants on type 2 diabetes and adaptive evolution. Nature Genet. 39, 218-225 (2007)
  • Field, S. F. et al. Analysis of the type 2 diabetes gene, TCF7L2, in 13,795 type 1 diabetes cases and control subjects. Diabetologia 50, 212-213 (2007)
  • Grant, S. F. et al. Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetes. Nature Genet. 38, 320-323 (2006)
  • Groves, C. J. et al. Association analysis of 6,736 U.K. subjects provides replication and confirms TCF7L2 as a type 2 diabetes susceptibility gene with a substantial effect on individual risk. Diabetes 55, 2640-2644 (2006)
  • Economou, M., Trikalinos, T. A., Loizou, K. T., Tsianos, E. V. & Ioannidis, J. P. Differential effects of NOD2 variants on Crohn's disease risk and phenotype in diverse populations: a metaanalysis. Am. J. Gastroenterol. 99, 2393-2404 (2004).
  • Hageman, G. S. et al. A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration. Proc. Natl Acad. Sci. USA 102, 7227-7232 (2005)
  • Haiman, C. A. et al. Multiple regions within 8q24 independently affect risk for prostate cancer. Nature Genet. 39, 638-644 (2007).
  • Yeager, M. et al. Genome-wide association study of prostate cancer identifies a second risk locus at 8q24. Nature Genet. 39, 645-649 (2007).
  • Stacey, S. N. et al. Common variants on chromosomes 2q35 and 16q12 confer susceptibility to estrogen receptorpositive breast cancer. Nature Genet. 2007
  • Hunter, D. J. et al. A genome-wide association study identifies alleles in FGFR2 associated with risk of sporadic postmenopausal breast cancer. Nature Genet. 2007
  • Easton, D. F. et al. Genome-wide association study identifies novel breast cancer susceptibility loci. Nature 2007
  • Helgadottir, A. et al. A common variant on chromosome 9p21 affects the risk of myocardial infarction. Science 2007
  • McPherson, R. et al. A common allele on chromosome 9 associated with coronary heart disease. Science 2007
  • National Library of Medicine's National Center for Biotechnology Information. "Database of Genotypes and Phenotypes" available at http://view.ncbi.nlm.nih.gov/dbgap
Evidence Behind Air pollution can greatly affect your immune system from early on.
The air we breathe, when polluted and contaminated, has been shown to affect our phenotype. Polycyclic aromatic hydrocarbons like phenanthrene, anthracene, fluoranthene, pyrene, benzo[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, BaP, dibenzo[a,h]anthracene, benzo[g,h,i]perylene, and indeno[c,d]pyrene has been associated with growth retardation of the fetus and exposure during the 14 days before birth was associated with reduced T-lymphocyte fractions CD3+, CD4+, and CD8+, and an increase in the B-lymphocyte fraction (CD19+).
Even the particles inhaled during a particular season (such as pollen or dust) can have an effect on the fetus. The fall season was found to be related to increased CD3+ and CD4+ cell fractions and a lower CD19+ cell fraction, whereas spring was associated with lower CD19+ but higher natural killer (NK) cell fractions.
Examining air particles in the home, it was found that newborns from homes using coal or wood for cooking or heating were associated with greater decreases in fractions of CD3+ and CD4+ and greater increases in the percentage of NK cells, and decreases of CD3+, CD4+, and CD8+ with a very significant increase in NK cell fractions were found in newborns exposed to cigarette smoke in the home.
Findings like these demonstrate how environmental factors, such as exposure to air pollutants or smoking habits of the family, can affect the immune system of a newborn that then remains a part of its phenotype.
References
  • Dejmek J, Selevan S, Benes? I, Solansky I, S?r?m R. 1999. Fetal growth and maternal exposure to particulate matter during pregnancy. Environ Health Perspect 107:475-480
  • Hertz-Picciotto, Irva, et al. "Air pollution and lymphocyte phenotype proportions in cord blood." Environmental health perspectives (2005): 1391-1398.
Evidence Behind Though obesity is related to many health issues, it's also related to asthma.
Obesity promotes a systemic inflammatory state in which proinflammatory hormones are released by adipocytes which can affect asthmatic conditions. Excess weight in the upper body can also lead to a reduction in expiratory reserve volume (ERV), functional residual capacity (FRC), and tidal volume as well as a reduced ability to take deep breaths due to bronchoconstriction. The effect this can have include a limitation of physical activity, breathlessness and wheezing, as well as sleep problems.
Further investigation showed that unlike typical asthmatics that may have Th type 2-mediated inflammatory pathways, there may be something related to corticosteroid resistance in the obesity-related asthmatic phenotype, which may be related to their increased exacerbations and decreased asthma control. It is also possible that the relationship between obesity and asthma is related to serum levels of leptin and adiponectin, which have been shown to have genetic predispositions.
So although there may be various factors that influence the existence and severity of asthma in general, genetic predispositions to lung problems and/or obesity may also be triggered by non-genetic conditions like induced obesity and therefore also ameliorated by weight gain in specific phenotypes.
References
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  • Boulet, LP, Des, CA The link between obesity and asthma: a Canadian perspective.Can Respir J2007;14,217-220
  • Boulet, LP, Turcotte, H, Boulet, G, et al Deep inspiration avoidance and airway response to methacholine: influence of body mass index.Can Respir J2005;12,371-376
  • Bustos, P, Amigo, H, Oyarzun, M, et al Is there a causal relation between obesity and asthma? Evidence from Chile.Int J Obes (Lond)2005;29,804-809.
  • Lessard, Andr?a, et al. "Obesity and asthma: a specific phenotype?." CHEST Journal 134.2 (2008): 317-323.
  • Lugogo, Njira L., Monica Kraft, and Anne E. Dixon. "Does obesity produce a distinct asthma phenotype?." Journal of applied physiology 108.3 (2010): 729-734.
  • Boulet LP, Franssen E. Influence of obesity on response to fluticasone with or without salmeterol in moderate asthma. Respir Med 101: 2240-2247, 2007
  • Sood A, Ford ES, Camargo CA Jr.. Association between leptin and asthma in adults. Thorax 61: 300-305, 2006
  • Sood A, Cui X, Qualls C, Beckett WS, Gross MD, Steffes MW, Smith LJ, Jacobs DR Jr.. Association between asthma and serum adiponectin concentration in women. Thorax 63: 877-882, 2008
  • Mai, Xiao?Mei, Yue Chen, and Daniel Krewski. "Does leptin play a role in obesity-asthma relationship?." Pediatric Allergy and Immunology 20.3 (2009): 207-212.
  • Shin, Joo Hwa, et al. "The expression of adiponectin receptors and the effects of adiponectin and leptin on airway smooth muscle cells." Yonsei medical journal 49.5 (2008): 804-810.
Evidence Behind Stress can unleash molecular signalling pathways leading to chronic inflammation and cancer.
Using a new technique called "ADPr-ChAP" that allows the identification of the chromatin sites that become modified after a cell stress and understand where and how ADP-ribosylation of the chromatin regulates its structure and chromatin-associated processes such as DNA replication, DNA repair or transcription.
Another stress-protective component in the body is called the transcription factor Nrf2 (NF-E2-related factor 2) that activates genes in response to oxidative and electrophilic stresses to protect the body against cancer through glutathione synthesis, elimination of reactive oxygen species (ROS) and detoxification of xenobiotics. Keap1 (Kelch-like ECH-associated protein 1) is essential for the regulation of activity of Nrf2 butu a disrupted NRF2-KEAP1 interaction has been shown to lead to cancer activation and cancer cell proliferation.
Understanding that Nrf2 is crucial for DNA's protection from oxidative and xenobiotic damage helps us understand that Nrf2 inhibitors should be effective for anticancer therapy. Unfortunately, research so far has found several Nrf2 inducers which have successfully shed light on cancer triggers and progressors, but specific inhibitors of Nrf2 have not yet been developed.
References
  • Althaus, Felix R., Helmuth Hilz, and Sydney Shall, eds. ADP-ribosylation of proteins. Springer Science & Business Media, 2012.
  • Taguchi, Keiko, Hozumi Motohashi, and Masayuki Yamamoto. "Molecular mechanisms of the Keap1-Nrf2 pathway in stress response and cancer evolution." Genes to Cells 16.2 (2011): 123-140.
  • Chen, W.M., Sun, Z., Wang, X.J., Jiang, T., Huang, Z.P., Fang, D.Y. & Zhang, D.D. (2009) Direct Interaction between Nrf2 and p21(Cip1/WAF1) Upregulates the Nrf2-Mediated Antioxidant Response. Mol. Cell 34, 663-673.
  • Komatsu, M., Kurokawa, H., Waguri, S., et al. (2010) The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1. Nat. Cell Biol. 12, 213-223.
Evidence Behind Obstructive sleep apnoea is a risk factor for cardiovascular disease.
Recent evidence indicates that inflammatory cytokines such as tumour necrosis factor (TNF)-α that are under the control of nuclear factor ?B actively participate in endothelial damage and chronically worsened with obstructive sleep apnea syndrome. Though this may be associated with an increased prevalence of left ventricular hypertrophy, diastolic dysfunction, or other sturctural issues, a molecular examination provides another perspective.
For instance, sleep apnea has been shown to worsen glucose metabolism in overweight, healthy, diabetic and non-diabetic people. A look at lipid metabolism and liver function revealed that sleep apnea can increase liver enzymes and steatohepatitis regardless of one's weight. Both C-reactive protein (CRP) and TNF-α (common markers of inflammation and disease) are increased with hypoxia, leading to oxidative stress that subsequently leads to left ventricular dysfunction due to reduced nitric oxide bioavailability, enhanced lipid peroxidation and the formation of isoprostanes.
The emerging evidence that inflammatory pathways and the molecular mechanisms of inflammation such as TNF-α, CRP and others are important in understanding atherogenesis and subsequent vascular disease and how obstructive sleep apnoea syndrome can be a risk factor for hypertension and heart disease. This is why sleep apnea caused by obesity, metabolic syndrome, poor liver function or lipid metablolism should be a focus on disease prevention.
References
  • Lavie, Lena, and Vsevolod Polotsky. "Cardiovascular aspects in obstructive sleep apnea syndrome-molecular issues, hypoxia and cytokine profiles." Respiration 78.4 (2009): 361-370.
  • McNicholas, W. T., M. R. Bonsignore, and Management Committee of EU Cost Action B26. "Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities." European Respiratory Journal 29.1 (2007): 156-178.
  • Meier-Ewert, Hans K., et al. "Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk." Journal of the American College of Cardiology 43.4 (2004): 678-683.
  • Oltmanns KM, Gehring H, Rudolf S, et al. Hypoxia causes glucose intolerance in humans. Am J Respir Crit Care Med 2004;169:1231-1237
  • Czupryniak L, Loba J, Pawlowski M, Nowak D, Bialasiewicz P. Treatment with continuous positive airway pressure may affect blood glucose levels in nondiabetic patients with obstructive sleep apnea syndrome. Sleep 2005;28:601-603
  • Tanne F, Gagnadoux F, Chazouilleres O, et al. Chronic liver injury during obstructive sleep apnea. Hepatology 2005;41:1290-1296.
  • Barcel? A, Miralles C, Barb? F, Vila M, Pons S, Agust? AGN. Abnormal lipid peroxidation in patients with sleep apnoea. Eur Respir J 2000;16:644-647
  • Chen L, Einbinder E, Zhang Q, Hasday J, Balke CW, Scharf SM. Oxidative stress and left ventricular function with chronic intermittent hypoxia in rats. Am J Respir Crit Care Med 2005;172:915-920.
  • Lavie L, Vishnevsky A, Lavie P. Evidence for lipid peroxidation in obstructive sleep apnea. Sleep 2004;27:123-128.
  • Carpagnano GE, Kharitonov SA, Resta O, et al. 8-Isoprostane, a marker of oxidative stress, is increased in exhaled breath condensate of patients with obstructive sleep apnea after night and is reduced by continuous positive airway pressure therapy. Chest 2003;124:1386-1392.
Evidence Behind Proper digestion means getting the right nutrients without the excess.
The stomach's hydrochloric acid breaks down proteins into amino acids, while gastric pepsin breaks down collagen. People who don't have a low enough pH in the stomach may experience problems with protein digestion at this level already. In the intestine, trypsin, chymotrypsin and carboxypolypeptidase come from the pancreas and continue to hydrolize proteins into even smaller amino acids. These are then absorbed into the capillaries of the intestine and brought into circulation to be delivered to other tissues. Underfunction of the pancrease or buildup in the intestine can hinder this process, causing fermentation and other issues. When there are too many amino acids brought to the liver, they undergo deamination through gluconeogenisis and are converted into glucose via the alanine cycle. Extra amino acids may also be created into fat through lipogenisis. The removal of the amine group of amino acids created nitrogen in the liver which is converted into urea and expelled from the body by the kidney.
This is why humans need to consider appropriate portions of protein and having complete proteins (meals that have a wide range of amino acids) for tissues to be well nourished without too much extra going into the body's storage system. All of these factors, and others, contribute to the way different proteins can have different effects on insulin levels, adipocytes, fatty acids, lipotoxicity, muscle building and organ function.
References
  • Friedberg, Errol C., Diego H. Castrillon, and Rene L. Galindo. New-opathies: An Emerging Molecular Reclassification of Human Disease. World Scientific, 2012.
  • Stadtman, E. R., and R. L. Levine. "Free radical-mediated oxidation of free amino acids and amino acid residues in proteins." Amino acids 25.3-4 (2003): 207-218.
  • Munro, Hamish Nisbet, ed. Mammalian protein metabolism. Vol. 4. Elsevier, 2012.
Evidence Behind A mother's health can change a child's genetic predisposition to disease.
Studies have shown that dispite a genetic predisposition to type 2 diabetes, body mass index (BMI), body fat index (BFI), family history, age, sex, HDL cholesterol, triglyceride levels, and other risk factors outperform our ability to predict diabetic onset. Studies using familial clustering of type 2 diabetes found that the risk for onset of this disease is not entirely due to genetic factors. Epigenetic processes can produce inherited risk over one or several generations.
For instance, pregnancy related factors, nutrition, toxins and infectious agents can also play a role in the activation of genes that may influence the risk of diabetes. Mechanisms like histone acetylation, DNA-methylation, RNA coding patterns and the regulation of gene expressions in response to environmental cues can be passed on generations later. But the one factor that has the most epigenetic impact remains obesity.
Studies focused on epigenetic markers found altered methylation and histone acetylation levels in genes involved in metabolic processes. For one, there is a huge influence of maternal obesity (including gestational and postnatal diet, maternal insulin resistance and metabolic syndrome) on changes in the biochemical structure of the baby's DNA that alter gene expression involved in the risk for developing metabolic syndrome in adulthood. The exact reason behind this is unclear, though leptin and adiponectin may play significant roles.
Leptin is a hormone secreted by fat tissues that travles from the mother's blood to the fetus and works on the development of the central nervous system. After birth, leptin regulates appetite and energy expenditure. Maternal hyperglycemia have been shown to be related to increased leptin levels in offspring.
Similarly, adiponectin should maintain insulin sensitivity but has been found to be significantly lower in children from mothers with high-fat diets. Meanwhile, a mother's insulin resistance can cause pregnancy complications due to impaired glucose transport, including an increased risk for metabolic disturbances, cardiovascular disease and even telomere length.
References
  • Talmud PJ, Hingorani AD, Cooper JA, Marmot MG, Brunner EJ, Kumari M, Kivim?ki M, Humphries SE. Utility of genetic and non-genetic risk factors in prediction of type 2 diabetes: Whitehall II prospective cohort study. BMJ. 2010;340:b4838
  • Skinner MK. Environmental epigenetic transgenerational inheritance and somatic epigenetic mitotic stability. Epigenetics. 2011;6:838-842
  • Burgio, Ernesto, Angela Lopomo, and Lucia Migliore. "Obesity and diabetes: from genetics to epigenetics." Molecular biology reports 42.4 (2015): 799-818.
  • Kaar JL, Crume T, Brinton JT, Bischoff KJ, McDuffie R, Dabelea D. Maternal obesity, gestational weight gain, and offspring adiposity: the exploring perinatal outcomes among children study. J Pediatr. 2014;165(3):509-515.
  • Smith, Caitlin J., and Kelli K. Ryckman. "Epigenetic and developmental influences on the risk of obesity, diabetes, and metabolic syndrome." Diabetes, metabolic syndrome and obesity: targets and therapy 8 (2015): 295.
  • Briffa JF, McAinch AJ, Romano T, Wlodek ME, Hryciw DH. Leptin in pregnancy and development: a contributor to adulthood disease? Am J Physiol Endocrinol Metab. 2015;308(5):E335-E350.
  • Hou M, Chu Z, Liu T, et al. A high-fat maternal diet decreases adiponectin receptor-1 expression in offspring. J Matern Fetal Neonatal Med. 2015;28(2):216-221.
  • Doblado M, Moley KH. Glucose metabolism in pregnancy and embryogenesis. Curr Opin Endocrinol Diabetes Obes. 2007;14(6):488-493.
  • West NA, Crume TL, Maligie MA, Dabelea D. Cardiovascular risk factors in children exposed to maternal diabetes in utero. Diabetologia. 2011;54(3):504-507.
  • Xu J, Ye J, Wu Y, et al. Reduced fetal telomere length in gestational diabetes. PloS One. 2014;9(1):e86161.
Evidence Behind About 70% of what causes aging can be modulated during the lifespan.
Epigenetics is the study of heritable phenotypic changes in the body without changes in the underlying gene sequence. For instance, chromatin, the nucleoprotein that allows the genome to be packaged inside the nucleus, can be influenced by the environment and lead to to long-lasting phenotypic effects. Although the precise role of chromatin's effect on biological aging is difficult to establish, scientists have been able to uncover many of the features that are directly related to the speed of aging on an epigenetic level.
Studies have mainly focused on diet, exercise, circadian rhythms, sex hormones and stress. More specifically, a healthy diet in which caloric restriction is integrated will prolong longevity. Factors that play a role in the influence diet has on chromatin modulation include nutrient-sensing pathways like insulin and insulin-like growth factor, protein kinase energy sensors, metabolites and metabolic enzymes, and maintaining a balanced Krebs cycle.
In humans, exercise seems to be associated with enhanced AMPK activity (responsible for cellular energy homeostasis), nuclear exclusion of HDAC4 and HDAC5 (genes that play a function in cell cycle progression and developmental events), and increased H3K36 acetylation in skeletal muscle tissue (improved skeletal-muscle metabolism). The circadian clock controls many physiological and behavioral systems and is highly linked to energy metabolism. And sex steroid hormones like estrogen that tends to decline with age, act mainly through nuclear receptors affecting chromatin states. Similarly, having a little bit of stress (called eustress) to keep the body active and alert, but then balancing this with regular rest cycles (like sleep or leisure) can also also affect the global chromatin landscape and thereby contribute to longevity.
All these factors, and certainly more, contribute to the heritable phenotypic changes throughout the lifespan. Accummulated DNA damage and mutations in DNA-repair enzymes contribute to aging.
References
  • Cournil, A. & Kirkwood, T. B. If you would live long, choose your parents well. Trends Genet. 17, 233-235 (2001).
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  • Vaquero, A. & Reinberg, D. Calorie restriction and the exercise of chromatin. Genes Dev. 23, 1849-1869 (2009).
  • Jiang, N. et al. Dietary and genetic effects on age-related loss of gene silencing reveal epigenetic plasticity of chromatin repression Aging 5, 813-824 (2013).
  • McGee, S. L., Fairlie, E., Garnham, A. P. & Hargreaves, M. Exercise-induced histone modifications in human skeletal muscle. J. Physiol. 587, 5951-5958 (2009).
  • Froy, O. Circadian rhythms, aging, and life span in mammals. Physiology 26, 225-235 (2011).
  • Janssen, I., Carson, V., Lee, I. M., Katzmarzyk, P. T. & Blair, S. N. Years of life gained due to leisure-time physical activity 23-29 (2013).
  • Sanchis-Gomar, Fabian, et al. "Physical exercise as an epigenetic modulator: Eustress, the "positive stress" as an effector of gene expression." The Journal of Strength & Conditioning Research 26.12 (2012): 3469-3472.
  • Gidday, Jeffrey M. "Extending injury-and disease-resistant CNS phenotypes by repetitive epigenetic conditioning." Frontiers in neurology 6 (2015).
Evidence Behind Epigenetic markers are often used to assess the rate of aging.
The CDKN2A gene encodes different transcripts involved in cell cycle regulation and cellular aging and its expression levels seem to increase with age, resulting in signs of aging like a reduction in the thickness and amount of hair on the head, greying of hair, curving of the spine, reduction in muscle mass, getting cataracts, etc). Studies have found that quieting this gene does delay various factors in aging because it slows down cellular aging and self-renewal, but it has been associated with many types of cancer.
Similarly, telomeres are the DNA-protein structures found at both ends of each chromosome that protect the genome from degradation and are crucial in preserving the information in the genome. Not only do telomeres shorten with age, but the rate at which this happens may indicate the pace at which the body ages.
Finally, the CpG islands are located around the promoters of housekeeping genes that regulate general cell functions and where many genes remain inactive till they need to be activated at specific points in life. Hypermethylation (over activation of these genes) occurs with age.
In simpler terms, there are several ways to see what effects various lifestyle choices have on the body and how they contribute to the speed at which the body ages.
References
  • Boquoi et al. (2015) "Reversible cell cycle inhibition and premature aging features imposed by conditional expression of p16Ink4a." Aging Cell 14(1):139-147
  • Baker et al. (2011) "Clearance of p16Ink4a-positive senescent cells delays aging-associated disorders." Nature 479(7372):232-236
  • Kamb et al. (1994) "A cell cycle regulator potentially involved in genesis of many tumor types." Science 264(5157):436-440
  • Shammas, Masood A. "Telomeres, lifestyle, cancer, and aging." Current opinion in clinical nutrition and metabolic care 14.1 (2011): 28.
  • Shin JS, Hong A, Solomon MJ, Lee CS. The role of telomeres and telomerase in the pathology of human cancer and aging. Pathology. 2006;38:103-113
  • Jiang H, Schiffer E, Song Z, et al. Proteins induced by telomere dysfunction and DNA damage represent biomarkers of human aging and disease. Proc Natl Acad Sci U S A. 2008;105:11299-11304.
Evidence Behind Metabolic and sleep disorders can affect your epigenome.
Many metabolic processes, such as glucose and cholesterol metabolism, or renal and liver function are regulated by the circadian clock. Scientists have shown that shift work and misalignment between appropriate hours of the day and behaviors (like eating at night) can cause metabolic disorders, decrease in leptin levels and increase in glucose and insulin levels.
Recent evidence has shown that the reverse is also true, in that eating behavior and times can affect the circadian rhythm. Factors that influence this include nuclear sensors and receptors, metabolites like phospholipids and amino acids, enzymes and even gene expression. For instance, blunting the enzyme responsible for glycogen degradation to produce glucose in mice resulted in deregulation of glycogen in the liver which increased fat mass and reduced muscle mass. Many such studies combined provide increasing evidence that restricting food intake to daylight times may help control unwanted weight gain.
References
  • Aguilar-Arnal, L. & Sassone-Corsi, P. The circadian epigenome: how metabolism talks to chromatin remodeling. Curr. Opin. Cell Biol. 25, 170-176 (2013).
  • Sahar S, Sassone-Corsi P. Regulation of metabolism: The circadian clock dictates the time. Trends Endocrinol Metab. 2012;23(1):1-8
  • Eckel-Mahan K, Sassone-Corsi P. Metabolism control by the circadian clock and vice versa. Nat Struct Mol Biol. 2009;16:462-467
  • De Bacquer D, Van Risseghem M, Clays E, Kittel F, De Backer G, et al. Rotating shift work and the metabolic syndrome: a prospective study. Int J Epidemiol. 2009;38:848-854.
  • Scheer FA, Hilton MF, Mantzoros CS, Shea SA. Adverse metabolic and cardiovascular consequences of circadian misalignment. Proc Natl Acad Sci U S A. 2009;106:4453-4458
  • Arble DM, Bass J, Laposky AD, Vitaterna MH, Turek FW. Circadian timing of food intake contributes to weight gain. Obesity (Silver Spring) 2009;17:2100-2102.
  • Costa MJ, So AY, Kaasik K, Krueger KC, Pillsbury ML, et al. Circadian rhythm gene period 3 is an inhibitor of the adipocyte cell fate. J Biol Chem. 2011;286:9063-9070
  • Eckel-Mahan, Kristin L., et al. "Reprogramming of the circadian clock by nutritional challenge." Cell 155.7 (2013): 1464-1478.
Evidence Behind The body wants to run like a swiss watch.
Many factors play a role in regulating the circadian clock, though it is mainly related to exposure to light during the day and darkness at night. For instance, darkness triggers an increase in melatonin which makes us feel sleepy. But more than just being a clock for sleepiness and wakefulness, it has an important affect on the body.
For instance, inflammatory responses are heightened at night (which is why fevers tend to spike at night). In contrast, responses that inhibit inflammation rise during the day. Similarly, early morning, signals the release of the stress hormone cortisol which puts our body into alertness so that we can be active for the day. This induces a rise in heart rate, blood pressure and body temperature. The body temperature, and consequent digestive process, peaks around late afternoon, only to slowly fall again as the body prepares itself for rest.
Maintaining a healthy circadian rhythm of 24 hours may promote healthy fundamental physiological functions in almost all organisms. Studies on the effects of shift work, for instance, has shown rise in blood pressure and heart rate variability which can lead to consequent cardiovascular issues. Though most people can adapt to regular shift work (eg: always working night shifts), shift rotation seems to have a more detrimental effect on the body and mind.
References
  • Buhr, Ethan D., and Joseph S. Takahashi. "Molecular components of the mammalian circadian clock." Circadian clocks. Springer Berlin Heidelberg, 2013. 3-27.
  • Partch, Carrie L., Carla B. Green, and Joseph S. Takahashi. "Molecular architecture of the mammalian circadian clock." Trends in cell biology 24.2 (2014): 90-99.
  • Wright, Kenneth P., et al. "Entrainment of the human circadian clock to the natural light-dark cycle." Current Biology 23.16 (2013): 1554-1558.
  • Su, Ta-Chen, et al. "Elevated blood pressure, decreased heart rate variability and incomplete blood pressure recovery after a 12-hour night shift work." Journal of occupational health 50.5 (2008): 380-386.
  • Haus, Erhard, and Michael Smolensky. "Biological clocks and shift work: circadian dysregulation and potential long-term effects." Cancer causes & control 17.4 (2006): 489-500.
  • MFJ, Martens, et al. "Flexible work schedules and mental and physical health. A study of a working population with non-traditional working hours." Journal of Organizational Behavior 20.1 (1999): 35-46.
Evidence Behind There is no perfect time to exercise.
The body's core temperature is at it's highest between 2pm and 8pm and is at its minimum around 5am, when we should be in deep sleep. Melatonin secretion is a major contributor to this, since it increases in the evening, which promotes a fall in body temperature and digestive activity as it prepares the body for rest. One of the ways the body cools itself down is through vasodilation. This is why exercise in the evening can cause more sweating and more blood flow throughout the body than it would earlier in the day. Muscles are therefore able to contract better in the evening with better hormonal response to resistance exercise, but tire more quickly.
But if sleep quality is an issue, evening workouts may not be ideal. Because early morning hours are when blood flow is poorer and joints are stiffer, it is the time when cardiovascular problems and joint or spine injury are most likely to occur and people with risks in these areas would be recommended to exercise later in the day. However, respiratory problems can increase with exercise late in the day and endurance exercises may be better earlier in the day when the core temperature is still low.
All of these factors, and many more, contribute to the ideal workout times recommended for an individual. It is important to consider what type of exercise to perform, its intensity, the health factors and personal needs.
References
  • Waterhouse, Jim, et al. "The circadian rhythm of core temperature: origin and some implications for exercise performance."?Chronobiology international22.2 (2005): 207-225
  • Nicolas, A., et al. "Time?of?day effects on myoelectric and mechanical properties of muscle during maximal and prolonged isokinetic exercise."Chronobiology international?22.6 (2005): 997-1011.
  • Bird, Stephen P., and Kyle M. Tarpenning. "Influence of circadian time structure on acute hormonal responses to a single bout of heavy-resistance exercise in weight-trained men."?Chronobiology international?21.1 (2004): 131-146.
  • Souissi, Mohamed, et al. "Effect of time-of-day of aerobic maximal exercise on the sleep quality of trained subjects."?Biological Rhythm Research?43.3 (2012): 323-330.
  • Atkinson, Greg, et al. "Chronobiological considerations for exercise and heart disease."?Sports Medicine?36.6 (2006): 487-500.
  • Reilly, T., et al. "Some chronobiological considerations related to physical exercise."?La Clinica terapeutica?157.3 (2005): 249-264.
  • Bessot, N., et al. "The effect of pedal rate and time of day on the time to exhaustion from high?intensity exercise."?Chronobiology international?23.5 (2006): 1009-1024.
Evidence Behind Exercise can keep the brain from aging poorly.
Exercise has been shown to be an important factor in maintaining neurological health. For example, voluntary exercise promotes neurogenesis and healthy cognitive aging in mice.
Studies on elderly with Alzheimer's disease found that exercise lowered levels of toxic tau proteins and increased blood flow in the brains of people with early memory changes that put them at risk for dementia. Four months of intense exercise improved symptoms like anxiety, irritability, and depression in people with Alzheimer's, though it didn't help their memories. But 6 months of exercise did improve memory and thinking in people diagnosed with vascular dementia. Neuroimaging of people with and without a genetic risk of Alzheimer's disease, based on the presence of APOE4 genes, found that people who exercised had brains that aged like unaffected adults whereas a sedentary lifestyle caused key brain structures to shrink and poorer performance on written tests of memory and thinking.
Whether it's the improvements in teh circulatory and microcirculatory system that maintains healthy brain function, the continuous use of neural functions to manage the body during and after exercise, the improved sleep quality that comes from exercising that improves neural detoxing, or other functions not yet discovered, the conclusion is simple: exercise keeps the mind as well as the body youthful.
References
  • Ahlskog, J. Eric, et al. "Physical exercise as a preventive or disease-modifying treatment of dementia and brain aging." Mayo Clinic Proceedings. Vol. 86. No. 9. Elsevier, 2011.
  • Smith, J. Carson, et al. "Interactive effects of physical activity and APOE-?4 on BOLD semantic memory activation in healthy elders." Neuroimage 54.1 (2011): 635-644.
  • Li, L. et al. Acute aerobic exercise increases cortical activity during working memory: a functional MRI study in female college students. PLoS ONE 9, e99222 (2014).
  • Gremeaux, V. et al. Exercise and longevity. Maturitas 73, 312-317 (2012).
  • Wu, C. W. et al. Exercise enhances the proliferation of neural stem cells and neurite growth and survival of neuronal progenitor cells in dentate gyrus of middle-aged mice. J. Appl. Physiol. 105, 1585-1594 (2008).
  • Lugert, S. et al. Quiescent and active hippocampal neural stem cells with distinct morphologies respond selectively to physiological and pathological stimuli and aging. Cell Stem Cell 6, 445-456 (2010).
Evidence Behind The epigenetic effect of exercise can be a life saver.
Studies on humans have found that exercise is associated with enhanced AMPK activity (activated protein kinase), which is important for balanced cellular energy. AMPK regulates metabolism by switching on catabolic pathways that generate adenosine triphosphate (ATP), while switching off anabolic pathways that consume ATP, including glucose uptake, fatty acid uptake, and fatty acid oxidation. ATP is essential for many metabolic pathways and provides the body the energy it needs.
AMPK activation also inhibits several anabolic pathways through a phosphorylation of key metabolic enzymes. This includes fatty acid synthesis, triglyceride and phospholipid synthesis and glycoden synthesis.
Although it is best known for its effects on metabolic pathways, recent research has found that AMPK also regulates cellular function, including autophagy and maintenance of mitochondrial homeostasis, cell polarity, and cell growth and proliferation and ultimately protecting the body against viruses and cancer formation.
References
  • McGee, S. L., Fairlie, E., Garnham, A. P. & Hargreaves, M. Exercise-induced histone modifications in human skeletal muscle. J. Physiol. 587, 5951-5958 (2009).
  • Hardie, D. Grahame. "AMP-activated protein kinase?an energy sensor that regulates all aspects of cell function." Genes & development 25.18 (2011): 1895-1908.
  • Richter, Erik A., and Neil B. Ruderman. "AMPK and the biochemistry of exercise: implications for human health and disease." Biochemical Journal 418.2 (2009): 261-275.
Evidence Behind Women should lift weights.
Research has found that even moderate weight training can increase a woman's strength by over 30%, the same rate as men or sometimes even outpacing them in strength gain. Yet because women have 10 to 30 times less of the hormones that cause muscle hypertrophy (increase size of muscle cells), they are unlikely to develop the bulky muscles men can and tend to develop a more slim and toned body instead.
As the body ages, skeletal muscle mass tends to decrease. But resistance exercises can slow down this process and help maintain a stronger body with better quality of muscle tissues and maintenance of bone mineral density as we age. There are many reasons for which the body becomes weaker with age (including hormonal changes, increase of proinflammatory cytokines, lipotoxicity, or metabolic changes), but staying physically active and working on strength training can attenuate this decline with age.
But for those who are not yet thinking of the later years and want to focus more on the here and now, thinking about the increased resting metabolic rate, decrease in leptin hormone release (hormone that controls hunger), increase in adiponectin hormone (regulates glucose and fatty acid breakdown) which helps with caloric management throughout the day and ultimately helps shed some fat.
References
  • Folland, Jonathan P., and Alun G. Williams. "Morphological and neurological contributions to increased strength."?Sports medicine?37.2 (2007): 145-168.
  • Kalapotharakos, Vasilios I., et al. "Effects of a heavy and a moderate resistance training on functional performance in older adults."?The Journal of Strength & Conditioning Research?19.3 (2005): 652-657.
  • Hubal, MONICA J., et al. "Variability in muscle size and strength gain after unilateral resistance training."?Med Sci Sports Exerc?37.6 (2005): 964-72.
  • Kim, Jeong-su, James M. Cross, and Marcas M. Bamman. "Impact of resistance loading on myostatin expression and cell cycle regulation in young and older men and women."?American Journal of Physiology-Endocrinology and Metabolism?288.6 (2005): E1110-E1119.
  • Phillips, Stuart M. "Physiologic and molecular bases of muscle hypertrophy and atrophy: impact of resistance exercise on human skeletal muscle (protein and exercise dose effects)."?Applied physiology, nutrition, and metabolism?34.3 (2009): 403-410.
  • Goodpaster, Bret H., et al. "The loss of skeletal muscle strength, mass, and quality in older adults: the health, aging and body composition study."?The Journals of Gerontology Series A: Biological Sciences and Medical Sciences61.10 (2006): 1059-1064.
  • Suominen, Harri. "Muscle training for bone strength."?Aging clinical and experimental research?18.2 (2006): 85-93.
  • Potteiger, Jeffrey A., et al. "Changes in resting metabolic rate and substrate oxidation after 16 months of exercise training in overweight adults."International journal of sport nutrition and exercise metabolism?18.1 (2008): 79.
  • Fatouros, I. G., et al. "Leptin and adiponectin responses in overweight inactive elderly following resistance training and detraining are intensity related."?The Journal of Clinical Endocrinology & Metabolism?90.11 (2005): 5970-5977.
Evidence Behind You can fight wrinkles with sleep.
In a study on people's judgment about a person's sleep quality, one of the tell tale signs for sleep deprivation was the presence of wrinkles and fine lines around the face, especially around the eyes. The mechanisms by which sleep deprivation causes wrinkles remain to be explored, but there are hypotheses being researched.
For instance, biopsies of forehead wrinkles had found lower skin thickness and less elastin, tropoelastin and collagen where wrinkles exist. Elastin, collagen and glycosaminoglycans give the skin its elasticity and flexibility. But sleep deprivation, with as little as 42 hrs in humans, can begin to break down the skin's integrity and mucous membranes due to an activated state of stress on the body.
Another sleep deprivation study showed that sleep loss is detrimental to the immune system and to the body's healing processes, which ultimately impairs the skin's integrity. Even sleep apnea has been shown to cause significant reductions in the amount of glycosaminoglycans and?collagen, which further substantiates this theory.
There are various approaches to improving sleep quality through diet, routine, meditation and exercise which may be recommended for the specific needs of an individual. But even if you've had a good night's sleep, researchers have found that sleeping faced down can increase facial wrinkles due to the pressure on the face by the pillow, so using a special pillow that distributes this pressure differently or avoiding this position at night could also help fight the appearance of wrinkles.
References
  • Sundelin, Tina, et al. "Cues of fatigue: effects of sleep deprivation on facial appearance."?Sleep?36.9 (2013): 1355.
  • El?Domyati, Moetaz, et al. "Forehead wrinkles: a histological and immunohistochemical evaluation."?Journal of cosmetic dermatology?13.3 (2014): 188-194.
  • Metcalfe AD, Ferguson MW. Tissue engineering of replacement skin: the crossroads of biomaterials, wound healing, embryonic development, stem cells and regeneration. J R Soc Interface 2007;4:413-37.
  • Altemus M, Rao B, Dhabhar FS, Ding W, Granstein RD. Stress-induced changes in skin barrier function in healthy women. J Invest Dermatol 2001;117:309-17
  • Zager A, Andersen ML, Ruiz FS, Antunes IB, Tufik S. Effects of acute and chronic sleep loss on immune modulation of rats. Am J Physiol Regul Integr Comp Physiol 2007;293:R504-509.
  • Kahan, V., et al. "Can poor sleep affect skin integrity?."?Medical hypotheses75.6 (2010): 535-537.
  • Drager, Luciano F., et al. "Early signs of atherosclerosis in obstructive sleep apnea."?American journal of respiratory and critical care medicine?172.5 (2005): 613-618.
  • Kotlus, Brett S. "Effect of Sleep Position on Perceived Facial Aging."Dermatologic Surgery?39.9 (2013): 1360-1362.
  • Poljsak, Borut, et al. "The influence of the sleeping on the formation of facial wrinkles."?Journal of Cosmetic and Laser Therapy?14.3 (2012): 133-138.
Evidence Behind Lack of sleep can create metabolic dysfunction.
Studies have found that frequent waking from breathing problems have been related to glucose intolerance and insulin resistance. Other studies have found that high altitude or hypobaric hypoxia are also associated with a decrease in insulin sensitivity, further confirming the relationship between breathing patterns, oxygen intake and glucose metabolism.
Some theories supposed that this could be related to a release of proinflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α, others suppose it could be an over activity of the sympathetic nervous system that influences glucose homeostasis by increasing glycogen breakdown and gluconeogenesis, or perhaps the hypothalamic-pituitary-adrenal axis increases levels of plasma cortisol and affects insulin secretions that way.
Although the underlying mechanisms behind this relationship is still uncertain, what remains clear is that there is a relationship between sleep deprivation and glucose intolerance which has been supported in various circumstances not related to nighttime breathing issues like shift work, short sleep hours (called sleep debt), and poor quality sleep.
References
  • Larsen JJ, Hansen JM, Olsen NV, et al. The effect of altitude hypoxia on glucose homeostasis in men.?J Physiol (Lond)?1997;504:241-9.
  • Braun B, Rock PB, Zamudio S, et al. Women at altitude: short-term exposure to hypoxia and/or alpha(1)-adrenergic blockade reduces insulin sensitivity.?J Appl Physiol?2001;91:623-31.
  • Liu H, Liu J, Xiong S, et al. The change of interleukin-6 and tumor necrosis factor in patients with obstructive sleep apnea syndrome.?J Tongji Med Univ2000;20:200-2.
  • Tasali, Esra, and Mary SM Ip. "Obstructive sleep apnea and metabolic syndrome: alterations in glucose metabolism and inflammation."?Proceedings of the American Thoracic Society?5.2 (2008): 207-217.
  • Buckley, Theresa M., and Alan F. Schatzberg. "On the interactions of the hypothalamic-pituitary-adrenal (HPA) axis and sleep: normal HPA axis activity and circadian rhythm, exemplary sleep disorders."?The Journal of Clinical Endocrinology & Metabolism?90.5 (2005): 3106-3114.
  • Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function.?Lancet?1999;354:1435-9.
  • Sookoian, S., et al. "Effects of rotating shift work on biomarkers of metabolic syndrome and inflammation."?Journal of internal medicine?261.3 (2007): 285-292.
  • Knutson, Kristen L., et al. "The metabolic consequences of sleep deprivation."?Sleep medicine reviews?11.3 (2007): 163-178.
  • Spiegel, Karine, et al. "Effects of poor and short sleep on glucose metabolism and obesity risk."?Nature Reviews Endocrinology?5.5 (2009): 253-261.
  • Schmid, Sebastian M., Manfred Hallschmid, and Bernd Schultes. "The metabolic burden of sleep loss." The lancet Diabetes & endocrinology 3.1 (2015): 52-62.
Evidence Behind Sleep function is related to the brain's health.
The lymphatic system of the brain is managed by glial cells and therefore galled the glymphatic pathway. Flushing the brains with CSF and ISF fluids, toxins are removed from the brain and sent to the liver to be eliminated from the body. Although this process does happen throughout the day, it is 10 times more active during sleep, causing brain cells to actually shrink up to 60% of their size.
Though details about how the brain's recuperation and detoxification process during sleep really works are still being, many studies on neurological diseases like Alzheimer's have revealed quite a bit about this phenomenon. For instance, disrupted sleep patterns have been shown to increase?amyloid plaques in the brain, a hallmark of the disease, as well as brain shrinkage and and irreversible, brain damage with a loss of neurons located in the locus coeruleus.
The national sleep foundation highly recommends adults get 7-9 hours of quality sleep each night for their brain and body's health. It is therefore important to consider sleep duration and sleep quality for better health and well being, especially for the brain.
References
  • Xie, Lulu, et al. "Sleep drives metabolite clearance from the adult brain."?science?342.6156 (2013): 373-377.
  • Iliff, Jeffrey J., et al. "Brain-wide pathway for waste clearance captured by contrast-enhanced MRI."?The Journal of clinical investigation?123.3 (2013): 1299-1309.
  • Ittner, Lars M., and J?rgen G?tz. "Amyloid-β and tau?a toxic pas de deux in Alzheimer's disease."?Nature Reviews Neuroscience?12.2 (2011): 67-72.
  • Sexton, Claire E., et al. "Poor sleep quality is associated with increased cortical atrophy in community-dwelling adults."?Neurology?83.11 (2014): 967-973.
  • Zhang, Jing, et al. "Extended wakefulness: compromised metabolics in and degeneration of locus ceruleus neurons."?The Journal of Neuroscience?34.12 (2014): 4418-4431.
  • Hirshkowitz, Max, et al. "National Sleep Foundation's sleep time duration recommendations: methodology and results summary."?Sleep Health?1.1 (2015): 40-43.
Evidence Behind The air you breathe could be killing you.
It is not news that people who live near high traffic areas (like in inner cities) are at a higher risk of asthma and respiratory conditions than people who live in rural areas where fresh air is plentiful. Particulate matter large enough to be seen (like as smoke or dust) or so small that an electron microscope is needed to know it's there.
Although bigger particles result in smog and haze that reduce visibility, it's the fine particles that stay in the air for days or weeks before they are removed, penetrating deep into our lungs, collecting in tiny air sacs called alveoli where oxygen enters the bloodstream. The particles that are smaller than 2.5μm in diameter (PM2.5) are the biggest danger to human health, with effects ranging from a runny nose and coughing, to bronchitis, asthma, emphysema, pneumonia, heart disease, and even cancer. That's because they come from the combustion of fossil fuels (like motor vehicle exhaust) and wood (like from woodstoves and fireplaces), industrial activity, garbage incineration and agricultural burning, meaning they can contain a number of harmful substances and cancer-causing chemicals.
People with pre-existing cardiovascular disease and diabetic and elderly individuals are considered to be more vulnerable, but the health effects of ultrafine particles can be detrimental to anyone. Despite the evidence of air pollution's negative effects on health, policies to clean the air and keep it clean are minimal and scientific health impact assessments often ignore this effect.
References
  • Knibbs, Luke D., Tom Cole-Hunter, and Lidia Morawska. "A review of commuter exposure to ultrafine particles and its health effects."?Atmospheric Environment?45.16 (2011): 2611-2622.
  • Moller, Winfried, et al. "Deposition, retention, and translocation of ultrafine particles from the central airways and lung periphery."?American journal of respiratory and critical care medicine?177.4 (2008): 426-432.
  • Wiebert, Pernilla, et al. "Negligible clearance of ultrafine particles retained in healthy and affected human lungs."?European Respiratory Journal?28.2 (2006): 286-290.
  • Nel, Andr?. "Air pollution-related illness: effects of particles."?Science308.5723 (2005): 804-806.
  • Terzano, C., et al. "Air pollution ultrafine particles: toxicity beyond the lung."Eur Rev Med Pharmacol Sci 14.10 (2010): 809-21.
  • Simkhovich, Boris Z., Michael T. Kleinman, and Robert A. Kloner. "Air pollution and cardiovascular injury: epidemiology, toxicology, and mechanisms."?Journal of the American College of Cardiology?52.9 (2008): 719-726.
  • Samet, James M., et al. "Concentrated ambient ultrafine particle exposure induces cardiac changes in young healthy volunteers."?American journal of respiratory and critical care medicine?179.11 (2009): 1034-1042.
Evidence Behind Reducing exposure to pesticides can prevent many health problems.
Sales of organic food and beverage has been growing exponentially over the years as people are becoming more aware of their benefits. Although there are numerous studies that claim that organic produce contains a greater number of beneficial vitamins and minerals, important antioxidant phytochemicals, and ultimately greater health benefits than their non-organic counterparts, one of the most important components is the absence of harmful chemicals in food products.
Despite the fact that there are rigorous tests that need to be done before a pesticide is considered legal and safe for consumer use, a European assessment on toxicity found that of the 276 legally marketed active substances in Europe indicate that 32 out of the 76 fungicides, 25 out of the 87 herbicides and 24 out of the 66 insecticides are related to at least one health effect (including cancer causing, endocrine disrupting, reproductive and developmental toxicity and acute toxicity). Europe has since imposed harsher cut-off criteria resulting in the removal of many pesticides proven to be harmful, but the long-terms effects of consumption of these pesticides before they were removed from the market is unknown. Similarly, we are unsure of the long term effects of pesticides currently approved that may not have yet been properly investigated.
And although Europe has imposed stricter regulations, there are many countries where harmful pesticides are still in use or products cultivated with such chemicals are imported into countries that have stricter regulations. Furthermore, people are often exposed to residues found on food made from non-organic foods and even drinking water and the true extent to which the cumulative effects of exposure affects human and environmental health is not yet known.
References
  • EPA. Registering Pesticides (2009). http://www.epa.gov/pesticides/regulating/re-gistering/index.htm
  • Karabelas, A. J., et al. "Impact of European legislation on marketed pesticides?A view from the standpoint of health impact assessment studies." Environment International 35.7 (2009): 1096-1107.
  • EMI.?Interpretation in Sweden of the Impact of the "Cut-off" Criteria Adopted in the Common Position of the Council Concerning the Regulation of Placing Plant Protection Products on the Market (Document No 11119/08); Swedish Chemicals Agency: Sundbyberg, Sweden, 2008; p. 14.
  • Matthews, Graham. Pesticides: health, safety and the environment. John Wiley & Sons, 2015.
Evidence Behind Reducing the risk for dementia is possible through exposomics research.
Exposomics is a relatively new approach to using big data to assess the gene-environment interaction in relation to a specific condition. Non-genetic exposures include variations within the body (like the metabolism and gut flora, the stability of the endocrine system and its relative hormones, the morphology of the body, levels of inflammation and oxidative stress, etc.) as well as outside the body (like chemical contamination, radiation, environmental pollution, etc). Pooling this giant amount of data isn't easy, but efforts like the Alzheimer's Disease Big Data DREAM Challenge which launched in 2014 have begin to pave the way.
The Toxin-Toxin-Target Database (T3DB) provides a summary on over 3000 toxic substances and their potential health effects. Recent evidence indicates that endogenous uremic toxins account for a significant portion of kidney-related dementia. Environmental toxins are another significant contributor to the risk of neurodegenerative diseases and can include heavy metals like mercury and arsenic, radiation, among many others. Finally, endocrine and metabolic dysfunction can expose the body to unwanted toxins it creates. Well outlined in Ghosh's review, these can include very high or very low thyroid stimulating hormones, high amounts of steroid hormones and carbon monoxide.
There is no simple exposomic link to dementia but we are becoming increasingly aware of the bits and pieces that can have direct, indirect and cumulative influences on dementia and neural health.
References
  • https://www.synapse.org/#!Synapse:syn2290704/wiki/60828
  • www.t3db.ca
  • Bugnicourt, Jean-Marc, et al. "Cognitive disorders and dementia in CKD: the neglected kidney-brain axis." Journal of the American Society of Nephrology 24.3 (2013): 353-363.
  • Olewe, Tom HAM. "Environmental Toxins as Causes of Brain Degeneration in Sub-Saharan Africa." Brain Degeneration and Dementia in Sub-Saharan Africa. Springer New York, 2015. 65-74.
  • Gerhardsson L, Lundh T, Minthon L, Londos E. Metal concentrations in plasma and cerebrospinal fluid in patients with Alzheimer's disease.?Dement Geriatr Cogn Disord.?2008;25:508?15.
  • Eicher T, Avery E. Toxic encephalopathies.?Neurol Clin.2005;23:353?76.
  • Brown PD, Buckner JC, Uhm JH, Shaw EG. The neurocognitive effects of radiation in adult low-grade glioma patients.?Neuro Oncol.2003;5:161?7.
Evidence Behind Depending on where you live, you may be exposed to toxic arsenic.
Arsenic contamination of groundwater is widespread and there are a number of regions where arsenic contamination of drinking-water is significant so knowing where you are and the quality of the water available is important in preventing potential ailments.
In the 1990's, for instance well-water in the Bengal delta became a major problem that caused massive exposure to high levels of arsenic in the drinking water. Thought there has been much improvement since, the WHO estimates that 45 million people in Bangladesh are still at risk of being exposed to levels higher than the guideline of 10 μg/litre.
Since arsenic in groundwater is largely the result of minerals dissolving from weathered rocks and soils, concentrations can be elevated almost anywhere and it's a matter of tracking these areas and implementing safety protocols to prevent exposure. In the United States, the West, the Midwest, parts of Texas, and the Northeast are reported to have areas of concern. High risk areas in China include the Xinjiang province and Hetao-Huhhot basin as well as some aras in the Quaidam basin.
But since arsenic enters the food chain mainly through contaminated water and soil, it is of no surprise that food sources may also be contaminated, meaning that a local issue can be spread across the world.
Dietary exposure to inorganic arsenic was extensively studied in Europe and found that the highest source of exposure for adults came from wheat-based breads, followed by rice. This reflects the water management needs of grains, especially rice from flooded paddies, and the unique physiology of plants that allows it to soak up and accumulate arsenic from ground water. Though scientists are examining cultivars and mapping grain arsenic sources while also looking at genetic modifications to reduce arsenic accumulation in grains, it may be worthwhile looking at PH360's shopping tips to easily know which types of rice are safest for now.
References
  • Flanagan, SV, Johnston RB and Zheng Y (2012). Arsenic in tube well water in Bangladesh: health and economic impacts and implications for arsenic mitigation. Bull World Health Organ?90:839-846.
  • Naujokas, Marisa F., et al. "The broad scope of health effects from chronic arsenic exposure: update on a worldwide public health problem."Environmental Health Perspectives (Online)?121.3 (2013): 295.
  • Rodriguez-Lado, Luis, et al. "Groundwater arsenic contamination throughout China." Science 341.6148 (2013): 866-868.
  • Zhu, Yong-Guan, Paul N. Williams, and Andrew A. Meharg. "Exposure to inorganic arsenic from rice: a global health issue?."?Environmental pollution154.2 (2008): 169-171.
  • European Food Safety Authority (EFSA) "Dietary exposure to inorganic arsenic in the European population". EFSA Journal 2014;12(3):3597
  • Yoon, Youngdae, Woo-Mi Lee, and Youn-Joo An. "Phytotoxicity of arsenic compounds on crop plant seedlings."?Environmental Science and Pollution Research?22.14 (2015): 11047-11056.
  • Rai A, Tripathi P, Dwivedi S, et al. Arsenic tolerances in rice (Oryza sativa) have a predominant role in transcriptional regulation of a set of genes including sulphur assimilation pathway and antioxidant system. Chemosphere 2011;82:986-95.
  • Norton, Gareth J., et al. "Genome wide association mapping of grain arsenic, copper, molybdenum and zinc in rice (Oryza sativa L.) grown at four international field sites." PloS one 9.2 (2014): e89685.
  • Song, Won-Yong, et al. "A rice ABC transporter, OsABCC1, reduces arsenic accumulation in the grain." Proceedings of the National Academy of Sciences 111.44 (2014): 15699-15704.
Evidence Behind The air you breathe at home could be contaminated.
The radiation dose provided by radon gas and its decay products is about 40% of the total exposure for the average population, but can be much greater for people living in areas with high uranium in the ground. In the USA radon in the indoor air contributes to about 20,000 lung cancer deaths each year. Only smoking causes more lung cancer deaths. Countries of great concern include Mexico, Sweden, Finland, Luxemburg, Slovakia, the Czech Republic, Montenegro, Albania, Armenia and Macedonia. However, other areas may be worth testing.
International efforts to map indoor radon levels, like the WHO's International Radon Project, are in effect but finding high quality reliable and up to date data on all countries has proven to be a difficult task. Additional efforts to help bring awareness of exposure risk to natural radioactivity caused by different sources, including cosmic radiation, terrestrial gamma radiation and water are also taking place in projects like the European Atlas of Natural Radiation. Though PH360 has not yet been able to include exposure to radioactivity in its algorithms, Shae's more mobile version will be able to include local data on exposure risks.
References
  • Appleton, D. J. (2005). Radon in air and water. In O. Selinus, B. Alloway, J. A. Centeno, R. B. Finkelman, R. Fuge, U. Lindh, & P. Smedley (Eds.), Essentials of medical geology?impacts of the natural environment on public health (pp. 227-262). London: Elsevier Academic Press.
  • Cosma, Constantin, et al. "Soil and building material as main sources of indoor radon in B?i?a-?tei radon prone area (Romania)."?Journal of environmental radioactivity?116 (2013): 174-179.
  • Carneiro, G. L., et al. "Radon in indoor concentrations and indoor concentrations of metal dust particles in museums and other public buildings."?Environmental geochemistry and health?35.3 (2013): 333-340.
  • Tollefsen, T., et al. "From the European indoor radon map towards an atlas of natural radiation."?Radiation protection dosimetry?162.1-2 (2014): 129-134.
  • Bossew, P., et al. "Status of the European Atlas of Natural Radiation."?Radiation protection dosimetry167.1-3 (2015): 29-36.
Evidence Behind Knowing air conditions contributes to health risk estimates.
Botswana, Mongolia, Pakistan, Senegal, Egypt, Bosnia, Saudi Arabia, Iran, United Arab Emirates, Nigeria, Nepal, Kuwait, India and Bangladesh are among the countries with the highest amount of air pollution, according to the World Health Organization. Using annual mean concentration of particulate matter (PM10 and PM2.5, i.e. particles smaller than 10 or 2.5 microns), outdoor air pollution from almost 1600 cities in 91 countries was compared between 2008 and 2013. Although some countries like America provide data on their air quality frequently and from a wide number of cities, relatively little known about other large countries like Russia and the heavily populated countries like China.
In addition, the data shows that air quality is not improving, rather deteriorating. This rise in city air pollution could be due to reliance on fossil fuels such as coal fired power plants, the high use of cars, moped and motorcycles instead of public transportation or non-polluting means like a bicycle, inefficient use of energy in buildings, and the use of biomass for cooking and heating. In April 2014, WHO issued new information estimating that outdoor air pollution was responsible for the deaths of some 3.7 million people under the age of 60 in 2012, resulting in one of the largest worldwide risks to health.
Knowing about local air pollution means having a better understanding of exposure risks that can become health risks, including lung problems and the potential development of diseases such as asthma, bronchitis, emphysema, and possibly cancer, as well a heart conditions, cerebrovascular and neurodegenerative conditions.
References
  • World Health Organization. "Ambient (outdoor) air pollution in cities database 2014."?World Health Organization, Geneva?(2014).
  • World Health Organization (WHO). "Air quality deteriorating in many of the world's cities."?WHO, Geneva, Switzerland?(2014).
  • Colvile, R. N., et al. "The transport sector as a source of air pollution."Atmospheric environment?35.9 (2001): 1537-1565.
  • Wilkinson, Paul, et al. "Energy, energy efficiency, and the built environment."The Lancet?370.9593 (2007): 1175-1187.
  • Zhang, Junfeng, and Kirk R. Smith. "Household air pollution from coal and biomass fuels in China: measurements, health impacts, and interventions."Environmental Health Perspectives?(2007): 848-855.
  • World Health Organization, and World Health Organization. "Burden of disease from ambient and household air pollution."?Retrieved from: http://www.who.int/phe/health_topics/outdoorair/databases/en/ (2015).
  • Adam, Martin, et al. "Adult lung function and long-term air pollution exposure. ESCAPE: a multicentre cohort study and meta-analysis."?European Respiratory Journal?45.1 (2015): 38-50.
  • Raaschou-Nielsen, Ole, et al. "Air pollution and lung cancer incidence in 17 European cohorts: prospective analyses from the European Study of Cohorts for Air Pollution Effects (ESCAPE)."?The lancet oncology?14.9 (2013): 813-822.
  • Hoek, Gerard, et al. "Long-term air pollution exposure and cardio-respiratory mortality: a review."?Environ Health?12.1 (2013): 43.
  • Shah, Anoop SV, et al. "Global association of air pollution and heart failure: a systematic review and meta-analysis."?The Lancet?382.9897 (2013): 1039-1048.
  • Mumaw, Christen L., et al. "Microglial priming through the lung-brain axis: the role of air pollution-induced circulating factors."?The FASEB Journal(2016): fj-201500047.
  • Anderson, Jonathan O., Josef G. Thundiyil, and Andrew Stolbach. "Clearing the air: a review of the effects of particulate matter air pollution on human health."?Journal of Medical Toxicology?8.2 (2012): 166-175.
Evidence Behind Chronic stress can cause chronic pain.
Chronic stress alters the hypothalamic-pituitary-adrenal axis (HPA) which is known as the body's "stress system". The HPA controls the body's cortisol and stress hormone levels. Among the various functions of the HPA, is the release of adrenocorticotrophic hormone (ACTH), which in turn causes the adrenal cortex to release cortisol, as well as beta-endorphin, a morphine-like hormone. Both ACTH and beta-endorphin are released together in response to stress.
Endorphins are thought to be important in reducing pain during times of stress. However, long-term stress can lead to the suppression of the HPA axis in the brain, which not only leads to burnout or exhaustion, but also less pain-killing beta-endorphins and hence both perceived and actual pain.
A study on the epigenetic impact of this phenomenon revealed that chronic stress can increase the DNA methylation of the?Nr3c1?that causes issues with neurons in the L6-S2 spinal vertebra affecting organs in the pelvic area, which include the large intestine, colon, bladder and genitals. It also affects Cnr1?transcription, which is related to peripheral pain pathways and resulting in chronic neuropathic and inflammatory pain where variance in the GAD65 gene may also play a role. Increased DNA methylation in?Nr3c1promoter is tightly linked to the down-regulation of NR3C1 expression in the brain, the glucocorticoid receptor gene that influences behavior, mood, learning and memory, which can also be hindered in chronic pain conditions.
Furthermore, studies on irritable bowel syndrome (IBS) showed changes in a specific noncoding microRNAs in intestinal mucosa which can also lead to a whole gamut of painful conditions. So understanding the effects chronic stress can have on the body provides clues as to how to mediate or prevent challenging conditiongs like IBS, fibromyalgia, chronic migraines and many other conditions.
References
  • Charmandari, Evangelia, Constantine Tsigos, and George Chrousos. "Endocrinology of the stress response 1." Annu. Rev. Physiol. 67 (2005): 259-284.
  • Hong, Shuangsong, Gen Zheng, and John W. Wiley. "Epigenetic regulation of genes that modulate chronic stress-induced visceral pain in the peripheral nervous system."?Gastroenterology?148.1 (2015): 148-157.
  • Denk F, McMahon SB. Chronic pain: emerging evidence for the involvement of epigenetics.?Neuron.2012;73:435-444.
  • Descalzi, Giannina, et al. "Epigenetic mechanisms of chronic pain."?Trends in neurosciences?38.4 (2015): 237-246.
  • Won, Eunsoo, and Byung-Joo Ham. "Imaging genetics studies on monoaminergic genes in major depressive disorder."?Progress in Neuro-Psychopharmacology and Biological Psychiatry?64 (2016): 311-319.
  • Jung, Seung Ho, et al. "Molecular mechanisms of repeated social defeat-induced glucocorticoid resistance: role of microRNA."?Brain, behavior, and immunity?44 (2015): 195-206.
  • Witzmann SR, Turner JD, Meriaux SB, Meijer OC, Muller CP. Epigenetic regulation of the glucocorticoid receptor promoter 1(7) in adult rats.?Epigenetics.?2012;7:1290-1301.
  • Zhou Q, Verne GN. miRNA-based therapies for the irritable bowel syndrome.?Expert Opin Biol Ther.2011;11:991-995.
Evidence Behind Stress can make you lose a kidney.
A recent American study has found that more than 50% of Americans will experience a moderate kidney disease in their lifetime, a risk that increases with age to the point that it is higher than diabetes,?coronary heart disease and invasive cancer. Not only does the risk increase a lot with age, with most cases being in late life, but the study showed it is higher in women than men and racial discrepancies also exist.
One important risk factor for kidney conditions is chronic stress. Chronic stress can increase sympathetic nervous system activity, increase glucocorticoid secretion, and increase levels of inflammatory cytokines. All of these factors also play a role in higher risks for hypertension, diabetes, and cardiovascular disease, which have also been found to be major risk factors for chronic kidney disease (CKD).
People with CKD seem to have lower levels of the hormone, renalase which is responsible for metabolizing products of the sympathetic nervous system. It is therefore believed that chronic stressors that cause an increased sympathetic nervous system activity can exhaust the body to the points than renalase is no longer adequately produced, which sets in motion a vicious cycle.
References
  • Grams ME, Coresh J, Segev DL, Chow EKH. Lifetime incidence of CKD stages 3-5 in the United States. Am J Kidney Dis. 2013;62(2):245-252.
  • Bruce, Marino A., Derek M. Griffith, and Roland J. Thorpe. "Stress and the kidney."?Advances in chronic kidney disease?22.1 (2015): 46-53.
  • Salman, Ibrahim M. "Cardiovascular autonomic dysfunction in chronic kidney disease: a comprehensive review."?Current hypertension reports?17.8 (2015): 1-20.
  • Malyszko, Jolanta, Hanna Bachorzewska-Gajewska, and Slawomir Dobrzycki. "Renalase, kidney and cardiovascular disease: Are they related or just coincidentally associated?."?Advances in medical sciences?60.1 (2015): 41-49.
Evidence Behind How you handle stress may be an epigenetic factor.
Animal studies have found that conditions in early life can change genetic expressions in the body, including increased expression of the Nr3c1 gene which affects the glucocorticoid receptor (GR) in the hippocampus of the brain and even corticotropin releasing factor (CRF) in the hypothalamus. Such changes in DNA methylation were also found in humans. Whether the study was based on environmental adversity, childhood abuse, parental depression, traumatic childhood experiences or other critical events, early life experiences have been shown to have an epigenetic effect on the glucocorticoid receptor gene methylation.
Not only can childhood environmental conditions have a profound effect on the epigenome, but its affect on the hypothalamic-pituitary-adrenal axis (HPA) not only changes the way the brain processes stress but also the body. The HPA axis is governed by corticotropin-releasing factor (CRF) and arginine vasopressin, both of which are subject to GR regulation. This explains the findings that childhood trauma can increase HPA response to stress and overall increased stress reactivity in both men and women. Dysfunctional release of adrenocorticotropic hormone (ACTH) by the pituitary gland can alter the metabolism of fats, carbohydrates, sodium, potassium, and protein as well as blood pressure, which can obviously lead to an array of diseases.
But studies have also found that can increase the desire for comfort foods, which we know can also contribute to an epigenetic influence. Epigenetic changes have been found to be related to various diseases ranging from allergy, asthma, rheumatoid arthritis, type 2 diabetes, obesity, bowel disease, cardiovascular disease and cancer. And certain conditions, like metabolic diseases, can even be passed down to other generations, further perpetuating the epigenetic effect.
Preventative medicine is not just about the next step, but looking several steps ahead. As stress increases in modern day, stress management becomes important to consider.
References
  • Weaver, I.C., Cervoni, N., Champagne, F.A., D?Alessio, A.C., Sharma, S., Seckl, J.R. et al.?Epigenetic programming by maternal behavior.?Nat Neurosci.?2004;?7:?847?854
  • McGowan, P.O., Sasaki, A., D?Alessio, A.C., Dymov, S., Labonte, B., Szyf, M. et al.Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse.?Nat Neurosci.?2009;?12:?342?348
  • Turecki, Gustavo, and Michael J. Meaney. "Effects of the social environment and stress on glucocorticoid receptor gene methylation: a systematic review."Biological psychiatry?79.2 (2016): 87-96
  • Heim, C., Mletzko, T., Purselle, D., Musselman, D.L., and Nemeroff, C.B.?The dexamethasone/corticotropin-releasing factor test in men with major depression: Role of childhood trauma.?Biol Psychiatry.?2008;?63:?398?405
  • Heim, C., Newport, D.J., Wagner, D., Wilcox, M.M., Miller, A.H., and Nemeroff, C.B.?The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis.?Depress Anxiety.?2002;?15:?117?125
  • Frodl, Thomas, and Veronica O'Keane. "How does the brain deal with cumulative stress? A review with focus on developmental stress, HPA axis function and hippocampal structure in humans."?Neurobiology of Disease?52 (2013): 24-37
  • Nagaraja, Archana S., et al. "SnapShot: Stress and Disease."?Cell metabolism?23.2 (2016): 388-388.
  • Kyrou, Ioannis, and Constantine Tsigos. "Stress hormones: physiological stress and regulation of metabolism."?Current opinion in pharmacology?9.6 (2009): 787-793.
  • Dallman, Mary F., Norman C. Pecoraro, and Susanne E. la Fleur. "Chronic stress and comfort foods: self-medication and abdominal obesity."?Brain, behavior, and immunity?19.4 (2005): 275-280.
  • Guil S, Esteller M. DNA methylomes, histone codes and miRNAs: tying it all together. Int J Biochem Cell Biol 2009;41:87-95
  • Godfrey KM, Gluckman PD, Hanson MA. Developmental origins of metabolic disease: life course and intergenerational perspectives. Trends Endocrinol Metab 2010;21:199-205
Evidence Behind Increasing good cholestorol may not lower cardiovascular risk in everyone.
Geneticists have found that a mutation in a gene called SCARB1 can result in a person having very high levels of high-density lipoprotein cholesterol (HDL cholesterol), which is considered the good kind of cholesterol to have, but also an 80% increased risk of heart disease which is comparable to the risk increase due to smoking and other unhealthy behaviors. This genetic mutation affects about 1 in 1,700 people and seems to prevent HDL cholesterol from dumping the fat collected in the liver for processing.
Apolipoprotein A-I (apoA-I), the principal protein constituent of HDL, is synthesized and secreted by the liver and intestine, which should increases macrophage-specific RCT and decrease atherosclerosis. But in some people, the process is hindered and genome wide studies have found many genes can negatively impact HDL metabolism, including ABCA1,?APOA1,?LIPG,?LIPC,?PLTP,?LPL?and?SCARB1.
Mutations in the?ABCA1?gene, for instance, prevent HDL from forming properly due to minimal amounts of pre-β HDL and no α-migrating particles in the blood, a condition associated with Tangier's Disease. Mutations in the LIPC gene may cause a deficiency of hepatic lipase which increases levels of total plasma cholesterol, triglycerides and HDL.
There are several examples of genetic mutations that can affect how cholesterol is process, but other non-genetic factors can also play a role. Though HDL particles possess anti-atherosclerotic properties, not everyone can benefit from simply adding more Omega 3 fatty acids to their diet to increase their HDL levels and assume their subsequent risk of cardiovascular issues is lowered, for the story can get much more complicated than that.
References
  • Hancock-Cerutti, W., et al. "A deleterious mutation in scarb1 significantly alters HDL level, composition, and biological function in humans."Atherosclerosis?235.2 (2014): e46-e47.
  • Yang, Xiaoping, et al. "SCARB1 Gene Variants are Associated With the New Lipid Phenotype of Combined High HDL-C and Lp (a)."?Circulation?132.Suppl 3 (2015): A16954-A16954.
  • Y. Zhang, I. Zanotti, M.P. Reilly, J.M. Glick, G.H. Rothblat, D.J. Rader Overexpression of apolipoprotein A-I promotes reverse transport of cholesterol from macrophages to feces in vivo. Circulation, 108 (2003), pp. 661-663.
  • S.J. Nicholls, E.M. Tuzcu, I. Sipahi, P. Schoenhagen, T. Crowe, S. Kapadia,?et al. Relationship between atheroma regression and change in lumen size after infusion of apolipoprotein. J Am Coll Cardiol, 47 (2006), pp. 992-997.
  • Brunham, Liam R., and Michael R. Hayden. "Human genetics of HDL: insight into particle metabolism and function."?Progress in lipid research?58 (2015): 14-25.
  • B.F. Asztalos, M.E. Brousseau, J.R. McNamara, K.V. Horvath, P.S. Roheim, E.J. Schaefer Subpopulations of high density lipoproteins in homozygous and heterozygous Tangier disease. Atherosclerosis, 156 (2001), pp. 217-225.
  • van Acker, Bernadette AC, et al. "High HDL cholesterol does not protect against coronary artery disease when associated with combined cholesteryl ester transfer protein and hepatic lipase gene variants."?Atherosclerosis200.1 (2008): 161-167.
Evidence Behind Iron for some biotrends can be a double-edged sword.
Hepcidin is a peptide hormone predominantly synthesized in the liver and secreted in response to increases in circulating iron. Hepcidin is the ligand for ferroportin, a transmembrane protein mainly found in the plasma membrane of hepatocytes, enterocytes, and macrophages. Hepcidin-ferroportin binding stimulates receptor (ferroportin) internalization and degradation. In this way, hepcidin regulates systemic iron via posttranslational modulation of iron export from cells positioned to regulate the body's iron levels in the blood and gastrointestinal system.
At a cellular level, the transferrin-transferrin receptor-ferritin axis regulates iron import and storage or iron. The transferrin receptor (TfRc) expression is regulated by cellular iron levels. Transferrin binds iron and delivers it to the TfRc for internalization and distribution of iron within the cell. An iron-rich diet should be expected to increase hepcidin secretion, and thus decrease ferroportin expression. This would lower iron export from targeted cells, favoring iron retention and cellular contrast.
However, this could be a problem if the body has cells that naturally handle iron well or are more sensitive to iron stores. Improper use of iron and maintenance of iron homeostasis can lead to issues like cardiac iron deposition, chronic inflammation, collagen and hepatic diseases, hereditary hemochromatosis who have a genetic HFE variant C282Y genotype, type 2 diabetes in carriers of the H63D variant and increased neurotoxicity leading to neurodegenerative diseases like Alzheimer's.
In PH360, Activators are more likely to fall into this category and though they are natural carnivores who need to make sure they have adequate protein in the diet, the corollary effects of dietary iron are considered.
References
  • Miret S, Simpson RJ, McKie AT. Physiology and molecular biology of dietary iron absorption.?Annu Rev Nutr.?2003;23:283-301.
  • Hentze M, Muckenthaler M, Galy B, Camaschella C. Two to tango: regulation of mammalian iron metabolism.?Cell.?2010;142:24-38.
  • Pantopoulos K, Porwal S, Tartakoff A, Devireddy L. Mechanisms of mammalian iron homeostasis.Biochemistry.?2012;51:5705-5724.
  • Ponka P, Lok C. The transferrin receptor: role in health and disease.?Int J Biochem Cell Biol.1999;31:1111-1137.
  • Goldhawk, Donna E., et al. "The Interface Between Iron Metabolism and Gene-Based Iron Contrast for MRI."?Magnetic resonance insights?8.Suppl 1 (2015): 9.
  • Gujja, Pradeep, et al. "Iron overload cardiomyopathy: better understanding of an increasing disorder."?Journal of the American College of Cardiology?56.13 (2010): 1001-1012.
  • Piperno A. Classification and diagnosis of iron overload. Haematologica. 1998;83:447-55.
  • Hanson EH, Imperatore G, Burke W: HFE gene and hereditary hemochromatosis: a HuGE review: Human Genome Epidemiology.?Am J Epidemiol (2001)154?:193?-206.
  • Qi, Lu, et al. "HFE genetic variability, body iron stores, and the risk of type 2 diabetes in US women."?Diabetes?54.12 (2005): 3567-3572.
  • Tao, Yunlong, et al. "Disturbed Iron distribution in Alzheimer's disease serum, cerebrospinal fluid and selected brain regions: a systemic review and meta-analysis." (2013).
Evidence Behind Short intestines require different nutrition protocols.
Unlike some biotrends that have longer intestines, digest foods slowly, and need to pay attention to fermentation and bacterial balance, the reverse applies to ectomorphic, lightweight Sensors. Though most academic research has been conducted on extreme cases with abnormally short bowels (possibly post surgical), healthy individuals with shorter than average intestines can benefit from some of the research that focuses on measures of preventing malnutrition due to malabsorption, fatigue, weakness or anemia, and other conditions that result from very quick metabolisms.
For instance, fat is absorbed over a longer length of the intestine than carbohydrate or protein and this distance increases as oral intake rises. If the digestive system is shorter than average, then fat-soluble vitamins and minerals (like vitamins A, D, E, and K as well as iron, calcium, and magnesium) may not be well absorbed. When too many ions and fluids are secreted in the small and large bowel, then water and electrolytes are not properly reabsorbed, directly affecting the pH levels in the body, muscle function, and tissue regeneration.
Similarly, increased carbohydrates will ensure proper glycogen storage by the liver and muscle. In contrast, a higher fat and protein diet in this biotrend may result in lower blood sugar, concentration and fatigue after exertion than a high carbohydrate diet would, potentially related to a typical difficulty in digesting proteins that require more time to fully digest.
References
  • Booth CC, Alldis D, Read AE. Studies on the site of fat absorption: 2 Fat balances after resection of varying amounts of the small intestine in man.?Gut.?1961;2:168-174.
  • Baidya, Keshaba Nanda. "Investigation of the Effect of Individual Metabolic Differences on Workers Musculoskeletal Disorders."?Advances in Physical Ergonomics and Human Factors: Part II?15 (2014): 331.
  • Brandlin, Christopher.?Your Body, Your Genes, Your Digestion, and Your Metabolism. Xlibris Corporation, 2013.
  • Hounnou, G., et al. "Anatomical study of the length of the human intestine."?Surgical and Radiologic Anatomy?24.5 (2002): 290-294.
  • Nightingale, J., and Jeremy M. Woodward. "Guidelines for management of patients with a short bowel."?Gut?55.suppl 4 (2006): iv1-iv12.
Evidence Behind Antioxidants are beneficial in preventing neurodegenerative diseases.
Oxidative stress occurs when reactive oxygen species (ROS) accumulate in the cell and cause damage to DNA, lipids, and proteins. This can happen either through excessive production or insufficient neutralization of ROS. Genetic mutations and environmental exposures can also increase the exogenous production of free radicals or decrease endogenous antioxidant defense systems.
Nutraceuticals in foods found to have antioxidant properties that protect again neurodegenerative diseases include resveratrol (found in pistachios, grapes, some berries and cocoa), carnosic acid ND rosmarinic acid (found in rosemary or sage), and 2-propenesulphenic acid (found in garlic), who seem to be effective scavengers of DPPH radicals (a most common way to evaluate potential antioxidant effects). One especially potent antioxidant is epigallocatechin 3-gallate (EGCG) from green tea because of its effect on a wide variety of ROS, including those specifically harmful to neuronal health, including superoxide, hydroxyl radical, hydrogen peroxide, and nitric oxide. Quercetin (found in capers and apples) protects cells from damage oxidative stress caused by hydrogen peroxide, linoleic acid hydroperoxide, tert-butyl hydroperoxide, interleukin-1β and tumor necrosis factor-α.
These are just a few examples of ongoing studies of antioxidants in common foods that protect the health of neural pathways. There is a remarkable potential in the use of nutraceutical antioxidants in the protection against neurodegeneration.
References
  • Shang, Y.J.; Qian, Y.P.; Liu, X.D.; Dai, F.; Shang, X.L.; Jia, W.Q.; Liu, Q.; Fang, J.G.; Zhou, B. Radical-scavenging activity and mechanism of resveratrol-oriented analogues: Influence of the solvent, radical, and substitution. J. Org. Chem. 2009, 74, 5025-5031.
  • Miura, K.; Kikuzaki, H.; Nakatani, N. Antioxidant activity of chemical components from sage (Salvia officinalis L.) and thyme (Thymus vulgaris L.) measured by the oil stability index method. J. Agric. Food Chem. 2002, 50, 1845-1851.
  • Alamed, J.; Chaiyasit, W.; McClements, D.J.; Decker, E.A. Relationships between free radical scavenging and antioxidant activity in foods. J. Agric. Food Chem. 2009, 57, 2969-2976.
  • Galano, A.; Francisco-Marquez, M. Peroxyl-radical-scavenging activity of garlic: 2-propenesulfenic acid versus allicin. J. Phys. Chem. B 2009, 113, 16077-16081.
  • Qi, X. Reactive oxygen species scavenging activities and inhibition on DNA oxidative damage of dimeric compounds from the oxidation of (-)-epigallocatechin-3-O-gallate. Fitoterapia 2010, 81, 205-209.
  • Schroeder, E.K.; Kelsey, N.A.; Doyle, J.; Breed, E.; Bouchard, R.J.; Loucks, F.A.; Harbison, R.A.; Linseman, D.A. Green tea epigallocatechin 3-gallate accumulates in mitochondria and displays a selective antiapoptotic effect against inducers of mitochondrial oxidative stress in neurons. Antioxid. Redox. Signal. 2009, 11, 469-480.
  • Scholey, Andrew, et al. "Acute neurocognitive effects of epigallocatechin gallate (EGCG)."?Appetite?58.2 (2012): 767-770.
  • Suematsu, Namiko, Miki Hosoda, and Ko Fujimori. "Protective effects of quercetin against hydrogen peroxide-induced apoptosis in human neuronal SH-SY5Y cells."?Neuroscience letters?504.3 (2011): 223-227.
  • Alia, Mario, et al. "Quercetin protects human hepatoma HepG2 against oxidative stress induced by tert-butyl hydroperoxide."?Toxicology and applied pharmacology?212.2 (2006): 110-118.
  • Bureau, Genevieve, Fanny Longpr?, and M?G. Martinoli. "Resveratrol and quercetin, two natural polyphenols, reduce apoptotic neuronal cell death induced by neuroinflammation."?Journal of neuroscience research?86.2 (2008): 403-410.
Evidence Behind Turmeric is great for cardiovascular health, but not for everyone.
Human clinical trials have found turmeric can have beneficial effects for dyspepsia, peptic ulcer, inflammatory bowel disease, rheumatoid arthritis, osteoarthritis, uveitis, orbital pseudotumor, and pancreatic cancer among many other conditions.
The main reason for this spice's anti-inflammatory and antioxidant properties is its polyphenol called curcumin. Curcumin has been found to be able to enhance cell viability by decreasing reactive oxygen species (ROS) and inhibiting pro-apoptotic signals, inhibit of several unwanted cell signaling pathways at multiple levels, have beneficial effects on cellular enzymes, the immune system, angiogenesis, gene transcription and apoptosis.
So why isn't it good for everyone? For instance, curcumin can inhibit cyclooxygenase (COX) activity in human platelets, which would otherwise lead to blood clots common in atherosclerosis, thrombosis, and acute coronary syndromes. In addition, curcumin can lower plasma fibrinogen levels with decreased the levels of lipid peroxides and oxidized lipoproteins, thus providing additional anticoagulant activity. However, though it may not inhibit platelet aggregation as much as eugenol and capsaicin, curcumin can still thin the blood enough to render it potentially harmful in some cases, especially if thin blood is of a concern.
Another example is that high doses of turmeric (far beyond what one would cook with but more like in masses of additional supplements) can be harmful to people with gastrointestinal disorders, gallstones kidney stones, or bile duct issues because it increases calcium oxalate absorption. The soluble oxalates in turmeric bind to calcium and form insoluble calcium oxalate that causes about 75% of all kidney stones. As a cholecystokinetic agent (one that helps the gallbladder pump to keep the bile from stagnating) it is great for improving bile flow but could be harmful in cases of gallbladder obstruction.
Whether one is undergoing chemotherapy, taking prescription medicines for their blood flow, pregnant or having menstruation problems, there are many other reasons for which high amounts of turmeric in the diet may not be ideal, even if it's great for most of us.
References
  • Asher, Gary N. "Clinical utility of curcumin extract."Alternative therapies in health and medicine?19.2 (2013): 20.
  • Aggarwal, Bharat B., Young-Joon Surh, and Shishir Shishodia, eds.?The molecular targets and therapeutic uses of curcumin in health and disease. Vol. 595. Springer Science & Business Media, 2007.
  • Raghavendra, R. H., and K. Akhilender Naidu. "Spice active principles as the inhibitors of human platelet aggregation and thromboxane biosynthesis."Prostaglandins, Leukotrienes and Essential Fatty Acids?81.1 (2009): 73-78.
  • Das, Sumana Ghosh, and G. P. Savage. "Total and soluble oxalate content of some Indian spices."?Plant foods for human nutrition?67.2 (2012): 186-190.
  • Rasyid, A., and A. Lelo. "The effect of curcumin and placebo on human gall-bladder function: an ultrasound study."?Alimentary Pharmacology and Therapeutics?13.2 (1999): 245-250.
Evidence Behind IBD can be treated through diet, but the diet is different for many.
There are many studies on various dietary recommendations for IBD, yet each has their pros and cons. Probiotics are often recommended because they can help regulate immune homeostasis and improve digestion but lactose-based probiotics (like yogurt) may increase abdominal discomfort in some people. Similarly, an increase in omega 3 fatty acids can reduce intestinal inflammation, but EPA and DHA, which are found in fish, are much more biologically active forms of Omega 3 than ALA found in flaxeed.
But you don't need to saturate your diet with Omega 3 to reap its benefits for an excess can still lead to oxidative damage leading to cancer. Though Omega 3 fatty acids are essential in the diet, too much of anything isn't good. Other known anti-inflammatory foods include plenty of fruits and vegetables.
However, people with diabetes need to watch for the glycemic index of fruits and juice that can spike their blood sugar levels, people with thyroid issues may need to reduce their intake of cruciferous vegetables despite their beneficial indole content, people with some auto-immune conditions may need to avoid nightshades, despite their cancer-fighting solanine, and people with kidney or gall stones may need to avoid oxalate-rich foods like spinach, okra and rhubarb. And considering that many people with this condition may have adipokine-releasing intra-abdominal fat that result in increased metabolic or inflammatory signals, visceral fat reduction may be another important consideration for IBD conditions. Whatever the condition may be, a personalized approach to managing IBD through diet is essential.
References
  • Chia, Mantak.?Advanced Chi Nei Tsang: Enhancing Chi Energy in the Vital Organs. Inner Traditions/Bear & Co, 2009.
  • Licht, Harvey. "Intestinal Gas."?The Clinician's Guide to Acid/peptic Disorders and Motility Disorders of the Gastrointestinal Tract?(2006): 437.
  • Mata, P., et al. "Effect of dietary fat saturation on LDL oxidation and monocyte adhesion to human endothelial cells in vitro."?Arteriosclerosis, thrombosis, and vascular biology?16.11 (1996): 1347-1355.
  • Brasky, Theodore M., et al. "Plasma phospholipid fatty acids and prostate cancer risk in the SELECT trial."?Journal of the National Cancer Institute105.15 (2013): 1132-1141.
  • Muraki, Isao, et al. "Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies." (2013): f5001.
  • Fares, F. A. "The anti-carcinogenic effect of indole-3-carbinol and 3, 3?-diindolylmethane and their mechanism of action."?Med chem S?1 (2014): 2161-0444.
  • Cho, Young Ae, and Jeongseon Kim. "Dietary factors affecting thyroid cancer risk: a meta-analysis."?Nutrition and cancer?67.5 (2015): 811-817.
  • Prousky, Jonathan E. "The use of Niacinamide and Solanaceae (Nightshade) Elimination in the Treatment of Osteoarthritis."?JOM?30.1 (2015): 13.
  • Sun, Hongwei, et al. "Solanine induces mitochondria-mediated apoptosis in human pancreatic cancer cells."?BioMed research international?2014 (2014).
  • Penniston, Kristina L. "Dietary oxalate and calcium oxalate stones: a theoretical or real concern?."?Practical Controversies in Medical Management of Stone Disease. Springer New York, 2014. 7-28.
  • Ortu?o Sahag?n, D., et al. "Modulation of PPAR-γ by nutraceutics as complementary treatment for obesity-related disorders and inflammatory diseases."?PPAR research?2012 (2012).
Evidence Behind Wellbeing can add 4 to 10 years to your life.
There are many factors that contribute to positive psychology, including positive moods such as joy, happiness, and energy, as well as characteristics such as life satisfaction, hopefulness, optimism, and sense of humor, all of which have been associated with a reduced risk in mortality in a meta analysis on 35 studies. This has been substantiated by other meta analyses on wellbeing and longevity.
One meta analysis on 24 studies out of 49 that passed quality standards estimated a 14% increase in longevity for happy versus unhappy people, even with the considerations of economic standards and other effects that may contribute to having a longer life. This matched another meta analysis on 225 papers that were reviewed. Of the longitudinal studies in this selection, the researchers found an 18% improvement in mental health, physical health and longevity for those who were defined as happy. They also found happiness preceded having fulfilling and productive work by 24% and having satisfying relationships by 21%.
One review on a small number of longitudinal studies estimated that the 7.5 to 10 years can be added to one's lifespan, thanks to happiness and its effect on preventative health care. To quote them, "Happy people live longer, probably because happiness protects physical health." This is where PH360 strongly falls in and emphasizes the need for happiness, self-satisfaction, overall wellbeing and positive mood and energy as a contributor to lifelong health and disease prevention.
References
  • Chida, Y., & Steptoe, A. (2008). Positive psychological well-being and mortality: A quantitative review of prospective observational studies. Psychosomatic Medicine, 70, 741?756.
  • Howell, R.T., Kern, M.L., & Lyubomirsky, S. (2007). Health benefits: Meta-analytically determining the impact of well-being on objective health outcomes. Health Psychology Review, 1, 83?136.
  • Lyubomirsky, S., King, L., & Diener, E. (2005). The benefits of frequent positive affect: Does happiness lead to success? Psychological Bulletin, 131, 803?855.
  • Veenhoven, R. (2008). Healthy happiness: Effect of happiness on physical health and the consequences for preventive health care. Journal of Happiness Studies, 9, 449?469.
Evidence Behind Depression and anxiety can literally break your heart.
In a meta-analysis of 11 studies examining whether depression predicts coronary heart disease, in was reported that depression predicted cardiovascular disease in initially healthy people. Those who were clinically depressed had a higher risk (2.69 risk ratio) than those who were considered to have a depressed mood (risk ratio of 1.49).
Anxiety seems to also be a contributor, much like depression. In a review of literature based on a rigorous quality filter, all of the 11 prospective studies on depression and anxiety predicted coronary heart disease in healthy people, and all of the 6 studies on people with existing cardiovascular disease predicted disease progression. However, a later study concluded that although depression is consistently related to impaired cardiovascular health, negative emotions may play a stronger role in disease development than in progression, meaning it could affect healthy people without a condition more than it could in those who already have an ailment. They also concluded that depression, anxiety, and anger can all influence health in unison, in interaction, or independently.
There is strong evidence that wellbeing is predictive of cardiovascular disease in healthy populations, affecting the neuroendocrine, cardiovascular, and inflammatory systems, with positive psychology and wellbeing being repeatedly found as protective factors and can even undo the effects of negative emotions.
References
  • Rugulies, R. (2002). Depression as a predictor for coronary heart disease. American Journal of Preventive Medicine, 23, 51?61.
  • Hemingway, H., & Marmot, M. (1999). Psychosocial factors in the aetiology and prognosis of coronary heart disease: Systematic review of prospective cohort studies. British Medical Journal, 318, 1460?1467.
  • Nabi, H., Kivimaki, M., De Vogli, R., Marmot, M.G., & Singh-Manoux, A. (2008). Positive and negative affect and risk of coronary heart disease: Whitehall II prospective cohort study. British Medical Journal, 337, 32?36.
  • Suls, J., & Bunde, J. (2005). Anger, anxiety, and depression as risk factors for cardiovascular disease: The problems and implications of overlapping affective dispositions. Psychological Bulletin, 131, 260?300.
  • Steptoe, A., Wardle, J., & Marmot, M. (2005). Positive affect and health-related neuroendocrine, cardiovascular, and inflammatory processes. Proceedings of the National Academy of Sciences, USA, 102, 6508?6512.
  • JK Boehm, LD Kubzansky (2012). The heart's content: the association between positive psychological well-being and cardiovascular health. Psych Bull, 138, 655?691
  • Fredrickson, B. L., Mancuso, R. A., Branigan, C., & Tugade, M. M. (2000). The undoing effect of positive emotions. Motivation and Emotion, 24, 237?258.
Evidence Behind Happiness can lead to success.
Success can be defined in many ways, including job satisfaction, income, productivity and contribution to what is deemed valuable by society, and so forth. Research has repeatedly found that happiness can be a great positive contributor to increased success in life on various domains.
In a meta-analysis of 27 studies, researchers found a 10%-25% of variance in job satisfaction was related to positive affect. Another meta analysis examining longitudinal studies found that social wellbeing, which includes life satisfaction, happiness, positive affect, can lead to job satisfaction (moreso than the other way around). Since studies have found that job satisfaction is related to increased pay, organizational commitment, job promotions and even feeling healthy, all of which are elements of overall success.
Furthermore, one meta analysis on cross-sectional, longitudinal, and experimental studies of the relationship between happiness and career success found no direct relationship but many indirect relationships. For instance, happiness was found to be related to job satisfaction, work autonomy, better performance, provision of support to coworkers and more cooperation, while it was also found to be mean one would be less likely to absent from work, unengaged in work or unemployed. All of these factors indirectly lead to one's potential for career success.
No matter how it's examined, happy people have an advantage over unhappy people in many aspects, including success. Promoting happiness, wellbeing and satisfaction are important considerations in the overall success one can have in life.
References
  • Connolly, J. J., & Viswesvaran, C. (2000). The role of affectivity in job satisfaction: A meta-analysis. Personality and Individual Differences, 29, 265?281.
  • Bowling, Nathan A., Kevin J. Eschleman, and Qiang Wang. "A meta?analytic examination of the relationship between job satisfaction and subjective well?being."?Journal of Occupational and Organizational Psychology?83.4 (2010): 915-934.
  • Judge, Timothy A., et al. "The relationship between pay and job satisfaction: A meta-analysis of the literature."?Journal of Vocational Behavior?77.2 (2010): 157-167.
  • Aziri, Brikend. "Job satisfaction: A literature review."?Management research and practice?3.4 (2011): 77-86.
  • Kosteas, Vasilios D. "Job satisfaction and promotions."?Industrial Relations: A Journal of Economy and Society?50.1 (2011): 174-194.
  • Fischer, Justina AV, and Alfonso Sousa-Poza. "Does job satisfaction improve the health of workers? New evidence using panel data and objective measures of health." (2008).
  • Boehm, Julia K., and Sonja Lyubomirsky. "Does happiness promote career success?."?Journal of career assessment?16.1 (2008): 101-116.
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