Wouldn’t it be nice if we had a set of genes that coded for the biochemicals of happiness? Imagine if every one of us possessed a gene collection that, when the right genes were turned off or on, made us happy.

Being happy is what virtually everyone says they want. Even miserable people seem to be happy being miserable. Many human activities revolve around the goal of creating the conditions in which happiness can flourish. Material wellbeing, safety and security, and physical health all contribute to happiness. Spiritual practices can change our brains in ways that promote happiness.

Yet happiness is not an on-off condition like a light switch. You aren’t either miserably depressed, or ecstatic, with nothing in between. It’s more like a the dimmer on a lamp, in which the position of the slider might be at any point between total lightness and total darkness, and is usually somewhere between those two extremes. In this way it’s like our fight-or-flight response. We aren’t either in total fight-or-flight mode, or totally passive. Most of the time we’re somewhere in between. Another spectrum is the production of cortisol and DHEA in the cortex of our adrenal glands. Your body isn’t going flat out producing either one or the other. It’s producing a ratio of both hormones. Prolonged stress will lead you to produce more cortisol. Prolonged relaxation will lead you to produce more DHEA. At any given moment, you’re somewhere between the extremes.

Happiness can also be found along a continuum. At any given moment, we’re somewhere on the spectrum between ecstasy and despair. The difference between feeling slightly content and slightly discontent might only be a few clicks along the slider, not very far apart at all. The trick that happy people have learned is to push their emotional state closer to the happy end of the scale, and further away from the dark side. How do our genes figure into these endlessly variable emotional states, and what can we do to nudge our experience closer to the light side of the spectrum?

Genes and Emotional States

When emotional changes occur in the psychospiritual realm, biochemical changes occur in the body.  These biochemicals are the products of gene expression. If your body is building more white blood cells, like AIDS patients who have spiritual transformations, or you’re boosting your immune markers, like people who master the art of producing coherent heart rate patterns, the genes that code for those physiological changes must be active. When we measure the boost in a feel-good neurotransmitter like serotonin that occurs during positive experiences, it stands to reason that the underlying genes that tell our cells how to produce serotonin must be expressed.

Researchers have now published a sizeable number of reviews of studies that show a link between emotional states and genes. 1, 2, 3 They have examined the correlations between emotional disturbances like schizophrenia, depression, panic and posttraumatic stress syndrome, and gene expression, especially in the brain. They have come up with startling and compelling evidence that the patterns of gene expression in the brains of these unhappy sufferers are different from those of happier people. Emotions, it turns out, are epigenetic, and can methylate genes in parts of our brain involved in the stress response.

The process is not a one-way street, with emotions turning genes on and off. People with certain genes are more prone to unhappy emotions, though the evidence suggests that most conditions require external epigenetic triggers to stimulate these genes. A 2008 study funded by the National Institute of Mental Health found that there are genes that predispose a person to posttraumatic stress disorder (PTSD) as an adult. But PTSD is much more likely to occur in these adults if they also have a history of abuse as children. 4 It’s an external environmental event, in the form of a traumatic childhood, that provides the epigenetic stimulus to the inner environment that triggers the gene changes. Such studies, using the new technology of DNA microarrays, or gene chips, are allowing scientists to peer into the gene expression in the fight-or-flight structures of the brain, and find out how genes are different in people with various flavors of unhappiness.

Unhappy Emotions, Unhappy Brain

Moshe Szyf, PhD, discovered that nurturing by mother rats provides an epigenetic stimulus to their offspring. Nurturing alters the expression of genes in the hippocampus and other parts of the brain that govern the fight-or-flight response, giving nurtured rats a better ability to manage stressful stimuli. 5 This made Szyf curious about whether human brains would show similar changes. He speculated that schizophrenics who had suffered abuse during their childhoods would show changes in the hippocampus too.

He dissected the brains of 24 people who had donated their organs to science. Eleven of these had happy childhoods. The other 13 were very unhappy indeed: they were schizophrenics who had committed suicide.

Szyf found that many of the stress-dampening genes in the hippcampi of the unhappy people were switched off. Although the unhappy people possessed all the right genes to dampen their stress response, the genes were methylated, which suppressed their activation. A Canadian study using brain tissue collected during autopsies also found that gene suppression in the brains of people who had committed suicide was much more prevalent than in happy people who had died accidental deaths. 6

Szyf calls these suppressed genes “frozen assets,” because while they are present in the brain, they are not accessible to its owner. In a part of the brain not involved with mood, called the cerebellum, there were no significant epigenetic differences between the happy and unhappy groups. This suggested that the methylation of the mood area was a response to the unhappy childhoods the schizophrenics had suffered. 7

In a study of 177 boys incarcerated in a juvenile detention center, psychological depression, plus a gene that transports the stress neurotransmitter dopamine, were linked to unhappy and neglectful mothering. 8 Another researcher compared pregnant women who were being treated for depression using SSRI drugs with women who were depressed but not receiving the drugs and also against happy women. They found increased secretion of stress hormones like cortisol in the babies three months after they were born, with a corresponding suppression of the infants’ stress-dampening genes. 9 This research provides a potent reminder that it’s not the presence or absence of genes, alone, that determines whether or not they build the proteins for which they’re designed. We can suppress or facilitate their expression by external environmental influences.

Stress-Induced Genetic Changes

What’s particularly interesting is to compare the genes of the same people before and after a stress experience. One study compared the gene expression of medical students to their anxiety scores on a standard psychological test. A measurement of their gene expression was taken just before their licensing examinations, a time of high test anxiety for the students. It was compared with a second gene chip sample and psychological test taken nine months earlier to provide a baseline. The researchers found that during the high-stress period, 24 genes were expressed differently. The expression of stress genes tracked the students’ scores on the psychological test. 10

Another set of researchers looked at people who were lonely and depressed, and compared the expression of their entire genome with a happier group. They found 209 genes that were differently expressed in the unhappy people. The nature of the affected genes is particularly interesting. They code for, amongst other things, markers of our levels of immunity from disease. 11 So unhappy people had weakened immune systems, and were more susceptible to illness.

A research team found that depression and elevated cortisol correlates with changes in the expression of many of the genes in the limbic system of the brain, which is central to our stress response. 12 Another group examined the link between a gene that for cortisol and other aspects of the fight or flight response, and the psychological trait of anxiety. Anxious children were more likely to have this gene strongly expressed, and the children of parents who had panic disorder, a very high degree of anxiety, showed an even stronger association between behavior and gene expression 13  To translate what the researchers are saying into plain English (a language carefully avoided in scientific papers), the crazier and unhappier your family is, the more likely it is that you will be anxious and unhappy yourself, with the gene modifications to prove it.

Not only do your genes change with unhappiness, your brain wiring changes too. Jeffrey Schwartz, PhD, a neuroscientist at the University of California at Los Angles, has studied a psychological illness called OCD or obsessive-compulsive disorder. He's tracked the changes that occur in bundles of neurons in the brain when OCD is treated. Successful treatment results, literally, in a rewiring of the neural connections inside the brain. Like a house that adds wiring to the electrical connections that are used most frequently, and strips wiring away from neglected circuits, the plastic brain is in constant motion, responding to stimuli by creating new neural pathways. Unhappiness reinforces our unhappy brain wiring, and vice versa. 14 Science is catching up to where spirituality has been for thousands of years; the Buddha urged us to maintain a calm state of desireless attention to the present moment, reminding us that, “We are what we think. All that we are arises with our thoughts. With our thoughts, we make the world.”

 Psychologist > Different Diseases; Biologist > Similar Disease

 It’s interesting to notice that these epigenetic signals were provided by a wide variety of unhappy psychological conditions. Test anxiety is different from loneliness which is different from PTSD which is different from schizophrenia which is different from OCD. Yet the body seems to interpret them all as similar epigenetic stress signals. Psychology has made an art of identifying and differentiating psychological conditions. The Diagnostic and Statistical Manual of the American Psychiatric Association, currently in its fourth edition, notes hundreds of classifications of distinct emotional maladies, from “vascular dementia with delirium” (290.41) to “factitious disorder with predominantly psychological signs and symptoms (300.16).

While reductionism, the act of differentiating mental disorders into so many categories, has its uses, it’s worth remembering that the body doesn’t work that way. While all these flavors of stressed-out unhappiness may look different to a psychologist analyzing the mind, they look biochemically similar to a biologist analyzing the body.

The term “stress” was coined by German physician Hans Selye in the 1930s. As he walked the wards of his hospital, he noted that most sick people had certain common symptoms, including aches and pains, looking and feeling unwell, digestive upsets, rashes, and fever. He called this syndrome stress. When there is enough environmental pressure, whether it’s physical, emotional, electromagnetic or chemical, to produce a surge of adrenaline and cortisol in the bloodstream, then what Selye called “an alarm reaction” follows. 15 Selye went in exactly the opposite direction from the reductionist approach in the DSM-IV. He didn’t seek the highest common multiple of symptoms, instead he identified the lowest common denominators.

This makes evolutionary sense. When a wooly mammoth charged at your distant ancestor, your ancestor fought back or ran away. Anyone who hesitated was maimed or killed. Any one of a thousand different environmental epigenetic inputs—from a snake to a thorn to a scream to a lion to a spear to a poison ivy bush—would result in a single epigenetic output: activate fight-or-flight. When the woolly mammoth appeared, your ancestor didn’t sit down on a log and wonder, “Gee, is this a Specific Phobia (300.29), a Panic Disorder Without Agoraphobia (300.01), or Mood Disorder (296.90)?” and then decide which course of action to take based on that diagnosis. He simply got out of Dodge as fast as his legs would carry him.

Stress Drives Gene Expression

Once Hans Selye had developed his insights into stress as the common denominator to much illness, a Harvard physician became famous for asking the logical next question, “How can we reverse stress?” His name was Herbert Benson, and he developed a method called the Relaxation Response. This stress antidote has practitioners sit quietly for 20 minutes, filling their minds with a positive phrase or belief, and focusing on relaxing their muscles from the feet all the way up to the head. Studies showed that the Relaxation Response was able to help with many different ailments, from high blood pressure to infertility to rheumatoid arthritis to pain. “How could a single simple stress-reduction technique affect so many different conditions?” researchers wondered.

The answer had to wait till the invention of DNA microarrays at the end of the twentieth century, which made possible the study of the Relaxation Response as an epigenetic intervention. Benson took healthy subjects, and compared the differences in gene expression patterns between long-term practitioners of the Relaxation Response and non-practitioners. Then, he put the non-practitioners through an eight week training, and found that their gene expression profile had changed to substantially resemble that of the long-term practitioners. He then replicated his findings before publishing them.

Among the genes that changed were those involved with inflammation, the rate at which cells regenerate, and the scavenging of free radicals, which are a prime contributor to aging. “For hundreds of years Western medicine has looked at mind and body as totally separate entities, to the point where saying something ‘is all in your head’ implied that it was imaginary,” said Benson of the study. “Now we've found how changing the activity of the mind can alter the way basic genetic instructions are implemented.” The Benson study’s co-author says, “This is the first comprehensive study of how the mind can affect gene expression, linking what has been looked on as a soft science with the hard science of genomics.” Psychology and spirituality have been regarded as less rigorous than biology and physiology, and the scientific world is having to rethink its priorities as it discovers that invisible human emotions have profound epigenetic effects.  18

Dean Ornish, PhD, who made the cover of Time magazine for his groundbreaking discovery that diet can reverse coronary artery disease, has taken his insights one step further in a gene study published in 2008. He examined the effects of lifestyle change, including an hour a day of a stress-reduction technique such as meditation, on men with prostate cancer. The subjects had decided not to undergo conventional surgery and radiation, or hormone-based cancer treatments. Instead, for three months, they changed their lifestyles. In addition to meditation and other stress management methods, they walked for a half hour a day, and ate a diet rich in legumes, soy, fruits, whole grains, and vegetables. It came as no surprise to the researchers to learn that the men lost weight and lowered their blood pressure. But when the researchers compared prostate biopsies taken before and after, they discovered that an astonishing 501 genes had been changed in just three months. Genes associated with breast cancer and prostate cancer had shut down.

Ornish observes, “It's an exciting finding because so often people say, ‘Oh, it's all in my genes, what can I do?’ Well, it turns out you may be able to do a lot!” 19 Meditation, prayer, spiritual practice and attendance at a house of worship are all stress-reducing activities. A vibrant spiritual social life also affects life span; the hospitalization rate of churchgoers is half that of non-churchgoers. 20

Stress, emotions, spirituality and disease are inextricably linked. Scientific papers have now documented the connection between stress and many organic diseases, including heart attacks, cancer and the progression of HIV/AIDS. 21 Emotional states such as panic, hostility, depression and anger all contribute to heart attack risk. 22 The link between cancer and stress is particularly interesting, and has been shown in much research. But a recent study found receptor sites on the outside of cancer cells for adrenaline, indicating a straight-line biochemical link between stress and tumors. When we’re stressed, our bodies are flooded with cortisol and adrenaline, and this study found that cancers grew 275% faster in stressed mice than in unstressed mice. 23 The scientific consensus is that only 5% to 10% of cancers are hereditary; the rest are due to environmental factors, including stress.

In a paper entitled Spirituality and Immunity, Stephen Marini, PhD lists studies that show the following results of stress at the cellular level:

Wound healing takes nine days longer

Intercellular communication is decreased

The immune system is suppressed

Poorer inflammation response at the site of injury

Increased bacterial infections

Increased susceptibility to autoimmune diseases

Decreased ability to handle invading toxins 24

“We don’t have a pill for this,” says Moshe Frenkel, M.D., medical director of the “Place of Wellness,” the integrative medicine department at the M. D. Anderson cancer clinic in Houston, Texas, one of the most advanced cancer treatment facilities in the country. “But we do have yoga, meditation, and guided imagery.” 25 Using a de-stressing technique doesn’t just activate your happy genes, it activates your healthy genes too!

Telomeres and Lifespan

Many of the genes found in these studies were regulatory genes, regulating the expression of other genes and proteins. Regulatory biochemicals can affect thousands other genes, and the synthesis of regulatory proteins and neurotransmitters. In fruit flies, PAX6, a regulatory gene that plays a role in the development of the insects eyes, has been artificially activated under laboratory conditions. When the expression of PAX6 is induced on a the antenna of a fruit fly, it triggers the expression of some 2,500 other genes, leading to the development of an extra eye on the antenna. 26 So regulatory genes are powerful, and the effects on the body go way beyond the changes in the roughly 1% of the genome noted in the group of studies with human subjects summarized above.

Telomeres are the “tails” of genes, and they get shorter each year, from birth to death, at a constant rate that averages 1% a year. They are a marker for aging; the older the person, the shorter their telomeres. Bad lifestyle habits accelerate the process, and good ones slow it down slightly. But a pilot study by my friend and mentor Norman Shealy, MD, PhD, has shown that the process can be reversed in human beings. Norm is the founder of the American Holistic Medical Association, and the coauthor, with me, of the book Soul Medicine (www.SoulMedicine.net), which explains the world of energy medicine, and how to find and work with your ideal practitioner. In his study of the epigenetics of aging, Norm measured the telomere lengths of six subjects, then put them on a healthy diet and exercise routine, including his patented Rejuvamatrix, which produces an electromagnetic field with the same frequencies as human DNA. After three months on Norm’s program, the telomeres of his subjects had stopped getting shorter. They actually began to lengthen! After ten months, they were 2.9% longer, suggesting that we can reverse many of the signs of cellular aging by a healthy electromagnetic environment and a supportive lifestyle. 27

Analysis of 30 studies by Dutch professor Ruud Veenhoven found that happiness adds between 7 and 10 years to your lifespan. He found that happy people were more likely to control their weight, perceive illness symptoms early on, and moderate their smoking and alcohol consumption. “Chronic unhappiness activates the fight-flight response, which is known to involve harmful effects in the long run such as higher blood pressure and a lower immune response,” Veenhoven observed. 28

Not only is happiness healthy, it’s contagious. You can catch it from the people sitting next to you. A large scale study of residents of Framingham, Massachusetts, from 1983 on, noted their degree of happiness, amongst other things. Since they had such a large group, the researchers were able to analyze how happiness spread throughout the population. They found that having a friend who’s happy increases your chances of happiness by 15%. A second-degree connection, such as the happy spouse of a friend, raises your chances by 10%. And a third-degree contacts, such as the friend of a friend, increases it by 6%, after which the effect tails off. And surrounding yourself by more happy friends increases the effect. 29 Since our social networks are largely under our control, this research presents us with yet another practical leverage point over our gene expression. While dumping negative friends and seeking positive ones may be difficult after a lifetime of association, it’s a strong signal of an intention to recreate our lives in a healthier mold. And if you find positive people avoiding you after they read the Framingham study, you might be one of the unhappy people they’re avoiding—and may need to undertake what Alcoholics Anonymous calls “a fearless moral inventory!”

Choices Reverse Childhood

If you had a lousy childhood, and your stress-dampening mechanisms were epigenetically compromised, are you doomed to a lifetime of unhappiness? Here again research has some encouraging answers for us. When scientists took mice that had been nurtured early on, and deprived them as adults, they undid most of the positive effects of maternal nurturing. But when they took mice that had been neglected as newborns, and provided them with a nurturing environment, the deficits they had shown were partially reversed. 30 Other studies reflect the same possibility. One found 27 genes upregulated by a good dose of laughter! 31 This suggests that it’s never too late to give yourself a happy childhood. Surrounding yourself by nurturing people and conditions can start to reverse the methylation and acetylization patterns in your stress system.

Every minute, about one million of your cells die. An equal number of cells are born each minute. Perhaps you implanted lousy epigenetic signals into your old cells through destructive habits and emotions. But your old cells are on their way out. If you start sending new epigenetic signals to the cells that are just getting born, filling your heart with love and your mind with positive thoughts, your new cells might be healthier than the ones they’re replacing. Every single molecule in your brain is replaced every two months. Every single cell in your body is replaced every seven years. So as you give yourself a psychospiritual makeover, you give yourself an epigenetic makeover too.

This kind of genetic drift over time shows up in identical twins. They start out with exactly the same genome, and at the age of three, their genes are indistinguishable from one another. But by age 50, there are many differences in methylation, and hence gene expression. 32 They have made different emotional and spiritual choices, their lifestyles are the habits they’ve cultivated, they have different stress levels, and every cell in their body has been replaced at least seven times. Though they began life with the same genome, on average identical twins die more than ten years apart! That’s a huge difference, indicating that the choices you make have powerful epigenetic effects, at all stages of your life.

So the scientific evidence continues to pour in, and it is compelling. It tells us that where we are on that happiness scale, our emotional state, has a powerful epigenetic effect on our bodies, affecting all the major systems of our body. It also provides us with a list of the practical things we can do to nudge us toward happiness. We can use:

Positive beliefs

Spirituality

Prayers

Positive images and visualizations

Electromagnetic shifts

Optimism

Energy Medicine

Energy Psychology

Positive attitude

Acts of kindness

Meditation

Happy social networks

Gratitude

Nurturing

The exciting implication of this research is that so many of the items in this list are under our conscious control. We can change our attitude by an act of choice. We can stop ourselves speaking an unkind word. We can volunteer for a charity. Every day presents us with opportunities for altruistic acts, if we’re awake to the possibility. We can say uplifting words to the people around us, and perform small acts of service. We can pray to whatever deity speaks to our deepest longings. We can meditate. We can join a house of worship, a club, a sports team, or a support group. We can use energy medicine and Energy Psychology to quickly dissipate the emotional charge of traumatic events. We can invent stories and imagine visualizations that are positive. We can turn off our TVs, and read books that enrich our hearts. We can watch inspiring movies and listen to soothing music.

Although these consciousness-based methods are different, they all can affect the stress response. Benson says that, “We found that no matter which particular technique is used different forms of meditation and yoga, breath focus, or repetitive prayer the mechanism involved is the same.” As we use these consciousness-based techniques to shift our emotional state from anxiety to serenity, we affect our gene expression. These are all behaviors we can choose deliberately, inducing happiness, and giving us active control over the genetic markers we place on the game board of life. Your happy genes are present as potentials, and what you do with them shapes your destiny.

1. Isles, A. R. & Wilkinson, L. S. (2008). Epigenetics: What is it and why is it important to mental disease? British Medical Bulletin, 85, p. 35-45.

 2. Higgins, E. S. (2008, June). The new genetics of mental illness. Scientific American Mind, p. 41-47.

 3. Stuffrein-Roberts, S., Joyce, P. R., & Kennedy, M. A., (2008). Role of epigenetics in mental disorders. Australian and New Zealand Journal of Psychiatry, 42, p. 97-107.

 4. Binder, E. B., Bradley, R. G., et. al. (2008, March 19). Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults. Journal of the American Medical Association. 299(11), p. 1291-1305.

 5. The Economist, (2006, September 23). Learning without learning, p. 89.

 6. Poulter, M. O., et. al. (2008). GABA receptor promoter hypermethylation in suicide brain: Implications for the involvement of epigenetic processes. Biological Psychiatry, 64, p. 645-652.

 7. McGowan P. O., et. al. (2008, May). Promoter-wide hypermethylation of the ribosomal RNA gene promoter in the suicide brain. PLoS ONE. 7:3(5), p. 2085.

 8 Haeffel, G. J., et. al. (2008, January). Association between polymorphisms in the dopamine transporter gene and depression: evidence for a gene-environment interaction in a sample of juvenile detainees. Psychological Science, 19(1), p. 62-9.

 9. Oberlander, T. F., et. al. (2008). Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses. Epigenetics, 3, p. 97-106. 

 10. Kawai, T., et. al. (2007, October). Gene expression signature in peripheral blood cells from medical students exposed to chronic psychological stress, Biological Psychology, 76 (3), p.147-155.

 11. Cole, S. W., et. al. (2007, September). Social regulation of gene expression in human leukocytes. Genome Biology, 8, p. R189.

 12. Karssen, A. M., et. al. (2007, September), Stress-induced changes in primate prefrontal profiles of gene expression, Molecular Psychiatry, 12, p. 1089.

 13. Smoller, J. W., et. al. (2003, December). Association of a genetic marker at the corticotropin-releasing hormone locus with behavioral inhibition. Biological Psychiatry. 54(12), p. 1376-1381.

 14. Kim, L. (2008). Healing the Rift. New York: Cambridge House Press, p. 122.

 15. Selye, H. (1974). The Stress of My Life: A Scientist’s Memoirs (New York: Van Nostrand Reinhold).

 16. Dusek, J. A., et. al. (2008, July). Genomic counter-stress changes induced by the relaxation response. PLoS ONE. 2:3(7), p. 2576.

 17. Ornish, D., et. al. (2008, June). Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proceedings of the National Academy of Sciences, 17:105(24), p. 8369.

 18. Koenig, H. (2007). Spirituality in Patient Care. Pennsylvania: Templeton Foundation Press.

 19. Cohen, S., Janicki-Deverts, D., Miller, G. E. (2007, October). Psychological stress and disease. Journal of the American Medical Association, 10;298(14), p.1685-7.

 20. Weil, A. (2007, December). How panic hurts the heart. Dr. Andrew Weil’s Self-Healing, p. 2.

 21. Thaker, P. H., Han, L.Y, Kamat, A. A., et. al., (2006, August). Chronic stress promotes tumor growth and angiogenesis in a mouse model of ovarian carcinoma. Nature Medicine, 12(8), p. 939-44.

 22. Marini, S. C. (2008). Spirituality and immunity. Philadelphia: Marini. Unpublished Monograph, p. 4.

 23. Crute, S. (2008). The best medicine. AARP magazine. March/April. p. 62.

 24. Gehring, W. J. (2005). New perspectives on eye development and the evolution of eyes and photoreceptors. Journal of Heredity. May-Jun 96(3), p. 171-84.

 25. Shealy, C. N. (2008). RejuvaMatrix—a fundamental key to health and longevity. Norm Shealy Self-Health Systems eLetter. Dec 17. 

26. Veenhoven, R. (2008, September). Healthy happiness: effects of happiness on physical health and the consequences for preventive health care. Journal of Happiness Studies, 9:3, p. 449-469.

 27. Fowler, J. H. & Christakis, N. (2008, December). Dynamic spread of happiness in a large social network: longitudinal analysis over 20 years in the Framingham Heart Study. British Medical Journal, 4;337, p. 2338.

 28. Champage, F. A., & Meany, M. J. (2007). Transgenerational effects of social environment on variations in maternal care and behavioral response to novelty. Behavioral Neuroscience, 121, p. 1353-1363. 

 29. Hayashi, T., et. al. (2006). Laughter regulates gene expression in patients with type 2 diabetes. Psychotherapy & Psychosomatics, 75, p. 62–65.

 30. Fraga, M. F., et. al. (2005, July). Epigenetic differences arise during the lifetime of monozygotic twins. Proceedings of the National Academy of Sciences, 26:102(30), p. 10604.

  NOT USED:

Adam EK, Hawkley LC, Kudielka BM, Cacioppo JT: Day-to -day dynamics of experience - cortisol associations in a population-based sample of older adults.  Proc Natl Acad Sci USA 2006, 103:17058-17063.