The Internet Journal of Biological Anthropology ISSN: 1939-4594
Investigating potential hormonal associations of grandmaternal care in Jamaica
Peter B. GrayDepartment of Anthropology, 4505 S. Maryland Parkway Box 455003, University of Nevada, Las Vegas, Las Vegas, NV, 89154-5003, USA
Maureen Samms-VaughanSection of Child Health, University of the West Indies, Mona, Jamaica
Citation: P.B. Gray, M. Samms-Vaughan: Investigating potential hormonal associations of grandmaternal care in Jamaica. The Internet Journal of Biological Anthropology. 2010 Volume 4 Number 1. DOI: 10.5580/104c
Keywords: Allocare, Caribbean, childcare, oxytocin, vasopressin, prolactin, social relationships, parenting
There has been increasing scholarly interest in the role of grandmothers in human evolution and cross-culturally. An unaddressed question is the proximate mechanisms associated with human grandmaternal care. Here, we report on results of a naturalistic study conducted in greater Kingston, Jamaica designed to test for between- and within-subject effects of grandmaternal care on women’s cortisol, oxytocin, vasopressin, and prolactin levels. We recruited 25 women who lived with and provided care for a biological grandchild aged five or younger (grandmothers) in addition to 20 women of similar ages, socioeconomic status, and health status who did not similarly provide such care (controls). Women were aged 50-67 and postmenopausal. Interviews and biological sample collection took place either in women’s homes or a nearby church. While control women participated on a single day, grandmothers participated on two days: one day when they had been caring for their youngest grandchild the previous four hours, and another day when not providing such care the previous four hours. Hormonal data revealed that grandmothers had significantly higher vasopressin levels than control women, but did not exhibit differences in cortisol, oxytocin, and prolactin compared with control women. Results also revealed no significant differences in hormone levels on days grandmothers provided vs. did not provide care the previous four hours. Findings from this first study investigating hormones associated with grandmaternal care can be situated in light of the comparative physiology of affiliative behavior and methodological considerations.
Wikipedia: Arginine vasopressin (AVP), also known as vasopressin, argipressin orantidiuretic hormone (ADH), is a neurohypophysial hormone found in mostmammals. Its two primary functions are to retain water in the body and to constrict blood vessels. Vasopressin regulates the body’s retention of water by acting to increase water absorption in the collecting ducts of the kidney nephron. Vasopressin increases water permeability of the kidney’s collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane. Vasopressin is a peptide hormone that controls the reabsorption of molecules in the tubules of the kidneys by affecting the tissue’s permeability. It also increases peripheral vascular resistance, which in turn increases arterial blood pressure. It plays a key role in homeostasis, by the regulation of water, glucose, and salts in the blood. It is derived from a preprohormone precursor that is synthesized in thehypothalamus and stored in vesicles at the posterior pituitary. Most of it is stored in the posterior pituitary to be released into the bloodstream. However, some AVP may also be released directly into the brain, and accumulating evidence suggests it plays an important role in social behavior, sexual motivation and bonding, and maternal responses to stress.
Web edition: March 20, 2013
Print edition: April 6, 2013; Vol.183 #7 (p. 18)
Now, animal studies and a smattering of human data suggest such prenatal effects could reach farther down the family tree: The vices, virtues, inadvertent actions and accidental exposures of a pregnant mother may pose health consequences for her grandchildren and great-grandchildren, and perhaps even their offspring.
Scientists have long known that radiation or certain chemicals can cause typos in a developing fetus’s genome — his or her genetic instruction book. Such mutations can get passed along to future generations in the DNA of sperm or egg cells. While exposure to sex hormones or a high-fat diet in the womb doesn’t directly change or damage DNA, those sorts of exposures can induce scribblings in the genome’s margins that can also be passed down.
The resulting health effects are not produced by altering DNA itself. Rather they stem from changes in chemical tags on DNA or its associated proteins, or to actions by RNA, another type of genetic molecule. All of these are exactly the types of changes that scientists have always assumed cannot be inherited. Their very name, epigenetic, literally means “over and above” or “beyond” genetics.
Source: M.K. Skinner/Nature 2010; Art: S. Egts
When these changes are inherited, scientists have found, the implications can be staggering. Part of your risk of disease may be determined by what your great-grandparents ate, not just the genes they passed on. Some researchers even believe that the long-lasting effects of these chemical marks helped shape human evolution.
Stuck for generations
Investigating how those marks travel to future generations is a new twist in the field of epigenetics. Originally, epigenetics researchers focused on the developmental processes that allow individual cells to specialize despite the fact that all the cells have the same DNA. It turned out that chemical tags that get stuck to DNA or to the proteins around which DNA is wound can influence gene activity without altering the genes themselves.
Some of those chemical tags highlight passages in the genome, typically so that particular genes will be turned on. Other tags work more like a censor’s black marker, redacting some genes so that they will be shut off. Chemically underscoring or crossing out different combinations of genes creates the various types of cells that populate the body.
Until fairly recently, scientists have thought that every new generation starts with its own freshly printed genome, devoid of epigenetic embellishments. That’s because shortly after fertilization, vestiges of epigenetic tags hanging from the DNA of eggs and sperm are wiped away, leaving a clean slate. New marks are made as the embryo develops, and over the course of a lifetime some can change. But then scientists began to document cases in which inheritance of a particular trait did not follow the usual rules of genetics, hinting that at least some epigenetic marks may be carried on to new generations.
Michael Skinner was among the first to document that certain chemicals could produce health effects across multiple generations without altering DNA. Exposing a pregnant rat to chemicals that disrupt the action of sex hormones could produce fertility problems that lasted at least to her great-great-grandchildren’s generation, his group reported in Science in 2005. Those problems were transmitted through the male line, apparently by way of chemical tags called methyl groups on DNA. (Many researchers study DNA methylation because it is more easily examined than other epigenetic tags, of which there are many.)
“At first everybody thought this was the greatest thing since sliced bread,” recalls Skinner, of Washington State University in Pullman. “But then the implications started to sink in.”
Introduction By Peter B. Gray. and Maureen Samms-Vaughan
The endocrine system plays a role in one’s hormone it is made up of several glands which are the pituitary gland, pineal gland, thyroid gland, and adrenal glands also the pancreas, gonads, and parathyroids. The pituitary gland also known as the “master gland” influences one’s blood pressure, thirst, sexual behavior, and the body growth. The pineal gland helps to regulate the sleep and wake cycle. The thyroid gland regulates the body’s rate of metabolism, it also alerts and energetic people on how the body should look like as in thin or fat. Adrenal gland has two parts the inner and outer which affects one’s body to stress. The gonads which are the testes in male and ovaries in females play a number of roles in the human development. Males between the ages 15 and 25 tend to show more aggressive behaviors while the female tends to show more signs of nesting. A parathyroid control and also helps balance the levels of calcium in the human body. Pancreas controls the level of sugar in one’s body which secrets’ two regulating hormones (Morris & Maisto 2010).
The human behavior is made up of several hormones that are a part of the genetic make- up of heredity. Heredity is already in our genes from conception. The hormones can be an uncontrollable chemical balance in one’s weight, lifestyle, and weight. The chemical sends messages to the brain which causes one to react in certain circumstances. Children inherit different things from their parents or great grandparents whether it is eye color, intelligent, or the way he or she acts. Some of these traits can reappear from generation to generation in a predictable pattern. Nucleus of each of the cells contains chromosomes which is a tiny thread like bodies that carry genes which is the basic unit of heredity. Heredity and hormones can influence an individual’s behavior. Genes do not affect the way a person acts it affects the development and operation of the nervous system along with the endocrine…[continues]
- Grandma’s Experiences Leave a Mark on Your Genes
Grandma’s Experiences Leave a Mark on Your Genes
Your ancestors’ lousy childhoods or excellent adventures might change your personality, bequeathing anxiety or resilience by altering the epigenetic expressions of genes in the brain.
By Dan Hurley|Tuesday, June 11, 2013
RELATED TAGS: GENES & HEALTH
And then, in 1992, two young scientists following in Freud’s and Darwin’s footsteps actually did walk into a bar. And by the time they walked out, a few beers later, they had begun to forge a revolutionary new synthesis of how life experiences could directly affect your genes — and not only your own life experiences, but those of your mother’s, grandmother’s and beyond.
Now, at the bar in Madrid, Szyf and Meaney considered a hypothesis as improbable as it was profound: If diet and chemicals can cause epigenetic changes, could certain experiences — child neglect, drug abuse or other severe stresses — also set off epigenetic changes to the DNA inside the neurons of a person’s brain? That question turned out to be the basis of a new field, behavioral epigenetics, now so vibrant it has spawned dozens of studies and suggested profound new treatments to heal the brain.
According to the new insights of behavioral epigenetics, traumatic experiences in our past, or in our recent ancestors’ past, leave molecular scars adhering to our DNA. Jews whose great-grandparents were chased from their Russian shtetls; Chinese whose grandparents lived through the ravages of the Cultural Revolution; young immigrants from Africa whose parents survived massacres; adults of every ethnicity who grew up with alcoholic or abusive parents — all carry with them more than just memories.
Like silt deposited on the cogs of a finely tuned machine after the seawater of a tsunami recedes, our experiences, and those of our forebears, are never gone, even if they have been forgotten. They become a part of us, a molecular residue holding fast to our genetic scaffolding. The DNA remains the same, but psychological and behavioral tendencies are inherited. You might have inherited not just your grandmother’s knobby knees, but also her predisposition toward depression caused by the neglect she suffered as a newborn.
Or not. If your grandmother was adopted by nurturing parents, you might be enjoying the boost she received thanks to their love and support. The mechanisms of behavioral epigenetics underlie not only deficits and weaknesses but strengths and resiliencies, too. And for those unlucky enough to descend from miserable or withholding grandparents, emerging drug treatments could reset not just mood, but the epigenetic changes themselves. Like grandmother’s vintage dress, you could wear it or have it altered. The genome has long been known as the blueprint of life, but the epigenome is life’s Etch A Sketch: Shake it hard enough, and you can wipe clean the family curse.
Meaney pursued the question of individual differences by studying how the rearing habits of mother rats caused lifelong changes in their offspring. Research dating back to the 1950s had shown that rats handled by humans for as little as five to 15 minutes per day during their first three weeks of life grew up to be calmer and less reactive to stressful environments compared with their non-handled littermates. Seeking to tease out the mechanism behind such an enduring effect, Meaney and others established that the benefit was not actually conveyed by the human handling. Rather, the handling simply provoked the rats’ mothers to lick and groom their pups more, and to engage more often in a behavior called arched-back nursing, in which the mother gives the pups extra room to suckle against her underside.
“It’s all about the tactile stimulation,” Meaney says.
In a landmark 1997 paper in Science, he showed that natural variations in the amount of licking and grooming received during infancy had a direct effect on how stress hormones, including corticosterone, were expressed in adulthood. The more licking as babies, the lower the stress hormones as grown-ups. It was almost as if the mother rats were licking away at a genetic dimmer switch. What the paper didn’t explain was how such a thing could be possible.
single picture, a photograph of two embryos in a womb.
Needing to write a thesis in the late 1970s for his doctorate in dentistry at Hebrew University of Jerusalem, Szyf approached a young biochemistry professor named Aharon Razin, who had recently made a splash by publishing his first few studies in some of the world’s top scientific journals. The studies were the first to show that the action of genes could be modulated by structures called methyl groups, a subject about which Szyf knew precisely nothing. But he needed a thesis adviser, and Razin was there. Szyf found himself swept up to the forefront of the hot new field of epigenetics and never looked back.
Until researchers like Razin came along, the basic story line on how genes get transcribed in a cell was neat and simple. DNA is the master code, residing inside the nucleus of every cell; RNA transcribes the code to build whatever proteins the cell needs. Then some of Razin’s colleagues showed that methyl groups could attach to cytosine, one of the chemical bases in DNA and RNA.
It was Razin, working with fellow biochemist Howard Cedar, who showed these attachments weren’t just brief, meaningless affairs. The methyl groups could become married permanently to the DNA, getting replicated right along with it through a hundred generations. As in any good marriage, moreover, the attachment of the methyl groups significantly altered the behavior of whichever gene they wed, inhibiting its transcription, much like a jealous spouse. It did so, Razin and Cedar showed, by tightening the thread of DNA as it wrapped around a molecular spool, called a histone, inside the nucleus. The tighter it is wrapped, the harder to produce proteins from the gene.
Consider what that means: Without a mutation to the DNA code itself, the attached methyl groups cause long-term, heritable change in gene function. Other molecules, called acetyl groups, were found to play the opposite role, unwinding DNA around the histone spool, and so making it easier for RNA to transcribe a given gene.
By the time Szyf arrived at McGill in the late 1980s, he had become an expert in the mechanics of epigenetic change. But until meeting Meaney, he had never heard anyone suggest that such changes could occur in the brain, simply due to maternal care.
“It sounded like voodoo at first,” Szyf admits. “For a molecular biologist, anything that didn’t have a clear molecular pathway was not serious science. But the longer we talked, the more I realized that maternal care just might be capable of causing changes in DNA methylation, as crazy as that sounded. So Michael and I decided we’d have to do the experiment to find out.”
Actually, they ended up doing a series of elaborate experiments. With the assistance of postdoctoral researchers, they began by selecting mother rats who were either highly attentive or highly inattentive. Once a pup had grown up into adulthood, the team examined its hippocampus, a brain region essential for regulating the stress response. In the pups of inattentive mothers, they found that genes regulating the production of glucocorticoid receptors, which regulate sensitivity to stress hormones, were highly methylated; in the pups of conscientious moms, the genes for the glucocorticoid receptors were rarely methylated.
Methylation just gums up the works. So the less the better when it comes to transcribing the affected gene. In this case, methylation associated with miserable mothering prevented the normal number of glucocorticoid receptors from being transcribed in the baby’s hippocampus. And so for want of sufficient glucocorticoid receptors, the rats grew up to be nervous wrecks.
To demonstrate that the effects were purely due to the mother’s behavior and not her genes, Meaney and colleagues performed a second experiment. They took rat pups born to inattentive mothers and gave them to attentive ones, and vice versa. As they predicted, the rats born to attentive mothers but raised by inattentive ones grew up to have low levels of glucocorticoid receptors in their hippocampus and behaved skittishly. Likewise, those born to bad mothers but raised by good ones grew up to be calm and brave and had high levels of glucocorticoid receptors.
Before publishing their findings, Meaney and Szyf conducted a third crucial experiment, hoping to overwhelm the inevitable skeptics who would rise up to question their results. After all, it could be argued, what if the epigenetic changes observed in the rats’ brains were not directly causing the behavioral changes in the adults, but were merely co-occurring? Freud certainly knew the enduring power of bad mothers to screw up people’s lives. Maybe the emotional effects were unrelated to the epigenetic change.
To test that possibility, Meaney and Szyf took yet another litter of rats raised by rotten mothers. This time, after the usual damage had been done, they infused their brains with trichostatin A, a drug that can remove methyl groups. These animals showed none of the behavioral deficits usually seen in such offspring, and their brains showed none of the epigenetic changes.
“It was crazy to think that injecting it straight into the brain would work,” says Szyf. “But it did. It was like rebooting a computer.
Despite such seemingly overwhelming evidence, when the pair wrote it all up in a paper, one of the reviewers at a top science journal refused to believe it, stating he had never before seen evidence that a mother’s behavior could cause epigenetic change.
“Of course he hadn’t,” Szyf says. “We wouldn’t have bothered to report the study if it had already been proved.”
In the end, their landmark paper, “Epigenetic programming by maternal behavior,” was published in June 2004 in the journal Nature Neuroscience.
Meaney and Szyf had proved something incredible. Call it postnatal inheritance: With no changes to their genetic code, the baby rats nonetheless gained genetic attachments due solely to their upbringing — epigenetic additions of methyl groups sticking like umbrellas out the elevator doors of their histones, gumming up the works and altering the function of the brain.
The Beat Goes On
Together, Meaney and Szyf have gone on to publish some two-dozen papers, finding evidence along the way of epigenetic changes to many other genes active in the brain. Perhaps most significantly, in a study led by Frances Champagne — then a graduate student in Meaney’s lab, now an associate professor with her own lab at Columbia University in New York — they found that inattentive mothering in rodents causes methylation of the genes for estrogen receptors in the brain. When those babies grow up, the resulting decrease of estrogen receptors makes them less attentive to their babies. And so the beat goes on.
As animal experiments continue apace, Szyf and Meaney have entered into the next great step in the study of behavioral epigenetics: human studies. In a 2008 paper, they compared the brains of people who had committed suicide with the brains of people who had died suddenly of factors other than suicide. They found excess methylation of genes in the suicide brains’ hippocampus, a region critical to memory acquisition and stress response. If the suicide victims had been abused as children, they found, their brains were more methylated.
Why can’t your friend “just get over” her upbringing by an angry, distant mother? Why can’t she “just snap out of it”? The reason may well be due to methyl groups that were added in childhood to genes in her brain, thereby handcuffing her mood to feelings of fear and despair.
Of course, it is generally not possible to sample the brains of living people. But examining blood samples in humans is routine, and Szyf has gone searching there for markers of epigenetic methylation. Sure enough, in 2011 he reported on a genome-wide analysis of blood samples taken from 40 men who participated in a British study of people born in England in 1958.
All the men had been at a socioeconomic extreme, either very rich or very poor, at some point in their lives ranging from early childhood to mid-adulthood. In all, Szyf analyzed the methylation state of about 20,000 genes. Of these, 6,176 genes varied significantly based on poverty or wealth. Most striking, however, was the finding that genes were more than twice as likely to show methylation changes based on family income during early childhood versus economic status as adults.
Timing, in other words, matters. Your parents winning the lottery or going bankrupt when you’re 2 years old will likely affect the epigenome of your brain, and your resulting emotional tendencies, far more strongly than whatever fortune finds you in middle age.
Last year, Szyf and researchers from Yale University published another study of human blood samples, comparing 14 children raised in Russian orphanages with 14 other Russian children raised by their biological parents. They found far more methylation in the orphans’ genes, including many that play an important role in neural communication and brain development and function.
“Our study shows that the early stress of separation from a biological parent impacts long-term programming of genome function; this might explain why adopted children may be particularly vulnerable to harsh parenting in terms of their physical and mental health,” said Szyf’s co-author, psychologist Elena Grigorenko of the Child Study Center at Yale. “Parenting adopted children might require much more nurturing care to reverse these changes in genome regulation.”
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Cliford Saron, PhD, at the UC Davis MIND Institute – his group and UCSF found changes in telomeres with meditation.
Volume 36, Issue 5, June 2011, Pages 664–681
Telomerase activity is a predictor of long-term cellular viability, which decreases with chronic psychological distress (Epel et al., 2004). Buddhist traditions claim that meditation decreases psychological distress and promotes well-being (e.g., Dalai Lama and Cutler, 2009). Therefore, we investigated the effects of a 3-month meditation retreat on telomerase activity and two major contributors to the experience of stress: Perceived Control (associated with decreased stress) and Neuroticism (associated with increased subjective distress). We used mediation models to test whether changes in Perceived Control and Neuroticism explained meditation retreat effects on telomerase activity. In addition, we investigated whether two qualities developed by meditative practice, increased Mindfulness and Purpose in Life, accounted for retreat-related changes in the two stress-related variables and in telomerase activity.
Retreat participants (n = 30) meditated for ∼6 h daily for 3 months and were compared with a wait-list control group (n = 30) matched for age, sex, body mass index, and prior meditation experience. Retreat participants received instruction in concentrative meditation techniques and complementary practices used to cultivate benevolent states of mind (Wallace, 2006). Psychological measures were assessed pre- and post-retreat. Peripheral blood mononuclear cell samples were collected post-retreat for telomerase activity. Because there were clear, a priori hypotheses, 1-tailed significance criteria were used throughout.
Telomerase activity was significantly greater in retreat participants than in controls at the end of the retreat (p < 0.05). Increases in Perceived Control, decreases in Neuroticism, and increases in both Mindfulness and Purpose in Life were greater in the retreat group (p < 0.01). Mediation analyses indicated that the effect of the retreat on telomerase was mediated by increased Perceived Control and decreased Neuroticism. In turn, changes in Perceived Control and Neuroticism were both partially mediated by increased Mindfulness and Purpose in Life. Additionally, increases in Purpose in Life directly mediated the telomerase group difference, whereas increases in Mindfulness did not.
The Lancet, Volume 366, Issue 9499, Pages 1769 – 1770, 19 November 2005
doi:10.1016/S0140-6736(05)67719-7Cite or Link Using DOI
Copyright © 2005 Elsevier Ltd All rights reserved.
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