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Epigenetics and the social work imperative.

Historically, social workers have been suspicious of the study of genetics, in part because of the malicious use of genetic knowledge in the eugenics movement, in which the profession played an unfortunate collaborative role (Kennedy, 2008). A partial rapprochement between social work and genetics occurred in the 1980s and 1990s, however, as new understanding of genetic diseases has highlighted the importance of the specialty practice area of genetic counseling (Rauch, 1988).

Knowledge about human genetics has grown at an astonishing rate, particularly since completion of the Human Genome Project (HGP) (National Human Genome Research Institute, 2010). The goal of the HGP was breathtaking: to map the entire human genetic code. The project was completed in 2003, and results demonstrate that humans have between 20,000 and 25,000 genes. Specific functions of many of those genes were identified, but it is not possible to identify the specific genes for most diseases, as most diseases are complex and related to the functioning of many genes. The most interesting findings of the HGP, however, turn out to be what it did not tell us: how and why specific genes are expressed.

THE HUMAN EPIGENOME

The human genome--that is, an individual's entire genetic code-is not a perfect predictor of his or her actual physiology (called the phenotype). Why do identical twins become less and less identical as they grow older (Gilbert, 2009)? Why do some women who carry the now well-known BRCA1 and BP, CA2 genetic mutations for breast cancer not develop breast cancer (Antoniou et al., 2003)? Why do only some members of monozygotic (identical) twin pairs develop schizophrenia and bipolar disorder, though a genetic connection is clear (Rosa et al., 2008)?

The answer to the above questions is epigenesis. Epigenesis is the transmission of information to new cells during cell division that determines how genes are expressed: which genes present are "turned on" and which are silenced. Experience and the environment (in the broadest sense) are major determinants of which genes are expressed and which are silenced, and as the environment changes, so may the epigenome, the system that regulates gene expression. Attention to the effects of the environment is, of course, social work's claim to fame, an attention we often cite (somewhat unfairly) as setting us apart from other professions. Nevertheless, our emerging understanding of epigenesis provides a new mandate and potential opportunity for social workers to focus on the environment.

EXPLAINING EPIGENESIS

Epigenesis occurs through biochemical processes, to which other genes, environmental exposures, experiences, and other factors contribute. Because it occurs during cell division, epigenesis may be most critical during periods of rapid growth: gestation, infancy, and puberty, as well as possibly during old age, when cells have divided many times and may be "wearing out" (Gilbert, 2009). Epigenesis causes changes in the structure of an organism (that is, the phenotype) without changing the underlying DNA (the double strand of nucleic acid that contains the genetic instructions) by altering gene expression. This point deserves emphasis: Epigenetic changes in the organism are not due to changes in the genes themselves, such as occur through mutation. Khan (2010) asserted that "epigenetics blurs the distinction between 'nature' and 'nurture' as experiences (nurture) become a part of intrinsic biology (nature)" (p. 259).

Genes direct development by determining which proteins are produced in the cells; although all cells have the same DNA, some produce proteins that direct them to become part of the eye, whereas others are directed to be liver or skin cells (Nafee, Farrell, Carroll, Fryer, & Ismail, 2007). Directions are transmitted primarily (though not exclusively) through two biochemical processes: methylation and chromatin remodeling.

In metkylation, a methyl molecule or group of molecules attaches to the DNA. Lower levels of methylation in a cell result in greater cell activity, so these added methyl groups reduce or cut off cell activity. For example, tumor suppressor cells, which intervene when cells begin to proliferate and create tumors, are highly active in the absence of methyl, but the addition of methyl groups to those cells reduces tumor suppressor activity and may contribute to cancer (Gilbert, 2009).

With chromation remodeling, there is a change in the shape of the chromatin, which is the substance that is wrapped around the DNA double helix, compressing it so some genes are inactive. When the chromatin "unwraps," the change in shape may allow some genes to be expressed that were silent before. The reverse process (deacetylation) may cause the "turning off" of some genes.

ENVIRONMENTAL INFLUENCES ON GENE EXPRESSION

That the environment is important to human development and behavior is well known to social workers, but it is useful to understand the mechanisms of this relationship. The environment is the major contributor to the two processes of epigenesis described earlier; indeed, epigenetic changes are arguably more susceptible to environmental influences than genetic changes such as mutation (Tang & Ho, 2007). Three of the most important environmental influences on gene expression are diet, exposure to chemicals, and the social environment. Each is briefly discussed in the sections that follow.

Diet

The social work profession certainly holds that adequate nutrition for all is important, but research on the connection between nutrition and gene expression clarifies just how important it is. Much of the important research has been done with animals because it is possible to use inbred strains of animals that are genetically identical and then to vary diet to observe the effects. For example, research on an inbred strain of mice (Agouti mice) has been productive for understanding obesity (Waterland & Jirtle, 2003). These mice are inbred to express a gene that causes extreme obesity and a tendency to diabetes and other diseases (in addition to a yellow coat instead of brown). However, supplementing pregnant Agouti mothers' diets with nutrients (including folate, B12, and other nutrients--not coincidentally, those included in human prenatal vitamins) leads to suppression of the Agouti gene through methylation, and resulting offspring show normal weight and disease risk and a brown coat color. These findings have led to further research demonstrating that maternal diet during gestation can lead to disease and poor health in offspring well into their adulthood (Prior, Head, & Armitage, 2011).

In humans, epidemiological research also points to significant differences in the health of populations with different types of diets. For example, a systematic review of epidemiological research around the world reveals that cultures favoring a diet that is typically consumed in the Mediterranean (rich in fruits, vegetables, legumes, and cereals; olive oil as the sole source of fat; moderate consumption of red wine, especially during meals; and low consumption of red meat) enjoy reduced cardiovascular and cancer mortality as well as lower rates of Parkinson's and Alzheimer's diseases (Soft, Cesari, Abbate, Gensini, & Casini, 2008). The differential effects of these foods on gene expression are likely to be the mechanisms for this relationship.

Nutrition matters, not just because adequate calories and protein are required to sustain life, but also because diet influences the expression of genes that either enhance or deter good health and development. Throughout the world, including the United States, poverty restricts access to nutritious food and takes its toll through higher morbidity and mortality among poor people (Drewnowski, 2009).

Moreover, Harper (2005) concluded that epigenetic changes due to diet can be passed on to future generations, and scientific evidence is mounting to confirm this conclusion (see Rothstein, Cai, & Marchant, 2009). Two natural experiments demonstrate this phenomenon. First was the famine imposed by the Nazis during World War II, in which 20,000 Dutch people starved to death (see Lumey & Van Poppel, 1994, for a discussion). Women who gave birth during this time delivered very underweight infants, as might be expected due to poor maternal nutrition and weight gain. However, when the famine ended and these children grew up to be parents, they, too, gave birth to underweight infants, despite having eaten sufficient diets most or all of their lives. These effects were then still visible in the third generation. Effects were strongest for the offspring of women who were in the third trimester of pregnancy during the famine.

The second natural experiment occurred in Overkalix, a geographically isolated Swedish village in the Arctic Circle. Analysis of meticulous records kept over hundreds of years (Kaati, Bygren, Pembrey, & Sj6str6m, 2007) demonstrated that variable food availability influenced morbidity and mortality of subsequent generations; the timing of bountiful versus scarce harvests affected rates of diabetes and cardiovascular disease in grandchildren. Moreover, effects varied by the gender of the grandparent in a process called parental imprinting; men's grandsons were most affected if the men had experienced a bountiful harvest right before puberty, whereas women's granddaughters were most affected if the bountiful harvest occurred during the grandmothers' gestations. It is important to note that accounting for the grandparents' social circumstances did not affect the results.

Both the Dutch famine and Overkalix are hypothesized to be examples of fetal imprinting, a process through which a developing fetus receives information about the environment in which it will live and adapts to survive in that environment. DNA itself is highly stable across many generations, but epigenesis might provide a means of adaptation to current environmental conditions. In times of scarce food, for example, mothers' reduced consumption results in smaller babies who will require fewer calories to survive. These infants' systems also might be "programmed" to store energy and fat for future famines, as demonstrated in Overkalix; in later years, when harvests are better, such an adaptation in fact may become detrimental, leading to increased obesity and disease (Nafee et al., 2007).

Tang and Ho (2007) generalized that when an epigenetic adaptation is consistent with the environment in which the organism lives, the organism will thrive. If there is a mismatch, however (as when the organism develops to adapt to scarcity but food is plentiful), the result is greater risk of morbidity and mortality.

Exposure to Chemicals

Exposure to chemicals is ubiquitous both outdoors and indoors; they are in the air we breathe, on the ground we walk on, and in the water we use to drink, bathe, and water crops and yards. Exposure derives from industrial, transportation, commercial, and agricultural processes, as well as from household and yard use of pesticides and other products. It is well known that exposure to toxic chemicals has major effects on gene expression. Chemical exposure has been shown to cause cancer, respiratory illnesses such as asthma, birth defects, and blood lead levels high enough to cause neurological damage. Heavy metals in particular, such as chromium, cadmium, arsenic, and nickel, are known to have damaging epigenetic effects, partly through reducing methylation (Tang & Ho, 2007). Exposure to these heavy metals is known to lead to increased risk of cancer and neurological disorders.

Baccarelli and Bollati (2009) summarized what is known from animal and human research about the epigenetic changes associated with several common toxic chemicals, including air pollutants, and endocrine disruptors, which are environmental chemicals that affect the function of the endocrine system by mimicking or blocking hormones, altering hormone signaling, or disrupting hormone production. Endocrine disruption can have profound consequences because of the crucial role hormones play in development and because they are some of the most common chemicals to which we are exposed (Skinner, Manikkam, & Guerrero-Bosagna, 2010).

Two common toxicants that have been in the news recently illustrate the risks of endocrine disruptors. Bisphenol A, or BPA, is frequently found in widely used plastic products such as baby bottles, and diethylstilbestrol (DES) is a medication that was given to many women between 1938 and 1971 to prevent miscarriages (see Tang & Ho, 2007). Both chemicals have been associated with reproductive cancers and infertility (Skinner et al., 2010). Because epigenetic changes occur in the germ line (that is the body's reproductive cells), they can be passed to subsequent generations, even when the effects are unexpressed in the parent. DES is no longer administered to prevent miscarriages, and recent campaigns have removed BPA from many products, especially baby bottles.

Toxic chemical exposure is more common for members of minority and disadvantaged populations, as their homes and neighborhoods may be targeted by industry because of the lack of political power in these populations. Thus, toxic chemical exposure is relevant to the social work profession and central to environmental justice concerns (for example, Rogge & Combs-Orme, 2003). Whereas the role of chemical exposure in genetic mutations has been referenced in social work (Rogge & Combs-Orme, 2003), Tang and Ho (2007) asserted that the epigenetic effects due to chemical exposure are more important than mutations. Moreover, as Rothstein et al. (2009) pointed out, epigenetic changes are more easily remediated (and sometimes reversed) than genetic mutations. For this reason alone, social workers should be well informed on this topic. Notably, illustrating Harper's (2005) point about fetal programming, the influence of toxic chemicals on human gene expression can persist for generations (Grandjean et al., 2007), long after chemicals have been cleaned up.

Social Environment

Perhaps of central interest to social workers is research demonstrating that the social environment can modify the expression of genes (see Meaney, 2001). Moreover, the effects may be passed to future generations.

The human response to threat occurs through a complex system of interactions in the hypothalamic--pituitary--adrenal (HPA) system. When the hypothalamus in the brain recognizes a threat, the sympathetic system communicates that information to the pituitary gland, which secretes glucocorticoids and adrenaline. These hormones lead to a cascade of effects: faster heart rate and higher blood pressure to deliver blood to the muscles (for running or fighting the threat), faster breathing to carry oxygen, and cessation of processes not necessary for immediate survival such as digestion and reproduction. The HPA system is an adaptive one that promotes survival in a dangerous environment.

One of the most valuable aspects of the stress response system is its feedback loop; when the threat subsides, the parasympathetic system returns the body to homeostasis, and the effects are reversed. In modern times, however, danger presented by wild animals has been replaced by psychological stress, which is often constant and unrelenting, and the feedback loop may become dysregulated. The physiological effects of stress continue for long periods of time, resulting in high blood pressure, rapid heartbeat, and the other physiological adaptations that are damaging and result in disease. Social workers may see this process when they work with individuals suffering from posttraumatic stress disorder such as veterans, adult survivors of childhood abuse, and others.

The stress response system begins to develop during gestation in interaction with the mother's own HPA axis. It is believed that the bath of chemicals resulting from the mother's chronic stress may result in up-regulation of the baby's own stress response system, resulting in higher baseline levels of stress hormones and a high level of reactivity (Lupien, McEwen, Gunnar, & Heim, 2009). The infant's stress system continues to develop in the first year of life, however, and a calm, nurturing environment can reduce some or all of the effects of high stress during gestation. In cases in which the mother's stress continues after the baby's birth, however, as in cases of poverty or domestic violence, for example, this remediation does not occur, and the infant may become even more reactive. High levels of stress in infancy set the infant up for poor health and are also damaging to the infant's brain, particularly the hippocampus, which plays an important role in learning (Lupien et al., 2009).

Of course, the most important environmental factor for infants is parenting, and animal research demonstrates that nurturing parenting plays a large part in the development of the stress response system, as the soothing provided by good nurturing (especially during times of stress) lowers the infant's stress response and helps the infant learn to self-regulate the response to stress.

Animal research is illustrative. Like humans, rats demonstrate a wide range of nurturing behavior, from "good" mothers who lick and groom their pups frequently to more "hands-off" mothers who seldom do so (Meaney, 2001). The offspring of more nurturing mothers are calmer and less reactive to stress than their counterparts because of the effects of the grooming (nurturing) on the rat pups' developing stress response system (as mediated by the HPA). That is, the mother rat's nurturing alters expression of the stress regulation gene inside the brains of her offspring. These offspring also later demonstrate their mothers' parenting styles. The researchers demonstrated that this behavior was brought about by the maternal grooming, and not the rat pups' genes, by "cross-fostering" the pups. That is, the babies of nurturing mothers were reared from birth by nonnurturing mothers and vice versa. In these cases, it was the type of nurturing received from the foster mothers that led to the pups' stress and later parenting behavior, rather than their genetic heritage (Meaney, 2001).

Similarly, McCrory, De Brito, and Viding (2010) suggested that epigenetic changes caused by variations in caregiving may be the mechanism behind well-demonstrated changes in brain functioning due to abuse (Roth, Lubin, Funk, & Sweatt, 2009). McCrory et al. pointed out that the genes demonstrated by research to be affected by methylation due to abuse were in the prefrontal cortex--the area that is known to be structurally and functionally altered in humans following abuse and that is so important to higher brain functions.

Research by McGowan et al. (2009) provides evidence that early life stress (in the form of childhood abuse in this case) results in epigenetic changes that damage the human stress response. They examined hippocampal tissue from the Quebec Suicide Brain Bank of 12 suicide victims with histories of childhood abuse, 12 suicide victims with no history of abuse but matched for psychiatric diagnoses, and 12 controls (matched for gender, age, and postmortem interval). Consistent with research on rats, they found methylation differences in suicide victims who had been abused but not in the two other groups. These methylation changes influence HPA activity by inhibiting the feedback loop that returns the body to homeostasis after a threat has passed. McGowan et al. asserted that their research "translate[s] previous results from rat to humans" (p. 342), suggesting a common effect of parental care on the physiology of response to stress.

POVERTY AND DISCRIMINATION: THE UNDERLYING PROBLEMS

Social workers have long been reluctant to accept the importance of the genetic influence on human development and behavior (see Strohman, 2003). How can a profession built on the idea of change accept that significant aspects of development result from something so immutable as the genetic code? Epigenesis is the bridge the profession can use to incorporate this science into practice because it demonstrates the power of the environment to regulate gene expression.

DNA does not predict destiny; it rather assembles a set of potentialities to be activated (or not) by experience and the environment. It suggests that every child may possess the raw material to make contributions to the world through music, science, art, or civic participation, or at least to learn and love and make positive contributions to society. It is quite literally true that realization of that potential depends in large part on a child's environment at home and in the family, neighborhood, and community, because elements in those environments shape which of the child's genes are expressed.

Poverty is the number-one threat to the expression of genetic potential (Guo & Stearns, 2002). Research evidence is overwhelming that poor children suffer disadvantages compared with their advantaged peers in virtually every arena, including health, cognitive and social development, mental and emotional health, and school achievement. Those disadvantages are clearly evident on the day poor children start school, and the gaps grow with each passing year (Holzer, Schanzenbach, Duncan, & Ludwig, 2007).

Moreover, the effects of poverty are long lasting; higher rates of delinquency, school dropout, and adolescent pregnancy clearly place poor children at a disadvantage with regard to achievement and quality of life as they enter adulthood (for example, Duncan, Brooks-Gunn, Yeung, & Smith, 1998). Throughout adulthood, poor individuals not only achieve and earn less, but they are less healthy and die sooner, and their contributions to society are greatly diminished (Holzer et al., 2007). In the past we have accepted that at least some of these disadvantages are genetic and, thus, outside the control even of a well-meaning society. But what if that is not the case?

We may think of epigenesis as the mechanism for how the rich get richer and the poor get poorer. That is, individuals carrying the same genetic potential (for example, tendencies toward violence or musical talent) who are exposed to vastly different environments (for example, violent neighborhoods or early musical training) are likely to experience very different outcomes as genes are expressed differentially in response to those environments. Offspring then share both the environment and the epigenetic markers of their parents, increasing the likelihood of stability of socioeconomic circumstances across generations. (Of course, this does not always happen. Our understanding of how genes are expressed is incomplete.) Remembering that the expression of genes (for good or for bad) is influenced by experience and the environment lends a new urgency to calls for social justice.

Racism, discrimination, and oppression are likely to have the same effects as poverty. (Of course, for many African Americans and other minorities, these forces are all at work.) Bums and Collins (2010) pointed to epigenesis as an explanation for the fact that rates of low-birthweight and infant mortality for African Americans are approximately twice those for their white counterparts (Heron et al., 2010). They suggested that the day-to-day realities of discrimination, such as crowded and violent housing, poor education, and poor diet may result in methylation of genes that increase the probability of premature labor. Geronimus (2002) termed this process weathering and invoked it to explain why birth outcomes are best for African American women at ages 15 to 19 (in contrast to the best rates for white women at ages 20 to 24) and deteriorate with each year of age thereafter. Although accounting for poverty reduces some of this disparity, birth outcome disadvantages (and health factors in general) are still striking for middle-class African Americans (Jackson & Cummings, 2011), who may suffer less from poverty but continue to experience racism.

Epigenetic effects of discrimination also might explain the violence in neighborhoods and communities with high concentrations of minority populations, the lower academic achievement levels of African American students, and the poorer health of African Americans, even holding social class constant. Waller's (2003) suggestion that years and generations of oppression and victimization (beginning in utero, as discussed previously, and indeed generations ago) may lower African Americans' threshold for response to stress in a process he called kindling. Again, it is possible that fetal imprinting occurs, as fetuses are programmed to be highly reactive to the stress in the dangerous, difficult world in which they will live. African Americans are only about five generations removed from slavery and fewer than 50 years from the end of Jim Crow laws.

CONCLUSION

Epigenesis provides a basis for understanding why poor and minority populations continue to lag behind in our nation, as it gives us an understanding of the mechanisms through which poverty, oppression, and disadvantage exercise their effects on physiology. Insights on epigenesis suggest that poor and minority children are not inherently inferior, damned by inferior genetics and condemned to poor health and low achievement. Indeed, Khan (2010) argued that epigenetic risk posed by poverty and racism is not merely a medical issue, but that it "more generally implicates the underlying fairness and .justice of our social contract" (p. 260).

Social work acknowledges the moral imperative of equal opportunity for all. The science is convincing that there is an economic imperative as well. Although the work we do in all arenas is important, epigenetics suggests that social workers can have their biggest influence through social policies that work hand in hand with nature to prevent the development of many of the problems that plague our nation and world, now and for generations to come. Increasingly, science is providing specific ways that epigenesis can be used to reverse some of the negative effects of poverty and discrimination; for example, Rothstein et al. (2009) described specific environmental regulations and new research on drugs that can reverse the damaging effects of chemical exposures. Prenatal vitamins demonstrate that supplements can correct some methylation problems that disadvantage poor infants before they are even born. When shown to be effective, interventions such as foster care and parent support and training can provide nurturing care to infants who have been exposed to high stress since conception and can reverse some of the negative effects on their stress response systems. The mandate for social work has never been clearer.

doi: 10.1093/sw/sws052

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Terri Combs-Orme, PhD, is professor, University of Tennessee, College of Social Work, 204 Henderson Hall, Knoxville, TN 37996; e-mail tcombs-ornte@utk.edu. This work was supported by the Urban Child Institute in Memphis, Tennessee.

Original manuscript received June 8, 2011

Final revision received July 21,2011

Accepted August 1, 2011

Advance Access Publication December 6, 2012
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