The psychology is relatively straightforward: being abused or otherwise traumatized is painful, and food can be a numbing or comforting escape. Hence, abused children may turn to overeating, which causes obesity. Indeed, ACEs are also strongly linked with other types of unhealthy "self-medication": for instance, cigarette smoking (which accounts for the increased rate of emphysema among high ACE scorers) and drug abuse (having four or more ACEs increases the risk of injectable-drug use by a factor of 10). As Felitti puts it, "Being fat [or having other unhealthy behaviors] is not the problem. It's the solution."
The psychological effects often exacerbate health problems that the physiological stress response has already caused. High ACE scorers who do not overeat, smoke or take drugs still have high rates of obesity, heart disease, depression and diabetes. The mechanism for these risks appears to lie in the biology of the stress-response system and in the way environment affects a person's genetic activity.
I am a bit confused. Assuming that there is a causal link between childhood sexual abuse and obesity, and obesity rates are rising, does that mean that childhood sexual abuse is also rising, or is the ready availability of "obesity-favoring food" just raising the numbers across the board?
Studies have also found that consistently elevated levels of stress hormones, like cortisol, can lead to permanent damage in certain brain regions linked to depression.
Recently, scientists have discovered that these changes can themselves be passed down from one generation to the next — a burgeoning new area of study called epigenetics. Such research may have significant and long-term implications for the prevention of obesity, addiction and other illnesses related to early life stress.
It is absolutely not true that sexual violence, either rape or childhood sexual assault, is motivated primarily by sexual attractionThis is pretty commonly understood. But I don't think it's being suggested that an aggressor commits the act of sexual abuse because of sexual attraction. Rather, that the victim may be reacting to the abuse, rational or not, in a way which he/she perceives will make him/herself appear an unattractive object of sexual desire, and therefore an unattractive target for further abuse.
It is absolutely not true that sexual violence, either rape or childhood sexual assault, is motivated primarily by sexual attraction
Have you actually read research into epigenetics?
Are you aware of what science disproved lamark and darwins early hypothesis that the body communicated adaptations in cellular functioning to the germline-- and how utterly crappy those studies "disproving" the theory actually were?
Ivan-- the reason I'm curious is that I spend a lot of time reading research in epigenetics, as an interested party, and I find that many conclusions about epigentic alterations being communicated to the germline quite common.
My sister, who has the same basic genetic material doesn't have the same issues that I have, nor does she have the same issues with weight-gain.
Really? So instead of removing some of the stigma of obesity, because much of it is due to horrible experiences that happened as a child, and over which the person had no control, you ADD more stigma because not only is it shameful to be fat, it's also shameful to be an abuse survivor? If that isn't what you are saying, please clarify, because WHAT THE HELL?
Telling someone "I'm impressed you're not shooting people from a bell tower, given what you've been through" might be interpreted as stigmatizing by that individual.
In my experience, people respond well to acknowledgmentthat they've been through a trauma and are handling it, however difficult it may be.
All in all, it seems like you're trying to have it both ways, where both ways end up being that stigmatization of being a survivor of childhood sexual violence is necessary and basically universal. Which is bullshit and rightly objected to here by numerous people.
Why the hell did fourteen people 'favorite' a sneering, derisive comment directed towards an innocent question?
Maybe you should recall that I wrote "In my experience.." for a reason and consider that in actual conversations, the statement has not been seen in the light you're conjecturing.
I'm talking about studies like this which show that early life stress alters the paternal germline of future offspring.
"Overall, these data support the existence of a sensitive period of early gestation when epigenetic programming of the male germline can occur, permitting transmission of specific phenotypes into subsequent generations."
Those who were exposed to the famine only during late gestation were born small and continued to be small throughout their lives, with lower rates of obesity as adults than in those born before and after the famine. However, as indicated above, those exposed during early gestation experienced elevated rates of obesity, altered lipid profiles, and cardiovascular disease.
... One of the predictions made by [this hypothesis] is that fetal adaptations to scarcity become maladaptive only when affected individuals are later exposed to an environment of plenty. This is dramatically shown by comparing those exposed to the Dutch Hunger Winter with babies born after the siege of Leningrad. In both cases, pregnant women were exposed to severe famine. However, whereas The Netherlands returned to a complete diet quite quickly after the time of severe restriction, there were continuing shortages in the U.S.S.R., where those exposed to famine in utero did not exhibit higher rates of either obesity or cardiovascular disease as adults (9).
Studies have also found that consistently elevated levels of stress hormones, like cortisol, can lead to permanent damage in certain brain regions linked to depression. Recently, scientists have discovered that these changes can themselves be passed down from one generation to the next — a burgeoning new area of study called epigenetics.
Maternal care influences hypothalamic-pituitary-adrenal (HPA) function in the rat through epigenetic programming of glucocorticoid receptor expression. In humans, childhood abuse alters HPA stress responses and increases the risk of suicide. We examined epigenetic differences in a neuron-specific glucocorticoid receptor (NR3C1) promoter between postmortem hippocampus obtained from suicide victims with a history of childhood abuse and those from either suicide victims with no childhood abuse or controls. We found decreased levels of glucocorticoid receptor mRNA, as well as mRNA transcripts bearing the glucocorticoid receptor 1F splice variant and increased cytosine methylation of an NR3C1 promoter. Patch-methylated NR3C1 promoter constructs that mimicked the methylation state in samples from abused suicide victims showed decreased NGFI-A transcription factor binding and NGFI-A–inducible gene transcription. These findings translate previous results from rat to humans and suggest a common effect of parental care on the epigenetic regulation of hippocampal glucocorticoid receptor expression.
In animal models, these types of effects, termed fetal programming, can be produced by exposing offspring in utero to a manipulation such as dietary restriction of the pregnant female. Although most studies of fetal programming only address effects in the first-generation offspring, there is strong evidence that, at least in some cases, these programmed phenotypes are maintained for several generations. For example, prenatal programming of birth weight by maternal food restriction or maternal exercise have been shown to last for more than one generation.
The molecular basis for these apparently nongenetic transgeneration effects is not known. One hypothesis is that it involves epigenetics. Epigenetics is the process by which patterns of gene expression are modified in a mitotically heritable manner by mechanisms that do not involve DNA mutation. Epigenetic modifications include, among others, the methylation state of the DNA and the proteins that package the DNA into chromosomes. The epigenetic state of the genome is established in early development and is generally thought to be cleared between generations.
The effects of environmental influences and the possibility that the resulting epigenetic alterations are heritable to the next generation are of considerable interest to those studying disease in humans. A recent study investigated the long-term effects of prenatal exposure to famine on DNA methylation at the imprinted IGF2 gene. Individuals conceived during the Dutch Hunger Winter (1944–1945) showed hypomethylation at the IGF2 differentially methylated region (DMR) when analyzed six decades later. Interestingly, no differences in DNA methylation were observed in individuals exposed to famine late in gestation. The finding suggests that the protein-deficient diet of the mother contributed to the loss of DNA methylation at the IGF2 DMR (Heijmans et al. 2008). It is difficult to tease out cause and effect. The loss of methylation in old age may be a consequence of some as yet unknown physiological changes. Unfortunately, in this study there is no record of DNA methylation patterns earlier in development. A prospective cohort study would be best, and epidemiologists are now collecting biospecimens from MZ twins at birth (Foley et al. 2009). This will provide us with exciting new data in the coming decades.
A large epidemiological study carried out in Sweden reported that early paternal smoking was associated with a greater body mass index in sons (Pembrey et al. 2006). Additionally, they found a correlation between mortality risk ratio of grandsons and paternal grandfather's food supply in mid-childhood. The mortality risk ratio of the granddaughters was linked to the paternal grandmother's food supply (Pembrey et al. 2006). While it is possible to explain these observations based on transgenerational epigenetic inheritance, other equally plausible explanations exist. In these types of studies, cultural confounders are almost impossible to rule out.
Multicellular organisms have evolved complex mechanisms to clear epigenetic states between generations. However, in some cases these mechanisms can be circumvented. Recent studies across a wide range of species have strengthened the idea that the direct inheritance of RNA molecules and of chromatin states does occur, making these plausible explanations. The development of high-throughput methods of sequencing both RNA and DNA in combination with antibodies specific to particular histone modifications will enable us to fully characterize the epigenetic marks across the entire genome of gametes and early embryos in the near future. Together, these studies will provide us with exciting new insights on how and to what extent transgenerational epigenetic inheritance occurs in various organisms. Certainly, we are only at the beginning, and most likely we will have to revise our current models about the nature and stability of the epigenetic marks to fully understand this mechanism.
Recently, scientists have discovered that these changes can themselves be passed down from one generation to the next — a burgeoning new area of study called epigenetics. Such research may have significant and long-term implications for the prevention of obesity, addiction and other illnesses related to early life stress. After all, reducing childhood exposure to trauma in one generation may further benefit that generation's children and grandchildren.
For most of human evolution, a stressful world would have been marked by famines or periods of starvation, and that environment might have resulted in a particular pattern of gene expression that would have prompted the body to store more fat in preparation for the next bout of scarcity. Today, of course, the same response to stress would result in obesity. This theory of a thrifty fat-storing system that kicks in under high levels of early stress was originally proposed by British physician David Barker.
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