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."This seems logical. Also, there are correlations between childhood sexual abuse and low self-esteem in adulthood, which can be a factor in obesity.
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?I think it mean that if you want to understand the world, you're going to have to be able to wrap your head around relatively complex systems of causality. If you really can't understand that there can be a causal link without something being the sole causal factor, then you should probably leave the thinking to other people.
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....the average reader will understand that to mean something that it doesn't.
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.
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?Well CLEARLY High fructose corn syrup turns people into child molesters. That's just logic.
Well, if someone did have traumatic experience with sex, they may be bothered by any kind of sexual attention, like flirting and being hit on. Getting fat will reduce that kind of attention, samizdat gave an example of that.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.
Have you actually read research into epigenetics?People read way more into epigenetics then is actually there. There seem to be a handful of traits that may be epigenetic. Obesity may actually be one of them. But this whole idea that it "proves lamark right" or whatever nonsense, it's completely ridiculous.
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.Reading the actual research papers, or popular science articles about it? Because there's a big difference.
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.It's not true that your siblings will have the same basic genetic makeup. Remember, each parent carries two different copies of the genome, and you end up with two 'remixes' of those two copies. There can be a ton of variation between siblings. Things like fraternal twins of different races happen. Not that maternal stress won't play a roll in the child's health.
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?You don't think there's a stigma associated with being an abuse survivor? It's not like people can 'chose' what stigmas other people associate with something.
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.Right exactly. If you assume that these people have some kind of mental problems, then that's a stigma, whether or not you think they 'earned' it is a stigma. Would you want to hire someone who you thought required incredible effort not to go on a shooting spree? Or date someone like that? Even if you're just making the assumption that they have PTSD or struggle with depression -- that still seems like a 'stigma' to me.
In my experience, people respond well to acknowledgmentthat they've been through a trauma and are handling it, however difficult it may be.Well, maybe they would really rather just have people think that they are 'normal', especially if it's something that they don't think traumatized them. Maybe you talk to people who are abuse survivors all the time and never tell anyone about it. The stats in this article are that 50% of obese women and 25% of normal sized women were abused as children.
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.What you're arguing about is the precise definition of 'stigmatized'. But that's not the issue at all. The issue is whether or not people are going to think 'bad' things about you, meaning things you would prefer they not think if they thought you were an abuse victim. It seems pretty obvious that the answer is yes. People will assume you're depressed, that you're one step away from going on a shooting spree, that you will have sexual dysfunction, and so on. Okay maybe the word "stigma" doesn't perfectly capture that if you restrict the definition to 'a mark of shame' because you think that people shouldn't be ashamed of those things. But clearly lots of people are ashamed of those things.
Why the hell did fourteen people 'favorite' a sneering, derisive comment directed towards an innocent question?I took that more as a "gotcha" than an innocent question, because it's the first thing people bring up, always, in metafilter fat discussions whenever anyone points out, for instance, that some people are predisposed to be fatter than others. It's a very common tactic of the fat-shaming brigade here. But if it was an innocent question, I apologize for being snide.
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.Yes, but here's the thing: They're talking about a handful of traits. Something like obesity, or some of these psychological disorders linked to stress might be epigenetic. If those things are epigenetically linked then they are linked due to mechanisms for triggering those changes that are coded in the genome.
"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.(emphasis mine)
... 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....and what xarnop is asserting exists.
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....which isn't, as is also not the case in your example, about transgenerational epigenetic inheritance. It's about regular epigenetic inheritance; and the possibility that this could become a transgenerational epigenetic inheritance is speculative and based upon the limited laboratory examples of transgenerational epigenetic inheritance.
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.Note the two sentences I bolded. Now, that's a six year old paper. However, here is a more recent 2010 survey paper about transgenerational epigenetics (fully available at the link), and it mentions both these studies:
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.Again, note my bolding.
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.This is very preliminary work and almost all of what we're discussing here is speculative. This is a very long way from something that overturns the CD and especially that transforms conventional contemporary understanding of evolutionary theory.
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.That's hedged pretty strongly, I think.
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.I guess I was just surprised to see such a strong negative reaction, since I thought this article did a lot of things right for a pop science column. Obviously, reasonable people can disagree.
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Come on. There's a correlation between poverty and obesity, and a correlation between poverty and neglect. Neither issue is confined to poverty, but both are more prevalent among the poor. Where do I apply for a grant? I'd like to buy a boat.
posted by Mayor Curley at 3:23 AM on February 27 [7 favorites]