People who grew up in Nazi-occupied countries who were malnourished as children also developed astoundingly high obesity rates as adults. From the evidence I’ve seen, genetics is over-emphasized as the missing factor in almost every medical theory before enough is known to know better. While income correlates with obesity, it does not explain the physiological mechanism through which poorer people (relative wealth may seem to mean much more than absolute wealth, interestingly) have a much harder time staying healthy.
It seems much more plausible that both semi-adaptable epigenomic variation and multi-generational lifestyle adaptions play bigger roles in generating familial and social trends of obesity. The nutrition, gut health, and overall health of BOTH parents contributes to the making of a child, and the mother’s health strongly affects it from then until birth, after which point colostrum and then breast milk will continue to play a direct parent-to-child role in the young one’s development.
Though there is no conclusive research that I’m aware of, it is probable that children establish certain growth limitations based on signals about nutrient availability received directly from their parents during conception and then from the mother during pregnancy and breastfeeding (variances of conveyed gut flora could be the mechanism here). Then, lifestyle and its epigenomic effects as normalized during childhood continues to play probably the same-seeming role since parents will tend to feed their children the same things they eat.
Anthropologically, going back a mere few hundred years there were no cultures anywhere in the world suffering obesity epidemics, so it doesn’t make sense to attribute variance too strongly to genetics. Historically, humans have survived healthfully on almost any combination of macronutrients while the main variant between healthy civilizations seems to have been micronutrients. Since studies generally don’t account in any fashion for idiosyncratic in-utero environment or for epigenetic variations among individuals, it could turn out that a vast amount of nutritional research is entirely worthless.
E.g. clinical studies of nutrition among populations could depend entirely on sociological factors about the last generation’s diet than about the objective value of macro-nutrients (which, in my opinion, should never be claimed as the object of a study as if removed from the context of the foods they are a part of).
The father’s health can play a role after conception as well since beneficial gut bacteria, in the least, can be transferred through saliva & sex. Additionally, since these gut bacteria build up multi-generationally, it could be that antibiotic treatment seriously impairs the functioning of newborns, especially if they don’t have probiotic sources in their diet (the best of which is breastmilk from a biotics-rich mother!).
The fact that metabolic privilege is conveyed via epigenetic vs genetic inheritance does not actually undermine the argument that privilege exists. No one is arguing that the effects of white male privilege come from the genetic components of being a white male. The discussion of where this metabolic privilege comes from is very useful, but let’s not confuse it with a discussion of whether or not it exists.
It is hard to debate the fact that certain people seem to have little difficulty maintaining a weight that is socially acceptable and others have a much harder time. I personally have a great deal of difficulty putting on weight and I am occasionally subjected to “skinny shaming” by my colleges at work. I take this in stride, knowing that I have the easier side of that coin. But is does seem to me that most individuals have a certain weight that they trend toward when they are not paying attention to what they eat. For a lucky few, that weight is in a socially acceptable range. Most are not so fortunate.
I don’t have a citation but I did read a paper which appeared to show that, while at first fat cells get smaller (and unhappier!), after about two years excess cells get culled. So if you can tough it out for two years it gets easier.
I acknowledge that there is also research that says otherwise. Not too easy to find, though journalism that says this is easy to find.
Both my wife and I lost about 15 kg of fat and did find after a couple of years life got easier, so maybe it’s true.
‘Good Calories, Bad Calories’ covers much of the research related to ‘Syndrome X’/Metabolic Syndrome. Some research seems to indicate that consumption of high glycemic index foods over an extended period can cause permanent damaging metabolic changes.
I think it is slightly misleading to equate damage to the metabolic system due to historical factors with a more general claim that healthy metabolisms vary widely however. The presence of Type 2 Diabetes is clearly a very relevant data point to be aware of when advising on diet and would lead to different advice than to a ‘normal’ healthy individual. I think the same is likely true of other types of metabolic damage that may have occurred in the past. Of course given the current state of understanding of the biology underlying all this it’s difficult to find unambiguous answers.
Children who overeat as kids have twice as many fat cells (large or small) for the rest of their life.
While I accept that this is literally true, I am very skeptical of the connotation—that greater numbers of fat cells is the mechanism responsible for the difficulty in losing weight and maintaining weight loss.
The hypothesis makes sense, since fat people who lose weight still have a lot of fat cells. But if it were true, one would expect that surgical removal of fat cells would have a significant positive impact on obesity. A couple studies have been done on this issue; I can try to find them if you like. There was not a significant positive impact.
So the inference is that (1) large numbers of fat cells; and (2) difficulty in losing weight and maintaining weight loss, are both the result of a third factor.
Children who overeat as kids have twice as many fat cells (large or small) for the rest of their life.
People who grew up in Nazi-occupied countries who were malnourished as children also developed astoundingly high obesity rates as adults. From the evidence I’ve seen, genetics is over-emphasized as the missing factor in almost every medical theory before enough is known to know better. While income correlates with obesity, it does not explain the physiological mechanism through which poorer people (relative wealth may seem to mean much more than absolute wealth, interestingly) have a much harder time staying healthy.
It seems much more plausible that both semi-adaptable epigenomic variation and multi-generational lifestyle adaptions play bigger roles in generating familial and social trends of obesity. The nutrition, gut health, and overall health of BOTH parents contributes to the making of a child, and the mother’s health strongly affects it from then until birth, after which point colostrum and then breast milk will continue to play a direct parent-to-child role in the young one’s development.
Though there is no conclusive research that I’m aware of, it is probable that children establish certain growth limitations based on signals about nutrient availability received directly from their parents during conception and then from the mother during pregnancy and breastfeeding (variances of conveyed gut flora could be the mechanism here). Then, lifestyle and its epigenomic effects as normalized during childhood continues to play probably the same-seeming role since parents will tend to feed their children the same things they eat.
Anthropologically, going back a mere few hundred years there were no cultures anywhere in the world suffering obesity epidemics, so it doesn’t make sense to attribute variance too strongly to genetics. Historically, humans have survived healthfully on almost any combination of macronutrients while the main variant between healthy civilizations seems to have been micronutrients. Since studies generally don’t account in any fashion for idiosyncratic in-utero environment or for epigenetic variations among individuals, it could turn out that a vast amount of nutritional research is entirely worthless. E.g. clinical studies of nutrition among populations could depend entirely on sociological factors about the last generation’s diet than about the objective value of macro-nutrients (which, in my opinion, should never be claimed as the object of a study as if removed from the context of the foods they are a part of).
The father’s health can play a role after conception as well since beneficial gut bacteria, in the least, can be transferred through saliva & sex. Additionally, since these gut bacteria build up multi-generationally, it could be that antibiotic treatment seriously impairs the functioning of newborns, especially if they don’t have probiotic sources in their diet (the best of which is breastmilk from a biotics-rich mother!).
-med student
The fact that metabolic privilege is conveyed via epigenetic vs genetic inheritance does not actually undermine the argument that privilege exists. No one is arguing that the effects of white male privilege come from the genetic components of being a white male. The discussion of where this metabolic privilege comes from is very useful, but let’s not confuse it with a discussion of whether or not it exists.
It is hard to debate the fact that certain people seem to have little difficulty maintaining a weight that is socially acceptable and others have a much harder time. I personally have a great deal of difficulty putting on weight and I am occasionally subjected to “skinny shaming” by my colleges at work. I take this in stride, knowing that I have the easier side of that coin. But is does seem to me that most individuals have a certain weight that they trend toward when they are not paying attention to what they eat. For a lucky few, that weight is in a socially acceptable range. Most are not so fortunate.
If parental health plays a role in this I would be interested in seeing if there’s a correlation between parental vaccination and obesity.
I don’t have a citation but I did read a paper which appeared to show that, while at first fat cells get smaller (and unhappier!), after about two years excess cells get culled. So if you can tough it out for two years it gets easier.
I acknowledge that there is also research that says otherwise. Not too easy to find, though journalism that says this is easy to find.
Both my wife and I lost about 15 kg of fat and did find after a couple of years life got easier, so maybe it’s true.
‘Good Calories, Bad Calories’ covers much of the research related to ‘Syndrome X’/Metabolic Syndrome. Some research seems to indicate that consumption of high glycemic index foods over an extended period can cause permanent damaging metabolic changes.
I think it is slightly misleading to equate damage to the metabolic system due to historical factors with a more general claim that healthy metabolisms vary widely however. The presence of Type 2 Diabetes is clearly a very relevant data point to be aware of when advising on diet and would lead to different advice than to a ‘normal’ healthy individual. I think the same is likely true of other types of metabolic damage that may have occurred in the past. Of course given the current state of understanding of the biology underlying all this it’s difficult to find unambiguous answers.
While I accept that this is literally true, I am very skeptical of the connotation—that greater numbers of fat cells is the mechanism responsible for the difficulty in losing weight and maintaining weight loss.
The hypothesis makes sense, since fat people who lose weight still have a lot of fat cells. But if it were true, one would expect that surgical removal of fat cells would have a significant positive impact on obesity. A couple studies have been done on this issue; I can try to find them if you like. There was not a significant positive impact.
So the inference is that (1) large numbers of fat cells; and (2) difficulty in losing weight and maintaining weight loss, are both the result of a third factor.