correlation does not merit causation. However, I believe that the study shows "thinner" children typically have thinner children/grandchildren.

This is almost the opposite of the Barker Hypothesis, "people who had low birth weight are at greater risk of developing coronary heart disease," which has been extended to diabetes and metabolic syndrome.

http://www.thebarkertheory.org/

I think a consensus is emerging that Lamarckian Evolution occurs through epigenetic mechanisms.

http://www.nature.com/nrg/journal/v14/n7/full/nrg3525.html

@Nutall, How these epigenetic mechanisms are inherited and what role they have in evolution is highly debatable; in the case of the study presented, dietary habitats are easily preserved across generations. Would this happen if these children had lived in different homes?

Hello friends, isn't it that the child himself/ herself has been over-eating or over-feeding? On the same great recipes that the family has enjoyed over generations. Another cause could be the feeding habits well-established in the family and has 'descended' / picked up by the younger generation.

I believe that the Y-gen have a greater problem with maintaining weight as compared to the baby boomers of a previous generation, who probably did more physical work and had more exercise, but that's only my observations within my community.

Biology is a balancing... if the balance is re-balanced in the other direction maybe diabetes decrease, maybe heart disease decrease... but what happen to all the other disorders?

By the way, it is not a kind of "selection" to take people who survived famine? It is not a way to keep more "resistant" individuals from a population?

Best

It is difficult to know if the transgenerational effects reported by Kaati et al. are mediated by inheritance of social patterns (eg. diet and exercise) or a biological mechanism. However, it is not obvious why social inheritance would pass down from the grandfather and not the grandmother. If this finding could be consistently replicated in different cultures, it is probably not social inheritance. If this were indeed an example of biological inheritance, classic natural selection is unlikely after only two generations. Lamarckian evolution has been demonstrated in mice, but it is a bit more challenging to demonstrate in humans. Lots of attention has focused on the prevention of obesity in the agouti mouse with a diet that increases DNA methylation. While this is consistent with the Barker hypothesis (ie. thrifty phenotype); the relevance of the agouti model to human nutrition remains unclear. However, the results by Kaati et al. are opposite of the thrifty phenotype/genotype. What would be the evolutionary benefit? I think I will take this with a grain of salt until I see more data.

In the case of the famine, most likely inheritance of social patterns is being witnessed; those that survive the famine passed on conservative dietary patterns to offspring; if the study was replicated with the respective grandmothers, similar results would probably be observed. Additionally, going through the different family lineages may make this concept more evident.

From a biological perspective, those that possessed genes associated with favorable eating behavior phenotypes would be more likely to survive food shortages; appropriate leptin, gherlin, CAD, CCK levels. These individuals would easily develop food selection habits that favored infrequent meal intake and smaller meal sizes.

Michael, how would infrequent meal intake and smaller meal size facilitate survival and/or reproduction during famine? The thrifty phenotype/genotype predisposes an individual to eat more and burn less.

I pointed out that the effect was specific to the paternal lineage because the study by Kaati et al. did look at the maternal lineage as well. If I were to believe that the statistically significant data from this correlation represented a causal association; the interpretation would be to starve your son and feed your daughter. Maternal exposure to famine increased CVD risk (consistent with David Barker's seminal work published in 1989). In contrast paternal or grandpaternal famine exposure decreased CVD risk. Grandmother's famine exposure was not significantly associated with CVD.

I can stretch my imagination to create a scenario. For example, if you eat less during a famine (as a male) and you allow your spouse and or sisters to eat more. However, this is nearly the opposite of the Barker hypothesis.

@Johnathan. During famines people tend to eat less, and less often.

Thus, some people whose natural eating behavior was "infrequent eating, and eating of smaller meals" would be better suited for the environment. My argument was not referring to the thrifty phenotype; there exists other phenotype for food intake.

The study demonstrates that different eating behavior phenotypes between men and women are selectively favored during famines; Heavier women/thinner men. This selectivity impacts the health of future generations. The possible disparity in weight between women/men during famines could be due to childbirth; heavier mothers were more likely to survive childbirth during famines.

However,I did not know that the Kaati study looked at maternal lineages.

Maternal exposure to famine increased CVD risk for the following reasons:

(1) possibly due to fetal development during famine; lack of certain nutrients

(2) heavier mothers would best survive childbirth during famines; these mothers would already be at a risk for CVD.

Already established that "thinner" grandfather/father best survive famine. These people would have a lower risk of CVD; so offspring might have lower as well.

It's not about the amount of food. It's about the type of food--period.

I think people are over-complicating this matter and trying to use reaching social explanations as means of discrediting the study results. I am not saying that those social explanations are inherently invalid but let's actually first consider the validity of this hypothesis on biological terms before we aim to discredit it with likely untestable (at least accurately) sociological phenomena. And I am not saying what follows may not be just as equally far-fetched and reaching (but it is at least testable!).

Many people here are familiar with the thrifty genotype/phenotype theory, and are also familiar with the Dutch and Chinese Famine studies showing an increase in Type 2 Diabetes and poor glucose tolerance in those were exposed to prenatal and childhood famine.

http://www.sciencedirect.com/science/article/pii/S0140673697072449

http://diabetes.diabetesjournals.org/content/59/10/2400.short

Low birth weight has been implicated in the prevalence of type 2 diabetes at a later age, and birth weight has an inverse relationship with type 2 diabetes, with a small u-curve near the highest strata of birthweights (so too large is still a problem, but moderately large is not):

http://jama.jamanetwork.com/article.aspx?articleid=183130

Please note that the exposure to famine and low birth weight implicates an environmental impact on the fetus or child, that translates into a later-in-life susceptibility to Type 2 diabetes. There is likely lasting inutero epigenetic (or otherwise undiscovered) alterations that occur in early life, that are retained into adulthood due to intense environmental stressors. Importantly, George Cahill and Faiman & Moorhouse separately demonstrated that Type 2 diabetics are better suited to combat bouts of starvation dating back to the 1960s, demonstrating that they retain nitrogen better, and produce more ketones during bouts of acute starvation.

So how do we reconcile this theory with the study results in the opening question?

It was observed that men who ate rich diets before puberty (and therefore before they could conceive) passed on higher likelihoods of developing CVD and diabetes, and there was even a small relationship of the opposite in women who were exposed to rich diets before puberty (lower development of CVD/diabetes in offspring).

This is no surprise, as women are the first environment a child is exposed to (fetal environment). I personally view the women in this context as the initial sanctuary for the fetus. If the women is highly susceptible to stress (ie: nutritional deprivation, psychological stress, etc) this will translate into increased resiliency to that stress and permanent epigenetic/other alterations in the child (which translates into an increased tendency towards CVD/diabetes).

Men, however, do not provide the initial environmental context, and instead likely pass on their genetic and epigenetic traits - but offer no environmental influence until later in life, postnatal and possibly even later in the form of teaching their child habits when the child has cognitive capacity to learn complex habits, but when the child is less malleable to environmental influence compared to prenatal and early childhood life. The older, more overweight, and less healthy the father is, likely translates into genetic or epigenetic (or something else) damage that unfavourably alters the offspring's genotype/phenotype, predisposing them to CVD/diabetes.

We have no evidence that exposure to famine later (post-childhood) in life predicts the development of diabetes/cvd (likely the opposite, as in low adult weight is inversely correlated to the development of diabetes/cvd), so it is very likely that the absence of poor health/overweight, and exposure to those mechanisms which may damage genetic/epigenetic/other unknown heritable mechanisms leads to favorable outcomes in the offspring of these men.

So in short, fat mothers and skinny fathers make healthy babies.... which also may explain why women are typically fattier, and less susceptible to the negative health effects of fat mass vs. men (because they are supposed to be fatter, for the health of any potential offspring).

Apologies for the long post, but this is of particular interest to me.

I can't find the original articles that are cited in these news articles, but they have done caloric restriction studies on animal models and found the effects on longevity can be inherited by their offspring.

http://www.technologyreview.com/news/425815/worm-offspring-inherit-longevity-even-without-the-genes/

https://www.fightaging.org/archives/2011/10/another-look-at-epigenetic-inheritance-of-longevity.php

Farhan—No, it has nothing to do with calories. Although calories can have an impact on health and weight, calories are not the driving force behind metabolic problems and weight gain.

 In my opinion excessive fat storage and the associated metabolic problems associated with obesity are mostly driven by the type of food that is eaten. Highly processed food is pro-inflammatory and pushes fat storage regardless of caloric intake.

Obesity is defined as excessive body fat, yet most people use weight or BMI as a measure. Neither metric tells you how much fat is in someone’s body. For years I have directly measured body composition on my patients and I have found that patients who under-eat yet eat process food tend to have a low BMI and weight yet they have excessive body fat. This is true of people with anorexia unless they are pre-terminal.

Thus I would suggest that you simply forget about calories because in my experience focusing on calories is a dead end street.

Wassim--By the way, your comments on epigenetics are spot on.