you could refer to this document of FAO-WHO to gain some information about prenatal determinants of chronic diseases in the adult age. It is no specifically dealing with obesity, but with some metabolic disorders associated with overweight

http://www.fao.org/docrep/005/ac911e/ac911e06.htm#bm06

A maternal high fat diet during pregnancy is implicated in offspring adult adiposity, but it is certainly not the only such developmental, predisposing nutritional factor. After all, maternal prenatal undernutrition has been clearly linked with low birth weight offspring who exhibit reduced muscle mass along with relatively high body fat at birth (the so called “thin-fat” Indian baby [Yajnik et al. 2003]). Beyond this, the maternal nutritional ‘window’ during which diet (and maternal phenotype) can affect offspring adiposity is larger than previously thought. Prepregnancy obesity has now been shown to be an independent risk factor for offspring overweight and abdominal obesity (Pirkola et al. 2010; Guenard et al. 2013). In addition, other studies have shown an independent relationship between maternal BMI during pregnancy and offspring BMI, adiposity, and insulin resistance (Koupil et al. 2008; Mingrone et al. 2008; Whitaker 2004), and between weight gain during pregnancy and greater offspring adiposity (Reynolds et al. 2010). But identifying maternal prenatal dietary factors alone is insufficient. Offspring adiposity (mass and distribution) is also partly the consequence of a complex interaction between maternal prenatal nutrition and postnatal nutrition in the first months and years of life – especially during critical periods of “catch up” growth prior to the adiposity rebound (see Benyshek 2007). Finally, recent animal studies and retrospective epidemiological research have revealed that adiposity can be influenced by developmental (e.g., epigenetic) processes associated with diet – in both the maternal and paternal lines – that reverberate for at least three generations beyond the original dietary insult/event (See Benyshek in press, Am J Phys Anth). All of these developmental factors, in addition to diet type and timing of nutiritional perturbations, must be considered in our efforts to understand the relationship between pre and postnatal nutrition and offspring adult obesity.

I'd recommend reading the work of Dana Dabalea and colleagues who have published work related to this question over the last 10 years.

As mentioned by others, therea are a variety of potential mechanisms through which fetal exposures can influence an array of adult outcomes.

The following referance may be useful: S Muhlhausler, B., and Z. Y Ong. "The fetal origins of obesity: early origins of altered food intake." Endocrine, Metabolic & Immune Disorders-Drug Targets 11.3 (2011): 189-197.

There is probably no critical prenatal period for adult obesity, but rather that the whole prenatal period is critical in the meaning tha maternal living conditions in combination with genetic factors throughout the pregnancy is vital. You have received many very relevant responses, and I will point out two other aspects trat are very much in focus at the present time:

Immunologic factors: There are a multitude of publicatins describing and discussing the association between intestinal microbiota composition, inmmunologic and metabolig developent, and adult adiposity. The composition of the intestinal microbiota inflict nutritional uptake, T-cell maturation and metabolig and energy-storing mechanisms thorughout life. The mechanisms are slowly beeing understood. One important factor is problably the loss in microbial diversity in westernized coutries as one of the reasons for the overveight epidemy in these counrtries.

Epigenetics: One of the former answers focused correctly on the fact that undernurtured mothers tend to have overveight children. Epigenetic mechanisms regulating genetig transcription and activation og genes can be transferred from mother to child during pregnancy and weaning (breast feeding), programming the individual for metabolic and energy-storing mechanisms leading to overveight and obesity. Particularly new knowledge on micro-RNA through breast feeding is beeing explored at the present time.

Congratulations all of the above on an interesting conversation thread. This topic has progressed since I last read about it!

I'm pretty sure you'll find your answers in one or more publications which came out of the Dutch 'Hungerwinter' (1944-45) research, here: http://www.hongerwinter.nl/index.php?id=31&language=en under publications.

btw: I hope ANYONE will take the trouble of respodning to my last three querry's!

You could read a recent study (Behavioral and Dietary Risk Factors for Noncommunicable Diseases, N Engl J Med 2013;369:954-64) to gain some information about determinants of chronic diseases in the adult age. It is no specifically dealing with overweight and obesity, but this article summarize the available data on trends in selected behavioral and dietary risk factors for noncommunicable diseases and examine the effects they have had, or may have in the future, on the health of populations around the world.

The entire gestational process its important for the correct development of the product. Adverse events or situatios, like undernourishment, during this life-period generate adaptative changes needed to survive the gestational period. However, these same adaptative mechanisms may be deleterious in the adult life.

I agree with your remarks Dr Ricardo Ramirez-Oseguera on the adaptive effects of under nutrition on the growth of the fetus. It would be wonderful to know some papers eliciting the specific adaptive responses to different types of under nutrition of the mother to the fetus at various stages of its development.

We know that exposure to over- or undernutrition in utero affects future metabolic status and adiposity, but the postnatal period may be equally important.

Early life programming and metabolic syndrome

Xiu-Min Wang

Metabolic syndrome (MS) has reached epidemic proportions worldwide among children. Early life “programming” is now thought to be important in the etiology of obesity, type 2 diabetes, cardiovascular disease and MS. Nutritional imbalance and exposures to endocrine disruptor chemicals during development can increase risk for MS later in life. Epigenetic marks may be reprogrammed in response to both stochastic and environmental stimuli, such as changes in diet and the in utero environment, therefore, determination of targets for early life effects on epigenetic gene regulation provides insight into the molecular mechanisms involved in the epigenetic transgenerational inheritance of a variety of adult onset disease phenotypes. The perinatal period is a crucial time of growth, development and physiological changes in mother and child, which provides a window of opportunity for early intervention that may induce beneficial physiological alternations.

Maternal nutritional status and dietary intake affects the composition of breastmilk. As lactation results in mobilization of maternal adipose tisse and bone remodeling, lifelong enviromental exposures may exert important influences on future obesity and metabolism in the offspring.

I sugest to read a very important paper recently publised iin NEJM (How Early Should Obesity Prevention Start? (in attachment)

I sugest to read a very important paper recently publised iin NEJM (How Early Should Obesity Prevention Start? (in attachment)

Thanks a lot Carlos for sending the above paper. I will go through it shortly.

The attached paper is a summary of a workshop held in 2009 about the potential link between exposure to endocrine disruptors and obesity, as well as diabetes. This working meeting was held by the US National Toxicology Program (NTP-NIEHS) and brought together scientists from all over the world to review the evidence and come to some conclusions. Several environmental exposures were considered: arsenic, POPs, maternal smoking, organotins, phthalates, bisphenol A, and pesticides. The working group concluded that there was enough scientific evidence to support the "developmental obesogen" hypothesis, such that exposure to chemicals that are endocrine disruptors during gestation may increase the risk of obesity later in life by altering the differentiation of adipocytes or the development of neural circuits that regulate feeding behavior. These effects are most likely to occur when the developmental exposure is combined with consumption of a high-calorie - high carbohydrate, or high-fat diet later in life. Children of mothers exposed to endocrine disruptors during their pregnancy are more likely to become obese as adults than children of mothers who did not have such exposures. As noted, adult diet impacts the development of obesity in these individuals exposed to endocrine disruptors in utero.