You Are What Your Mother Eats
The old adage used to indicate that you are what you eat. And certainly for someone suffering from obesity, type 2 diabetes, and/or the metabolic syndrome that person is definitely an unfortunate example of the truth of that statement.
However, recent research into epigenetics (se earlier posting from January 31, 2011) is clearly demonstrating that a person is "what their mother ate" while she was carrying said person in her uterus.
There is now evidence demonstrating a clear correlation between poor nutritional status of the mother during fetal development and the potential for an increased risk that her child will develop the metabolic syndrome (MetS) later life. MetS (also once referred to as Syndrome X), is a disorder that defines a combination of metabolic and cardiovascular risk determinants. These risk factors include insulin resistance, hyperinsulinemia, central adiposity (obesity associated with excess fat deposits around the waist), dyslipidemia, glucose intolerance, hypertension, pro-inflammatory status, and microalbuminemia. The hallmark feature of MetS is indeed insulin resistance.
These correlations have also been observed in animal studies where prenatal diets in mothers impacts their offspring. Overfeeding during of the mother during fetal development as well as excessive nutritional intake by the mother during the pre-weaning period of postnatal development results in increased obesity, adipocyte hypertrophy, reduced activity, insulin resistance, elevated blood pressure, endothelial cell dysfunction, and altered cardiovascular and renal function in offspring. When mothers are obese and fed high-fat diets during fetal development their adult offspring exhibit impaired glucose tolerance, hyperinsulinemia, dyslipidemia, hypertension, resistance to the anorexic actions of the leptin on the hypothalamus, and develop non-alcoholic fatty liver disease (NAFLD). Additional evidence indicates that manipulation of fetal protein access leads to modified pancreatic islet cell expansion resulting in reduced pancreatic β-cell mass and persistent deficits in glucose homeostasis.
There is now a clear link between maternal dietary status and future development of MetS in adult offspring. Likewise, because the risks of metabolic syndrome in the general population, due to identified inherited polymorphisms is relatively small, the huge increase in the numbers of individuals with the disorder is most likely due to epigenetic changes that occur during early fetal development. The role of epigenetics in transgenerational disease manifestation has been outlined in several studies on the outcomes of children born to parents who experienced famine while pregnant. These children are far more likely to develop diabetes, obesity, and cardiovascular disease than children from parents of similar backgrounds who were not nutritionally deprived. Of striking significance is that the second generation children (grandchildren of the starved mothers) were more likely to be born with low birth weight regardless of the nutritional status of their mothers. The potential for diet and nutrition to effect epigenetic changes in offspring on multiple generations has been conclusively demonstrated in animal models. In mice, the lack of adequate fetal nutrition results in a reduction in the methylation status of the promoter regions of several transcriptional regulators. Hypomethylation of genes is most often associated with increased transcriptional activation. One transcriptional regulator of key metabolic significance whose promoter has been found to be hypomethylated in offspring of nutritionally deprived mothers is PPARα. PPARα is highly expressed in the liver, skeletal muscle, heart, and kidney. Its function in the liver is to induce hepatic peroxisomal fatty acid oxidation during periods of fasting. Expression of PPARα is also seen in macrophage foam cells and vascular endothelium. Its role in these cells is thought to be the activation of anti-inflammatory and anti-atherogenic effects.
The take home from the results of these types of experiments is that doctors should be doing a better job of educating their female patients that their bad dietary behaviors are not only bad for them but very bad for their babies who, as fetuses, have absolutely no control over what their mothers are doing to them. And what they are doing is dooming their children to a life of horrible metabolic disease, costly health care, and early death.
However, recent research into epigenetics (se earlier posting from January 31, 2011) is clearly demonstrating that a person is "what their mother ate" while she was carrying said person in her uterus.
There is now evidence demonstrating a clear correlation between poor nutritional status of the mother during fetal development and the potential for an increased risk that her child will develop the metabolic syndrome (MetS) later life. MetS (also once referred to as Syndrome X), is a disorder that defines a combination of metabolic and cardiovascular risk determinants. These risk factors include insulin resistance, hyperinsulinemia, central adiposity (obesity associated with excess fat deposits around the waist), dyslipidemia, glucose intolerance, hypertension, pro-inflammatory status, and microalbuminemia. The hallmark feature of MetS is indeed insulin resistance.
These correlations have also been observed in animal studies where prenatal diets in mothers impacts their offspring. Overfeeding during of the mother during fetal development as well as excessive nutritional intake by the mother during the pre-weaning period of postnatal development results in increased obesity, adipocyte hypertrophy, reduced activity, insulin resistance, elevated blood pressure, endothelial cell dysfunction, and altered cardiovascular and renal function in offspring. When mothers are obese and fed high-fat diets during fetal development their adult offspring exhibit impaired glucose tolerance, hyperinsulinemia, dyslipidemia, hypertension, resistance to the anorexic actions of the leptin on the hypothalamus, and develop non-alcoholic fatty liver disease (NAFLD). Additional evidence indicates that manipulation of fetal protein access leads to modified pancreatic islet cell expansion resulting in reduced pancreatic β-cell mass and persistent deficits in glucose homeostasis.
There is now a clear link between maternal dietary status and future development of MetS in adult offspring. Likewise, because the risks of metabolic syndrome in the general population, due to identified inherited polymorphisms is relatively small, the huge increase in the numbers of individuals with the disorder is most likely due to epigenetic changes that occur during early fetal development. The role of epigenetics in transgenerational disease manifestation has been outlined in several studies on the outcomes of children born to parents who experienced famine while pregnant. These children are far more likely to develop diabetes, obesity, and cardiovascular disease than children from parents of similar backgrounds who were not nutritionally deprived. Of striking significance is that the second generation children (grandchildren of the starved mothers) were more likely to be born with low birth weight regardless of the nutritional status of their mothers. The potential for diet and nutrition to effect epigenetic changes in offspring on multiple generations has been conclusively demonstrated in animal models. In mice, the lack of adequate fetal nutrition results in a reduction in the methylation status of the promoter regions of several transcriptional regulators. Hypomethylation of genes is most often associated with increased transcriptional activation. One transcriptional regulator of key metabolic significance whose promoter has been found to be hypomethylated in offspring of nutritionally deprived mothers is PPARα. PPARα is highly expressed in the liver, skeletal muscle, heart, and kidney. Its function in the liver is to induce hepatic peroxisomal fatty acid oxidation during periods of fasting. Expression of PPARα is also seen in macrophage foam cells and vascular endothelium. Its role in these cells is thought to be the activation of anti-inflammatory and anti-atherogenic effects.
The take home from the results of these types of experiments is that doctors should be doing a better job of educating their female patients that their bad dietary behaviors are not only bad for them but very bad for their babies who, as fetuses, have absolutely no control over what their mothers are doing to them. And what they are doing is dooming their children to a life of horrible metabolic disease, costly health care, and early death.
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