New research on obesity predispositions through the female bloodline has found that a mother’s metabolic problem can be inherited through the egg’s mitochondrial DNA.
The study, conducted by Washington University, also points out that certain dietary interventions may represent an aggravating factor in the transmission of the condition from mother to offspring.
Researchers already knew that a woman’s health in pregnancy determined her child’s weight later in life, but what these findings reveal is that elements of her lifestyle, in particular her diet, could also influence the health outcomes of the new-born.
The St. Louis University School of Medicine’s team first made the astonishing discovery that genetic abnormalities caused by a woman’s obesity, and its related conditions such as type 2 diabetes and heart disease, can be passed on to at least three generations.
The research, published in the journal Cell Reports, described the mechanism behind the inheritance of these genetic modifications as a transfer of altered DNA from the powerhouses of cells, known as mitochondria, to the unfertilized egg.
The scientists also established that mitochondria have their own set of genes, which can only be inherited from mothers, not fathers.
The data collected on the propagation of genetic mitochondrial dysfunction throughout the entire organism emanated from a six weeks controlled dietary study on mice.
The hypothesis tested by researchers was whether the quality of a pregnant woman’s diet can also predict the development of similar metabolic disorders in offspring.
From six weeks prior to conceptio, pregnant mouse mothers with metabolic syndrome were fed a high-fat (60%), high-sugar (20%) diet. The control group of animals were given a standard rodent chow which was high in protein and low in fat and sugar.
The results showed that despite the healthier diet, the three generations of mice produced developed insulin resistance and other metabolic problems. For Kelle H. Moley, the senior author of the study, however, the effects of diets that closely mirror those of their parents may be greater in human maternal metabolic syndrome than in a mouse model.
Further research is needed to determine with more precision if a low-fat, low-sugar diet combined with regular exercise can reverse genetic metabolic abnormalities.

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