Diet Success may Depend on Your DNA

Perhaps as could be expected, both in earlier research and in anecdotal evidence in humans, the animal models tended not to do great on the American-style diet. A couple of the strains became very obese and had signs of metabolic syndrome. Other strains showed fewer negative effects, with one showing few changes except for having somewhat more fat in the liver. With the Mediterranean diet, there was a mix of effects. Some groups were healthy, while others experienced weight gain, although it was less severe than in the American diet. Interestingly, these effects held, even though the quantity of consumption was unlimited.

The results demonstrated that a diet that makes one individual lean and healthy might have the complete opposite effect on another. “My goal going into this study was to find the optimal diet,” Barrington said. “But really what we’re finding is that it depends very much on the genetics of the individual and there isn’t one diet that is best for everyone.”

Read the source article here.

This is the first research study I’ve come across exploring genetics and diet.  This supports a belief I have about diet.  Eat what your ancestors ate.

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Gila Monster News – From Lizard to Laboratory… and Beyond

While studying the effects of exendin-4 on the pancreas, Dr. Egan and her colleagues found that it also seemed to have beneficial effects on the brain. Specifically, GLP-1 stimulates the growth of neurites (developing neurons) in cell culture, and both GLP-1 and exendin-4 protect mature neurons against cell death. In fact, research increasingly suggests that there may be a link between some neurodegenerative disorders and metabolic dysfunction. The hope is that drugs, such as exendin-4, that enhance metabolic function may also be useful in the treatment of neurologic disease.

Building on these findings, Dr. Egan and others in the NIA Intramural Research Program have tested exendin-4 in cellular and mouse models of several neurodegenerative diseases. The results are promising. For example, using a mouse model of Huntington’s disease, they found that exendin-4 reduces the accumulation of the mutant huntingtin protein, which is implicated in the disease’s onset and progression. The treatment also improved motor function and extended the survival time of the Huntington’s disease mice.

In other studies, investigators found that exendin-4 significantly reduced levels of amyloid beta protein (a hallmark of Alzheimer’s disease) and its precursor molecule in mice models of the disorder. It also proved beneficial in cellular and animal models of another neurodegenerative disorder, amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease.

via National Institute on Aging | The Leader in Aging Research.