Even if you do everything right – exercise, healthy eating, no smoking– whether or not you’ll make it to the century mark depends to some extent on your genes.

One of the important longevity genes seems to be FOXO3A.  It’s been linked to lifespan in several experimental animal models. In humans, studies have shown that certain variations in the FOXO3A gene increase the odds of being extremely long-lived.

(See SNPwatch: Mounting Evidence That FOXO3A Contributes To Human Longevity for more about FOXO3A variation and, for 23andMe Complete Edition customers, a link to your data.)

It’s not exactly clear how FOXO3A affects longevity because it’s known to play a part in several important cellular functions, including cell growth, cell specialization, response to oxidative stress and  the regulation of cell death.  Two studies published last month in the journal Cell Stem Cell added to the list of the FOXO3A’s talents.  Renault et al. and Paik et al. showed that in mice FOXO3A and related FOXO genes are involved in maintaining the brain’s ability to generate new cells, a function critical for both normal brain functions and repair in response to natural degeneration or injury.

New brain cells arise from a pool of specialized self-renewing cells called neural stem cells.  The FOXO genes appear prevent the brain from burning through its supply of these important cells prematurely.

“Because [neural stem cells] have been shown to be important for learning, memory, and mood regulation, our findings could give insight into the decline in cognitive function that occurs during aging,” Renault et al. wrote in their report.

More research will be needed to fully understand the role of the FOXO genes in neural stem cells.  Experiments will also be needed to test whether these findings can be extended to humans.

Despite the work that is left to be done, Paik et al. optimistically suggest the new understanding of the importance of the FOXO genes in neural stem cells may help guide the development of drugs that could help improve central nervous system health in the elderly and people suffering from neurodegenerative disease or brain injury.

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Our bodies need iron: to form the oxygen-carrying hemoglobin for our red blood cells, maintain our immune systems and keep our muscles and brains functioning properly.

But not too much.  Excess iron can build up in tissues like the liver, heart and pancreas, causing damage and possibly organ failure.

Other than blood loss, there’s no way for the human body to rid itself of excess iron.  The only way to regulate iron levels is by adjusting how much is taken in from food. Low iron levels in the body lead to more absorption in the gut, high iron leads to less.

There are several known genetic mutations that interrupt this iron absorption control mechanism, leading to a condition called hereditary hemochromatosis.  But there are some forms of this disease for which the causative mutation isn’t known, and not everyone with one of the known mutations actually ends up having hemochromatosis.  These observations suggest there are genetic factors affecting iron level control that have yet to be identified.

Two reports published online yesterday by the journal Nature Genetics may have identified one of these additional genetic factors.  Researchers working with mice have found that disrupting the function of the BMP6 gene can lead to iron overload much like that seen in the severe childhood-onset forms of human hemochromatosis.

“Although no human patients with BMP6 mutations have yet been described, our data …suggests that BMP6 mutations or BMP6 gene variants may function as another cause of hereditary hemochromatosis or a modifier of disease penetrance,” write the authors of one of the studies.

23andMe customers can learn whether they are carriers of the mutations that cause adult-onset hemochromatosis using the Health and Traits feature.

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