The life spans of lower animals, such as the flies and the nematode worms commonly used in exploratory studies of the biochemistry of aging, are very plastic. They can be considerably lengthened by environmental circumstances and altered metabolism that have very little effect on longer-lived mammals. Where we have direct comparisons that are easy to make, such as for calorie restriction and growth hormone receptor dysfunction, we know that while mice with those circumstances life half again as long as usual, we humans certainly don't. Evolution has made short lives much more reactive to circumstances than long lives. So when you read about life extension in worms or flies of 10% or 30% or even a doubling or more, bear in mind that, when based on altered states of metabolism, this will not translate to any meaningful extension of human life. The degree of extension isn't anywhere near as important as the methodology of extension when it comes to whether or not it can produce usefully large effects on human longevity. This is made particularly clear by the fact that, say, aspirin produces significant life extension in lower animals. So too does vitamin D, as demonstrated here, and I think that most people are fairly comfortable acknowledging that life-long intake of either aspirin or vitamin D does not have profound effects on human longevity - if it did give us a third again as much life, that would certainly have been noted by now.
Vitamin D has much wider effects regulating calcium absorption and promoting bone growth - at least in the nematode worm, C. elegans. Research shows that vitamin D works through genes known to influence longevity and impacts processes associated with many human age-related diseases. The study may explain why vitamin D deficiency has been linked to breast, colon and prostate cancer, as well as obesity, heart disease and depression. "Vitamin D engaged with known longevity genes - it extended median lifespan by 33 percent and slowed the aging-related misfolding of hundreds of proteins in the worm. Our findings provide a real connection between aging and disease and give clinicians and other researchers an opportunity to look at vitamin D in a much larger context."
The study shines a light on protein homeostasis, the ability of proteins to maintain their shape and function over time. It's a balancing act that goes haywire with normal aging - often resulting in the accumulation of toxic insoluble protein aggregates implicated in a number of conditions, including Alzheimer's, Parkinson's and Huntington's diseases, as well as type 2 diabetes and some forms of heart disease. "Vitamin D3, which is converted into the active form of vitamin D, suppressed protein insolubility in the worm and prevented the toxicity caused by human beta-amyloid which is associated with Alzheimer's disease. Given that aging processes are thought to be similar between the worm and mammals, including humans, it makes sense that the action of vitamin D would be conserved across species as well. Vitamin D3 reduced the age-dependent formation of insoluble proteins across a wide range of predicted functions and cellular compartments, supporting our hypothesis that decreasing protein insolubility can prolong lifespan. We've been looking for a disease to associate with vitamin D other than rickets for many years and we haven't come up with any strong evidence. But if it's a more global marker of health or longevity as this paper suggests, that's a paradigm shift. Now we're talking about something very different and exciting."
Given adequate funding, researchers plan to test vitamin D in mice to measure and determine how it affects aging, disease and function - and hope that clinical trials in humans will go after the same measurements. "Maybe if you're deficient in vitamin D, you're aging faster. Maybe that's why you're more susceptible to cancer or Alzheimer's. Given that we had responses to vitamin D in an organism that has no bone suggests that there are other key roles, not related to bone, that it plays in living organisms."
Link: http://buckinstitute...ew-its-benefits
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