Are Humans Aging at Different Rates?

Do we age at different rates? At the American College of Nutrition conference today, we are being treated on this subject entitled “Nutritional and Hormonal Influences on Aging” by Nir Barzilai, MD, of Albert Einstein College of Medicine.

“Aging is the major risk factor for death from all chronic diseases,” Dr. Barzilai says, so we should be focused on strategies to modulate aging.

Is lifespan determined by genes or the environment? This is not a really good question, he says. It’s about “50 50” because it’s really “genes in an environment.” But even if it was 20 percent genetics, then you can still change the environment and increase lifespan.

He gives an example about how caloric restricted animals decreases all causes of death. In calorie-restricted animals fat is melted away, so this caused Barzilai to question, “what is the role of adipose tissue in aging.”

In an experiment on Zucker diabetic fatty rats, those with visceral fat removed lived significantly longer. The visceral fat removal prevented diabetes in the rats, which clearly shows that visceral fat is biologically active and causes diabetes.

So, can a study design depict the challenges of genetics in aging? There is a major barrier, however, in conducting a study of centenarians. You don’t have controls. As a control, you could use offspring of centenarians (Ashkenazi Jews).

Barzilia goes to a centenarian’s home and always asks, “Why do you think you lived so long?” In one example, there was a whole set of siblings who were centenarians. He put some data together on what was found.

(He shows the data and compares it to NHANES and it appears similar. In fact, some smoked and overall they exercised less.

“If anything, this group was worse,” said Barzalai. From age-related disease perspective, however, their age had been delayed for about 30 years.

Now, he says, we have an opportunity that no one else has because we can study specific genotypes and look at modeling changes in the frequency of a genotype as a function of age.

We can track the frequency trends of favorable longevity genotypes, which all have phenotypes. The best thing, obviously, is to have longevity running in the family. Plus, high HDL is a very good marker of a longevity genotype.

An interesting theory is the “rate of living” theory of aging that the more metabolically active you are, the shorter the life.

We’ve showed that a CETP-W genotype is protective. Merck is also developing a CETP inhibitor, which he is anxiously awaiting.

Dr. Barzilai is now showing images of several centenarians, who are so very cute, and some of the interactions they have.

In summary, the fact is that we all have different rates of aging and that both genetics and environment play factors, but it can be different for each of us.

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