Some People Have a Better Insulin Metabolism Than Others

It is an unfortunate fact of life that some people are dealt a better hand by chance and happenstance. This includes the biology we are born with, and its contributions to our life expectancy: for example, some people have better mitochondrial DNA than others, which does seem to be correlated with inherited longevity.

By way of a different example, let me point out recent research that shows a correlation between better insulin metabolism and inherited longevity. You might look back into the Fight Aging! archives for an introduction to insulin and its relationship with aging. It's a much-studied area:

Mainstream research on the biochemistry of aging and longevity - with an eye to slowing down aging rather than repairing it - is at this time primarily focused on a small number of areas. One is the cluster of mechanisms and signaling pathways associated with insulin and insulin-like growth factor 1 (IGF-1). You might recall that a tenfold increase in nematode life span was engineered via manipulation of IGF-1, for example.

Here is the research paper that caught my eye. The authors look at insulin sensitivity in long-lived families - how well the body's glucose metabolism operates, and whether that correlates well with longevity.

Familial longevity is marked by enhanced insulin sensitivity:

Insulin resistance is a risk factor for various age related diseases. In the Leiden Longevity study, we recruited long-lived siblings and their offspring. Previously we showed that, compared to controls, the offspring of long-lived siblings had a better glucose tolerance. Here, we compared groups of offspring from long-lived siblings and controls for the relation between insulin and glucose ... After adjustment for sex, age and fat mass, the insulin-mediated glucose disposal rate was higher in offspring than controls ... Furthermore, glucose disposal rate was significantly correlated with the mean age of death of the parents. In conclusion, offspring from long-lived siblings are marked by enhanced peripheral glucose disposal. Future research will focus on identifying the underlying biomolecular mechanisms, with the aim to promote health in old age.

Folk like you and I do in fact have a great deal of control over the course of our own insulin and glucose metabolisms. We can laze around and grow fat, or we can exercise and eat a diet that keeps us thin - type 2 diabetes, and the unseen biochemical damage that precedes it, is largely a choice. The Leiden offspring have a helping hand in this game in comparison to the rest of us, but it is only a helping hand, not a get out of jail free card. They can still damage themselves and become diabetic if they choose to take poor care of their health.

To me, it has long seemed that one of the more noble goals of longevity science is to make all the human variability in DNA and metabolism irrelevant when it comes to our life spans. Medicine of the near future will add far more healthy years to life - and far greater resistance to age-related disease - than even the best natural human metabolism. Longevity-enhancing therapies will make it possible for even the most genetically disadvantaged people to live in youthful vigor for far, far longer than we presently can.


The IGF pathway may not have to do with glucose and insulin with regard to obesity and diabetes per se, but with integrity and responsiveness of the immune system. By way of background, several studies aiming to identify longevity genes in model organisms such as the nematode C. elegans and the fruit fly D. melanogaster have shown that defense (i.e., immune system) genes are important players. Keep the free of disease with a healthy immune system and live longer.

I recently heard Shai Shen-Orr of Stanford Univeristy speak on networks of cytokine responses during aging. This involves immunosenescence and longevity. The group identified in samples of immune cells of elderly humans those that responded to cytokine activation and those that did not. The differences between cytokine responders and non-responders in those older subjects are enriched for longevity-associated genes. They found 151 genes including IGFR1 and FOXO1. Importantly, these two genes and others he listed are part of the insulin-response network.

Posted by: Larry Parnell at November 23rd, 2010 1:39 PM
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