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Aging fat as a cause for diabetes – the role of short telomeres

Older coupleOver the past couple of days, I have dug pretty deep into the metabolic associations between obesity, diabetes, and short telomeres. The end result is of course, accelerated aging.

But, more and more I have to tell you, I think aging is the real cause, or at least a major contributing factor to many of the diseases we associate with aging.  In other words, I think we have it ‘bass acwards’.  Fix aging and you’ll probably get rid of heart disease, Alzheimer’s, diabetes, arthritis and cancer, to name a few.

Now understand, we can accelerate the process greatly by eating poorly, sleeping poorly, exercising poorly, or not at all and stressing out more frequently.

From my clinical experience, there is a certain inevitability to many of these diseases and even people who seem to age well eventually get nailed by one or more of them when they run out of telomeres!

So, today I want to share with you a bit about diabetes and how aging fat may cause, or at the very least, contribute to it.

If you look at my most recent blogs, I talk about a hormone-like chemical made by fat cells called adiponectin.  The actions of adiponectin limit appetite, improve sugar control and insulin secretion and are generally anti-inflammatory and anti-obesity.

When fat cells get old, they have the same choices that other cells have. Either kick back in the rocking chair and wait for the grim reaper (senescence), or blow up from the inside out (apoptosis).

It’s pretty easy to imagine an exploding cell being the cause of inflammation, but it’s less clear about the rocking chair senescent ones.  Well, if you’ve read my stuff before, then you are aware of something called senstatic activation or more recently SAPs – the senescent activated phenotype.

Bottom line is, those cells sitting in the rocking chair are fairly oozing pus in terms of inflammatory chemicals.  In the process, they not only become non functional, but they support aging as an inflammatory process all by itself.  The only place I know where you may have heard this before is right here in my blog or my newsletters.  Mark my words, you’ll hear much more about it.

As a consequence of aging, fat cells make less adiponectin and take up less sugar – all of which can lead to or worsen age-related diabetes.

The consequence of all of this is shortened telomeres and a vicious cycle of more inflammation, less adiponectin and more destabilization of blood sugar.

Now here is the kicker.  Depending on the following — genetics, epigenetics and lifestyle — the same processes happen in every other cell and every other disease we associate with aging, including Alzheimer’s, cancer and heart disease, all of which are inflammatory.

Short and sweet: Do everything you can to keep your telomeres longer. I won’t belabor those steps here; you’ve heard them all before if you’ve read our book The Immortality Edge or read any of my blogs in the past three years.

Hint: fish oil and TA-65!

Doc

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