Finding the anti-aging sweet spot

Aging might be said, to paraphrase von Clausewitz, to be a mere continuation of growth by other means.

The growth-longevity trade-off

The process of aging still holds many mysteries, but we can say with some certainty that there is a trade-off between growth and longevity. The more growth that occurs, the faster and greater the aging. Within species, bigger animals age faster and die younger, and this holds true in humans. This is probably why men age faster and die younger than women: men are bigger, and as such have experienced more and faster growth. Shorter men live longer.

Professional (American) football players, who are known for their huge size, die at the average age of 55. Or it might even be 51. (There’s lots of talk about head injuries, which football players undoubtedly suffer from, but the idea that that kills them in their 50s strikes me as implausible. Muhammad Ali is still alive, and I’d bet he’s taken a lot more and more powerful shots to the head than almost any football player. N=1 of course.)

The average age of death of a sumo wrestler is around 63, about 15 years younger than the average Japanese man.

Whatever the mechanism of action or even whatever the ultimate truth is about the relationship between growth and longevity, plenty of evidence for it exists.

Growth hormone and aging

It seems that one of the reasons for the relationship lies with the growth hormone IGF-1. This hormone causes increased growth, but at later ages, increases the rates of cancer. IGF-1 activates mTOR (Nature Cell Biology), which in turn is implicated in “cancer, atherosclerosis, hypertension, heart hypertrophy, osteoporosis, type II diabetes, obesity, Alzheimer’s and Parkinson’s diseases, age-related macular degeneration, osteoarthritis and other diseases.” (Cell Cycle.)

Higher levels of IGF-1 make for a robust human being, able to survive the threats of infectious disease and wounds. But most of us are no longer in an environment where these threats are paramount. Those football players would likely be able to survive a battle or a plague better than others, but the consequence is that they age faster. In fact, one of the reasons humans are living longer is probably because the threats of infection and wounds are low, and slow-growing people with less robust constitutions who may not have been able to survive those threats now live longer, and age slower. (Aging.) In essence, there are more slow-aging people around because we’ve reduced the threats of infections and wounds.

Wasting away

On the other hand, with age comes a lack of vigor, susceptibility to infection, atrophy of muscles, bones, and brain, all around general deterioration of the body and of quality of life. Much of this can be traced to an increasing inability to repair and regenerate tissues.

Sarcopenia, or muscle wasting, is a very common affliction in the old, and can be devastating. Osteoporosis, the wasting of bone, is another common affliction.

As it happens, IGF-1, the same growth hormone that appears to increase aging, may also treat the diseases of atrophy seen in old age. Circulating levels of IGF-1 directly regulate bone density (Journal of Clinical Investigation), and therefore higher levels of this hormone may help prevent osteoporosis. Sarcopenia may be ameliorated with higher levels of IGF-1. (Mechanisms of Ageing and Development.)

Levels of IGF-1 are inversely correlated with measures of cognitive decline; the more IGF-1, the better the mental function in people aged 65 to 86. (Neuropsychobiology.)

So, I’d say we need balance. Intermittent fasting can lower levels of IGF-1, and hence slow the aging process and improve health biomarkers. But, if fasting isn’t done carefully, and followed by periods of adequate protein nutrition and exercise, preferably resistance training, it could potentially lead to muscle and bone loss and frailty.

Successful implementation of anti-aging must be carefully done. A useful analogy might be with exercise; too little leads to poor health, and too much – such as extensive distance running – can lead to damage.

The program I outlined in my anti-aging book seeks to balance the increase in autophagy brought on by fasting with a renewal of lean tissue through diet and exercise.

We want to slow or reverse the aging process so we can live longer lives in robust health, not so we can spend more years in a nursing home.



Leave a Comment:

Shawn says August 3, 2015

It seems like professional wrestlers tend to die really young too.

John says November 15, 2015

You mentioned your workout/fasting schedule in this book. Mine is different, and I wonder if you could comment on it. Here would be a typical (ideal) schedule:
M-W-F weight lifting in the am.
Tu-Th-Sa jogging 2.5 miles/day.
Before workout I eat yogurt with whey (appx 30g). This is when I break my fast. After workout, lunch; and eating within the next 8 hours, then fast for 16hrs. The reason I ask, is that you mentioned a 24 hr eating period after a workout. How should I prioritize: is regular intermittent fasting more important than feeding after exercise, or visa versa.? Or maybe I’m overthinking it? BTW I don’t always get to the gym that much, more like: weights M-Th, Jog Tu-Fri, nothing on Wed. At any rate, thanks to your books, I’m exercising more than I have in a loooooong time.

    P. D. Mangan says November 16, 2015

    Hi John, I think you’re doing OK with that schedule. Veteran lifters experience increased muscle synthesis for about 24 hours after a workout. But if you get enough calories and protein during your feeding window, you ought to be good. Martin Berkhan of Leangains has everyone (his clients) doing this, and it works well for them. So that’s the bottom line: not that you eat for exactly 24 hours after a workout, but sufficient quantity and quality of food.

Catching Up with Rogue Health - Rogue Health and Fitness says March 1, 2016

[…] So, does a ketogenic diet result in less muscle growth because of lower IGF-1? No, because muscle growth does not depend on systemic IGF-1. […]

Ben says March 2, 2016

Hi, could you clarify the explanation on why lower IGF-1 does not result in less muscle growth? Especially since higher IGF-1 ameliorates sarcopenia

    P. D. Mangan says March 2, 2016

    Ben, you’ve probably read that some of the “big” exercises, mainly squats and deadlifts, increase growth hormone acutely, which they do. So some studies have undertaken to see if that increases growth of other muscles. For instance, have one group of men do heavy squats and biceps curls, the other group do only biceps curls; result, the biceps grows and strengthens to the same extent in both groups, despite higher growth hormone in the squats group.

    The sweet spot is enough IGF-1 (which is promoted by GH) to prevent sarcopenia, but not too much to promote aging.

      Ben says March 4, 2016

      Alright. Do you think IGF-1 levels on a ketogenic diet are optimal/sufficient?
      Also do you know how IGF-1 secretion works? I’ve read that IGF-1 is elevated due to excess carbs, but I also read that in low-carb more HGH will be produced (as HGH is negatively correlated with blood glucose) which increases IGF-1. What is your take on this?

        P. D. Mangan says March 4, 2016

        IGF-1 secretion is promoted by protein and carbs. HGH does stimulate its production in the liver, but overall it looks like a ketogenic diet lowers IGF-1 levels. Is it optimal? Lots of bodybuilders claim they can’t gain muscle without carbs, but protein alone stimulates insulin and probably IGF-1 to the threshold level necessary for max protein synthesis and raising it further doesn’t do anything.

        Have you bought my books by any chance?

          Ben says March 4, 2016

          Understood, thanks. I haven’t bought any of your books. I am reading Body By Science atm, will probably get your book on iron once I’m done.

          P. D. Mangan says March 4, 2016

          OK, well, how many of your questions have I answered in the past few weeks? And you can’t be bothered to buy any of my books, but you have plenty of money for others apparently. I won’t be answering any more questions. Jesus. I’m doing this for free, I must be crazy.

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