Obesity is a major risk factor for a list of diseases that seems to be getting longer every week. Recent additions include metastasizing prostate cancer and cirrhosis of the liver. Over the past few years, brain shrinkage and Alzheimer’s disease have been added, as have arthritis, various cancers, and even incontinence. Scanning the multitude of woes linked to obesity, you can’t help but think that getting fat does more than make people sick—it may actually speed up the fundamental aging process, greatly increasing the risks of every single thing that can go wrong as we age. If so, you could view your bathroom scale as a kind of crude speedometer for your rate of biodegrading.
This is more than a personal health issue. As I recently wrote on the Miller-McCune website, obesity is a leading contributor to ballooning healthcare costs, and more than any other factor such costs are responsible for busting government budgets. Thus, it’s arguable that one of the main drivers of our nation’s fiscal malaise is a little-recognized phenomenon: The obesity epidemic has prematurely aged a third or more of the population by a couple of decades, presenting us with huge medical bills for a myriad “old-age” diseases that we had once expected would come due gradually with population aging over the next few decades. Indeed, you might say this issue is the hidden elephant in the room as policymakers furiously debate what to do about exploding entitlement costs and the federal deficit.
This idea that obesity is tantamount to accelerated aging makes sense in light of what’s known about calorie restriction: In general, the more calories that are cut from animals’ diets (without causing malnutrition or starvation), the longer they live in good health. This suggests that, roughly speaking, the richer the diet, the faster the aging. (I say roughly because various studies indicate that unusually thin people have higher mortality rates than normal-weight ones, which probably rules out the existence of a simple relationship between calorie intake, body-mass index and aging. On the other hand, it may be that many thin people are thin because they suffer from subtle, long-term health problems—former smokers, for example, may seem perfectly healthy in midlife but harbor subtle lung damage whose ill effects are manifested many years later in the form of wasting diseases such as chronic obstructive pulmonary disease. Thus, in many cases unusual thinness may well be an effect of subtle, underlying health problems that play out over many years to increase the risk of early death—not a cause of them.)
There’s also growing evidence that obesity engenders many of the same changes that aging does at the cellular and molecular levels. For instance, potbellies, formally called visceral fat, have a strong pro-inflammatory effect, and hundreds of studies over the past two decades have suggested that low-level, body-wide inflammation, which tends to increase with age, is a key driver of just about every major disease of aging, from Alzheimer’s to arthritis. (It appears that such inflammation even increases the risk of chronic stress and depression.)
Fascinating connections between obesity and aging have also come to light as in recent research on a gene called mTOR (mammalian target of rapamycin). Mikhail Blagosklonny, a researcher at the Roswell Park Cancer Institute in Buffalo, has elucidated these connections in a compelling new theory of aging. Briefly, the theory rests on the fact that mTOR’s main mission is to gear our cells’ growth to food intake—mTOR is activated in tandem with rising nutrient levels, giving cells a green light to grow and divide when inner resources are adequate for that; when they’re scarce, mTOR is deactivated and its pro-growth signal wanes. Here’s the key thing: Suppression of mTOR by reduced food intake also activates metabolic pathways whose combined effect both conserves energy and opposes the aging process. They include “stress-response” pathways, which help fend off cellular damage, and a cellular recycling function, called autophagy, which clears away molecular gunk that tends to build up as we age and contribute to everything from neuronal decay to wrinkles. As Blagosklonny explains, mTOR activation is essential to foster growth and development early in life. But after that, its unchecked pro-growth activity—he compares mTOR to a brakeless car barreling toward disaster as we age—fosters various forms of damaging cellular hyperactivation, leading to atherosclerosis, accumulation of fat, low-level inflammation, insulin resistance, and other pro-aging processes that culminate with the onset of cancer, heart disease, dementia, and other killer diseases. Add rich diets and sedentary lifestyles to this picture and the brakeless mTOR car speeds up and goes over the cliff faster than ever.
In an extended riff on Blagosklonny’s theory, I recently proposed in a paper in the journal Aging that the relentlessly rising prevalence of obesity is behind a trend toward increasingly rapid sexual maturation in recent decades—in effect, the aging process has been starting ever earlier as kids have gotten fatter. This phenomenon, which I speculate has roots in our species’ evolutionary past, has especially dismaying implications about our society’s oncoming tsunami of obesity-associated diseases and skyrocketing healthcare costs.
To be sure, the detailed physiological effects of obesity are probably different in some important respects from those of normal aging. In particular, it seems likely that obesity accelerates the decay of certain organs more than others, and that this organ-specific pattern of deterioration is somewhat different from the deterioration caused by aging without obesity—normal aging, for example, isn’t known as a risk factor for liver cirrhosis. But the ultimate fallout from these two, somewhat different patterns of decay is remarkably similar—as one researcher put it, when it comes to chronic diseases, being obese is roughly the same as being aged by a couple of decades.
In sum, you might say that obesity doesn’t so much speed up our journey toward late-life decrepitude as forcibly steer us onto a short-cut toward it. I can’t think of a better example of haste making waste.
Does obesity speed up aging?
Obesity is a major risk factor for a list of diseases that seems to be getting longer every week. Recent additions include metastasizing prostate cancer and cirrhosis of the liver. Over the past few years, brain shrinkage and Alzheimer’s disease have been added, as have arthritis, various cancers, and even incontinence. Scanning the multitude of woes linked to obesity, you can’t help but think that getting fat does more than make people sick—it may actually speed up the fundamental aging process, greatly increasing the risks of every single thing that can go wrong as we age. If so, you could view your bathroom scale as a kind of crude speedometer for your rate of biodegrading.
This is more than a personal health issue. As I recently wrote on the Miller-McCune website, obesity is a leading contributor to ballooning healthcare costs, and more than any other factor such costs are responsible for busting government budgets. Thus, it’s arguable that one of the main drivers of our nation’s fiscal malaise is a little-recognized phenomenon: The obesity epidemic has prematurely aged a third or more of the population by a couple of decades, presenting us with huge medical bills for a myriad “old-age” diseases that we had once expected would come due gradually with population aging over the next few decades. Indeed, you might say this issue is the hidden elephant in the room as policymakers furiously debate what to do about exploding entitlement costs and the federal deficit.
This idea that obesity is tantamount to accelerated aging makes sense in light of what’s known about calorie restriction: In general, the more calories that are cut from animals’ diets (without causing malnutrition or starvation), the longer they live in good health. This suggests that, roughly speaking, the richer the diet, the faster the aging. (I say roughly because various studies indicate that unusually thin people have higher mortality rates than normal-weight ones, which probably rules out the existence of a simple relationship between calorie intake, body-mass index and aging. On the other hand, it may be that many thin people are thin because they suffer from subtle, long-term health problems—former smokers, for example, may seem perfectly healthy in midlife but harbor subtle lung damage whose ill effects are manifested many years later in the form of wasting diseases such as chronic obstructive pulmonary disease. Thus, in many cases unusual thinness may well be an effect of subtle, underlying health problems that play out over many years to increase the risk of early death—not a cause of them.)
There’s also growing evidence that obesity engenders many of the same changes that aging does at the cellular and molecular levels. For instance, potbellies, formally called visceral fat, have a strong pro-inflammatory effect, and hundreds of studies over the past two decades have suggested that low-level, body-wide inflammation, which tends to increase with age, is a key driver of just about every major disease of aging, from Alzheimer’s to arthritis. (It appears that such inflammation even increases the risk of chronic stress and depression.)
Fascinating connections between obesity and aging have also come to light as in recent research on a gene called mTOR (mammalian target of rapamycin). Mikhail Blagosklonny, a researcher at the Roswell Park Cancer Institute in Buffalo, has elucidated these connections in a compelling new theory of aging. Briefly, the theory rests on the fact that mTOR’s main mission is to gear our cells’ growth to food intake—mTOR is activated in tandem with rising nutrient levels, giving cells a green light to grow and divide when inner resources are adequate for that; when they’re scarce, mTOR is deactivated and its pro-growth signal wanes. Here’s the key thing: Suppression of mTOR by reduced food intake also activates metabolic pathways whose combined effect both conserves energy and opposes the aging process. They include “stress-response” pathways, which help fend off cellular damage, and a cellular recycling function, called autophagy, which clears away molecular gunk that tends to build up as we age and contribute to everything from neuronal decay to wrinkles. As Blagosklonny explains, mTOR activation is essential to foster growth and development early in life. But after that, its unchecked pro-growth activity—he compares mTOR to a brakeless car barreling toward disaster as we age—fosters various forms of damaging cellular hyperactivation, leading to atherosclerosis, accumulation of fat, low-level inflammation, insulin resistance, and other pro-aging processes that culminate with the onset of cancer, heart disease, dementia, and other killer diseases. Add rich diets and sedentary lifestyles to this picture and the brakeless mTOR car speeds up and goes over the cliff faster than ever.
In an extended riff on Blagosklonny’s theory, I recently proposed in a paper in the journal Aging that the relentlessly rising prevalence of obesity is behind a trend toward increasingly rapid sexual maturation in recent decades—in effect, the aging process has been starting ever earlier as kids have gotten fatter. This phenomenon, which I speculate has roots in our species’ evolutionary past, has especially dismaying implications about our society’s oncoming tsunami of obesity-associated diseases and skyrocketing healthcare costs.
To be sure, the detailed physiological effects of obesity are probably different in some important respects from those of normal aging. In particular, it seems likely that obesity accelerates the decay of certain organs more than others, and that this organ-specific pattern of deterioration is somewhat different from the deterioration caused by aging without obesity—normal aging, for example, isn’t known as a risk factor for liver cirrhosis. But the ultimate fallout from these two, somewhat different patterns of decay is remarkably similar—as one researcher put it, when it comes to chronic diseases, being obese is roughly the same as being aged by a couple of decades.
In sum, you might say that obesity doesn’t so much speed up our journey toward late-life decrepitude as forcibly steer us onto a short-cut toward it. I can’t think of a better example of haste making waste.