Intelligent Medicine®

Why is it harder to keep the fat off as you grow older?

Mature Mexican couple enjoying the view during a hike through the woods. They both carry hiking poles and wear backpacks. He is in a plaid shirt and light colored pants, while she wears a gray long-sleeved top and patterned leggings.
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You’re 48, 59, or 72. You exercise vigorously and follow a disciplined low-carb diet. Yet the scale keeps ticking upward. Try as you might, those love handles enlarge, a muffin top appears, that former six-pack disappears, and back fat becomes your nemesis.

What’s worse is that the less cosmetically obvious fat that lines our intestinal organs—visceral fat—tends to accumulate. That’s bad news for blood sugar regulation, leading to insulin resistance and eventual outright diabetes.

It’s been nearly 10 years since I wrote an article entitled “10 reasons why it’s not your fault you’re fat”

The theme was that, contrary to conventional wisdom, maintaining weight is not just a matter of calories in, calories out; unlike machines, humans don’t conform to the traditional Law of Thermodynamics. Other factors are at play: Insulin resistance, inflammation, hormones, certain medications, even environmental toxicity, all play roles mediating the impact of caloric intake and energy expenditure. 

Surely, as we age, we slow down. Decreased endurance and musculoskeletal pain may limit our ability to harness exercise to expend calories. 

But there’s more to the story of why we inexorably gain fat as we age. An intriguing new study in Science“Distinct adipose progenitor cells emerging with age drive active adipogenesis”—suggests that our fat cells proliferate as a natural consequence of aging.

The paper notes that, as we age, our stem cells—the source of our tissues’ regenerative capacities—tend to decline. Hence the potential of stem cell therapies—not yet entirely realized—to restore function and rejuvenate failing organs.

But contrary to stem cells that reside in our muscles, brains, livers, hearts, bone marrow, etc., stem cells that are precursors to adipocytes, the cells that are repositories of fat, follow a different path: they increasewith age. 

The researchers’ experiments with mice revealed “adipogenesis is unlocked during middle age”, particularly in males. The same held true for human fat cells. Hello Dad-bod!

The editors of Science offer this perspective (“The cellular basis of middle-aged spread”) on the findings:

“Body fat in humans tends to increase in middle age (approximately 40 to 65 years old), with a preferential expansion of visceral adipose tissue (VAT) around internal organs in the abdominal cavity rather than subcutaneous adipose tissue (SAT) that is stored just beneath the skin. This increase in VAT-selective deposits is linked to declines in insulin sensitivity and a heightened risk of metabolic diseases. Total energy expenditure in humans remains relatively stable from ages 20 to 60 years old. However, if caloric expenditure is roughly constant, it is unclear how VAT continues to grow with age. On page 378 of this issue, Wang et al. report that a population of adipocyte progenitor cells (APCs) emerges in middle-aged VAT that drives adipogenesis. This APC subpopulation exhibits a high potential for differentiation into adipocytes, which suggests that adipose tissue in middle age is biologically primed for spread.” [my emphasis]

Admittedly, this is a rather fatalistic view. It implies that middle-aged people are simply programmed to store fat. Maybe natural selection favors modest fat accumulation in older adults as a hedge against famine or disease? It may have helped our ancestors, but it works against us in our modern obesogenic environment surrounded by plenty.

Another new study explains why, once overweight sets in, a vicious cycle ensues. Obesity drives intestinal inflammation, which in turn worsens insulin resistance, a feature of which is proliferation of fat stores. Ultimately diabetes sets in. 

The authors conclude: “The present study revealed a potentially novel role of the gastrointestinal tract in the maintenance of β cell regulation.”

But unlike the first study, the discovery of an intestinal link to metabolic derangements offers a path to remediation: Targeting colonic inflammation with medications reversed the insulin resistance. So, too, might a healthier diet, anti-inflammatory botanicals, and probiotics, I would maintain.

Studies like these may provide some consolation to the many middle-aged Americans who are valiantly fighting the Battle of the Bulge. Be merciful to yourselves and understand that maintaining a perfectly svelte figure as you get older can be challenging. Starving yourself with pharmaceuticals might yield dramatic short-term results, but it’s ultimately unsustainable. Instead, “Be all you can be” with the best possible diet, exercise, and lifestyle, and you will enjoy a long healthspan regardless of some hits to your ideal body image.

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