What Happens Inside Your Body After a Doughnut

Metabolism is ultimately about energy flow—how your body decides where every calorie goes. Take a simple doughnut, for example. Once eaten, the carbohydrates are broken down into glucose, and the body must decide what to do with it.

Some glucose becomes glycogen, a form of short-term energy storage. About 75 percent of this glycogen goes into skeletal muscle and the remaining 25 percent into the liver—enough to fuel roughly two hours of intense exercise. The liver, meanwhile, acts as a regulator, converting glycogen back into glucose to keep blood sugar levels steady.

Here’s the delicate balance: the average adult has only about five grams—just a teaspoon—of glucose circulating at any moment. Only two extra grams can push levels into diabetic territory, showing how finely tuned our system is.

When glycogen stores are full, excess energy moves into fat storage, especially subcutaneous fat, the layer just under the skin. Contrary to popular belief, this fat is not inherently harmful—it’s the body’s safest energy reservoir. It functions as a metabolic buffer, soaking up surplus calories and releasing them when needed. Problems arise only when this storage buffer is overwhelmed, pushing fat into other organs like the liver, muscle, or pancreas—the key tipping point in metabolic diseases.

The Cell’s Cleanup Crew: How Autophagy, the Liver, and Fat Work Together to Keep You Alive
Inside every living cell, an intricate workshop operates around the clock. It builds, repairs, recycles, and reuses. One of its most remarkable mechanisms is autophagy—a process that represents the “cleanup” or catabolic side of metabolism.

Autophagy literally means “self-eating,” but it’s not as alarming as it sounds. When the cell stops producing new proteins for a while, it begins to break down old or damaged proteins and structures into their basic components, such as amino acids. These parts are then reused to build new cellular materials or to produce energy. Think of it as cellular recycling: the cell tears down its worn-out house and uses the salvaged bricks and lumber to make repairs or build anew.

If autophagy ever completely stopped, the organism would die. Just as neglecting to take out the garbage eventually turns a house unlivable, failure to clear out cellular junk suffocates the cell. Specialized organelles called lysosomes perform this cleaning job—they’re tiny sacs filled with enzymes that dismantle old proteins, invading pathogens, and toxic aggregates of damaged material. These aggregates are especially dangerous, as they’re linked to neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and ALS. In fact, mice lacking key autophagy genes suffer severe neurodegeneration within months.

As we age, however, autophagy slows down. The result? Cells become less efficient at handling stress, and the buildup of junk contributes to conditions such as osteoarthritis and cognitive decline. Understanding how to restore or improve autophagy could be a key to healthier aging.

The Role of mTOR: The Cell’s Master Regulator
Autophagy doesn’t act alone. It is tightly regulated by another important cellular pathway known as mTOR—short for “mechanistic Target of Rapamycin.”

mTOR exists in two complexes: mTORC1 and mTORC2, each handling distinct cellular duties. When mTORC1 is active, cells emphasize growth and building; when it’s inhibited, autophagy kicks in, allowing cleanup and renewal. Certain drugs, like rapamycin (originally used in transplant medicine), can inhibit mTORC1, which may help simulate some of the cellular benefits of fasting or calorie restriction—enhancing longevity and cellular efficiency.

The nuance lies in dosage and timing. Continuous inhibition of both complexes can cause side effects, but short or cyclic dosing that targets only mTORC1 seems to unlock protective, longevity-related effects. Scientists have long speculated that a drug selectively targeting mTORC1—without affecting mTORC2—could one day optimize these benefits without unintended drawbacks.

The Liver: The Body’s Metabolic Powerhouse
If autophagy is the cell’s janitor, the liver is the body’s processing plant. Among its many roles, the liver maintains blood-sugar balance, processes nutrients, and performs detoxification. It is also one of the most resilient organs known to science—capable of regenerating itself almost completely within weeks. After partial donation during a transplant, both donor and recipient can grow back near-full-sized, functional livers in just two months.

However, this metabolic hub can come under strain. Two related conditions—NAFLD (nonalcoholic fatty liver disease) and NASH (nonalcoholic steatohepatitis)—represent a growing modern epidemic. NAFLD occurs when the liver accumulates excess fat, while NASH adds inflammation to the mix, causing scarring similar to hepatitis. Although symptoms are subtle, these conditions are reversible through lifestyle interventions like weight loss. Once the excess liver fat is reduced, inflammation subsides and liver function can normalize.

The Bigger Picture: Balance and Renewal
Autophagy, mTOR, liver metabolism, and fat storage may seem like separate topics, but they are closely intertwined. Together, they form a dynamic system of building, recycling, and energy management. When balanced, this system supports clean, efficient cellular function and long-term health.

Our modern lifestyles—often high in calories and low in physical exertion—can easily disrupt this harmony. Supporting autophagy through intermittent fasting, moderate exercise, or balanced nutrition may help restore some of the natural rhythm our bodies evolved to maintain.

Ultimately, longevity is not just about adding years to life—it’s about keeping the microscopic machinery of life itself running smoothly. Each cell, every organ, every process plays its part in the symphony of renewal.

Source : Outlive: The Science & Art of Longevity by Peter Attia, Bill Gifford

Goodreads : https://www.goodreads.com/book/show/61153739-outlive

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