Why We Need Body Fat
Body fat is a highly specialized organ, critically important for health and longevity.
The following is an excerpt from Always Hungry? by David Ludwig.
In our weight-obsessed culture, it’s common to disparage the fat in our bodies. But body fat (scientifically termed “adipose tissue”) is a highly specialized organ, critically important for health and longevity.
Among its many functions, fat surrounds and cushions vital organs like the kidneys and insulates us against the cold. Body fat also signifies health, conferring beauty when distributed in the right amounts and locations. But critically, fat is our fuel tank—a strategic calorie reserve to protect against starvation.
Compared to other species our size, humans have an exceptionally large brain that requires an enormous amount of calories. The metabolic demands of the brain are so great that, under resting conditions, it uses about one of every three calories we consume. And this calorie requirement is absolute. Any interruption would cause immediate loss of consciousness, rapidly followed by seizure, coma, and death. That’s a problem, because until very recently in human history, access to calories had always been unpredictable. Our ancestors faced extended periods of deprivation when a hunt or a staple food crop failed, during harsh winters, or when venturing out across an ocean. The key to their survival was body fat.
If we go for more than a few hours without eating, the body must rely on stored fuels for energy, and these come in three basic types, familiar to anyone who reads a nutrition label: carbohydrate, protein, and fat. The body stores accessible carbohydrate in the liver and protein in muscle, but these are in dilute forms, surrounded by lots of water. In contrast, stored fat is highly concentrated, since fat tissue contains very little water. In addition, pure carbohydrate and protein have less than half the calories of pure fat, making them relatively weak sources of energy. For these reasons, liver and muscle contain only a small fraction of the calories in fat tissue (less than 600 compared to about 3,500 per pound). In the absence of body fat, even a muscular man would waste away in days without eating, whereas all but the leanest adults have enough body fat to survive many weeks.
And these fat cells aren’t just inert storage depots. Fat cells actively take up excess calories soon after meals and release them in a controlled fashion at other times, according to the body’s needs.
Fat tissue also responds to and emits a multitude of chemical signals and neural messages, helping fine-tune our metabolism and immune system. But when fat cells malfunction, big problems ensue.
We generally think that weight gain is the unavoidable consequence of consuming too many calories, with fat cells being the passive recipients of that excess. But fat cells do nothing of consequence without specific instructions—certainly not calorie storage and release, their most critical functions.
Insulin: The Fat Cell Fertilizer
Many substances produced in the body or contained in our diet directly affect fat cell behavior, chief among them the hormone insulin.
Insulin, made in the pancreas, is widely known for its ability to lower blood sugar. Problems with the production or action of insulin lead to the common forms of diabetes, specifically type 1 (previously called juvenile diabetes) and type 2 (a frequent complication of obesity).
But insulin’s actions extend well beyond blood sugar control, to how all calories flow throughout the body.
Soon after the start of a meal, insulin level rises, directing incoming calories—glucose from carbohydrate, amino acids from protein, and free fatty acids from the fat in our diet—into body tissues for utilization or storage. A few hours later, decreasing insulin level allows stored fuels to reenter the blood, for use by the brain and the rest of the body. Although other hormones and biological inputs play supporting roles in this choreography, insulin is the undisputed star.
Insulin’s effects on calorie storage are so potent that we can consider it the ultimate fat cell fertilizer. For example, rats given insulin infusions developed low blood glucose (hypoglycemia), ate more, and gained weight. Even when their food was restricted to that of the control animals, they still became fatter. Conversely, mice genetically engineered to produce less insulin had healthier fat cells, burned off more calories, and resisted weight gain, even when given a diet that makes normal mice fat.
In humans, high rates of insulin release from the pancreas due to genetic variants or other reasons cause weight gain. People with type 1 diabetes who receive excess insulin predictably gain weight, whereas those treated inadequately with too little insulin lose weight, no matter how much they eat. Furthermore, drugs that stimulate insulin release from the pancreas are also associated with weight gain, and those that block its release with weight loss.
If too much insulin drives fat cells to increase in size and number, what drives the pancreas to produce too much insulin? Carbohydrate, specifically sugar and the highly processed starches that quickly digest into sugar. Basically, any of those packaged “low-fat” foods made primarily from refined grains, potato products, or concentrated sugar that crept into our diet as we single-mindedly focused on eating less fat.
Our Fat Cells Make Us Overeat
All this is just Endocrinology 101, well-established information every first-year medical student should know. But it leads to a stunning possibility. The usual way of thinking about the obesity epidemic has it backward. Overeating hasn’t made our fat cells grow; our fat cells have been programmed to grow, and that has made us overeat.
Too much refined carbohydrate causes blood glucose to surge soon after a meal, which in turn makes the pancreas produce more insulin than would have ever been the case for humans in the past. High insulin levels trigger fat cells to hoard excessive amounts of glucose, fatty acids, and other calorie-rich substances that circulate in the blood. It’s like those floor‑to‑ceiling turnstiles you might see at a ballpark or in the subway.
People can pass freely in one direction, but horizontal crossbars prevent movement the other way. Insulin ushers calories into fat cells, but restricts their passage back out. Consequently, the body starts to run low on accessible fuel within a few hours, more quickly than normal.
When that happens, the brain registers a problem and transmits an unmistakable call for help—in the form of rapidly rising hunger. Eating is a sure and fast way to increase the supply of calories in the blood, and processed carbohydrates act the fastest. The brain exploits this fact, making us crave starchy, sugary foods, more so than anything else.
What would you rather have when your blood sugar is crashing: a bowl of fruit, a tall glass of full-fat milk, a large chicken breast, or a cinnamon sticky bun (each with the same number of calories)?
As usually happens, we give in to temptation and have the sticky bun, or the myriad other formulations of processed carbohydrate so readily available today. But this solves the “energy crisis” only temporarily, sets up the next surge-crash cycle, and, over time, accelerates weight gain.
Excerpted from the book Always Hungry? by David Ludwig, MD, PhD. Copyright © 2015 by David Ludwig, MD, PhD. Reprinted by permission of Grand Central Publishing. All rights reserved.
David Ludwig is author of Always Hungry (Grand Central, 2016). He’s a practicing endocrinologist at Boston Children’s Hospital and a professor of nutrition at the Harvard School of Public Health in Boston, Massachusetts.