obesity -- 4/13/22

Today's selection -- from The Story of the Human Body by Daniel E. Lieberman. The quest to understand obesity:
"Putting the evidence together, the key point is that excessive weight gain relative to height during childhood is a strong risk fac­tor for future diseases associated with metabolic syndrome. A major reason that overweight children have a propensity to become over­weight or obese adults is that they develop and then retain for life more fat cells than average-weight children. Crucially, these extra fat cells are often inside the abdomen, packed around organs such as the liver, kidneys, and intestines. These visceral (belly) fat cells behave differently than fat elsewhere in the body in two important ways. First, they are several times more sensitive to hormones and thus tend to be more metabolically active, which means they are capable of storing and releasing fat more rapidly than fat cells in other parts of the body. Second, when visceral cells release fatty acids (something fat cells do all the time), they dump the molecules almost straight into the liver, where the fat accumulates and even­tually impairs the liver's ability to regulate the release of glucose into the blood. An excess of belly fat (a paunch) is therefore a much greater risk factor for metabolic disease than a high BMI.

"Although we still don't understand why some people store fat more readily than others, it is uncontroversial to state that all humans are adept at storing extra energy as fat and that all of us inherited trade-offs in the ways we use energy to grow and repro­duce that did not adapt us to thrive in conditions of too much energy. However, if you look at any graph of obesity rates over the last few decades, it is evident that the percentage of overweight people has remained constant while the percentage of obese people started rising rapidly in the 1970s and 1980s. What changed?

"The most widespread, partly true, yet overly simplistic explana­tion for why more people than ever are getting fatter is that more people than ever are eating more and being less active. As chapter 9 described, there is plenty of evidence that food industrialization over the last few decades has increased portion sizes and made food denser in calories. Other industrial 'advances,' such as the prolif­eration of cars and labor-saving devices, as well as more sitting, cause people to be less active. If you add up how many extra calo­ries people consume and how many fewer they expend, then you get larger energy surpluses, which translate into more fat.

"The 'calories in versus calories out' explanation for the obesity epidemic is not entirely wrong, but the situation is more compli­cated because we have also changed what we are eating. Remember that energy balance is regulated by hormones, especially insulin. Insulin's chief function is to shuttle energy from the food you have digested into your body's cells. It bears repeating that insulin rises when blood glucose levels rise, causing muscle and fat cells to take up and store some fraction of that sugar as fat. Insulin also causes fat (triglycerides) in the bloodstream to enter fat cells and simultaneously inhibits fat cells from releasing triglycerides back into the bloodstream. Insulin thus makes you fatter, regardless of whether the fat comes from eating carbohydrates or fat. According to some estimates, twenty-first-century adolescents in the United States secrete far more insulin than their parents produced when they were the same age in 1975.  It's no wonder more of them are overweight. Since insulin rises only after you eat foods that con­tain glucose, one obvious culprit for higher levels of insulin and more fat must be eating more glucose-rich foods, such as soda and cake. There are, however, many other factors that promote obe­sity, including two additional factors related to sugar. One is the rate at which you break foods down into glucose, which determines how quickly your body produces insulin. The other factor, which is more indirect, is how much fructose you eat, and how fast it hits your liver.

"To explore these effects of sugar on obesity let's compare how your body responds to eating a raw apple that weighs 100 grams (3.5 ounces) and a 56 gram (2 ounce) pack of fruit rolls that once upon a time were apples but then were industrially processed with sugar added for sweetness and any fiber removed (along with the apple's nutrients) to improve the product's shelf life. If we focus only on the sugar, one major difference evident between these two foods is that the apple has about 13 grams (a bit less than half an ounce) of sugar, whereas the fruit rolls have been packed with 21 grams (three quarters of an ounce) of sugar, hence nearly twice the calories. A second difference is the percentage of sugar types. The apple is about 30 percent glucose: the fruit roll is about 50 percent glucose. So eating the fruit rolls yields about the same amount of fructose and more than twice the glucose. Finally, the apple comes with a skin, and the apple's sugar resides within cells, both of which contain fiber. Fiber, also known as roughage, is the portion of the apple you cannot digest, but it plays a crucial role in how you digest the apple's sugars. Fiber makes up the walls of the cells that encase the sugars in the apple, slowing the rate at which you break down carbohydrates into sugars. Fiber also coats the food and the walls inside your gut, functioning as a barrier to slow the rate at which your intestine transports all those calories, especially the sugar, from your gut to your bloodstream and organs. Finally, fiber speeds the rate at which food passes through your gut, and it makes you feel full. As a result, when we compare the two apple products, the real apple not only supplies less sugar, but it makes you feel more sated and causes you to digest those sugars at a much more gradual rate. In contrast, the fruit rolls are termed high glycemic because they rapidly and markedly elevate blood sugar levels (a condition known as hyperglycemia).

"It is possible to get fat by eating too many apples, but you now have enough information to appreciate why the fruit roll is so much more likely to cause weight gain. Most obviously, the fruit roll has more calories. A second problem is the rate at which you get those calories. When you eat the apple, your insulin levels rise, but they rise gradually because the apple's fiber slows the rate at which you extract the glucose. As a result, your body has plenty of time to fig­ure out how much insulin to make to keep your blood glucose levels steady. In contrast, the fruit roll's double load of glucose passes rap­idly into your bloodstream, causing your blood sugar levels to sky­rocket, in turn causing your pancreas to frantically pump out lots of insulin, often too much. This overshoot commonly causes your blood sugar levels to subsequently plummet, and you then become ravenous, causing you to crave more fruit rolls or other calorie dense foods to raise your blood sugar quickly back to normal again. Put simply, foods rich in rapidly digested glucose supply lots of calo­ries and make you hungrier sooner. People who eat meals with a higher percentage of calories from protein and fat are less hungry for longer and thus eat less food overall than people whose calories come mostly from sugary and starchy foods. Less processed food with more fiber also induces hunger less quickly because the food remains longer in the stomach, which releases appetite-suppressing hormones.

"Glucose, however, is not the whole story, and the other sweet elephant in the room (or apple) is fructose. It has become common (sometimes justifiably) to demonize fructose, in large part because the invention of high fructose corn syrup has made sugar ridicu­lously cheap and abundant. But I hope you noted that the apple and the fruit roll contain about the same dose of fructose. In fact, chimps eat a diet of almost entirely fruit, so they must digest lots of fructose. Yet they and other fruit lovers don't get fat. Why is the fructose in raw fruit less likely to promote obesity than the fructose in the processed fruit or other fructose-laden foods like soda and fruit juice?

"The answer again has to do with the combination of the quantity and the rate at which the fructose is handled by the liver. In terms of quantity, one factor is domestication. Most of the fruits we eat today have been heavily domesticated to be much sweeter than their wild progenitors. Until recently, most apples were like crab apples and had considerably less fructose. In fact, almost all the fruits our ancestors ate were about as sweet as carrots -- hardly a food that promotes obesity. Even so, domesticated fruits are not pumped up on fructose compared to processed foods like fruit rolls and apple juice, and they also contain lots of fiber, which as we have discussed is removed from many industrial foods. Because of fiber, a raw apple's fructose is digested gradually and thus arrives more slowly at the liver. As a result, the liver has plenty of time to cope with the apple's fructose and can readily burn it at a leisurely pace. However, when processed foods deluge the liver with too much fructose too quickly, the liver is overwhelmed and converts most of the fructose into fat (triglycerides). Some of this fat fills up the liver, causing inflammation, which then blocks the action of insulin in the liver.

"This sets off a harmful chain reaction: the liver releases its stores of glucose into the bloodstream, which in turn drives the pancreas to release more insulin, which then shuttles the extra glucose and fat into cells. The rest of the fat the liver produces from rapid doses of fructose gets dumped into the bloodstream, where it, too, ends up in fat cells, your arteries, and other potentially bad places.

"If fructose sounds dangerous, it can be, but only in fast and large doses. For most of human evolution the only big, rapidly digest­ible source of fructose that our ancestors could acquire was honey. As chapter 9 described, gargantuan, cheap quantities of fructose first became available in the 1970s because of high fructose corn syrup. Before World War I, the average American consumed about 15 grams of fructose (half an ounce) a day, mostly from eating fruits and vegetables that surrender the fructose slowly; the aver­age American today consumes 55 grams (almost 2 ounces) per day, much of it from soda and processed foods made with table sugar. All in all, the chief reason why more people are getting fatter, especially in our bellies, is that processed foods are supply­ing them with too many calories, many from sugar -- both glucose and fructose -- in doses that are both too high and too rapid for the digestive systems we inherited. Although we evolved to eat plenty of carbohydrates and to store them efficiently, we are not well adapted to consume them so plentifully in the raw form that is found in sweet beverages like soda and juice (yes, fruit juice is a junk food), as well as cake, fruit rolls, candy bars, and countless other indus­trial foods. The problems caused by industrial diets explain why many traditional diets that evolved independently in different farm­ing societies around the globe all seem to do a good job of pre­venting weight gain. Classic Asian and Mediterranean diets, for example, seem to have little in common and both include plenty of starch (rice, or bread and pasta), yet both cuisines incorporate lots of fresh vegetables that contain fiber, and both are rich in protein as well as healthy fats, such as fish and olive oil (more on fats later). These diets also tend to be rich in other health-providing nutrients (another important topic). In short, it is harder to become over­weight and easier to keep weight off if you get your carbohydrates from an old-fashioned, commonsensical diet with lots of unpro­cessed fruits and vegetables.

"Diet plays a dominant role in explaining why more people around the globe are getting fatter, but there are several additional factors that are also important: genes, sleep, stress, the bacteria in your gut, and exercise."

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Daniel E. Lieberman


The Story of the Human Body




Copyright 2013 by Daniel E. Lieberman


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