Book Notes: 'Why We Get Fat' by Gary Taube
As I explained in that post, I find it helpful to do a ‘deep dive’ on some of the books I want to be deeply influenced by. For a variety of reasons, I have a tolerably high degree of physical fitness. I’d like to retain this fitness for a long time. Much of the fitness equation is “don’t have extra body fat”, so to that end, I’ve been doing reading on the topic.
Given how prevalent being overweight or obese is in our society, the small investment of reading a few books that might point one towards a proper course of action has ludicrously high returns.
Notes on formatting
I will be freely interjecting my thoughts throughout the rest of this review. When I quote the author, it will be denoted like such:
These are words the author has written
Sometimes they’ll extend for several paragraphs
I may choose to italicize or make bold portions of the quotations from the books. In general, these are my decisions, not the author’s.
If there are
[words wrapped in brackets]
it’s me editorializing to load the context of the quote.
My collected notes from Why we get fat: and what to do about it
Getting fat is not a “calories-in/calories-out” problem, or “eat too much, exercise too little” problem. It’s a hormonal regulation problem.
In honor of the laws of thermodynamics that they’re replacing, we’ll call these the laws of adiposity. The First Law:
Body fat is carefully regulated, if not exquisitely so.
This is true even though some people fatten so easily that it’s virtually impossible to imagine.
What I mean by “regulated” is that our bodies, when healthy, are working diligently to maintain a set amount of fat in our fat tissue — not too much and not too little — and that this, in turn, is used to assure a steady supply of fuel to the cells.
The implication (our working assumption) is that if someone gets obese it’s because this regulation has been thrown out of whack not that it’s ceased to exist.
Lots of Taube’s assessment of nutrition comes from research done in Europe, specifically Germany and Austria. It got lost to the modern medical establishment, though.
Anti-German sentiment in the postwar medical community, understandable as it may have been, assuredly didn’t help matters.
The authorities writing about obesity in the United States after the war treated the German medical literature as though it didn’t exist, even though it was Germans and Austrians who had founded and done most of the meaningful research in the fields of nutrition, metabolism, endocrinology, and genetics, which means all the fields relevant to obesity.
(The one notable exception was Hilde Bruch, a German herself, who discussed this prewar literature extensively.)
Once the psychologists took over in the 1960s and obesity officially became an eating disorder — a character defect but in kinder words — any hope that these authorities would pay attention to how the fat tissue was regulated effectively vanished.
The science I’ll be talking about was worked out by researchers between the 1920s and the 1980s. At no point was it particularly controversial. Those who did the research agreed that this was how it worked, and they still agree.
The problem, though, as I hope I’ve made clear, is that the “authorities” on obesity, even those who weren’t psychologists or psychiatrists, came to believe that they knew what makes people fat: overeating and sedentary behavior.
As a result, nothing else on the subject really mattered to them, including the science of how fat tissue is regulated. They either ignored it entirely or actively rejected it because they didn’t like its implications (which I’ll discuss later). Despite their head-in-the-sand attitude, the regulation of our fat tissue does matter. Whether we get fat or stay lean depends on it.
Why fat accumulates
Simple question: Why do we store fat in the first place? What’s the reason? Okay, some of it provides insulation to keep us warm, and some of it provides padding to protect the more fragile structures within, but what about the rest? The fat around the waist, for instance? The way the experts typically see it is that fat storage works as a kind of long-term savings account — like a retirement account that you can dip into only in dire need.
The idea is that your body takes excess calories and stashes them away as fat, and they remain in the fat tissue until you someday find yourself sufficiently underfed (because you’re now dieting or exercising or perhaps stranded on a desert island) that this fat is mobilized. You then use it for fuel.
But it has been known since the 1930s that this conception is not even remotely accurate.
As it happens, fat is continuously flowing out of our fat cells and circulating around the body to be used for fuel and, if it’s not used for fuel, returned to the fat cells.
This goes on regardless of whether we’ve recently eaten or exercised.
In 1948, after this science was worked out in detail, Ernst Wertheimer, a German biochemist who had emigrated to Israel and is considered the father of the field of fat metabolism, put it this way: “Mobilization and deposition of fat go on continuously, without regard to the nutritional state of the animal.”
Insulin is the “god-level” hormone that regulates fat accumulation or fat loss
Since insulin is the primary regulator of fat metabolism, it’s not surprising that it’s the primary regulator of LPL activity. Insulin activates LPL on fat cells, particularly the fat cells of the abdomen; it “upregulates” LPL, as researchers say.
The more insulin we secrete, the more active the LPL on the fat cells, and the more fat is diverted from the bloodstream into the fat cells to be stored.
Insulin also happens to suppress LPL activity on the muscle cells, assuring that they won’t have many fatty acids to burn. (Insulin also tells muscle cells and others in the body not to burn fatty acids but to continue burning up blood sugar instead.)
This means that when fatty acids do escape from a fat cell, if insulin levels happen to be high, these fatty acids won’t be taken up by the muscle cells and used for fuel. They’ll end up back in the fat tissue.
Insulin also influences an enzyme that we haven’t discussed, hormone-sensitive lipase, or HSL for short. And this may be even more critical to how insulin regulates the amount of fat we store.
Just as LPL works to make fat cells (and us) fatter, HSL works to make fat cells (and us) leaner.
It does so by working inside the fat cells to break down triglycerides into their component fatty acids, so that those fatty acids can then escape into the circulation. The more active this HSL, the more fat we liberate and can burn for fuel and the less, obviously, we store.
Insulin also suppresses this enzyme HSL, and so it prevents triglycerides from being broken down inside the fat cells and keeps the outward flow of fatty acids from the fat cells to a minimum.
And it takes just a little bit of insulin to accomplish this feat of shutting down HSL and trapping fat in our fat cells. When insulin levels are elevated, even a little, fat accumulates in the fat cells.
In short, everything insulin does in this context works to increase the fat we store and decrease the fat we burn. Insulin works to make us fatter.
If insulin matters so much, how do we use that to our advantage?
The bottom line is something that’s been known (and mostly ignored) for over forty years.
The one thing we absolutely have to do if we want to get leaner — if we want to get fat out of our fat tissue and burn it — is to lower our insulin levels and to secrete less insulin to begin with.
Here’s how Yalow and Berson phrased it back in 1965:
“releasing fat from our fat tissue and then burning it for energy”, they wrote, “requires only the negative stimulus of insulin deficiency.”
If we can get our insulin levels to drop sufficiently low (the negative stimulus of insulin deficiency), we can burn our fat.
If we can’t, we won’t. When we secrete insulin, or if the level of insulin in our blood is abnormally elevated, we’ll accumulate fat in the fat tissue. That’s what the science tells us.
But another important factor is just how sensitive to insulin your cells happen to be and how quickly they become insensitive — the property called “insulin resistance” — in response to the insulin you secrete.
This idea of being resistant to insulin is absolutely critical to understanding the reasons we get fat and also many of the diseases associated with it. I’ll return to it frequently.
As I said, it’s carbohydrates that ultimately determines insulin secretion and insulin that drives the accumulation of body fat.
Not all of us get fat when we eat carbohydrates, but for those of us who do get fat, the carbohydrates are to blame; the fewer carbohydrates we eat, the leaner we will be.
A comparison with cigarettes is apt. Not every longtime smoker gets lung cancer. Only one in six men will, and one in nine women. But for those who do get lung cancer, cigarette smoke is far and away the most common cause.
In a world without cigarettes, lung cancer would be a rare disease, as it once was. In a world without carbohydrate-rich diets, obesity would be a rare condition as well.
Not that all foods that contain carbohydrates are equally fattening. This is a crucial point. The most fattening foods are the ones that have the greatest effect on our blood sugar and insulin levels.
These are the concentrated sources of carbohydrates, and particularly those that we can digest quickly:
- anything made of refined flour (bread, cereals, and pasta)
- liquid carbohydrates (beers, fruit juices, and sodas)
- starches (potatoes, rice, and corn)
These foods flood the bloodstream quickly with glucose. Blood sugar shoots up; insulin shoots up. We get fatter. Not surprisingly, these foods have been considered uniquely fattening for nearly two hundred years (as I’ll discuss later).
Total sugar consumption (“caloric sweeteners,” as the Department of Agriculture calls them, to distinguish them from “non-caloric” artificial sweeteners) promptly increased from roughly 120 pounds per capita yearly to 150, since Americans didn’t realize that high-fructose corn syrup was just another form of sugar.
The message of Adiposity [aka “getting fat”] 101 is simple enough: if you’re predisposed to get fat and want to be as lean as you can be without compromising your health, you have to restrict carbohydrates and so keep your blood sugar and insulin levels low.
The point to keep in mind is that you don’t lose fat because you cut calories; you lose fat because you cut out the foods that make you fat — the carbohydrates.
If you get down to a weight you like and then add these foods back to the diet, you’ll get fat again.
That only some people get fat from eating carbohydrates (just as only some get lung cancer from smoking cigarettes) doesn’t change the fact that if you’re one of those who do, you’ll only lose fat and keep it off if you avoid these foods.
This isn’t the only injustice involved here. It’s not even the worst of them. As I said in the introduction, the implications of Adiposity 101 do not include the ability to lose weight or maintain it without sacrifice. So far, the message is that carbohydrates make us fat and keep us fat.
But the precise foods responsible for making us fat are also the ones we’re likely to rank highest on a list of foods we crave and would never want to live without—pasta, bagels, bread, French fries, sweets, and beer among them.
Low-carb/high-fat diets are not bad for you
Late-1900’s and early-2000s research on diet was often championing the exactly wrong approach to weight management. Something was going wrong then, given the skyrocketing rate of obesity.
The Times article, “New Diet Decried by Nutritionists: Dangers Are Seen in Low Carbohydrate Intake,” quoted Harvard’s Jean Mayer as claiming that to prescribe carbohydrate-restricted diets to the public was “the equivalent of mass murder.”
Mass murder. Mayer’s logic? Well, first, as the Times explained, “It is a medical fact that no dieter can lose weight unless he cuts down on excess calories, either by taking in fewer of them, or by burning them up.”
We now know that this is not a medical fact, but the nutritionists didn’t in 1965, and most of them still don’t.
Second, because these diets restrict carbohydrates, they compensate by allowing more fat.
It’s the high-fat nature of the diets, the Times explained, that prompted Mayer to make the mass murder accusation. This is how such diets have been treated ever since.
The belief that dietary fat causes heart disease — saturated fat, particularly — led directly to the idea that carbohydrates prevent it.
By the early 1980s, Jane Brody of The Times, the single most influential journalist on the nutrition beat for the last forty years, was telling us “we need to eat more carbohydrates” and advocating starches and bread as diet foods. “Not only is eating pasta at the height of fashion,” she wrote, “it can help you lose weight.”
In 1983, when British authorities compiled their “Proposals for Nutritional Guidelines for Health Education in Britain,” they had to explain that “the previous nutritional advice in the UK to limit the intake of all carbohydrates as a means of weight control now runs counter to current thinking.”
This logic may have reached the pinnacle of absurdity in 1995 (at least I hope it did), when the American Heart Association published a pamphlet suggesting that we can eat virtually anything with impunity — even candy and sugar — as long as it’s low in fat: “To control the amount and kind of fat, saturated fatty acids and dietary cholesterol you eat,” the AHA counseled, “choose snacks from other food groups such as … low-fat cookies, low-fat crackers … unsalted pretzels, hard candy, gum drops, sugar, syrup, honey, jam, jelly, marmalade (as spreads).”
When we pay attention to how HDL tracks with heart disease — not just LDL and total cholesterol — we learn something about the purported risks and benefits of the foods we might choose to eat instead of fattening carbohydrates: red meat, say, or eggs and bacon, even lard and butter.
It’s important to understand that the fat in these foods is not all saturated. Rather, these animal fats are mixtures of saturated and unsaturated fats, just as vegetable fats are, and these fats all have different effects on our LDL and HDL cholesterol.
Take lard, for example, which has long been considered the archetypal example of a killer fat. It was lard that bakeries and fast-food restaurants used in large quantities before they were pressured to replace it with the artificial trans fats that nutritionists have now decided might be a cause of heart disease after all.
You can find the fat composition of lard easily enough, as you can for most foods, by going to a U.S. Department of Agriculture website called the National Nutrient Database for Standard Reference. You’ll find that nearly half the fat in lard (47 percent) is monounsaturated, which is almost universally considered a “good” fat. Monounsaturated fat raises HDL cholesterol and lowers LDL cholesterol (both good things, according to our doctors).
Ninety percent of that monounsaturated fat is the same oleic acid that’s in the olive oil so highly touted by champions of the Mediterranean diet. Slightly more than 40 percent of the fat in lard is indeed saturated, but a third of that is the same stearic acid that’s in chocolate and is now also considered a “good fat,” because it will raise our HDL levels but have no effect on LDL (a good thing and a neutral thing).
The remaining fat (about 12 percent of the total) is polyunsaturated, which actually lowers LDL cholesterol but has no effect on HDL (also a good thing and a neutral thing).
In total, more than 70 percent of the fat in lard will improve your cholesterol profile compared with what would happen if you replaced that lard with carbohydrates. The remaining 30 percent will raise LDL cholesterol (bad) but also raise HDL (good). In other words, and hard as this may be to believe, if you replace the carbohydrates in your diet with an equal quantity of lard, it will actually reduce your risk of having a heart attack.
It will make you healthier. The same is true for red meat, bacon and eggs, and virtually any other animal product we might choose to eat instead of the carbohydrates that make us fat. (Butter is a slight exception, because only half the fat will definitively improve your cholesterol profile; the other half will raise LDL but also raise HDL.)
What counts as “sugar” for the purposes of this book (and your life)
In an attempt to use the knowledge contained within this book, I want to be better at parsing information in ingredient lists and the nutritional panel included on the back of most food items. If one wants to avoid sugar, one needs to be aware of the many different words used to describe sugar.
Biochemically, the term “sugar” refers to a group of carbohydrate molecules consisting, as the word “carbohydrate” implies, of atoms of carbon and hydrogen. The names of these carbohydrates all end in “-ose”—glucose, galactose, dextrose, fructose, lactose, sucrose, etc. All of these sugars will dissolve in water, and they all taste sweet to us, although to a greater or lesser extent. When physicians or researchers refer to “blood sugar,” they’re talking about glucose, because it constitutes virtually all of the sugar circulating in our blood.
The more common usage of “sugar” refers to sucrose, the white crystalline variety that we put in our coffee or tea or sprinkle on our morning cereal. Sucrose in turn is composed of equal parts glucose and fructose, the two smaller sugars (monosaccharides, in the chemical lingo) bonded together to make the larger one (a disaccharide).
Fructose, found naturally in fruits and honey, is the sweetest of all these sugars, and it’s the fructose that makes sucrose particularly sweet. Lately, researchers have been asking whether fructose is toxic, because it’s the significant amount of fructose in sugar (sucrose) that differentiates it from other carbohydrate-rich foods, such as bread or potatoes, which break down upon digestion to mostly glucose alone. Because we never consume the fructose without the glucose, though, the appropriate question is whether sucrose, the combination of roughly equal parts fructose and glucose, is toxic, not one alone.
This would be confusing enough without the introduction in the 1970s of high-fructose corn syrup (HFCS), which replaced a significant part of the refined sugar (i.e., sucrose) consumed in the United States over the decade that followed. High-fructose corn syrup comes in different formulations; the most common one is known as HFCS-55, because it’s 55 percent fructose and 45 percent glucose.
Sugar by any other name is still sugar! All of these are forms of sugar:
- agave syrup
- high-fructose corn syrup
- maple syrup
- brown-rice syrup
- evaporated cane juice
- cane juice
- fruit-juice concentrate
- corn sweetener