A Synopsis of Gary Taubes’ “Why We Get Fat And What To Do About it”

I just finished reading Gary Taubes’ book Why We Get Fat and What To Do About It and have summarized it for the benefit of those who have not had an opportunity to read this treatise of nutritional and metabolic intriguing and contrarian thoughts and ideas. The book is well worth your time and effort, but if you do not have the inclination to read it, my synopsis will give you the essential points.

A 1998 National Institute of Health report provided an excellent definition of obesity: a complex, multi-factorial chronic disease that develops from an interaction of genotype and the environment, involving the integration of social, behavioral, cultural, physiologic, metabolic and genetic factors. Taubes expands upon the NIH definition and not only rethinks and debunks conventional wisdom about weight gain and obesity, but literally decimates dogma into dirt, dust and debris. Be prepared to throw by the wayside much of what you understand as nutritional and metabolic givens! I will boldface his iconoclastic statements to make it easier for the reader.

Taubes’ premise is that obesity—the most prevalent form of “malnutrition,” is not a caloric imbalance (more calories in than out), but a hormonal imbalance, with a strong genetic component. If we happen to be born with a fat regulatory system that is efficient at turning calories into fat as opposed to burning them as fuel, and we stoke the genetic edict with a diet high in carbohydrates, then we are likely to get fat. Carbohydrates—particularly refined carbs, starchy vegetables and sugar/high fructose corn syrup—promote insulin release and hence fat storage, largely driving this pathway. Major culprits are carbs in liquid form including sodas, juices and beer as well as any refined, fiber-poor, easily digestible source of carbs.

He posits that it is not gluttony, sloth nor excessive caloric intake that are responsible for the majority of us being overweight or obese, but the way we process energy. Based upon genetic decree, some of us have a propensity to store calories as fat and at the other extreme there are the energy consumers, those who easily burn calories. So, energy regulation is responsible for gluttony and sloth—we are not fat because we overeat, but overeat because we get fat. Those with a predilection for storing calories as fat have fewer calories left to run the body. The more calories fat cells sequester, the more eating there must be in order to compensate—the body figures a way to get calories by increasing appetite or decreasing expenditure or both, promoting gluttony and sloth.

Taubes’ intriguing theory is that moderate eating and maintaining a physically active lifestyle are the metabolic benefits of a body that is programmed to remain lean, not evidence of moral rectitude. If our fat tissue is regulated so that it will not store significant calories as fat or our muscle tissue is regulated to take up plenty of calories to use for fuel, then we’ll either eat less, be more physically active, or both. This implies that elite athletes like marathoners and cyclists are not lean because they train vigorously and burn calories readily; rather, they are driven to expend calories because they are wired to burn calories and be lean. Analogous to greyhound dogs as opposed to basset hounds, genetics dictate how fuel gets partitioned to lean tissue or fat, and drives a propensity to exercise or not.

A central theme of the book is that our body fat (fuel) is carefully regulated, and hormones play a key role in this regulation—think how women fatten differently then men. Local factors also are relevant as some parts of our body are fat-free and others have a propensity for fat storage—think our hands vs. our abdomens. The importance of genetic factors has been discussed above. Essentially, genes regulate lipophilia (an affinity for stockpiling fat) to cause obesity. Fat tissue in obese individuals can be thought of in a similar way to malignant tumors, both of which have own agendas and grow regardless of food intake or exercise. If we can accept that our body fat is carefully regulated, obesity can be explained by a regulatory defect so small that it would be undetectable by any technique we know. If a laboratory animal that is genetically programmed for fat storage is put on a restricted diet from the get go, it responds by compromising its organs and muscles to satisfy its genetic drive to grow fat

Our fat stores are not static, but are dynamic with continuous mobilization (as fatty acids) and deposition (as triglycerides). Our pancreatic hormone insulin is the principal regulator of fat metabolism. Insulin controls how fuel is “partitioned” in our body—if we are “storers” of energy or “burners” of energy.
After a meal, insulin is released to get energy into our cells and when we go without food, as happens when we are asleep, insulin levels decrease and fat is released to be used as fuel. Insulin levels are determined primarily in response to carbohydrate intake in order to keep our blood sugar regulated. Everything insulin does promotes fat storage and decreases fat burning—this is why diabetics on insulin therapy get fat.

Insulin resistance occurs in response to chronic carbohydrate overload—the more insulin secreted, the more likely that the cells and tissues will become resistant to that insulin (as cells already have enough fuel within). As we age, our muscles get relatively insulin-resistant yet our fat cells always remain more sensitive than muscle. Insulin-resistant muscles partition more energy into fat, leaving less available for muscles and organs to use as fuel, so our cells adapt and use less energy. In Taubes’ mode of thinking, we don’t get fat because our metabolism slows, but our metabolism slows because we’re getting fat.

Taubes opines that energy consumption and energy expenditure are not independent but are dependent variables—cells burn less energy because they have less energy to burn. He believes that diets do not work because they result in us becoming hungry, cranky, depressed and lethargic and are therefore not sustainable. One of the most remarkable things about humans is our ability to adapt and compensate to changes in our environments. When we “starve” ourselves, we go into energy-conservation mode that essentially slows our metabolism. Ultimately, our bodies compensate for eating less and exercising more. Exercise makes us hungry and causes us to reduce our energy expenditure when we’re not exercising.

Excessive insulin secretion and insulin resistance causes metabolic syndrome. Metabolic syndrome is a spectrum of risk factors that increase the risk for diabetes, heart disease and stroke. It is defined as having three or more of the following:
• Blood pressure equal to or higher than 130/85
• Fasting blood sugar equal to or higher than 100
• Large waist circumference:
o Men – 40 inches or more
o Women – 35 inches or more
• Low HDL cholesterol:
o Men – under 40
o Women – under 50
• Triglycerides equal to or higher than 150

Insulin causes fat accumulation and stimulates fat cells to release inflammatory cells called cytokines. Insulin works in the liver to convert carbs to fat; this fat is sent off on particles that become small, dense LDL cholesterol, the dangerous kind that promote plaque formation in our arteries. Insulin causes our kidneys to resorb sodium, promoting hypertension; insulin impairs secretion of uric acid and stiffens our arterial walls. Chronically elevated blood sugars engender oxidative stress with accumulation of advanced glycation end products and provoke premature aging.

Now a bit of nutritional anthropology: For 99.5% of human existence (the Paleolithic era): mankind were hunter-gatherers subsisting on a diet in which 2/3 of calories were of animal origin and 1/3 of plant origin—a high protein, high fat, low carb diet that was of low glycemic index foods (carbs that are rather slowly absorbed), high fiber, slowly-digesting plants including seeds, nuts, roots, tubers and bulbs. For only 0.5% of our existence (the last 12,000 years), we have been in the agriculture era—so carbohydrate-rich foods are relatively new to our diet and in Taube’s opinion, it just might be that insufficient time has passed to allow us to evolve to be able to handle this carb-rich diet appropriately.
Studies on ethnic groups such as the Inuits and Maasai who are meat and fish eaters with no vegetable or fruit intake have interestingly shown that they have not suffered with diseases of Western civilization. We know that there are essential amino acids (building blocks of proteins) and fatty acids (building blocks of fats), but no such thing as an essential carbohydrate. All of the aforementioned suggest that a diet that primarily consists of protein and fat with limited carbohydrates, as has been the norm for many years, is a healthy diet that can help avoid the ravages of Western diseases. Taubes reports that wild animals maintain a stable weight no matter how abundant their food supply. Carnivorous animals never get fat, but herbivores (on a carb diet) can get fat, for example, the hippopotamus.

Dietary fats do not elevate our trigylceride levels and make us fat, but carbohydrates do. In the world according to Taubes, the predisposition for obesity is beyond our control, but is set off by the carbs we consume. The higher glycemic index foods—carbs that break down rapidly during digestion and release glucose swiftly into our blood, also typically the cheapest foods—promote fat deposition more so than lower glycemic index foods.

If we want to get leaner, we must lower our insulin levels and to do so requires carbohydrate restriction. Even if we don’t reduce our quantity of carb intake, we can improve the quality of our carb intake by eating healthier carbs—whole grains, fruits, vegetables, etc. There are numerous health benefits that accrue from a low carb diet. If we replace a high carb diet with a diet high in protein and fat and low in carbs, we end up with weight loss, higher HDL cholesterol , lower triglycerides, lower blood pressure, stable total cholesterol, higher LDL cholesterol and overall a decreased risk of heart disease.


This is the kind of information you will find in my book: Promiscuous Eating: Understanding and Ending Our Self-Destructive Relationship with Food. The website for the book is: www.promiscuouseating.com.   It provides information, a trailer, excerpts, ordering instructions, as well as links to a wealth of excellent resources on wellness and healthy living.  Promiscuous Eating is now available on Amazon Kindle.

Andrew Siegel

4 Responses to “A Synopsis of Gary Taubes’ “Why We Get Fat And What To Do About it””

  1. Judi Says:

    Great info..

  2. energy conservation Says:

    energy conservation…

    […]A Synopsis of Gary Taubes’ “Why We Get Fat And What To Do About it” « Promiscuous Eating[…]…

  3. Marilyn Monroe Says:

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  4. John Says:

    Thank you so much…I have heard that he takes several chapters before getting to the ‘meat’ of his book. Great summery

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