Good Calories, Bad Calories

by Matthew Kent | Nov 20, 2017

If you want a deep dive into the science of obesity and chronic disease, this is it.

Gary Taubes is a journalist who started out wanting to be a scientist. He was studying physics at Harvard, but was forced to find a new major when he got a bad grade in a quantum mechanics class.

He switched to journalism and started writing about science and how hard it is to do it well and wrote about physicists who thought they had discovered phenomena that they hadn’t actually discovered.

Eventually one of his physicist friends told him that if he liked doing exposes, he needed to go into public health where the science was terrible.

His first story ended up exploring the popular myth that eating salt causes hypertension. He basically concluded that the evidence was so weak that the only people who could believe it were people who were already 100% convinced.

After that he was looking for a new story and happened to see the man who he regarded as one of the worst scientists ever get on some television show and claim credit for awakening America to the dangers of salt and fat.

He knew then that his next article needed to be about fat. Bad scientists he reasoned, almost never get the right answer.

So he started researching the diet-heart hypothesis, the notion that eating fat and/or cholesterol is what is responsible for heart disease. That also led him to the closely historically related hypothesis known as the energy balance hypothesis, the notion that we get fat because we eat too much and exercise too little.

He spent years researching how these ideas came about and what the evidence for them is. What he discovered was that not only is the evidence for the diet-heart hypothesis and the energy balance hypothesis virtually non-existent, there is another hypothesis for why we get fat that existed before these two faulty ideas came about, one that has stuck around in one form or another right up until today and which does a much better job explaining all the observations.

This “alternative” hypothesis is that the cause of the chronic diseases of society –including obesity, type two diabetes, and heart disease–is the quantity and quality of carbohydrates in the diet. Too much sugar and starch.

The completely bizarre thing is that this hypothesis is simultaneously ridiculed as quackery and universally agreed upon depending on how you frame the question.

Anyway, here are my notes. There are a lot of them and they may seem to jump around. This is a dense book and a few notes written in a notebook don’t come close to doing it jusctice:

Among animals, carnivores are never fat, but herbivores often are (e.g. the Hippo who lives off of rice, millet, and sugar cane).
In the early 1960’s, Sir Stanley Davidson and Reginald Passmore note in their classic textbook Human Nutrition and Dieteics that obesity was more common among the poor than among the rich. They speculated it was because starchy foods were cheaper.
The low fat diet came not from scientific evidence, but from the diet-heart hypothesis, which proposes that the level of fat (especially saturated fat) in the diet increases serum (blood) cholesterol leading to atherosclerosis, heart disease, and early death.
According to the USDA, we have been eating less red meat, fewer eggs, and more poultry and fish since the 1960’s. Our average fat intake has dropped from 45% of total calories to less than 35%.
Doctors are getting better at treating heart disease and the deaths are starting to go down, but the number of adverse events is not.
In Great Britain, researchers proposed another hypothesis for heart disease, diabetes, colorectal and breast cancer, tooth decay, obesity, etc. It was based on the consistent observation that these “diseases of society” where rare to non-existent in isolated populations, but would become common once the population adopted a “Western diet” of sugar, flour, white rice, and maybe beer (in other words, refined carbs that have been machine processed to make them more easily digestible).
Fiber has little to no effect on the incidence of chronic disease.
Eisenhower had a heart attack at age 64 setting off a panic about coronary heart disease. He had no family history, and virtually no risk since he had stopped smoking in 1949.
Eisenhower started dieting and exercising religiously, but started to gain weight and his cholesterol started increasing,
In the 1900’s, physicians did such a good job fighting infectious diseases that people lived long enough to succumb to degenerative and chronic diseases
Ancel Keys’s “7 Country Study” launched the Mediterranean Diet craze and helped popularize the notion that saturated fat leads to elevated cholesterol which leads to heart disease.
Controlled diet studies are tricky to carry out because they can’t be double-blind and you can’t change the macronutrient content without changing calories.
In 1977, George McGovern, the chair of the Senate Select Committee on Nutrition and Human Needs, published his dietary goals which essentially agreed with Keys’s hypothesis.
Francis Bacon distinguished between good science and wishful science saying that good science would evolve and the case for it would grow. Bad or wishful science looks its best with its original authors then devolves to the point where it is only kept alive by the refusal to admit that it is wrong.
The notion that statins (cholesterol lowering medications) prevent heart attacks and lower cholesterol has become well-established, but here is now way of knowing if they prevent heart attacks because they lower serum cholesterol.
During the time this was being worked out, researchers also found that having cholesterol that was low was associated with early death. They assumed that on the low end of cholesterol levels, chronic disease was the cause and low cholesterol was the effect. On the high end of cholesterol levels, they assumed that cholesterol was the cause, and heart disease was the effect.
White flour is basically all the starch and carbs removed from the wheat.
Sugar is harvested by extracting the syrup from the husk of the sugar cane.
Before insulin was discovered, researchers were already speculating that sugar caused diabetes. The physician George Campbell proposed the idea of an incubation period for diabetes. It takes a population eating more than 70 pounds of sugar per person per year for 18-22 years for diabetes to start running wild (that sounds like a lot of sugar, but it’s less than half of what the average American eats today).
The greatest single change in the American diet has been the increase in the consumption of sugar from the mid 19th century onward: annual consumption was under 15 lbs/person in the 1830’s, It was 100 lbs/person by the 1920’s and (including high-fructose corn syrup, a form of sugar that is usually 55% fructose 45% glucose instead of the traditional 50-50 split of table sugar, it was 150 lbs/person by the end of the 20th century.
Ancel Keys held up Japan as a model of a heart-healthy diet, but he didn’t seem to notice the low sugar consumption in Japan as significant. In Japan, annual sugar consumption was <40 lbs/person per year in 1963, and <50lbs/person in 1980, the equivelent to what US consumption had been about a century earlier.
The “Mediterranean Diet” was really only successful in Crete and Corfu. Their sugar consumption was 16 lbs/person per year and their was no white flour in the diet. So despite conventional wisdom, we don’t know whether the health benefits they experienced were due to their consumption of olive oil and vegetables or if it had more to do with the lack of sugar consumption.
Most of the triglycerides in the the blood (triglycerides are three fatty acids bound with a glycerol molecule) are found in VLDL (very low density lipoprotein). Much of the cholesterol is found in LDL (low-density lipoprotein. Cholesterol isn’t soluble in water, so lipoproteins are kind of like boats that carry it around the blood stream. Cholesterol is the cargo).
In the 1950’s Goffman proposed an atherogenic index (LDL +VLDL) as the best predictor of atherosclerosis
Goffman also reported that carbs raise VLDL
Ahrens observed carbohydrate-induced lipemia: an excessive concentration of fat in the blood. When he gave lectures, he would show photos of two test tubes of blood from the same patient. The one taken when the patient was on a high fat diet diet was clear, and the one one taken when the patient was on a high-carb diet was white with lipids.
High triglycerides are significantly more common in heart disease patients than high cholesterol
When HDL is high, triglycerides are low and vice-versa.
Monounsaturated fat can both raise HDL and lower LDL
The principle fat in red meat, eggs, and bacon is not saturated fat, but monounsaturated fat. In fact it is the same oleic acid that is found in olive oil.
The number of apo-B particles (LDL and VLDL combined) is elevated in heart disease patients (my note: LDL particle count is different from the normal LDL cholesterol measurement you get at a cholesterol screening. Remember, LDL is a lipoprotein which is kind of like a boat that transports cholesterol around the cell. Having a high LDL particle count means there are a lot of metaphorical boats. This could lead to having high LDL Cholesterol, but that can also be cause by a normal amount of “boats” carrying a high amount of cholesterol “cargo”).
Some people have large, fluffy LDL particles with lots of cholesterol (big “boats” with lots of “cargo”), others have small, dense LDL particles. The small dense particles are like grains of sand that get stuck everywhere and are the real problem
Lipoproteins need to be oxidized to cause atherosclerosis and small, dense LDL oxidizes more easily.
There are two patterns: Pattern A is large, fluffy LDL, Pattern B is low HDL accompanied with small, dense LDL particles and high triglycerides. Pattern B is the one that is associated with atherosclerosis.
Patterns A and B are partly genetic, but are also influenced by diet, exercise, and lifestyle.
Less carbs in the diet + more fat = better likelihood of having Pattern A
The more saturated fat in the diet, the larger and fluffier the LDL
Half the people that dies of heart attacks have normal LDL cholesterol, but high apo-B (the particles)
There are two ways to increase LDL (LDLE Cholesterol, not particle count): increase secretion or decrease disposal. Saturated fat does the latter, hence why it can raise LDL.
Overproduction of VLDL is the most common reason for elevated LDL
Insulin resistance: cells become resistant to the effects of insulin with the result being that you need to release more insulin to achieve the same effect.
Heart attacks survivors tend to have high triglycerides and to be glucose intolerant (meaning that if they take a glucose tolerance test where they consume a concentrated dose of glucose, their blood glucose levels are higher after two hours than they should be).
Except for pancreatic and prostate cancer, the incidence of all cancers increases with weight gain.
In developed nations, the poorer people are, the heavier they are likely to be.
In 1965 Albert Stunkard and his colleagues surveyed 1,660 New Yorkers and found that obese women were 6x more common at the lowest economic level than the highest. 30% of the poorest women were obese compared to 16% of the middle class and 5% of rich women. Poor men were twice as likely to be obese as rich men, 32% to 16%
In non-industrialized countries, obesity is often coupled with malnutrition and undernutrition.
In a 1959 study of African Americans living in Charleston, South Carolina, nearly 30% of adult women and 20% of adult men were obese despite living on incomes of $9-$53/week.
In 1966, a team of US Physicians reported that in Trinidad, 1/3 of women older than age 25 were obese, and that this happened despite the fact that they were eating less than 2,000 calories a day, below the amount recommended by the United Nations Food and Agricultural Organization recommended to avoid malnutrition. 21% of their diet was fat and 65% was carbohydrate
A 200lb man will burn just 3 extra calories climbing a flight of stairs
Many obese people are sedentary, but that doesn’t men that being sedentary is the cause of obesity; obesity might be the cause of being sedentary or some third factor might be could be the cause of both. Harvard researcher John Mayer noticed that among teenage girls, obese girls ate less than thin girls, but were also less active. Therefore he assumed that laziness and sedentary behavior was the cause of obesity.
University of Vermont endocrinologist Ethan Sims did a famous study where he raised the caloric intake of convicts at Vermont state prison to 4,000/day. They gained a few pounds but then their weight stabilized. He then upped it to 7,000/day and finally 10,000/day, all while making sure they stayed sedentary. Out of his eight subjects, two gained weight easily and six did not, with one guy managing to only gain 9 pounds going from 134-143. When the 200 day experiment ended, all the subjects lost the weight easily.
In other similar studies, weight gain has been shown to differ dramatically. Twins gain weight similarly, but pairs of twins do not.
“overeating” is a tautology because the only way you can say someone has overeaten is if they have excess adipose tissue.
People who gain weight don’t tend to gain it indefinitely, they reach a certain point and then their weight stabilizes.
Positive energy balance (calories in>calories out) must be associated with weight gain, but that doesn’t mean that positive energy balance is the cause, rather than the effect.
Caloric balance is positive in children who are growing, but they don’t grow because they east voraciously, the eat voraciously because they are growing. Voracious eating is a compensatory effect to satisfy the demands of growth. The growth is induced by growth hormone.
Pregnant women are similarly driven but hormonal changes to gain weight.
In the 1970’s a hypothesis developed called the “set point hypothesis” that said that over the long term our body preferred a certain level of fat storage and would adjust to achieve it.
Lean people run marathons because they are lean and have excess calories to burn.
What matters is not how many calories you eat, but how they are distributed. It’s not the energy balance that drives this distribution of energy; it’s the demand for energy at a cellular level.
In 1976 the University of Tokyo published an article on the diets of Sumo wrestlers. In the “upper group” (the highest division of wrestlers) they consumed 5,500 calories a day of “chankonabe” (a pork stew). They ate 780 grams of carbs, 100 grams of fat, and 365 grams of protein,a 57% carb 16% fat split. The lower group weighed just as much as the upper group, but was fatter and less muscular. The ate just 5,120 calories of chankonabe a day, but had 1000 grams of carbs, 165 grams of protein, and 50 grams of fat. These were men in their early 20’s. If you want to make a man in his prime fat, a high-carb, low-fat diet is the way to go.
Nitrogen equilibrium: you need to eat enough protein every day so that the nitrogen taken in through the protein matches the nitrogen in the urine from the breakdown of muscle protein.
Potatoes are “20% vegetables,” meaning they are 20% carbs by weight, and the rest is mostly water. Green peas and artichokes are 15% vegetables, onions, carrots, beets, and okra are 10%, most of the green veggies including lettuce, spinach, cucumbers, asparagus, broccoli, and kale are 5%.
For experiments with a short duration, it’s difficult to evaluate weight loss because a large percentage of what is lost is water.
People assume that you need a “balanced diet” because it was demonstrated that you could cure scurvy with vitamin c. While it’s true that this means that fruits and vegetables can be used to ameliorate scurvy, it doesn’t mean it is the only way, nor does it mean that scurvy was caused by a lack of fruits and vegetables in the diet. The Inuit don’t get scurvy and they don’t eat fruits or vegetables at all (they don’t consider fruits and vegetables to be food fit for humans).
A researcher with the last name Kemp theorized that carbohydrate tolerance varied from person to person, and that for the same person it could vary across their lifetime.
As Pennington observes: the first law of thermodynamics has to apply to the fat cell as well as the organism.
According to Pennington, when the metabolic defect that leads to obesity is present, the body will store calories as fat, robbing the person of nutrients. The cells will be semi-starved even if the person is theoretically getting enough calories.
When a calorie-restricted diet is implemented, the starved tissue of the obese person become more starved.
The three propositions of the “alternative hypothesis”:

Obesity is caused by a regulatory defect of fat metabolism; a defect in the distribution of energy rather than an imbalance of intake and expenditure.
Insulin plays the primary role in this fattening process. Hunger and lethargy are compensatory behaviors.
Carbohydrates, especially refined carbohydrates, and the consumption of sugars are the prime suspects in the chronic elevation of insulin and are the root cause of common obesity.

Through the beginning of WWII, the first proposition above was known as the “lipophelia” (“love of fat”) hypothesis.
Lipodystrophy is a condition where you lose the ability to store subcutaneous fat. Progressive lipodystrophy is where eventually you lose the ability to store fat above the waist. Your upper body can be very skinny while your legs are visibly obese. What do calories in, calories out have to do with where a person with this disorder stores fat? Do we say their top half undereats and their bottom half overeats?
When a child is growing, it will set aside the calories needed for growth and will eat extra to obtain the energy they need. It’s the same with someone who is fattening.
Men who are castrated develop a fattening pattern similar to women. Testosterone plays a major role in preventing fattening n certain areas.
Van Norden suggested that obesity and diabetes were both symptoms of the same underlying root cause.
Insulin was first discovered in 1921.
When insulin was injected into animals, human adults, or human children, they gained weight. Insulin was even used as a treatment for anorexia.
Insulin stimulates the appetite for carbohydrates and the consumption of carbohydrates raise insulin levels. It’s a viscous cycle.
Adipose tissue is interlaced with blood tissue such that no marked quantity of fat cells escapes close contact with at least one capillary.
The German Biochemist Rudolf Schoenhimer developed a technique to measure serum cholesterol. He also discovered a way to label or tag molecules with a form of hydrogen known as deuterium so that we could track them through the body. He found that both dietary fat and carbohydrates are stored as triglycerides in the fat cells.
Fat accumulates in the adipose tissue not when there is an excess of calories, but when there are more deposits than there is fatty acid mobilization (in other words when more fat is entering than exciting the fat cell).
lipogenic means anything that acts on the fat cell causing it to store fat.
lipoletic means anything that works to mobilize the fatty acids (get fat out of the fat cells).
The body will burn carbohydrates as fuel as long as blood sugar is high and the reserve of glycogen (the storage form of glucose) in the liver and muscles is not depleted.
Some of the carbs and all of the fat that we eat gets stored as fat and will be metabolized as needed. In an average diet, this supplies 50-70% of our energy needs.
Triglycerides and free fatty acids are both forms that fat takes in our bodies. Triglycerides are the fat that gets stored in our adipose tissue (fat cells) and the fat that is found in our food. Oleic acid, the monounsaturated fat found in Olive Oil, is a fatty acid, but in meat it exists as a triglyceride. Triglycerides are three fatty acids bonded with a glycerol. Some of the triglycerides in our body are from the fat we eat, and some are from the carbohydrates that we eat through a process called “de novo lipogenesis” (Latin for “the creation of new fat”).
Roughly 30% of the carbs in a meal will end up as triglycerides stored in the fatty tissue.
Fat is stored as triglycerides, but enters and exits the fat cell as free fatty acids, the form of fat that gets burned for energy.
Triglycerides getting broken down into free fatty acids is a process called “lipolisis.”
When the free fatty acids enter the fat cell they are rebuilt into triglycerides in a process called estrification
The Randall cycle (aka the glucose/fatty acid cycle): As blood sugar decreases, more fat is released from fat cells raising the level of fatty acids in the blood. This leads to a series of reactions in the muscle cells that inhibit the use of glucose for fuel and use fatty acids instead. When the availability of blood sugar decreases fatty acids in the the blood, you start to burn glucose instead of fat.
The release of fatty acids from fat cells and their diffusion into the circulation require only the negative stimulus of insulin deficiency.
The only necessary requirement to shut down the release of fatty acids from the fat cells is the presence of insulin.
Eating carbs not only promotes insulin, but suppresses growth hormone.
Dr. Atkins diet revolution can be distilled to three assertions:

Weight can be lost without hunger or calorie restriction
A low carb diet is inherently more healthy than a low fat diet. He implicate triglycerides over cholesterol as being responsible for heart disease
Calorie restricted diets are a cruel hoax that don’t really work

During sleep we mobilize fat for energy, this is why we can sleep for eight hours without getting up to eat.
Anything that acts to mobilize fatty acids from the fat cells to be used as fuel will cause satiety. Anything that stores fatty acids as triglycerides will cause hunger, since there is less food available in circulation.
We eat to maintain caloric homeostasis, the flow of energy to the cells, rather than to maintain body stores or some preferred weight.
Satiety is more than the absence of hunger, it is a depression of interest in food.
Both weight gain and hunger are promoted by factors that deposit fatty acids in the fat tissue and decrease their mobilization (in other words, by anything that elevates insulin which does both of those things). Satiety and weight loss will be promoted by factors that increase the release of fatty acids from the fat tissue and direct them to the cells of the tissues and organs where they are oxidized: i.e. anything that lowers insulin.
Nicotine is arguably the most successful weight loss drug in history. Smokers weigh on average 6-10 pounds less than non-smokers and they gain this weight back and sometimes more if they quit. It’s true that smokers usually eat more when they qyuit, but only for a couple of weeks. Smokers are less active than non-smokers, so physical activity does not explain the weight gain associated with quitting. Nicotine decreases LPL (Lipoprotein Lipase) in the fat cells and increases it on muscles (this is the opposite of what insulin does). Since LPL is what puts fatty acids into fat cells, this means that smokers are burning more fatty acids since the fatty acids are going to the muscles to be burned instead of the fat cells to be stored. Drugs that boost your metabolism aren’t helpful for weight loss since they will just make you hungry for carbs. Drugs like Nicotine that promote fatty acid mobilization will help lose weight (that’s not to suggest that you start smoking to lose weight. Stop smoking, stop eating and drinking sugar and you should be fine).
Insulin is naturally high in the late fall and winter and low in early spring
Insulin comes in waves. The first wave is as soon as the body starts eating a palatable food. This is to prime the body for what is coming. The next wave is more slow and steady.
This is why as the French say: “The appetite comes with eating.”
Even the thought of food can promote insulin secretion. The perceived taste of sweetness can cause insulin secretion.
The thought of eating makes us hungry because the pre-release of insulin shuts down our access to energy from both glycogen and fatty acids.
High insulin prevents the liver from releasing the glucose that is stored as glycogen.
It is important to distinguish two types of “hunger”: the hunger that accompanies semi-starvation is a real physiological phenomenon. Cravings for carbohydrates are psychological symptoms of withdrawal from addiction.
One thing that low-carb deniers constantly miss is that the side effects that sometimes accompany low-carb diets are the short-term symptoms of withdrawal, not long-term, chronic conditions.
Serum levels of cholesterol can initially increase on a low-carb diet because the body starts rleasing fat to be burned and cholesterol is released as well. Eventually, cholesterol levels normalize.
The Authors main conclusions:

Dietary fat, whether saturated or unsaturated, is not a cause of obesity, heart disease, or any other chronic disease of civilization.
The problem is the carbohydrates in the diet: their effect on insulin secretion, and thus the hormonal regulation of homeostasis. The more refined and easily digestible the carbohydrates, the greater the effect on our health, weight, and well being.
Sugars (specifically sucrose and high fructose corn syrup) are particularly harmful. Probably because the combination of fructose + glucose simultaneously elevates insulin while overloading the liver with carbohydrates.
Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of Coronary Heart Disease, and diabetes. They are the most likely dietary causes of cancer, alzhiemers, and the other chronic diseases of civilization.
Obesity is a disorder of excess fat accumulation, not of some combination of overeating and sedentary behavior.
Consuming excess calories does not cause us to grow fatter any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss, it leads to hunger.
Fattening and obesity are caused by an imbalance, a disequilibrium in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.
Insulin is the primary regulator of fat storage. When insulin levels are elevated (either chronically or after a meal), we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and we use it for fuel.
By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.
By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy expended by our metabolism and in physical activity.

The longer humans have been eating a particular food for and the closer it is to its natural state, the more likely it is to be good for us.
Nutritionists insist that a diet needs at least 120-130 grams of carbohydrates a day because this is the amount of glucose the brain and central nervous system will metabolize when the diet is carbohydrate-rich. But what the brain uses and what it requires are two different things. Without carbs in the diet, the brain will run on ketone bodies converted from dietary fat and from the fat released by the adipose tissue, on glycerol released from the breakdown of triglycerides and on glucose converted from the protein in the diet.
Animal products contain all the essential amino acids, vitamins, and minerals necessary for health. The only point of controversy is vitamin C, but the evidence is that as long as there is no sugar in the diet, you probably won’t have a vitamin C deficiency on a diet of only animal products.

Whew, that was a lot of info. If it was at all interesting (I’m guessing it was or you wouldn’t have made it this far) and you’re looking for further reading, you can also check out my review of Gary’s book Why We Get Fat as well as my post What Really Makes You Fat?

Of course, you can also get the book below. I listened the audio book for this one, but there is a link to the physical copy below as well:

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The most thorough book on the science of the relationship between diet and health that I have ever read.

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