Calorie

On Industrial Myths, Dr. Robert Lustig and Metabolical

• Food writer Mark Bittman has said that since food is defined as “a substance that provides nutrition and promotes growth” and poison is “a substance that promotes illness,” then “much of what is produced by industrial agriculture is, quite literally, not food but poison.” He was talking primarily about pesticide use versus sustainable farming, arguing that we have laced our food with poison. Yes, pesticides are one aspect of food toxicity—but only the tip of the iceberg, maybe about 10 percent of what ails us. The other 90 percent is due to the procedures of the processing, which has morphed what was food into this new slow-acting poison. Your box of cereal may tout that it’s “organic” and “all natural”—but it still may be poison. What’s important is the alchemy of how the food itself has become poison. Until you understand that, you can’t understand what has happened to our food—and to us. – Metabolical by Dr. Robert Lustig

I’ve wondered about calories for quite some time.

I accepted the simple (fast thinking) elegance of “calorie in, calorie out.”

But I always suspected that it was a bit too linear for a complex biological system.

I asked several people whether a calorie from a carb, fat or protein was the same. Never found an answer.

Then I stumbled onto this video with Dr. Robert Lustig

I’d never come across Lustig before. I like him.

He understands industrial narrative and mythology and its protective value for industry. Tick.

He is well aware of industries’ desire to victim blame. Tick.

He can explain things simply and well. Tick.

He talks about the importance of the gut microbiome. Tick.

He seems, at least to me, and at least within this domain, to be a truth teller. Tick.

Here is a detailed summary of the 13-minute video, but it’s definitely worth listening to him explain how to think about calories.

1. Fundamental Flaw in the Calorie Concept: The narrative begins by challenging the food industry's claim that managing weight is simply about balancing calories - calories in versus calories out. This idea leads to a chain of assumptions: obesity is due to gluttony and sloth; it's the individual's fault; diet and exercise are the sole solutions; and any calorie can fit into a balanced diet. Lustig criticizes this viewpoint as overly simplistic and misleading, arguing that it shifts responsibility onto the consumer while absolving the food industry.

2. The Big Lie in Medicine: Lustig, with a background from Brooklyn, New York, vehemently argues that the equivalence of all calories is the biggest lie in medicine. This lie, he says, benefits the food industry as it diverts attention from the quality of calories to their quantity.

3. Evidence Against the Calorie Myth: Lustig offers evidence to debunk this myth by examining four different food items - almonds, protein, fats, and sugars (fructose and glucose).

   1. Almonds: When one consumes 160 calories of almonds, only 130 are absorbed due to the fiber content. The fiber in almonds forms a barrier in the intestines, preventing the absorption of certain calories and sugars, thereby protecting the liver and reducing insulin response. The unabsorbed calories benefit the gut microbiome rather than the individual.

   2. Protein: Protein, when not needed for muscle building, is metabolized by the liver. This process of converting protein to energy is inefficient compared to carbohydrates, resulting in fewer ATPs (energy molecules) produced per calorie.

   3. Fats: The speaker contrasts omega-3 fatty acids (beneficial) with trans fats (harmful), both containing nine calories per gram. This stark difference in their health impacts illustrates that not all calories have the same effect on the body.

   4. Fructose and Glucose: These two sugars, both with four calories per gram, have vastly different effects on the body. Glucose is described as essential, while fructose is labeled a toxin.

4. Implications for the Food Industry: Lustig suggests that acknowledging the truth about calories - that their source and nature matter - would significantly impact the food industry. It would challenge the industry's narrative and potentially lead to legal consequences.

5. Impact of Fiber on Sugar Absorption: The fiber in almonds, both soluble and insoluble, creates a barrier in the duodenum, which is the first part of the small intestine. This barrier inhibits the absorption of simple sugars like glucose, fructose, and sucrose. This process helps in maintaining liver health and preventing the liver from turning excess sugar into fat.

6. Gut Microbiome and Calorie Utilization: The unabsorbed calories from almonds, owing to their fiber content, pass further down the intestine to the jejunum, where they become available to the gut microbiome. The gut bacteria then utilize these calories for their own purposes. Lustig emphasizes that the human gut is home to a vast number of bacteria, which play a crucial role in overall health.

7. Fiber's Role in Metabolic Health: By influencing the absorption of calories and sugars, fiber plays a significant role in maintaining metabolic health. It prevents excessive insulin response by reducing serum glucose response, thus keeping insulin, which can drive chronic metabolic diseases, at lower levels.

8. The Misleading Nature of Calorie Counting: Lustig argues that the focus on calorie counting is misleading because it ignores the critical aspect of how different foods and their components, like fiber, are processed by the body. He emphasizes that it’s not just about the number of calories consumed but also about what the body does with these calories.

Essentially, all you need to know are two precepts, six words total: 1) protect the liver, 2) feed the gut. Those foods that satisfy both precepts are healthy; those that do neither are poison, and those that do one or the other are bad (but less bad)—no matter what the USDA and FDA allow to be stated on the package. Only items that meet both of these criteria qualify as Real Food, i.e., that hasn’t been stripped of its beneficial properties and sprinkled with toxins that will hasten our demise. – Metabolical

He has a functionally low opinion of doctors and what they are taught (indoctrinated).

As an interesting sidenote.

Doctor: The word "doctor" originally comes from the Latin word "docēre," which means "to teach." Over time, the term evolved to refer to someone who is educated or trained in a particular field, especially medicine. In academic contexts, a doctor is someone who has obtained a doctoral degree, signifying a high level of expertise in their subject area. The term has become synonymous with medical professionals, although it is also used in academia.

Indoctrinated: The word "indoctrinated" derives from the Latin "indoctrinatus," past participle of "indoctrinare," which means "to teach" or "to instruct." The prefix "in-" in this context can be understood as "into," and "doctrina" means "teaching." Thus, "indoctrinare" means to instruct or to teach thoroughly. In modern usage, "indoctrinated" often carries a connotation of being taught to accept a set of beliefs uncritically.

Only 28 percent of medical schools have a formal nutrition curriculum; even fewer than in 1977 when Congress passed the law that created the Dietary Guidelines and called for more nutrition science in the medical classroom. Now, medical students receive on average 19.6 contact hours of nutrition instruction during their four-year medical school careers, about 0.27 percent of the time spent in class. How is your doctor supposed to provide nutrition advice if they never learned it in the first place? – Metabolical

[Unbekoming: Someone should tell Lustig how much they are taught about vaccines.]

I will leave you with this section from Metabolical on Calories.

With thanks to Dr. Robert Lustig

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A Calorie Is Not a Calorie

This myth is all that is left of the legacy of Wilbur Atwater. It argues that all calories possess the same heat generation, equivalent to 4,184 joules of energy. From a physics standpoint, a calorie is a calorie. But so what? This has nothing to do with what happens to those calories in the human body, because weight gain is only about how those calories are stored.

The efficiency of capturing all those calories and transforming them into chemical energy in the human body is highly uneven. Understanding these various phenomena shows that in fact “a calorie is not a calorie,” and there’s an actual difference between eating a handful of almonds and a donut, even if their calorie count is the same.

The “calorie is a calorie” myth can be disproven through five examples:

1.   Fiber. You eat 160 calories in almonds, but you only absorb 130. The other 30 are prevented from early absorption because the fiber in them prevents early absorption in the duodenum (early intestine), so the bacteria in the jejunum and ileum (middle and late intestine) will chew the 30 up for their own purposes. You ate them, so they’re considered “calories in,” but you didn’t get them (your bacteria did).

2.   Protein. If an amino acid is to be prepared for energy metabolism, the amino group must be removed by the liver to convert it into an organic acid (e.g., aspartate to oxaloacetate). It costs two ATPs to do this, as opposed to preparing carbohydrate, which costs one ATP. This is known as the thermic effect of food (TEF). Fats generate about 2 to 3 percent of TEF, carbohydrate about 6 to 8 percent, and protein about 25 to 30 percent—meaning it takes more energy to burn a protein than a carbohydrate. If a calorie isn’t recouped because it’s burned, it can’t be stored.

3.   Fat. All dietary fats would liberate 9 calories per gram if you burned them. But omega-3 fatty acids aren’t burned—they’re hoarded, as they’re needed for cell membranes and neurons in the brain (see Chapters 7 and 19). Furthermore, trans-fats can’t be burned, as humans don’t have the enzyme to cleave the trans-double bond. They instead will clog your arteries and kill you, unrelated to their calories. All in all, neither are burned, but one will save your life and the other will kill you.

4.   Sugar. Added sugar is made up of equal amounts of glucose and fructose. Both provide the same number of calories, but are metabolized differently in the liver and perform different jobs in the brain. Glucose can be metabolized by all of your body’s tissues and only 20 percent of a glucose load goes to your liver, and even then insulin tells the liver to turn it into glycogen (liver starch). On the other hand, fructose can only be metabolized by the liver, so the whole load goes to your liver, insulin doesn’t have an effect, the mitochondria are overwhelmed, and the rest is turned into liver fat, driving insulin resistance (see Fig. 2–1). And on the third hand, fructose drives glycation seven times faster than glucose (see Chapter 7), doesn’t shut off the hunger hormone ghrelin, and is addictive (see Chapter 21).

5.   Different fat depots. It’s not just if the calorie is stored, it’s where it’s stored. There are three fat depots, but they confer different risks for development of metabolic disease: 1) subcutaneous (butt) fat: you need about 22 pounds to worsen your health; 2) visceral (belly) fat: you need about 5 pounds to worsen your health; and 3) liver fat: you only need about 0.3 pounds to worsen your health. And almost all calories from added sugar are going to liver fat. If a calorie stored were a calorie stored, it wouldn’t matter which fat depot was doing the storage—but it does. Protecting the liver is the prime directive.

But It’s Zero Calories . . . ?

Sugar sweetened beverages (SSBs) are causative for at least three diseases of metabolic syndrome—type 2 diabetes, heart disease, and fatty liver disease—plus tooth decay. So, what about noncaloric diet sweeteners, for those with a “sweet tooth”? Stevia, sucralose, aspartame, acesulfame-K, allulose, xylitol, erythritol, and others would seem the obvious choices—no calories, so no heart disease, right? No fructose, so no liver fat or diabetes, right? Not so fast. Though the US has slowly turned to diet drinks because of the obesity epidemic—as of 2010, 42 percent of Coca-Cola sales in the US were of the no-sugar variety—33 percent of all sugar consumption is in drinks, and 42 percent of drinks are now no-sugar, so someone somewhere should be losing weight, right?

Unfortunately, diet sweetener consumption is also correlated with metabolic syndrome. Studies of switching out sugar for diet sweeteners don’t show beneficial effects on weight loss. Rather, the data show that sugar is a direct cause of metabolic syndrome—though thus far we only have correlation with diet sweeteners. So, do diet sweeteners cause metabolic syndrome, or do people with metabolic syndrome consume more diet drinks? The question really is if the substitution of diet sweeteners for sugar actually reduces caloric intake, body fat, and metabolic disease. Here are five reasons to be concerned:

1.   There’s a difference between pharmacokinetics (what your body does to a drug) and pharmacodynamics (what a drug does to your body). We have pharmacokinetic data on diet sweeteners to determine acute safety, which is part of the FDA’s charter (see Chapter 24), but none of the pharmacodynamics. This has to do with chronic effects, which is not in the FDA’s charter. The fact of the matter is, we don’t know what any of these diet sweeteners do to your long-term food intake, weight, body fat, or metabolic status. The food industry doesn’t do these studies because such studies are expensive and could have detrimental effects on sales. The NIH won’t do them, saying it’s the food industry’s job. So the studies aren’t done.

2.   You drink a soda. The tongue sends a signal to the hypothalamus that says, “Hey, sugar is coming, get ready to metabolize it.” The hypothalamus then sends a signal along the vagus nerve to the pancreas, saying, “A sugar load is coming, get ready to release the insulin.” If the “sweet” signal is from a diet sweetener, the sugar never comes. What happens next? Does the pancreas say, “Oh, well . . . I’ll just chill until the next meal,” or does it say, “WTF? I’m all primed for the extra sugar. Let’s eat more to get it.”

In one study, four groups of Danish men ate their normal diet for six months plus a liter of sugared soda per day, a liter of diet soda per day, a liter of milk per day, or a liter of water per day. No surprise, the sugared soda group gained 22 pounds. The diet soda group gained 3.5 pounds. The milk group stayed the same. The water group lost 4.5 pounds. Now, 3.5 is better than 22 pounds, but they still gained weight even without the calories. And the milk has as many calories as the sugared soda, so why didn’t that group gain weight? It all has to do with insulin—meaning the diet sweetener still caused insulin release, while the lactose and fat in the milk didn’t. Plus the fat was satiating, so people ate less.

A second study took diet soda drinkers and switched them to water. They lost another 6 pounds. If there are no calories in either case, why did their weight change? Insulin again. Insulin response to oral glucose tolerance testing was performed in seventeen morbidly obese adults without diabetes, both with and without a diet sweetener pretreatment. After the diet soda, the insulin response was 20 percent higher than with the seltzer control. The sweet taste alone can both stimulate appetite and insulin release, which drives energy storage.

3.   Diet sweeteners might change the composition of intestinal bacteria, which could cause leaky gut, generate inflammation, increase deposition of visceral fat, and drive metabolic syndrome, unrelated to calories (see Chapter 7). The intestinal microbiome plays a role not only in what the tongue tastes, but also what the brain senses.

4.   Early studies suggest that certain diet sweeteners act directly on fat cells grown in a petri dish to promote energy transport inside the cell. In other words, diet sweeteners may have insulin-like properties of their own, but this has yet to be confirmed.

5.   We don’t know the role that diet sweeteners may play in sugar addiction (see Chapter 21), as this field is in its infancy. However, there are animal studies that suggest brain pathways react similarly to sucrose and diet sweeteners.

Recent studies argue that artificially sweetened beverages are associated with diabetes, cardiovascular issues, and dementia. Thus far, all of these studies have been correlative—we don’t yet have causation. Nonetheless, quantitatively, the data suggests that the toxicity of two diet sodas is equivalent to one sugared soda, and that they’re way worse than water in terms of obesity and diabetes development. As an example, take the case of aspartame (NutraSweet), which in animal models affects three of our eight subcellular pathologies: oxidative stress, membrane integrity, and inflammation (see Chapter 7). These health concerns are just swept under the rug—a University of Sussex report looked at the original approval of aspartame by the European Food Safety Authority (EFSA). They documented that the EFSA discounted fully 100 percent of the seventy-three studies that showed aspartame caused harm, while accepting 84 percent of the studies that showed no harm.

While none of this research closes the book on diet sweeteners in either direction, it should certainly give us pause. In the last fifteen years, American sugar consumption has dropped from 120 to 94 pounds per year, yet obesity and metabolic syndrome persist unabated. Could diet sweeteners be playing a role? The only surefire way to find out is for Americans to de-sweeten their food across the board—drinks, too. And don’t start thinking juice is the answer (see Chapter 19).

Instead of worrying about calories, we should instead focus on the interaction between genetics and sugar consumption, as this determines insulin levels and where that fat will develop and deposit. Understanding the role of different foods in generating different insulin responses is paramount, and that includes diet sweeteners.

Here is my own very recent example of how this kind of skepticism works to everyone’s detriment, except the academician. I first aired the “sugar is toxic” message in public in 2009. In 2011, Gary Taubes wrote his New York Times article “Is Sugar Toxic?,” followed by my 2012 Nature comment (written with UCSF colleagues Laura Schmidt and Claire Brindis), “The Toxic Truth about Sugar.” We then published our landmark fructose restriction study (see Chapter 20) in the journal Obesity in 2016, which demonstrated causation between sugar consumption and metabolic syndrome.

Despite all the information and science gleaned by myself and others, an incredulous WebMD video appeared online asking Joslin Diabetes Center CEO Ron Kahn the question, “Can eating a lot of sugar cause my diabetes?” Kahn responded (and I quote): “Eating a lot of sugar definitely does not cause diabetes if you don’t eat so much sugar that you gain weight. And in fact, sugar to a certain extent is OK because it stimulates the pancreas to make more insulin, which actually helps to control the blood sugar . . .”

This is the head of the Joslin Diabetes Center, saying in 2015, “a calorie is a calorie,” “it’s about obesity,” and “insulin is good.” With all we knew at that point, to be that unabashed about one’s stance on a seminal point that has such important clinical implications—think about that. – Metabolical

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