Part 3: Diet Changes: Based on the book “Metabolical”
There are three commonalities to all the diseases that we call metabolic syndrome: 1) despite all efforts, these diseases are all increasing in incidence, prevalence, and severity at a faster rate than obesity; 2) they’re all exacerbated by obesity, although not specifically caused by it; and 3) while there are drugs to treat the symptoms of each one (including obesity), there are no drugs to either treat, cure, or prevent the diseases themselves. However, every single one of these pathologies can be prevented, mitigated, and in many cases reversed, by changes in diet. And none of these changes in diet have anything to do with calorie restriction. In most cases, reversal can be accomplished just by removing processed food and substituting Real Food. It’s the consumption of refined carbohydrates that’s associated with type 2 diabetes. In particular, dietary sugar, even more than starch, drives the metabolic reactions that lead to type 2 diabetes, especially because of effects in the mitochondria. The glucose in the dietary sugar drives the insulin release, which drives the weight gain, while the fructose drives the liver fat accumulation that drives the insulin resistance. Processed food is the primary vehicle. The discovery of our symbiotic relationship with our intestinal microbiome changed everything. We now know that we have to feed it to stay healthy. When we don’t feed it right (e.g., depriving it of dietary protein), those bacteria send blood-borne and neural signals that tell our brains to alter our behavior so that they can get the nutrition that they do need. Whether you like it or not, you’re eating for two—you’re in a symbiotic relationship with your gut, and if you hurt your gut, your gut will hurt you back. The key to fending off chronic disease is to keep those eight subcellular pathways running right—and each and every one of them can be made to run right with two simple dictates: Protect the liver. You have to protect the liver from fructose, glucose, branched-chain amino acids, omega-6 fatty acids, iron, and other oxidative stresses —all of which end up causing fat accumulation and liver damage, and generate insulin resistance. This can be done by either reducing the dose of dietary liver stressors (e.g., a low-sugar diet) or their flux (e.g., a high-fiber diet, which blocks sugar absorption, thus reducing the rate by which fructose and branched-chain amino acids reach the liver). Feed the gut. If you don’t feed your microbiome, your microbiome will feed on you; it will literally chew up the mucin layer that protects your intestinal epithelial cells, which increases the risk for leaky gut, inflammation, and more insulin resistance. The goal is to deliver more nutrients farther down the intestine (e.g., a high-fiber diet). The word “weight”—when did it become a synonym for health? When we decided that health was the new morality. Political correctness meant you couldn’t shame people for poverty or race—but fat-shaming continues to this day, because “it’s your fault you’re a glutton and a sloth.” But the data shows that it’s your liver and visceral fat that determines your health, not your weight or total body fat. Liver fat tops out at about one pound, and visceral fat at about six pounds. You can’t see that on the scale. Normal weight people have liver fat, too. It’s not the fat you can see, it’s the fat you can’t see that matters. The word “fat”—does it mean body fat or dietary fat? Or fatty acid? Or, “do these pants make my butt look fat?” Two-thirds of the US populace continue to believe and perpetuate the myth that “fat makes you fat.” While it’s true that dietary fat could become body fat, it does so only in response to insulin. And so weight isn’t driven by dietary fat, which doesn’t raise insulin, but rather by dietary refined carbohydrate and sugar, which do. The word “sugar”— does it mean blood sugar (glucose) or dietary sugar (glucose-fructose)? The food industry says “you need sugar to live”—but while you do need a blood glucose level to live, you don’t have to consume that glucose. In fact, your liver can make glucose from the glycerol released from the breakdown of triglycerides in either dietary fat or body fat, or from amino acids, a process called gluconeogenesis. Conversely, you don’t need fructose (the molecule that makes food sweet) to live at all. In fact, there’s no biochemical reaction in any animal cell on the planet that requires dietary fructose. Which means you may want dietary sugar, but you don’t actually need it. What happens to those calories in the human body, because weight gain is only about how those calories are stored. The “calorie is a calorie” myth can be disproven through five examples: 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). 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 carbohydrates, 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. 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.. 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. 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. And on the third hand, fructose drives glycation seven times faster than glucose, doesn’t shut off the hunger hormone ghrelin, and is addictive. 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.
