Part 5: Food Chemicals

Part 5: Food Chemicals: Based on the book “Metabolical”

Butylated Hydroxyanisole (BHA) and Butylated Hydroxytoluene (BHT). These are standard preservatives for chips and meats. However, the International Agency for Research on Cancer categorizes BHA as a possible human carcinogen, and it’s listed as a known carcinogen under California’s Proposition 65. These designations are based on consistent evidence that BHA and BHT causes tumors in animals—but data in humans are hard to come by. Propyl Gallate. Propyl gallate is a preservative in products that contain fats, such as sausage, vegetable oil, soup bases, and even chewing gum. There’s some evidence that suggests it may also have estrogenic activity. It’s been implicated in a rat model of Parkinson’s disease, but not with any human disease at this point. Nitrates and Nitrites. Nitrates and nitrites are the preservatives in cured meats, such as bacon, salami, sausages, and hot dogs. Although they can prolong a food’s shelf life and give it an attractive hue, they’re directly implicated in human disease. Nitrates turn into nitrites, which react with amino acids to form nitrosamines, which then react with nitrogen to form nitrosoureas. These are among the most potent carcinogens around and are associated with virtually every cancer of the alimentary tract: stomach, intestine, and colon. In 2010, the WHO declared nitrates as probable human carcinogens, and there are now regulations as to how many can be added to your cured meats, though we still don’t know what a safe amount actually is. Trans fats. Trans-fats were probably the single most important reason for the advent and success of processed food. Invented in 1911, the first trans-fat, called Crisco, hit the market, and by 1920 virtually every bakery product sold in America was laced with it, since it acts as a preservative and a hardening agent. Trans-fats can’t go rancid, because the trans-double bond can’t be oxidized by bacteria, as they don’t possess the enzyme to cleave it. The problem is that our mitochondria are refurbished and repurposed bacteria—they even have their own DNA—meaning they don’t produce the enzyme either, so trans-fats line our arteries and generate oxygen radicals, leading to metabolic syndrome. The first glimpse of the danger of trans-fats came in 1957, when an immigrant German biochemist at the University of Illinois named Fred Kummerow demonstrated their presence in arterial plaques of rats. This finding was ignored for thirty years, until corroboration in 1988. It was then that Kummerow launched a scientific campaign against trans-fats, and he was laughed at until 2006, when the FDA agreed that the science was strong enough to warrant a warning label on foods. Kummerow filed a petition with the FDA to ban trans-fats, while Big Food was kicking and screaming. He was ninety-nine years old when he sued the FDA in 2013, and finally trans-fats were taken off the generally recognized as safe (GRAS) list. The processed food industry vociferously argues that sugar is a required and necessary ingredient in their recipes. And that’s true, because if it weren’t for the sugar, you wouldn’t eat it, and their profits would dwindle. Here are five of the industry’s pro-sugar arguments, and why it’s good for them and bad for you. Sugar adds bulk. Kellogg’s Honey Smacks are 56 percent sugar. Sugar makes food brown. Indeed, we love the brown color and caramel taste from the Maillard reaction, glycation, browning, or aging reaction. Every time this reaction occurs, it throws off an oxygen radical that can damage the cell. Sugar raises the boiling point. This allows for caramelization to occur, which like we said is very tasty, but again this is just the Maillard reaction, which, over time, can cause your cells to age. There’s also data to suggest that fructose could “caramelize” your hippocampus, which might contribute to memory decline. Sugar is a humectant (attracts and maintains moisture). How soon does fresh bakery bread become stale? Maybe two days? How about grocery store commercial bread? More like three weeks. Ever wonder why? In commercial bread, the baker adds sugar to take the place of water, known as water activity. Sugar doesn’t evaporate, but instead takes up space in the bread while holding onto water during baking so the loaf stays moist. Sugar is a preservative. Have you ever left a soda at room temperature? Of course, after the carbonation escapes, it goes flat. But do bacteria or yeast ever grow in it? Never. That being said, if insulin and leptin were the only problems, then we would overeat all types of foods—but we don’t usually over consume fruits, vegetables, or beans/legumes/lentils. The foods we overeat are all found as components of fast food. Often we’re not consuming food just because we’re hungry. It’s become an easy “reward” and a balm for chronic stress. Which begs the question: is fast food addictive, and if so, what about it is addictive? Recent revelations in popular literature have alluded to this signature aspect of the Western diet, driving excessive consumption. Addiction is one of those bandied-about terms that changes meaning based on context. There is a phenomenon called reward eating drive (RED), which induces people to consume “tasty” foods unrelated to hunger or caloric needs. In a series of clinical research experiments, they showed that some people experience a loss of control with certain foods, and those that do tend to binge on high sugar/high-fat foods (think chocolate cake). This aberrant behavior is driven by dysfunction of the reward system. Fast food contains four specific chemicals that have been examined for addictive qualities: salt, fat, caffeine, and sugar. 

Part 4: Fiber and Food

Part 4: Fiber and Food: Based on the book “Metabolical” 

The fiber in food is perhaps the most important nutrient for health, because it single handedly protects the liver and feeds the gut in six different ways: Both kinds of fiber together form a gel on the inside of the duodenum to reduce the rate of absorption of monosaccharides and disaccharides, as well as slow the breakdown of starches. Reduced absorption means reduced transport to the liver, thus preventing the liver from turning excess energy into fat—in turn preventing liver insulin resistance. The reduction in the rate of absorption also reduces the glycemic excursion in the blood, keeping the insulin response down, and reducing energy deposition into fat tissue. There are two flavors of bacteria that live in your gut: the white hat and the black hat bacteria—and it’s a daily struggle to see which will prevail. The white hat bacteria (e.g., Bacteroides) need more energy to survive and grow in order to battle the black hat bacteria (e.g., Firmicutes). Thankfully, the good bacteria can proliferate and maintain a balanced intestinal ecosystem, but need a greater and more robust supply chain to ward off the bad guys. What’s that supply chain made of? Fiber—both types. The fiber transits the food through the intestine faster, generating the satiety signal (the gut hormone peptide YY3–36, which is released into the bloodstream and goes to the brain) sooner, thus reducing second portions. Soluble fiber is metabolized by gut bacteria into short-chain fatty acids like butyrate. They uniquely feed the microbiome of the colon (large intestine) and are absorbed into the bloodstream where they are anti-inflammatory as well as suppress insulin secretion from the pancreas. Insoluble fiber acts as a mild abrasive in the lumen of the colon, which dislodges and sluffs old dead cells, thus reducing cancer risk. There are three inherent myths about carbohydrates that play a role as to whether they’re causative of, or preventative against disease: Sugar vs. starch. Sugars are monosaccharides and disaccharides (one or two molecules), while starch is a complex polymer (many molecules). Sugars either have one bond or no bonds to break, so they’re digested and absorbed quickly in the duodenum, especially when they’ve been liberated from a food matrix, as they often are (e.g., soda, fruit juice, alcohol). Starch has more bonds to break, and is digested and absorbed slower. All of this adds up to a more rapid and higher insulin response with sugar, which drives weight gain. Type of starch (the two “Amys”): But “a starch is not a starch.” There are two kinds of starch: amylose (brown foods including beans, lentils, and legumes; carbs that are digested and absorbed slowly) and amylopectin (white foods including wheat, pasta, rice, and potatoes; carbs that are digested and absorbed rapidly). Amylose is better for you, as it’s a string of glucoses with two ends; therefore, only two enzymes at a time can chew it up, resulting in slow digestion and absorption. Amylopectin is more like a tree of glucoses, with lots of branch points. Many more enzymes can chew it up at once, releasing glucose more rapidly, which is more likely to be absorbed early, flood the liver, and generate a bigger insulin response. Carbs are rarely ingested in isolation. A slice of white bread is straight glucose. But Real Food is glucose plus protein plus fat plus fiber. Those other macronutrients, or lack thereof, influence the glucose’s absorption in the intestine, the insulin response that follows, and risk for weight gain. The important parameter is glycemic load (GL). GL is different from glycemic index (GI)—how much food do you have to eat to get the 50 grams of carbohydrate? GL takes into account the beneficial effect of fiber. A good example is carrots, which are high-GI (lots of carbohydrate) but low-GL (even more fiber). More fiber means a larger portion, because there’s less digestible carbohydrate. You can turn any high-GI food into a low-GL food by eating it with its original fiber. Real Food is by definition low-GL. Protein. Your kidneys have a limited capacity to excrete the metabolic by-products of protein metabolism, and overexcretion can cause kidney damage. Therefore, protein quality is as important as protein quantity. For example, eggs and beans both contain protein, but are very different in quality. You have a spectrum of macronutrient compositions to choose from, from one end to the other: vegan, Ornish, flexitarian, pescatarian, Japanese, Mediterranean, low-carb, paleo, keto. They all work, if you’re eating Real Food. Real Food is low-sugar and high-fiber, which lowers insulin; it protects the liver and feeds the gut. The caveat is that each of us has different genetic predispositions, intestinal microbiota, and livers, so it’s likely that there are specific diets that will work better for some and not for others. Fats. Omega-3s are fish oil, not snake oil. Omega-3s might just be the healthiest thing you can put in your mouth. There are two kinds—docosahexaenoic (DHA) and eicosapentaenoic acids (EPA)—both of which reduce the inflammatory response in the fat cell and prevent the release of free fatty acids. This keeps them from hitting the liver, where they would be packaged into triglyceride. What’s in our processed foods? The ultra-processed food industry adds chemicals at various points. They may add it to the animal while it’s maturing to prevent infection, or they may add it to the plant while it’s growing to prevent infestation. They may also add chemicals to the food during processing for flavor, color, texture, and/or preservation. In any case, when they add it to the animal or plant or food, they add it to you as well. Many of these chemicals act directly on those eight subcellular pathologies to increase your burden of chronic disease. Natural Flavors. Did you ever wonder what a “natural” or “artificial” flavor was? Aside from salt, sugar, and water, natural or artificial flavor is the most commonly listed item, appearing on one out of seven food ingredient lists on the Nutrition Facts label. But what are they exactly? They’re chemicals, and the company doesn’t have to tell you what’s in it, and the FDA doesn’t require them to. Since most flavors are nonpolar, it usually means there’s an emulsifier (e.g., polysorbate 80), a solvent (e.g., propylene glycol), and a preservative (e.g., butylated hydroxyanisole; BHA), although it could be several of one hundred different items. The companies that make flavors also make fragrances. In general, the dose is small, so disease is unlikely—unless you have an allergy. But we don’t know for sure. Emulsifiers. Lecithin (chocolate), polysorbate 80 (shortening), carboxymethylcellulose (salad dressing), and carrageenan (ice cream) are added to foods to maintain food consistency upon storage. After all, who wants clumpy ice cream? These molecules have one polar end and another nonpolar end, so they’re able to bind fat and water together to keep them from separating. However, emulsifiers are also detergents, and can strip away the mucin layer that sits on top of and protects intestinal epithelial cells from the bacteria, thus predisposing individuals to intestinal disease, food allergy, or leaky gut. Thus far, however, the FDA states they haven’t found cause for human concern. 

Part 3: Diet Changes

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.

Part 2: What the doctor orders

Part 2: What the doctor orders: Based on the book “Metabolical”

There are a few branches of Modern Medicine that have recognized both the problems and the importance of nutritional therapy; for instance, integrative and functional medicine and psychiatry. Their charge is to treat the upstream causes of disease, not the downstream symptoms. Many of these doctors and healthcare professionals eschew medications, rather opting to use food as medicine. And this makes sense the cellular pathways that lead to chronic disease are not druggable, but they are foodable. Unfortunately, such doctors are still few and far between. There are a few courageous practitioners who’ve spoken up, but most of them have been marginalized by the medical establishment for all the reasons stated above. However, this new wave of physicians has some guiding lights and the data to make inroads into the medical debacle we find ourselves in. Decades ago, the ability to dispense nutritional advice was “claimed” by dietitians. The field of modern dietetics was borne out of two concepts, both of which turned out to be false. The first is the idea that a “calorie is a calorie,” which was espoused by the Atwater system, developed by agriculturist Wilbur Olin Atwater in 1916. His claim to fame was that he standardized how much heat energy (i.e., how many kilocalories, or kcal) three specific macronutrients would liberate when burned in a bomb calorimeter (a device that measures heat release of organic substances), and he calculated the ratios, which computes the number of kcal in a given food by its protein (4 kcal/gm), carbohydrate (4 kcal/gm), and fat (9 kcal/gm) content. As fat was the most calorie-dense, Atwater thought it was the most egregious in terms of weight gain. Since then, dieticians have clung to the idea that a patient’s food plate can be calculated using this arithmetic. The problem is that our bodies are a bit more complicated. The Atwater equation neglected to account for the intestinal microbiome and its inherent metabolism of approximately 25 to 30 percent of everything you eat, as well as the role of fiber in altering that percentage. Since fiber doesn’t contribute any calories to your total but alters the percentage of the total that you absorb, the number of calories you eat versus how many you metabolize are completely disparate. Nowhere is this more true than for nuts such as almonds, where the amount of calories absorbed is a full 30 percent less than those generated from a bomb calorimeter; in fact, some manufacturers are now ratcheting down the labeling of caloric content of their products specifically to reflect this fact. Corporate dietitians have continued to exonerate processed food over the decades, as has the American Nutrition and Dietetics Department (AND). They do this for three reasons. The first is that they espouse calories, and virtually all food has calories, so what makes an individual food a problem? The Atwater system was, is, and always will be defective. Where those food calories come from determines where they go. It’s not physics, it’s nutritional biochemistry. My hope is that you will see past this fallacy. They also claim it’s what’s in the food that matters—this is clear from their support of the Nutrition Facts label. Except that it’s not what’s in the food, it’s what’s been done to the food, which doesn’t appear on the food label. They’ve missed the mark on both counts. And, last, 90 percent of their operating budget comes from Big Food, as documented by public health lawyer Michele Simon. They exonerate dietary sugar even to this day because they can’t possibly kill the goose that lays the golden eggs. Calories are the industry’s shield; it’s how they hide from culpability. What can you do to advocate for yourself? Get the proper testing! Here’s the list of the tests you need to make sure your doctor orders: lipid profile (LDL-C, HDL-C, TG), homocysteine (Hcy) level, alanine aminotransferase and aspartate aminotransferase (ALT and AST), uric acid, fasting insulin, fasting glucose, and hemoglobin A1c. Once you have these results, take a look at the HDL. If it’s over 60, it almost doesn’t matter what the other fractions are, as this is a sign of good cardiovascular health. If the HDL is under 40 (men) or under 50 (women), then your predisposition for heart disease is much higher. Then look at LDL-cholesterol. If it’s below 100, the small dense fraction can’t be high enough to be harmful. If it’s between 100 and 300, then you need to look at the TG level. If the TG level is above 150, that’s metabolic syndrome until proven otherwise. You need to assess diet and liver function. The liver enzyme alanine aminotransferase (ALT) is easy to assess and reasonably sensitive and specific for measuring the degree of liver fat. If it’s over 25, you definitely should investigate further. If the AST is elevated, you can assume your liver is either under acute (infectious, alcohol-, or toxin-related) assault, and if your ALT is elevated, then it’s likely under chronic metabolic assault (e.g., liver fat). If both are elevated, you then want to know whether there’s been any liver damage. Uric acid is a by-product of liver carbohydrate metabolism, especially when it metabolizes sugar. This prevents the mitochondria from metabolizing pyruvic acid to carbon dioxide, which forces the liver to turn excess energy into liver fat. Levels above 5.5 indicate mitochondrial dysfunction and insulin resistance. Fatty liver disease: ALT >25 in Caucasians, >20 in African Americans, >30 in Latinos, GGT >35, Uric acid > 5.5. Glucose intolerance: Fasting glucose > 100 or 2-hour, glucose > 140; HbA1c > 6.0 percent. Type 2 diabetes mellitus: Fasting glucose > 125 or 2-hour glucose > 200; HbA1c > 6.5 percent. Dyslipidemia and heart disease Lipid profile: TG > 150, HDL < 40, TG:HDL > 2.5, LDL-C >300, LDL-P >1000 Homocysteine > 15. Insulin resistance: Fasting insulin > 15, Insulin hypersecretion 3-hour OGTT with insulin levels; measure insulin secretion and resistance indices. Signs of poor mitochondrial function are high uric acid and high homocysteine. Signs of liver fat are high ALT and high fasting insulin. Signs of poor peripheral clearance of fat are a high triglyceride and a low HDL. This pattern would argue for reducing your refined carbohydrate and sugar consumption. Conversely, signs of poor liver clearance of fat include a high LDL without a concomitant high triglyceride, as well as a normal fasting insulin levels.