I recently traveled back in a time capsule to watch Guns N’ Roses sing Knockin’ on Heaven’s Door in 1992 at the Freddy Mercury tribute concert. If you’ve been on this planet as long as I have, this song will likely touch your soul! One thing that caught my eye was that everyone, including the band, the backup girls, and the audience, was thin and trim. If you go anywhere in this country or any other modern society today, see how long it takes to find a large group of thin, healthy-appearing young people. Good luck with that! The most tragic part of this story is the recent report from the Centers for Disease Control and Prevention stating that despite decades of efforts to lower the rate of obesity in children, from 2017 to March 2020, the prevalence of obesity among U.S. children and adolescents was 19.7%. This means that approximately 14.7 million U.S. youths aged 2–19 years already have obesity. You know we’ve hit rock bottom when we can’t protect our children! It’s an even worse trajectory for adults in this country.
This dire situation led to writing this post about the six types of obesity. When the appearance and health of most members of society dramatically change in a few short decades, there must be obvious underlying reasons. To date, I haven’t seen anyone, from man on the street to the world’s top scientists, come up with a viable explanation. This suggests that the medical and scientific communities have missed one or more pieces of this puzzle. The current obesity theory is that because we have so much cheap, ultra-processed food available, virtually everyone has managed to consume too many calories and failed to exercise to compensate, leading to obesity. As a physician and empirical scientist, I find this concept to be short-sighted.
Define the Problem
Let me walk you through my perspective on this critical topic. If we discuss obesity, we first must define the term. The scientific definition of obesity has always been “excessive body fat”, indicating that excessive fat is present in the body relative to other components such as organs, muscles, and water. Thus, obesity is a body composition issue rather than a size issue.
Decades ago, when I noticed the beginning of the onslaught of obesity in my primary care practice patients, I studied the topic in detail. In 1996, a group of experts published this consensus report on obesity. The report used these definitions: “Overweight is defined as a body mass index (BMI) of 25 to 29.9 kg/m2. Obesity is defined as an excess of total body fat that is documented by a BMI of ≥30 kg/m2.” They acknowledged that the scientific definition of obesity is excessive body fat. Yet, they stated: “Even though accurate methods to assess body fat exist, measuring body fat content by these techniques is often expensive and is not readily available clinically.” They instructed us dummies in primary care to use BMI to diagnose obesity. Although BMI and percent body fat tend to correlate in populations, this isn’t the case in individuals. As a clinician, I treat individuals, not populations.
I ignored their advice and purchased several pieces of FDA-approved equipment that measure body composition. Over many decades in primary care, I took over 10,000 such measurements. I measured the body composition of every patient at every visit. By carefully making empirical observations on these patients and studying the medical literature, I eventually outlined six separate types of obesity, each with its unique treatment protocols. I learned that if you tried to treat the wrong kind of obesity with an inappropriate treatment protocol, the patients tended to become more obese. This trend reflected what we were seeing in all developed populations worldwide.
Now, let’s move on to the six different types of obesity. These are primarily separate conditions, each defined by its unique pathology, although there is some overlap between several of the categories. In the real world, most obese individuals are suffering from multiple forms of obesity.
- Sumo wrestler obesity.
This relatively rare form of obesity is due to the purposeful consumption of excessive calories in a conscious attempt to become obese. The main dish consumed by sumo wrestlers is a one-pot stew called Chankonabe. It is made from reasonably healthy ingredients, but they purposely consume large amounts to gain weight. Their diet tends to be reasonably low in sugar and ultra-processed foods.
All sumo wrestlers are morbidly obese when based on BMI. When you measure their body composition, most of their fat is subcutaneous, with very little abdominal or visceral fat. They also tend to have standard metabolic markers and normal cholesterol levels. Maintaining this type of body requires a great deal of physical exercise, and when sumo wrestlers retire, they almost always quickly revert to the metabolic form of obesity.
- Hereditary Obesity.
Genetic causes of obesity can be grouped into syndromic, monogenic, and polygenic causes. Prader-Willi Syndrome is an inherited form of obesity that closely mimics sumo wrestler obesity. A dysfunctional satiety system characterizes this brain disorder, so there is no on/off switch to turn off feeding when fullness is reached. These individuals will consume anything organic in their environment, so food must be kept under lock and key to prevent them from eating themselves to death. Prader-Willi patients also have minimal visceral obesity, relatively normal metabolic parameters, and insulin sensitivity. These individuals also suffer from hypotonia, delayed development, poor growth, and various deformed body parts. The primary treatment for this syndrome is using growth hormones and restricting food. There is no effective treatment for most forms of hereditary obesity, but thankfully, they are infrequent conditions.
- Secondary Obesity.
Secondary obesity is a broad class of obesity secondary to other factors such as certain medications or excessive alcohol intake. The drugs associated with weight gain include various diabetic medications, antipsychotics, corticosteroids, anti-seizure medications, beta-blockers, and antidepressants. The characteristic weight gain from each drug tends to be unique, often a combination of increased total body fat and increased metabolic dysfunction. There appears to be some association between alcohol intake and obesity, but the association’s nature is somewhat unclear. The treatment for secondary obesity is somewhat variable, depending on the underlying triggers. When it comes to weight-inducing medications, it’s essential to use the lowest possible effective dose and consider stopping the drug if it doesn’t seem to be effective or is no longer needed. Recent research has identified a long list of chemicals and toxins that seem to trigger obesity, likely acting as endocrine disrupters. A full discussion of this topic is beyond this post’s scope, but there is one substance that merits close attention–plastics. Plastics are products manufactured from petroleum, which have only entered our environment during the past 70 years. Correlation doesn’t equal cause and effect, but there is a concern that microplastics are playing a role in excessive fat storage. Their introduction and rapid increase in production seem to match our current obesity epidemic. Plastic never wholly degrades; once produced, it never leaves the environment. Plastic is then gradually degraded into microplastic particles that enter our food chain at various points. We end up ingesting microplastic particles that tend to reside in our bodies. There is mounting evidence that microplastics and various other toxins act as endocrine disrupters, stimulating the body to store more fat. There is a concern that microplastics tend to combine with the other five forms of obesity to create our current massive obesity epidemic. My friend and colleague Barry Sears believes that bacteria in the gut break the polymers in plastic into monomers that travel to the brain through the vagal nerve. Trust me, you don’t want a brain full of monomers! Eating a healthy, whole-food diet and regular exercise are essential to effective treatment protocols for this form of obesity.
- Metabolic Obesity.
Metabolic obesity is the most common form of obesity. It is characterized by excessive visceral body fat and metabolic disorders like insulin resistance, metabolic syndrome, and type 2 diabetes. This form of obesity is strongly associated with excessive sugar intake, especially the fructose portion of sucrose. More than 20 grams of fructose from any source is converted to fat by the liver, contributing to insulin resistance and steatohepatitis. Uric acid also appears to play a role in metabolic obesity, but its exact role is unclear. For more information on fructose and uric acid’s complex biology, I recommend reading “The Sugar Fix” or “The Fat Switch” by Richard Johnson. For more information on the adverse effects of sugar and ultra-processed food, I recommend reading Robert Lustig’s “Fat Chance” or “The Hacking of the American Mind.”
This form of obesity is mainly characterized by visceral rather than subcutaneous fat. However, many individuals have excessive amounts of both types of fat, often indicating a combination of CARB syndrome (see below) and metabolic obesity. Metabolic obesity is triggered by consuming ultra-processed food over a period of time. This type of food is composed of three elements:
–Excessive fructose, mainly from sugars.
–Excessive high glycemic carbohydrates, especially from grains.
–Excessive omega-6 fatty acids relative to omega-3 fatty acids.
People with metabolic obesity also tend to have disruption of the complex neurological and hormonal mechanisms that help to maintain a healthy body composition without conscious efforts at restricting calories. Metabolic obesity and CARB syndrome obesity lie along a spectrum, with metabolic obesity at one end and CARB syndrome obesity at the other end.
Shifting to a healthy, Mediterranean-style diet composed of high-quality protein, complex carbohydrates, and healthy fats, along with regular exercise and limiting caloric intake without micromanaging it, is the recommended treatment for metabolic obesity. Low-carb or ketogenic diets may be helpful for some people. Restricting calories without focusing on the type of food consumed is not a very effective long-term treatment for metabolic obesity. Because unresolved inflammation is critical in metabolic obesity, suppressing inflammation is crucial in treating this disorder. One of the best ways to counter inflammation is to balance the consumption of omega-3 and omega-6 fatty acids properly. We need both types of fat to maintain health, and the AA/EPA ratio is the best way to measure unresolved inflammation. This ratio should be between one and three for optimal health. Most Americans must supplement this with a high-quality omega-3 supplement to reach this goal. I had to take eight capsules daily to get my ratio to 1.9. For more information about resolving inflammation, I recommend reading “The Resolution Zone” by Barry Sears. Numerous FDA-approved medications can help some patients, and various forms of surgery can also be very effective, especially for morbid metabolic obesity.
- Hypothalamic obesity.
This form of obesity is caused by damage to the hypothalamic pituitary axis. This area of the brain can be damaged by various infections, tumors, or trauma. In this type of obesity, the satiety switch is damaged, so you never feel full after eating a reasonable amount of food.
Treatment for this form of obesity is very challenging. The GLP-1 receptor agonist medications are helpful for some patients. Restricting access to ultra-processed food is important, as you don’t want to add metabolic/CARB syndrome obesity to hypothalamic obesity.
- CARB Syndrome Obesity.
The medical and scientific communities have only recently been exposed to this rather complex concept. CARB syndrome obesity is similar in many ways to metabolic obesity, but its defining characteristic is the presence of 22 brain dysfunction symptoms. For reasons we don’t fully understand, in some individuals, the long-term consumption of ultra-processed food seems to deplete key brain monoamine neurotransmitters such as dopamine, norepinephrine, and serotonin. This seems to stimulate the body to store more fat, likely because the brain is misreading the environment and signals to the body that a famine is underway. Evolution likely hard-wired these signals into the human brain. Throughout our evolutionary history, folks storing the most fat tended to survive famines better than their skinny comrades. Hereditary factors likely play a vital role in the pathology of this form of food-induced brain dysfunction.
Hudson and Pope from Harvard were the first to hint at this condition when they published their Affective Spectrum Disorder (ASD) concept in 2003. They proposed that 14 common brain disorders are part of the same disease process. Because they never identified the pathology or triggers of this condition, their ASD concept never made it out of academic medicine. Now that we know that ultra-processed food is the trigger and we understand quite a bit about the underlying pathology, we have renamed the disorder Carbohydrate Associated Reversible Brain syndrome or CARB syndrome. As mentioned above, CARB syndrome obesity and metabolic obesity appear along a spectrum. Those with CARB syndrome obesity have significant brain dysfunction symptoms, whereas those with more metabolic obesity lack these symptoms.
This concept also received support from a paper published in Science by an organization called “The Brainstorm Consortium,” an organization made up of many of the top neuroscientists in the world. Their primary goal is to figure out how the brain works. Good luck with that! We know what the brain does when it’s working as intended, yet we have little understanding of how the brain performs these tasks. They found that ten common brain disorders seem to be somehow connected. These geniuses failed even to match the 14 disorders found by Hudson and Pope.
Follow The Science
People with CARB syndrome are often misdiagnosed with traditional brain disorders like major depression, ADHD, bipolar disorder, eating disorders, anxiety disorder, and others. A good example is major depressive disorder (MDD). Since ancient Greece, major depression or melancholia has always been associated with a loss of appetite and weight loss. Without these parameters, you couldn’t make a diagnosis of major depression. Over the past 50-75 years, we have seen many folks who appear to be depressed but have an increased appetite and weight gain. The “experts” at DSM who determine the criteria of mental disorders noticed this trend and were initially uncertain about what to do. They finally decided to include both types of depression under major depression—”melancholia” or depression associated with loss of appetite and weight loss, and “atypical depression” associated with an increased appetite and weight gain. Even a 7th-grade science student knows that if a parameter qualifies you for a diagnosis throughout the spectrum of the parameter (say appetite or weight), then you need to throw it out because it can’t possibly help you to make a diagnosis. We now know that atypical depression is CARB syndrome, and it has no connection to classical major depression.
When given traditional treatments for these established disorders, over time, people with CARB syndrome tend to get worse rather than better. CARB syndrome also seems to be associated with excessive fat storage (both visceral and subcutaneous), as mentioned above, and traditional treatments tend to lead to worsening symptoms and increased fat storage regardless of caloric intake.
The most noticeable characteristic of CARB syndrome is the apparent impairment of brain function, impairing a person’s ability to function in virtually all settings. It’s also interesting to note that increases or decreases in brain dysfunction symptoms precede changes in body composition, suggesting that the brain calls the shots regarding fat storage, consistent with known physiology.
The Nuances of Body Composition
The diagnosis of CARB syndrome is a bit complex. There are numerous ways of measuring body composition. The most accurate techniques include DEXA scans, bioelectrical impedance, and underwater weighing. These methods are expensive and not readily available except in research settings. I do not recommend using body mass index (BMI) because it’s merely a size measure that tells you nothing about the fat in your body. Because visceral fat is the most dangerous type of fat, using a waste-to-height ratio is probably the most meaningful measurement. You can also use the Body Adiposity Index (BAI). There are commercial scales that estimate body fat, but they aren’t very accurate. My favorite technique is “Wilson’s Naked Mirror Test”. You take off your clothes and stand in front of a mirror. If you have a typical pot belly, you have visceral or metabolic obesity. If you can’t see well-defined muscles in your arms and legs, you have subcutaneous obesity. To diagnose CARB syndrome, go through the 22 symptoms listed above. If you have many of them, especially cravings for sweet and starchy food and excessive hunger, you have CARB syndrome. If you effectively reverse the disease, these symptoms will subside, you will automatically lose excessive body fat, and you won’t have to measure anything!
The Treatment of CARB Syndrome
The treatment for CARB syndrome involves suppressing the brain dysfunction symptoms that make lifestyle changes virtually impossible. The lead symptoms of CARB syndrome are excessive hunger and powerful cravings for sweet and starchy food. If you throw in some of the other 22 CARB syndrome symptoms, people can’t comply with healthy lifestyle changes. Decades ago, I learned the key to successfully treating CARB syndrome is to first suppress these symptoms by sometimes using low-dose medications combined with monoamine neurotransmitter precursors L-tyrosine and 5-htp in a ratio of 10 to 1. Carb-22 is the supplement product I currently recommend. It also contains co-factors and L-glutamine, an amino acid that effectively suppresses food cravings.
I was likely the first primary care physician in the world to prescribe the notorious Fen-Phen combination. I never prescribed these drugs as “weight loss” drugs because I learned that when people ate less than their bodies’ metabolic needs, they lost mainly lean body mass rather than fat. The same often happens when you use the new GLP-1 receptor agonist drugs. However, these medications are highly effective at suppressing or eliminating CARB syndrome symptoms, so patients can easily comply with the needed lifestyle changes. With these medications, patients often report that they feel “normal” virtually overnight for the first time in years. I also learned that to keep the medicines working long-term, people must take the precursors discussed above to help maintain dopamine, norepinephrine, and serotonin levels. Over time, I would taper the drugs and leave them on the precursors. In the past, I measured body composition at every visit, and if a patient was losing lean body mass rather than fat, I would tell them they needed to increase their caloric intake, especially protein, or I would stop the drugs.
Eventually, fenfluramine (the Fen in FenPhen) was withdrawn from the market due to heart valve deformities. As far as I know, none of the patients I treated with this combination developed heart valve problems. I suspect it’s because I used low doses and precursors, and I didn’t use the drugs long-term. If a patient needs medication, I now use low-dose phentermine, which is still available, along with a low dose of an SSRI medication like Prozac, Celexa, and Lexapro or drugs like lorcaserin, topiramate, metformin, and zonisamide. These medications should always be used with a precursor supplement. If the patient is taking an SSRI, cut the dose of CARB-22 to 1-2 capsules twice daily to avoid the rare complication of serotonin syndrome. I also sometimes use a low dose of a GLP-1 receptor agonist like semaglutide (Wegovy) for a period of time, along with CARB-22. When the symptoms improve, I slowly reduce the dose of the medication. In today’s world, many patients cannot access the new “miracle” weight loss medications like Wegovy, or their insurance won’t cover it, and it’s costly. Elon Musk has used Wegovy, so it must be doing something if the wealthiest guy in the world uses it! Unfortunately, unless your provider has read this post, they likely won’t understand the most effective way to use these medications. Even the FDA is relatively clueless in this regard because they don’t approve or study combinations of drugs and supplements. If you know Elon, please let him know I will treat him for free so he can remain buff while tapering the Wegovy. I will need another blog post to address his brain function!
Most people with obesity have a combination of metabolic obesity and CARB syndrome, so that’s where we need to focus our attention. If you seem to fit this pattern, the information in this post will give you and your healthcare provider a roadmap back to optimal brain and metabolic health.
