I was greatly saddened when Little Richard, one of the most talented singers in modern history, passed away on May 9th. In honor of his memory, I pulled up this version of his classic song “Lucille” on YouTube. Other than the raw talent of this great singer, the next thing that caught my eye was that all eight band members were thin and healthy appearing. Go anywhere in this country or any other modern society and see how long it takes you to find eight thin, healthy appearing young people of any race. Good luck with that! The most tragic part of this story is the recent report from the Centers for Disease Control and Prevention that despite decades of efforts to lower the rate of obesity in children, the rate has increased to where 1 in 5 children in the U.S. are now obese. You know we’ve hit rock bottom when we can’t even protect our children!
That led to my decision to write 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, processed food available, virtually everyone has managed to consume too many calories, and failed to adequately exercise to compensate, leading to obesity. As a physician and empirical scientist, I find this concept to be rather outlandish.
Let me walk you through my perspective on this critical topic. If we are going to 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 the patients in my primary care practice, I decided that I should study the topic in detail. In 1996 a group of experts got together and 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 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 more or less 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.
Thus, I ignored their advice and purchased several pieces of FDA approved equipment that measure body composition. Over many decades I took over 10,000 such measurements in primary care. By carefully making empirical observations on these patients and studying the medical literature, I eventually outlined six separate types of obesity, each with their unique treatment protocols. I learned that if you tried to treat the wrong kind of obesity with the wrong treatment protocol, the patients tended to become more obese. This trend reflected what we were seeing in all developed populations around the world.
Now let’s move one to the six different types of obesity. These are separate diseases, each defined by their unique pathology. 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 highly processed foods.
Of course, 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 normal metabolic markers and cholesterol. 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.
There are several types of rare hereditary obesity. The best known is likely Prader-Willi Syndrome, 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 satiety 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 and 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 hormone and restricting food.
- 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. Each drug’s characteristic weight gain 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 important to use the lowest possible effective dose and consider stopping the medication if it doesn’t seem effective or no longer needed. Eating a healthy, whole foods diet and regular exercise seem to be essential parts of effective treatment protocols.
- 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 would recommend reading “The Sugar Fix” or “The Fat Switch” by Richard Johnson. For more information on the adverse effects of sugar and highly processed food, I recommend reading “Fat Chance” or “The Hacking of the American Mind.”
This form of obesity is mainly characterized by visceral fat rather than subcutaneous fat, although many individuals have excessive amounts of both types of fat, indicating a combination of sumo wrestler obesity and metabolic obesity, a rather common finding. As previously mentioned, sumo wrestler obesity is primarily driven by excessive caloric intake of any type of food, including food that is generally considered to be quite healthy. Metabolic obesity is triggered by consuming highly 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.
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 caloric intake, is the treatment for metabolic obesity. Restricting calories without focusing on the type of food consumed is not a very effective long-term treatment for metabolic obesity. Ketogenic diets and intermittent fasting also appear to be very effective at reversing metabolic obesity. For a more complete discussion of these topics, I recommend reading Joseph Mercola’s excellent books including “Fat for Fuel”, “Super Fuel”, and “Ketofast”.
Because unresolved inflammation seems to play a critical role in metabolic obesity, suppressing inflammation plays a crucial role in treating this disorder. One of the best ways to counter inflammation is to properly balance consumption of omega 3 and omega 6 fatty acids. We need both types to maintain health, and the arachnoid acid (AA)/EPA ratio is the best way to measure unresolved inflammation. This ratio should be between one and three for optimal health. Most Americans need to supplement 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.
There are numerous FDA approved medications that can help some patients, and various forms of surgery can be very effective, especially for morbid metabolic obesity.
- Obesity driven by exposure to toxins.
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, and they only entered our environment over 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, and 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 take in our body. There is mounting evidence that microplastics and various other toxins act as endocrine disrupters, stimulating the body to store more fat. Correlation doesn’t equal cause and effect, but 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 then travel to the brain through the vagal nerve. Trust me, you don’t want a brain full of monomers.
Avoiding exposure to microplastics and removing them from your body are significant challenges for most people living in modern society. I like this article that outlines many ways to detox from microplastics. I have been a gum chewer for decades. It somehow seems to help me relax. I have chewed Mentos gum for years until I realized that it is packed in plastic and made from plastic! I recently switched to sugar-free and plastic-free Glee gum, likely resulting in a considerable decline in my exposure to plastic.
- 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 that we don’t fully understand, in some individuals, the long-term consumption of highly processed food seems to deplete key monoamine neurotransmitters such as dopamine and norepinephrine and serotonin. These depletions seem 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 seems to have hard-wired these signals into the human brain. The folks storing the most fat tended to survive famines better than their skinny comrades. Hereditary factors likely place 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 highly processed food is the trigger and understand quite a bit about the underlying pathology, we have renamed the disorder Carbohydrate Associated Reversible Brain syndrome or CARB syndrome.
This concept also received support from a recent paper published in Science by an organization called “The Brainstorm Consortium,” an organization made up of all the top neuroscientists globally, and their 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.
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 depression. Since ancient Greece, major depression or melancholia was always associated with a loss of appetite and weight loss. Without these parameters, you simply couldn’t make a diagnosis of major depression. Over the past 50-75 years, we have been seeing many folks who appear to be depressed but have an increased appetite and weight gain. The “experts” at DSM who determine mental disorders’ criteria noticed this trend and were initially uncertain 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, people with CARB syndrome tend to get worse rather than better over time. 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 that impairs a person’s ability to function in virtually all settings. It’s also interesting to note that increases or decreases in brain dysfunction symptoms seem to precede changes in body composition, suggesting that the brain calls the shots when it comes to fat storage, consistent with known physiology.
The treatment for CARB syndrome is relatively complex, but the key to effective treatment is to suppress 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 simply can’t comply with healthy lifestyle changes. Decades ago, I learned the key to the successful treatment of CARB syndrome is to suppress these symptoms using low dose medications combined with the monoamine neurotransmitter precursors L-tyrosine and 5-htp in a ratio of 10 to 1.
I was also probably 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 they lost mainly lean body mass rather than fat when people under ate below their bodies’ metabolic needs. However, these two drugs were extremely effective at suppressing or eliminating CARB syndrome symptoms, so patients could easily comply with the needed lifestyle changes. Patients would report that they felt “normal” virtually overnight for the first time in years after taking Fen-Phen. I also learned that to keep the medications working long term, they need to take the precursors discussed above to help maintain dopamine, norepinephrine, and serotonin levels. Over some time, I would taper the drugs and leave them on the precursors. I measured their 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, or I would stop the drugs.
Eventually, Fen-Phen 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. I later switched to using low dose phentermine, which is still available along with a low dose of an SSRI medication like Prozac, Celexa, Lexapro, and precursors.
I find it enlightening that even today, I can prescribe drugs known to cause heart valve problems, including dopamine agonists and ergot alkaloids. Of course, Parkinson’s disease and migraine headaches are “real” diseases, unlike obesity, which is seen as a choice. Sad, very sad.
The pathology, diagnosis, and treatment of CARB syndrome are a bit complex. For more details, please read my book, “Brain Drain.” Once you understand that there are six forms of obesity, each with their unique pathology and treatment, our current worldwide obesity mess becomes quite clear.
I find it interesting that the talent and genius that Little Richard bought to the world of music is sharply contrasted by the lack of talent and inspiration that the medical and scientific communities brought to our understanding of obesity. It is my mission to correct this tragic situation.