When it comes to critical public health issues, there is one fact that’s hard to dispute. We are now in the clutches of a massive, world-wide obesity epidemic. The United States has been at the vortex of this dramatic development. There are virtually endless academic articles and statistics to support this assertion, but if you are 50 years old or older, you have had a front row seat to witness this tsunami of fatness. Throughout history, true obesity has been a fairly rare phenomena. Just look at a photo of groups of people before 1970, and just about everyone will appear to be fit and trim. Peer at a similar photograph of groups of people in today’s world, and the majority will be oversized or obviously obese.
To better understand this disturbing trend, we first need to understand the scientific definition of obesity. Obesity is defined as “excessive body fat” relative to other tissues in the human body. To determine the level of fatness in someone’s body, you need to measure their body composition. There are several technologies to do so, including underwater weighing, bioelectrical impedance, and near-infrared light. Because weighing people underwater is a hassle and is mainly used in research settings, the other two technologies are the most practical for clinical applications. When I was working full time in front-line Family Practice during the 1970s, I noticed this obesity trend in my patient population. I decided that I needed to get a handle on this problem, and my first priority was to find the most accurate parameter to measure obesity in my patients.
I always caution people to be skeptical about so-called “expert” consensus. During the 1990s with this obesity epidemic in full swing, the experts published an article in the prestigious New England Journal of Medicine telling us dummies in primary which parameter to use for diagnosing obesity. They recommended that we use Body Mass Index (BMI), a height/weight formula that is essentially a size measure. If you’re a large person your BMI will be high and likewise if you are a smaller person, your BMI will be low. What does BMI tell you about the amount of fat in your body? Nada, zippo, nothing! Although BMI and percent body fat correlate in populations, this doesn’t hold up for individuals, and I treat individuals, not populations. I eventually decided to purchase two expensive pieces of equipment to measure the body composition of my patients—a Futrex 5000 machine using near infrared light technology and a Tanita machine using bioelectrical impedance. Over many years I eventually took over 10,000 body composition measurements using these technologies. I measured body composition on every patient at every visit. All of the available technologies to measure body composition have their limitations, and the readings often vary between the different methodologies. Even though the Tanita and Futrex readings were often slightly different, their strong point is their ability to accurately reflect changes in body composition over time. They would accurately tell me if a given patient was losing or gaining body fat. Based on my experiences following changes in body composition in my patients over time, I sent a letter to the editor of the NEJM challenging their BMI recommendations and it was published in 1999.
The so-called obesity experts also postulated the cause of this sudden surge in obesity over the past 50 years. They asserted that obesity only occurs when there is an excess in calorie consumption often combined with a reduced level of physical activity. This is the “diet/exercise” theory of obesity.This perspective fails to explain why it wasn’t until relatively recently that calories suddenly increased and physical activity suddenly decreased to the level necessary to trigger massive obesity. Why didn’t this ever occur in the previous eons of human existence? To date the experts have failed to come up with an explanation for this dilemma that makes any sense.
I also had a strong interest in neuroscience during this period of time and I joined Stephen Stahl’s Neuroscience Education Institute. Dr. Stahl is considered one of the world’s top experts when it comes to brain pathology. Thus I always paid careful attention to my patient’s brains and symptoms suggesting some degree of brain dysfunction. Over time I noticed a curious correlation between the onset and progression of certain brain dysfunction symptoms and changes in body composition. I also noted that changes in brain dysfunction symptoms seemed to precede changes in body composition. It appeared to me that the brain was in the driver’s seat when it comes to fat storage. Of course, this makes sense from an evolutionary standpoint. If fat stores were totally dependent on caloric intake, our ancient ancestors would have eventually come up short on the evolution survival scale.
Over time I noticed that 22 distinct brain dysfunction symptoms seem to be driving the bus when it comes to fat storage. At the time I also stumbled across the research of Hudson and Pope from Harvard. They developed a concept called Affective Spectrum Disorder (ASD) that included a diverse list of 14 common brain disorders, and they suggested that these conditions were somehow linked through a shared pathological process. Their list correlated very closely with the symptoms that I was observing in my patients. These patients would usually be diagnosed by their physicians with one of the conditions listed under the ASD concept.
At the time I also had access to urine tests that measured certain monoamine neurotransmitter levels such as serotonin, norepinephrine and dopamine. At the time it was unclear how to use the results of these tests, but I noticed an unusual trend. Shortly after consuming food with sugar and rapidly absorbed carbohydrates, urine neurotransmitter levels would dramatically increase, as is the brain was for some reason dumping these valuable chemical. This trend was very dramatic when patieints were undergoing glucose tolerance test screening for type 2 diabetes. The symptoms of ASD also reflected low levels of brain monoamine neurotransmitters, suggesting a dietary trigger to many of the conditions under the ASD label. During the ravages of our current obesity epidemic, the incidence of the common brain disorders like those associated with ASD also began to dramatically increase. I then knew that I was likely dealing with some type of food-induced brain dysfunction that had yet to be described by the medical and scientific communities. I decided to call this new disease model Carbohydrate Associated Reversible Brain syndrome or CARB syndrome.
During this time my brilliant medical school classmate Richard Johnson unraveled the physiology of fructose metabolism that was driving obesity at the cellular level. Although fructose has always been a part of the human diet, consuming more than 20 grams of fructose daily results in excessive fat production and storage leading to insulin resistance and metabolic syndrome. The pieces of the obesity puzzle were rapidly falling into place to the point where I could envision a model to successfully treat patients who fit the CARB syndrome disease model.
At this time I began to question the concept that excessive calories and lack of physical exercise were the driving forces behind our obesity epidemic. Let me provide a more likely scenario. Folks with CARB syndrome have depletion of the two activating neurotransmitters—dopamine and norepinephrine. When someone lacks these key chemical messengers, they tend to lack energy and the motivation to get up and move. They prefer to sit and rest. Thus lack of energy is a result rather than a cause of food induced brain dysfunction and resulting obesity. Low serotonin is associated with cravings for sweet and starchy food, especially those thata are rapidly absorbed and thus have a high glycemic index.
Over several years I learned to successfully treat my patients who fit the CARB syndrome model by targeting the presumed pathology of the disorder. These are the guiding principles that seemed to be the most effective:
- To jump start their depleted brains, I used low doses of medication that magnified the low levels of monoamine neurotransmitters. The most potent combination of such drugs was the notorious phen/fen combination that was eventually promoted as a “weight loss” combination
- I increased levels of monoamine neurotransmitters by providing the precursors of dopamine, norepinephrine and serotonin: L-tyrosine, dl-phenylalanine, and 5-htp.
- I worked to dramatically reduce intake of excessive fructose, sucrose and rapidly absorbed carbohydrates in my patients.
- In order to radically change their diets, I used the amino acid L-glutamine to suppress the strong cravings for starch and sugar that drives this disease process.
- I eventually combined all these supplement together in a product called CARB-22 that I sold to my patients at cost.
I also listened to my good friend Barry Sears of Zone Diet fame. Barry is an expert on systemic inflammation, and like virtually all chronic diseases, inflammation on a cellular level plays a central role in the pathology of CARB syndrome. Based on his recommendations, I encourage my CARB syndrome patients to measure their AA/EPA ratio. A ll you need is an inexpensive fingerstick test available from the Zone web site or Omegaquant. The optimal AA/EPA ratio is between 1 and 3, and most people in modern societies eating processed food need to take a relatively high dose of omega 3 fatty acid to get in this range. I had to take 8 capsules daily to get my ratio to 1.9. I take Omega Rx2 available from Dr. Sears web site. Unlike many cheaper brands that are of poor quality, Omega Rx2 is extremely high quality and pure—just what the doctor ordered!
I successfully used this approach to treat thousands of my patients who fit the CARB syndrome model. Fenfluramine was eventually removed from the market when the relatively high doses used to treat obesity were associated with rare cases of valvular heart disease. I only used low doses of this drug, and I never noticed this side effect in any of my patients. When the serotonin enhancing drug fenfluramine was withdrawn from the market, when a. patient needed medication, I switched to low doses of other serotonin enhancing drugs like Prozac, and this seemed to work quite well. Many patients did quite well with supplements alone without medications.
When I measured the body composition of my patients, I noticed that our obesity epidemic is even worse than most contemporary estimates. That’s because some of the folks who were normal or under weight, had increased body fat when their body composition was measured. These thin but obese folks also had typical CARB syndrome brain dysfunction symptoms. Many people diagnosed with anorexia nervous and other eating disorders fit this pattern.
It’s also important to remember that some patients have traditional brain disorders that are not part of the CARB syndrome disease model. Their symptoms will fit the traditional disorder, they won’t have strong cravings for sweet and starchy food, and their body composition will be normal. These patients should be treated with standard psychiatric protocols which often included various medications, usually in much higher than I might initially use to treat CARB syndrome. If patients only had CARB syndrome, I would try to taper and discontinue medications as soon as possible, and rely on supplements, dietary changes, and exercise to move them back to optimal health.
To summarize, I believe that our current obesity epidemic is driven by the consumption of excessive amounts of fructose, sucrose, high glycemic carbohydrates, and omega 6 fatty acids present in the modern diets now consumed by most people around the world. Although some of these obese folks are consuming excessive calories driven by their cravings, many others are not and some are consuming well below average amounts of calories. Thus, our obesity epidemic is likely caused by food-induced brain dysfunction or CARB syndrome, not an excessive amount of calories and a reduction in physical activity promoted by current experts. In order to successfully combat this tsunami of obesity, we need to understand the true pathology of the disorder. Because individuals who fit the CARB syndrome pattern often have no access to professionals who understand their disease and thus can effectively treat them, I have written a book titled “Bran Drain” where I teach people to diagnose and treat their own CARB syndrome. I know this is not an ideal situation, but it’s the best I can do until the medical and scientific communities come to their senses.
I am also not afraid of being wrong. In science when new theories are proposed, it is the job of the scientific community to prove the theory to be wrong. Only when they fail to do so can the new theory take its place in established science. To date the CARB syndrome model has rebuffed all challenges. Feel free to take your own shot at the concept. If you succeed, it will certainly give me a bit more free time than I currently enjoy! If you do decide to follow my advice, please enjoy your new journey to optimal health and improved quality of life. I will be rooting for you!