You go to your physician or psychiatrist and give them a list of unusual symptoms that you have noticed. Something is wrong, and you want it to be fixed. Your health care provider will then group your symptoms into categories that coincide with mental health disorders that have been defined by the “experts” in the Diagnostic and Statistical Manual of Mental Disorders or DSM V, the latest version. They will then label you with one or more of these disorders. Because there are no objective tests for mental disorders, symptoms determine the diagnosis. Historically most of these various disorders did seem to coincide with real illnesses. Still, something has changed over the past 50 years.
The History of Depression
Major depression is a good example. The ancient Greeks were the first to describe depression or what they called melancholia. The symptoms included loss of appetite, excess sleeping, lack of motivation to even bathe, constant weeping, chronic exhaustion, and a sense of helplessness. Because of the loss of appetite, people with depression wasted away and lost a lot of weight. The description of depression stayed that way for the past 2,000 years. Without loss of appetite and weight loss, you simply couldn’t make a diagnosis of melancholia or depression. That suddenly began to change in the middle of the last century. All of a sudden, we started to see a lot of depressed people who seemed to have an increased appetite and weight gain, the exact opposite of classic depression. Can you think of anything else that changed in the 1950s and 60s that might also drive a significant increase in obesity that then began to show up a few decades later? It’s pretty apparent to me that it was the dramatic increase in highly processed food that took over our diet at that time.
The Toxic Triad
You may wonder what qualifies as “highly processed food”? It consists of three neurotoxic elements:
- Excessive fructose mainly from sugars.
- Excessive high glycemic carbohydrates mainly from grains.
- Excessive omega 6 fatty acids relative to omega 3 fatty acids mainly from vegetable oils.
To me, this looks like your average modern pizza, breakfast cereal, or baked goods. So, what did our experts at DSM think of this dramatic change? They were likely sitting around drinking coffee and eating donuts. They then decided in their great wisdom to include both parameters for the criteria of obesity: increased and decreased appetite and weight loss and weight gain. Huh? Even a seventh-grade science student knows if criteria qualify you for a diagnosis throughout the spectrum of the requirements (say appetite or weight), then you must discard the criteria. That’s because these requirements can’t possibly help you to make a diagnosis! The experts apparently left their thinking caps at home that day, and you and your loved ones will be the ones to suffer the consequences if any of you have ever faced a diagnosis of depression.
The DSM V Depression Fiasco
So now in DSM V we have two subcategories of depression. “Melancholia” or classic depression is associated with loss of appetite and weight loss as described by the ancient Greeks and “atypical depression” that is associated with an increased appetite and weight gain. They propose treating both types of depression the same way, mainly with high dose SSRI type medications, the ones that can make you gain weight. Do you see a problem here for people with atypical depression?
Let’s put on our thinking caps and see if we can figure out this mess made by the goofballs at DSM. To do so, we need to go back to 2003 when two prominent psychiatrists from Harvard, James Hudson, and Harrison Pope, published a series of elegant articles. They suggested the radical notion that 14 common brain disorders are part of the same disease process. The called this disease Affective Spectrum Disorder or ASD. The conditions under the ASD banner included:
- Major depression.
- Attention-deficit/hyperactivity disorder.
- Bulimia nervosa.
- Dysthymic disorder.
- Generalized anxiety disorder.
- Irritable bowel syndrome.
- Obsessive-compulsive disorder.
- Panic disorder.
- Posttraumatic stress disorder.
- Premenstrual dysphoric disorder.
- Social phobia.
Holy smokes! These guys just blew up the field of psychiatry! So, what happened? A big nothing. Because they never discovered the triggers and pathology of ASD, and because their concept was so radical, their idea never made it out of academic medicine. It also more or less died on the vine. If you ask a physician or psychiatrist today what they know about ASD, you will likely respond with a blank stare.
Follow the Body Fat
During this same time, I was wrestling with the emerging obesity epidemic. I knew that obesity was defined as excessive body fat, so I wondered why everyone was talking about BMI and weight, two parameters that tell you zippo about the fat inside your body. I decided to purchase two FDA approved instruments that measure body composition, and I started to measure the body composition of all my patients. After thousands of such recordings that I took in my solo practice on the Iron Range in Northern Minnesota, I noticed an odd trend. At the time, I had a keen interest in neuroscience, and I belonged to Stephen Stahl’s Neuroscience Education Institute. Stahl’s Psychopharmacology was the bible for all practicing psychiatrists then and today. I started to notice an odd correlation between specific brain dysfunction symptoms and changes in body composition. It seemed that when these symptoms increased, within 3-4 weeks, the patient’s percent body fat would start to rise. If I managed to suppress these brain dysfunction symptoms, within 3-4 weeks, their percent body fat would start to drop slowly. It also became apparent to me that the primary driver of this process with highly processed food, but when it came to fat storage, the brain was calling the shots.
It soon dawned on me that I was witnessing a new form of food-induced brain dysfunction that had symptoms that overlap with many traditional brain disorders. The light bulb brightly burned when I realized that I was witnessing the same phenomena described by Hudson and Pope with their ASD concept. Because I had figured out the primary trigger of the disorder, I changed the name to Carbohydrate Associated Reversible Brain syndrome or CARB syndrome. I eventually identified 22 symptoms of CARB syndrome. Through trial and error, I figured out some very effective treatment protocols that had nothing in common with the typical psychiatric approaches used to treat these patients. I also realized that atypical depression is CARB syndrome, and it has nothing to do with classic melancholic depression.
Neurotransmitters Down the Drain
It became clear to me that patients with CARB syndrome were depleted of the key monoamine neurotransmitters dopamine, norepinephrine, and serotonin. It appeared likely that glucose spikes from eating highly processed food caused excessive dumping of neurotransmitters from neurons, overwhelming the reuptake system. Most of these neurotransmitters would be taken up by the blood supply and cleared by the kidneys to show up in the urine. At one point, we used urine neurotransmitter tests during glucose tolerance tests, where subjects were given a pure glucose load. Soon large amounts of monoamine neurotransmitters would show up in their urine. Mother Nature doesn’t like to waste valuable chemicals like neurotransmitters, so this was clearly a pathological rather than a physiological process.
The Fen-Phen Pioneer
I know that the drugs usually used for major depression called selective serotonin reuptake inhibitors or SSRI medication acted by blocking the reuptake of neurotransmitters already in the synaptic space. This process magnified the effects of the low levels of neurotransmitters in your brain. It seemed like people with CARB syndrome had even lower levels of these chemicals than people with classic depression. I realized I needed to increase the levels of these chemicals dramatically. I had read the work of Julia Ross who had worked with neurotransmitter precursors or the building blocks of neurotransmitters for years. I also studied the work of Judith and Richard Wurtman from MIT, who did much of the original research of precursors. I soon realized that if I gave my patients with CARB syndrome the precursors for all the monoamine neurotransmitters, all boats would rise. Over time I determined that when I combined the precursors L-tyrosine (the precursor of dopamine and norepinephrine) and 5-htp (the precursor of serotonin) in a ratio of 10 to 1, all monoamine neurotransmitters would rise together. By combining a low dose of magnifying drugs that targeted both the dopamine/norepinephrine side and the serotonin side, I could dramatically relieve the patient’s brain dysfunction symptoms. This approach would allow them to comply with the dietary and lifestyle changes that they needed to make.
Over several decades I treated thousands of patients who fit the CARB syndrome disease model, and most of them did exceptionally well. I found that the most effective combination of drugs to treat CARB syndrome was the infamous Fen-phen combination of phentermine and fenfluramine. I was the first practitioner in the world to prescribe these drugs in clinical practice, yet I never used them at “weight loss” drugs. I used them to control the symptoms of CARB syndrome so patients could comply. If a patient tried to diet and under-eat while taking these drugs, I would immediately catch them, because they would lose lean body fat rather than fat. I warned them that if they didn’t start eating more healthy whole foods, I would stop the medications. Shortly after taking Fen-Phen, patients with CARB syndrome stated that almost overnight, they felt completely normal for the first time in many years. The claimed I had found some type of magic switch in the brains.
Mickey Mouse Wins the Day
At one point, because my approach was so unusual, I had to defend myself against the Minnesota Board of Medical Practice. I presented the physicians who presided over the hearing with a hundred and ten-page referenced report supporting what I was doing. My attorney told me he thought I would lose my medical license. When I finished my lecture, jaws had dropped throughout the room, and all charges were immediately dismissed. They felt they had Osama Bin Laden, and they ended up with Mickey Mouse!
Don’t Wait for the Goofball Experts to Get Up to Speed
Despite my successes at managing these complex patients, the folks at DSM and the medical profession continue to plod along using the same flawed approaches that are guaranteed to make these patients worse rather than better. I decided it would likely take several lifetimes for these clowns to get up to speed, and I didn’t think it was fair for you, your family and your loved ones to wait until they did. Thus I recently published a book called “Brain Drain” that teaches people how to make their own diagnosis of CARB syndrome and arrange for their own treatments. All of these treatments are relatively inexpensive, safe, and effective, so I have no problem promoting them.
After reading this article and possibly the book, if you feel that you might have CARB syndrome, don’t look to your physician or psychiatrist to help you. Simply follow the directions in the book, leading you back to a life of health and optimal brain function. After all, what could be better than that?
By the way, the DSM fiasco didn’t end with their depression blunder. In recent years, they noticed that some people who previously had anorexia nervosa were now obese. They decided to call these folks “atypical anorexia.” Because I measure body composition and apparently they don’t, I learned early on that virtually all anorexics, unless they are preterminal, have excessive body fat. In essence, they are thin but obese. Even though they eat very little, when they do eat they eat the same crap that all folks with CARB syndrome eat, driven by their strong cravings for sweet and starchy food. They just don’t eat very much of it early on, so they stay skinny with their increased body fat hidden. Later some of them start to eat more food, and they quickly become visually obese, but they have the same disease the whole time—CARB syndrome. The concept of atypical anorexia or obese anorexia blows me away. Maybe the experts at DSM need a few more cups of coffee and a little less vino! You might also consider sending them this blog post if you want to stir things up!
Good luck and be healthy!