Or “Honey, I Just Blew up the Field of Psychiatry!”
A “humongous” study was recently published in Lancet that supposedly laid to rest the issue of whether or not antidepressants are effective. The study was titled “Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis.” Talk about a mouth full! Since then, headlines around the world have blasted out the message that we are now certain that all 21 anti-depressants are at least somewhat effective. Don’t get me wrong, I was excited when Prozac first hit the market. Up until that time all we had to treat depression were tricyclic anti-depressants and MAO inhibitors. Even though they were effective for treating depression, both classes of drugs tend to have a lot of side effects, some of which are very serious. Since then dozens of new SSRI (selective serotonin reuptake inhibitors) and SNRI (serotonin and norepinephrine reuptake inhibitors) have hit the market and they all seem to have about the same clinical efficacy.
This study ranked all 21 drugs for efficacy (they all worked) and also by their dropout rates reflecting adverse side effects. Because there was so little difference between most of the drugs, the quality of the data was critical for the validity of this study. This study was necessary because over the years many different studies of variable quality have been published, some showing that these drugs are effective and others showing that they are no more effective than taking a placebo or sugar pill. Those of us in clinical practice didn’t need to wait for this study to tell us that in general, most of these drugs worked. I have prescribed these medications thousands of times over the past few decades and in most cases, they worked quite well with only mild to moderate side effects.
I do have a specific criticism about this massive new study generating all the headlines. Although I think it’s overall conclusion that antidepressants work is likely accurate, the way they presented their date is seriously flawed. The study is based on the ideas that all drugs were treating patients with major depressive disorder (MDD). In my opinion, the major flaw in this study revolves around the definition of MDD. This classic disorder has been around since the dawn of civilization. In ancient Greece, they called it Melancholia. Since those days the diagnostic criteria for MDD have been fairly precise:
- Depressed mood.
- Loss of appetite or weight loss.
- Decreased interest or pleasure.
- Poor sleep.
- Psychomotor agitation or retardation.
- Feelings of guilt.
- Diminished ability to concentrate.
- Suicide thoughts,
Up until the past 50 years this list held up fairly well. Let me make it clear, that throughout history loss of appetite and weight loss were two absolutely critical elements of MDD and without them you simply couldn’t make a diagnosis of depression. A few decades ago somebody threw a monkey wrench into the works and noticed that a lot of folks who appeared to be depressed also had an increased appetite and weight gain. Of course, this had the good old boys at DSM (Diagnostic and Statistical Manual of Psychiatric Disorders) in a tizzy. They were sitting around a table in a room eating donuts and drinking coffee trying to decide what to do.
Depression Gets Sliced Down the Middle
When DSM IV and V came out, they came up with an ingenious solution—they decided to include both increased and decreased appetite and weight gain and weight loss as criteria for MDD. They even went so far as to develop two subcategories of MDD: Melancholic depression for those with a diminished appetite and weight loss and Atypical Depression for those with an increased appetite and weight gain. There’s only one slight problem with their “solution” to the appetite/weight dilemma. Even a seventh-grade science student knows that if a parameter qualifies you for a diagnosis throughout the spectrum of that parameter (say appetite or weight), you must throw it out because it cannot possibly help you to make a diagnosis!!!!
Despite the fact that the experts totally screwed up this issue, we still need a rational and scientific based explanation for these two types of depression. I am fairly certain that I do have the answer.
A Revolutionary New Disease Model
Over decades I also noticed that many common psychiatric disorders were increasing at about the same rapid rate, suggesting there might be a connection between them. Hudson and Pope, two prominent Psychiatrists from Harvard, conducted several experiments that support this idea. They grouped together about a dozen conditions and called this new disease Affective Spectrum Disorder (ASD). Their ASD concept included major depressive disorder (MDD), attention-deficit/hyperactivity disorder, bulimia nervosa, cataplexy, dysthymic disorder, fibromyalgia, generalized anxiety disorder, irritable bowel syndrome, migraine, obsessive-compulsive disorder, panic disorder, posttraumatic stress disorder, premenstrual dysphoric disorder, and social phobia. Because they never identified the triggers or pathology of ASD, their concept never made it out of academic medicine.
At the time Hudson and Pope were conducting their studies, I was trying to make sense of the rapidly emerging obesity epidemic. When I was doing my basic research on the topic of obesity, I found out that obesity is defined as excessive body fat. Our bodies are made up of three main components: lean body mass (bones, muscles and organs), fat mass and water. Obesity occurs when the percent of fat in your body rises to an abnormal level relative to the other components. In other words, it is clearly a body composition issue. Normal percent body fat numbers vary by sex and age and there are charts you can refer to concerning whether or not you are obese. It then made sense to me that we should be measuring body composition on all our patients rather than using weight or BMI, essentially a size measure. Neither parameter tells you anything about the amount of fat in your body so I decided to follow the science and I purchased a Futrex 500 Near Infrared Light machine and a Tanita scale that measures bioelectrical impedance. There is no perfect way to measure body composition, but both of these technologies give you a fairly accurate recording of body composition and unlike underwater weighing and other highly technical methods, they are easy to use in a clinical setting. Over time I measured over 10,000 such readings.
The Association of Excessive Body Fat and Brain Dysfunction Symptoms
I made several key observations over the decades of taking these measurements. First of all, percent body fat readings correlate very poorly with BMI and weight in many individuals. This suggests that studies that rely on BMI or weight as measures of obesity are likely fatally flawed. Because of my interest in Neuroscience, I also noticed that people with excessive body fat always seemed to have some or many brain dysfunction symptoms, many of which are typical for traditional psychiatric disorders, the same disorders that Hudson and Pope had lumped together in their ASD concept. Yet many of these folks didn’t qualify for a formal psychiatric diagnosis using DSM criteria.
I also had patients with a normal body composition and they never seemed to have any of these symptoms. Over time some of them would slowly start to develop these brain dysfunction symptoms which worsened over time. After 4-6 weeks, something strange also began to occur—their percent body fat readings would slowly start to rise into the obese range. As I learned to successfully treat patients with CARB syndrome, I also noticed the opposite trend. The symptoms would start to improve and within 4-6 weeks their percent body fat would slowly start to drop. To me this suggested when it comes to fat storage, the brain calls the shots! At this point I decided to change the name ASD to Carbohydrate Associated Reversible Brain syndrome or CARB syndrome.
The 22 Symptoms of CARB Syndrome
Over time I identified 22 symptoms that are associated with CARB syndrome. The lead symptom of CARB syndrome is having increased hunger. Their increased appetite actually consists of two components: increased hunger and an increase in intense cravings for sweet and starchy foods. Such cravings are not normal or physiological, but rather they are pathological symptoms of CARB syndrome. The primary trigger of CARB syndrome is long-term exposure to highly processed food and these cravings push people to consume more of the very food that is frying their brain. Women frequently experience such cravings in the 7-10 days prior to their menstrual cycle. Hudson and Pope were wise and observant enough to place premenstrual dysphoric disorder as part ASD and thus it is also a part of CARB syndrome. If they do not receive effective treatment these symptoms will gradually cover the entire month and this usually occurs at menopause.
People with CARB syndrome can gradually develop these 22 symptoms and because many of these symptoms overlap with traditional psychiatric disorders, this has created massive diagnostic confusion in the medical profession and scientific communities and this often results in treatment choices that are bound to make these people worse rather than better. It has been well documented that the incidence of common brain disorders seems to be rapidly increasing for no obvious reason. When we ask the medical professionals and scientists what is behind this rapid increase in these diseases, their answer is usually “We don’t know.” Of course, “we don’t know” is not a satisfactory answer in the face of so much grief and suffering caused by these common disorders which include:
- ADHD, ADD.
- Bipolar II.
- Social phobia.
- Eating disorders.
- Multiple chemical sensitivities.
- Oppositional defiance disorder (ODD).
- Obsessive-compulsive disorder (OCD).
- Panic disorder and other anxiety disorders.
- Premenstrual dysphoric disorder.
- Migraine headaches.
It is obvious that the incidence of common metabolic disorders is also rapidly increasing at about the same rate as the above conditions. These common disorders include:
- Metabolic syndrome.
- Type II diabetes.
Although it has been well-documented that these disorders seem to be increasing at about the same rate, nobody to date has come up with an adequate explanation for this troublesome phenomenon. Hudson and Pope came close but they missed the important metabolic connection.
The Eureka Moment
After treating thousands of patients, I came to the conclusion that Hudson and Pope were spot on. I simply added metabolic problems to the list and identified the primary trigger of the disorder: long-term consumption of highly processed food. As I mentioned, I changed the name to Carbohydrate Associated Reversible Brain syndrome or CARB syndrome. As with major depression, I also recognized that all of the above conditions can be broken down into two subparts. The first group are those with the true disorder such as ADHD, panic disorder, fibromyalgia, etc. These people need to be managed according to standard treatment protocols and in most cases, this involves using fairly high doses of psychiatric medications. The second larger subpart are those folks who actually have CARB syndrome that is mimicking a traditional disorder and the treatment for this CARB syndrome is much different than the treatment for traditional disorders.
This reflects the major flaw in this Lancet article. In reality, they were likely treating two completely different diseases—classic MDD and CARB syndrome. Even though antidepressants can be used for both disorders, the way they are used is radically different for the two conditions. For example, when I use antidepressants to treat MDD, I always use fairly high doses for prolonged periods of time because of high relapse rates.
The Magic of Effective CARB Syndrome Treatment
When using drugs to treat CARB syndrome, the most effective approach involves using very low doses of and SSRI or SNRI medication (for example Celexa or Lexapro 5 mg) along with a low dose of a drug that enhances dopamine/norepinephrine such as Adderrall XR 5-10 mg, Ritalin 5mg or Provigil 50 mg. I then always combined the medications with the precursors of dopamine/norepinephrine and serotonin (L-tyrosine and 5-htp in a ratio of 10 to 1). I learned about precursors from Julia Ross and I highly recommend reading her books “The Mood Cure”, “The Diet Cure” and “The Craving Cure.” In my opinion Julia is one of the world’s top experts in managing complex brain problems with simple and safe dietary changes and monoamine precursor supplements. I have added low dose medications to the mix for patients with advanced CARB syndrome because this seems to “jump start” their malfunctioning brain. In other words, these medications are merely compliance enhancers. This would in turn improve brain function to the point where the person could actually comply with the dietary and exercise components of treatment. As they improved I would gradually wean them off the medications and continue the supplements. They would never experience serotonin withdrawal when stopping the drugs when they were used with precursors. There are other components to treating CARB syndrome, but these parameters form the core of treatment and they are very effective at reversing the illness and improving brain function.
I admit that I could be wrong about all of this, but every time I move away from the above diagnostic and therapeutic principles, my results take a nose dive and as practicing front line primary care physician I live for the best possible results for my patients. If you can show me as disease model that results in better treatments and improved outcomes, I will be the first to adopt it but I am still patiently waiting for this to happen.
Don’t Look Now, But I Think I Just Blew Up the Field of Psychiatry
If the CARB syndrome model is correct, then this large study concerning the effectiveness of antidepressants is quite flawed and likely worthless. They are treating two different diseases: classic MDD and CARB syndrome and each of these responds completely different treatment protocols. Now that I think about it, virtually all research on the above conditions included in Hudson and Pope’s ASD concept is likely invalid for the same reasons. For example, there are two type of ADHD—the classic type and the CARB syndrome type. Each disease has its own unique treatment protocols.
Remember that old move from 1989: “Honey, I Shrunk the Kids!” You might want to avert your eyes because I think I just completely and thoroughly blew up the field of Psychiatry! Do you have my back as we try to put it back together in a way that better serves our patients?