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I felt this sensation in the pit of my stomach – it was a combination of sympathy and anger – listening to Annie tell me, through tears, about her postpartum journey into the world of psychiatry.
Three separate psychiatrists dismissed me when I expressed concerns about taking an addictive medication like Klonopin. It's been two years, I can't get off it, I'm on 4 psych meds and I feel worse than I ever did before I started this treatment.
Annie was ushered into the promise-filled halls of psychiatry 3 months after the birth of her first baby when she began to experience racing heart, insomnia, vigilance, irritability, and a host of physical complaints including joint pain and hair loss. No one did bloodwork, asked about her diet, or cared about any of the myriad observations about her body and its changes in functioning. This was a "head-up" intervention. I believe women deserve better. People deserve better.
Most patients who come to me for treatment of depression and anxiety do so because they want answers. They want to know WHY they are struggling. The closest they will be offered by their prescribing psychiatrist or primary care doc is some reductionist hand waving about serotonin imbalances. I think it is time to speak to these patients with respect, truthfulness, and to offer them more than a life-long relationship with a pill (or pills as it will inevitably become over the years). First, let's review some basics:
Depression is Not A Serotonin Deficiency
Thanks to direct-to-consumer advertising and complicit FDA endorsement of evidence-less claims, the public has been sold an insultingly oversimplified tale about the underlying driver of depression. Here's how we know depression is not a serotonin deficiency corrected by Zoloft:
- There has never been a single study, in humans, to validate the theory of low serotonin in depression. Low levels are found in a minority of patients.
- An antidepressant marketed as Stablon, increases reuptake of serotonin (reducing serotonin activity) and appears to be equally effective as those that decrease it or have no effect on it at all.
- Manipulation of serotonin levels (depletion or enhancement) do not consistently result in a depressive syndrome.
- These medications are used to treat an impossibly non-specific and broad array of illnesses from obsessive compulsive disorder to anorexia to premenstrual dysphoria to bipolar depression to irritable bowel syndrome.
- Antidepressants of all categories seems to work about the same regardless of their presumed mechanism of action with about 73% of the response unrelated to pharmacologic activity.
You might wonder: Well, then how is it that antidepressants are a billion dollar industry and I have all these friends who are so much better on them? Some pioneering individuals have investigated the data supporting antidepressant efficacy and have made compelling arguments for what is called the "active placebo" effect accounting for "breaking blind" in placebo-controlled trials. In short, the expectation of relief and subsequent change in symptoms experienced by "responders" is related to perception of side effects. This analysis suggests that antidepressants may only have 10% efficacy above and beyond the placebo effect. When you also consider the suppression of negative studies (permission of sedatives in trials, replacement of non-responders, and allowance of placebo washout) by pharmaceutical companies, you may start to worry that you have been sold a bill of goods. When inefficacy, long-term risks, increase in suicidality and violent behavior are taken into account, it is a marvel to observe the star-power of these medications.
What Is It Then? Inflammation!
Inflammation is a buzzword, and a 41 million+ Google hit for a reason: it appears to underlie just about every chronic disease plaguing Americans today. A contribution of genetic vulnerabilities likely determines who develops heart disease or cancer or obsessive compulsive disorder, but many researchers are convinced that depression may have a significant inflammatory component. Just as a fever is one of your immune system's mechanism for eradicating intruders, suppressing a fever, in no way, serves to resolve the underlying infection or to support the body's return to balance. Similarly, suppressing symptoms of depression does not achieve rebalancing, and will likely result in the Whack-a-Mole phenomenon of shifting symptoms, and protracted resolution.
There appears to be a specific subset of non-responders to medication who have measurable markers of inflammation as explored in this study. We know that medications such as interferon given to patients with Hepatitis result in significant levels of depression and even suicide, and we know that anti-inflammatory agents such as infliximab or even aspirin can result in resolution of symptoms. Investigators like Miller and Raison have discussed, in a series of wonderful papers, the conceptualization of depression as "sickness behavior" with accompanying social withdrawal, fatigue, loss of appetite, decreased mobility. Recent meta-analyses have identified at least 24 studies which have correlated levels of inflammatory cytokines like CRP, IL6, and TNFalpha with states of depression.
What Drives Inflammation?
What causes inflammation in the body that can affect the brain? This is the subject of an excellent book, and, it turns out the list is long, but these are the contributors that I see most commonly in my practice:
It's in almost every packaged food. Seriously. Look for it and you will find it. It may come with different labels – cane sugar, crystalline fructose, high fructose corn syrup – but it's all sugar. The way the body handles fructose and glucose is different; however, which may account for why fructose is 7x more likely to result in glycation end products or sticky protein clumps that cause inflammation. In addition to the above mood and anxiety rollercoaster, sugar causes changes in our cell membranes, in our arteries, our immune systems, our hormones, and our gut as I discuss here.