I read a chilling book recently, called “The Anatomy of an Epidemic,” by Robert Whitaker.  Here are the highlights, and I’ve included references at the bottom.

We tend to think of antidepressants and anti-anxiety meds (benzodiazepines) as “silver bullets,” much in the same way that we originally viewed antibiotics as silver bullets against infectious diseases.  The idea that depression and anxiety are caused by chemical imbalance in the brain is so widespread that it almost goes without question… and antidepressants especially (and benzodiazepines as well) supposedly correct those chemical imbalances, helping such afflicted individuals function normally in society.

But there isn’t any evidence for that hypothesis.

Lack of Evidence for the Chemical Imbalance Theory

The theory of depression as a chemical imbalance in the brain was first postulated by Bernard Brodie.1 But when depressed patients and normal controls were tested for the breakdown products of serotonin (5-HIAA), researchers failed to find a statistically significant difference between the two – nor did there appear to be any correlation between 5-HIAA levels and depressive symptoms.2,3 Further studies showed that depressed patients who had not taken antidepressants had normal 5-HIAA levels.4

Stanford psychiatrist David Burns said in 2003, “I spent the first several years of my career doing full-time research on brain serotonin metabolism, but I never saw any convincing evidence that any psychiatric disorder, including depression, results from a deficiency of brain serotonin.” 5

Colin Ross, associate psychiatry professor of Southwest Medical Center in Dallas, said, “There is no scientific evidence whatsoever that clinical depression is due to any kind of biological deficit state.” 6

Iatrogenic Chemical Imbalance

Depressed patients treated with SSRIs end up with a chemical imbalance as a result of the drugs, though. Here’s how it works.

Your body is a living system, designed to find balance (homeostasis) with its environment.  SSRIs (Selective Serotonin Reuptake Inhibitors) prevent serotonin from being recycled, so it sticks around to re-stimulate its receptors longer.  Your brain responds to this by saying, “Hey, we’ve got too much serotonin stimulation going on, stop making so many receptors.”  So your body drops the production of serotonin receptors by 25% within four weeks,7 and up to 50% with chronic use.8 This may also be the reason why it takes 3-4 weeks for SSRIs to “work.”

Antipsychotics do essentially the same thing with the dopamine system instead of serotonin, but instead they block the dopamine receptors, forcing the body to flood the system with more and more dopamine.

Benzodiazepines increase the affinity of receptors for the calming neurotransmitter GABA. This leads to a decrease in the inhibitory effects of GABA, as well as an increase in the excitatory neurotransmitter glutamate to compensate.

In other words, you may not have had a chemical imbalance before, but you do now.  (That’s why you can’t abruptly stop any of the psych drugs without potentially severe consequences.)

Downhill With Benzos

The introduction of these drugs to the public has corresponded with a dramatic decline in American mental health.

In 1955, only one in every 468 Americans was considered to be mentally disabled, and there were only 5,415 “psychoneurotic” (anxiety disorder) patients in state mental hospitals.9

Then Valium (a benzodiazepine) hit the market in 1963. It was the bestselling drug in the Western world until 1981, touted as perfectly safe. It works very quickly to calm anxiety, but the clinical trials demonstrate (and most people can attest) that these benefits are pretty much gone by 4-6 weeks.10 But the withdrawal symptoms were so horrific and in many cases so lingering11 that in 1975, the U.S. Justice Department made it a controlled substance (schedule IV drug). Patients who remain on benzos long-term have a four-fold increase in depressive symptoms, as well as a gradual increase in panic attacks and agoraphobia.12 The “higher the intake, dose and period of use

[of benzodiazepines], the greater the risk of impairment.”13

By 2006 more than 300,000 adults in the US were on SSI (government disability) for anxiety disorder alone – that’s about 60 times the number hospitalized for psychoneurosis (anxiety) in 1955.14

Downhill with Prozac

In the 1930s and 1940s, less than one in a thousand adults suffered clinical depression yearly.9 Around 60 percent of such individuals suffered only a single episode of depression in their lifetimes, and only 13 percent suffered three or more episodes.15 Dean Schuyler, head of the depression section at the NIMH in 1974, noted that spontaneous recovery rates for depression exceeded 50 percent within a few months.16

Then Prozac was approved in 1987. While depression had previously been associated with a high rate of spontaneous recovery within a few months to a year and a low relapse rate, studies show that the longer the duration of treatment with SSRIs, the higher the rate of relapse.17 In fact, those treated for depression were three times more likely than untreated depressed patients to “suffer a cessation of their principle social role, and nearly seven times more likely to become incapacitated.” 18

All told, in 2007 the disability rate had soared to one in every 76 Americans, from one in every 468 Americans in 1955.19  This includes children – in 1987, pre-Prozac, only 5.5 percent of American kids were on disability rolls for mental health issues.  By 2007 that number rose THIRTY FIVE FOLD, and is now the leading cause of disability in children.20  By June 2008, one in every sixteen young adults is now considered to be mentally ill.21

I could go on – I have not even mentioned the studies that demonstrate SSRIs are not significantly better than placebo for the treatment of mild to moderate depression, nor have I mentioned the side effects of any of these drugs. The book goes on to cite similar research for medications for schizophrenia, bipolar disorder, and ADD/ADHD.

So I reiterate the initial question. Are we making ourselves sicker?

References:

  1. Valenstein, Blaming the Brain, 70-79. Also see David Healy, The Creation of Psychopharmacology (Cambridge, MA: Harvard University Press, 2002), 106, 205-206. 
  2. M. Bowers, “Lumbar CSF 5-hydroxyindoleacetic acid and homovanillic acid in affective syndromes,” Journal of Nervous and Mental Disease 158 (1974):325-30.
  3. J. Mendels, “Brain biogenic amine depletion and mood,” Archives of General Psychiatry 30 (1974):447-51. 
  4. M. Asberg, “Serotonin depression: A biochemical subgroup within the affective disorders?” Science 191 (1976): 478-80; M. Asberg, “5-HIAA in the cerebrospinal fluid,” Archives of General Psychiatry 33 (1976):1193-97. 
  5. J. Lacasse, “Serotonin and depression: a disconnect between the advertisements and the scientific literature,” PloS Medicine 2 (2005): 1211-16.
  6. C. Ross, Pseudoscience in Biological Psychiatry (New York: John Wiley & Sons, 1995),111.
  7. D. Wong, “Subsensitivity of serotonin receptors after long-term treatment of rats with fluoxetine,” Research Communications in Chemical Pathology and Pharmacology 32 (1981):41-51.
  8. J. Wamsley, “Receptor alterations associated with serotonergic agents,” Journal of Clinical Psychiatry 48, suppl. (1987):19-25.
  9. C. Silverman, The Epidemiology of Depression (Baltimore: Johns Hopkins Press, 1968), 139.
  10. Social Security Administration, annual statistical reports on the SSI program, 1996-2008; and Social Security Bulletin, Annual Statistical Supplement, 1988-1992.
  11. U.S. Government Accountability Office, “Young adults with serious mental illness” (June 2008).
  12. K. Solomon, “Pitfalls and prospects in clinical research on antianxiety drugs,” Journal of Clinical Psychiatry 39 (1978):823-31.
  13. H. Ashton, “Protracted withdrawal syndromes from benzodiazepines,” Journal of Substance Abuse Treatment 9 (1991):19-28.
  14. A. Pelissolo, “Anxiety and depressive disorders in 4,425 long term benzodiazepine users in general practice,” Encephale 33 (2007):32-38.
  15. Schuyler, The Depressive Spectrum, 47
  16. G. Fava, “Can long-term treatment with antidepressant drugs worsen the course of depression?” Journal of Clinical Psychiatry 64 (2003):123-33.
  17. W. Coryell, “Characteristics and significance of untreated major depressive disorder,” American Journal of Psychiatry 152 (1995):1124-29.
  18. A. Zis, “Major affective disorder as a recurrent illness,” Archives of General Psychiatry 36 (1979):835-39.
  19. Social Security Administration, annual statistical reports on the SSDI and SSI programs, 1987-2008.
  20. M. Barker, “Cognitive effects of long-term benzodiazepine use,” CNS Drugs 18 (2004):37-48.
  21. Government Accountability Office, Young Adults with Serious Mental Illness, June 2008.

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