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,9 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