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Serotonin Depression Myth

Simplified research sounds very impressive, writen in language flowing with anatomical nomenclature and statistical gobbledygook. Looking at SEROTONIN as a simple single molecular unit, and then reasoning that serotonin is the primary cause of various depressions and Seasonal Affective Disorder (SAD), is wrong.

The article on the serotonin depression complex explaines how serotonin can naturally be used to fight depression.

There are a few problems with these oversimplified studies. Serotonin is more than a molecule looking for a few synapses to bounce between in the brain. It is a part of a system of neurotransmitter systems. Serotonin is used by the body for more than keeping depression at bay. only 5% of serotonin is in the brain. The rest, 95%, is busy doing what serotonins do, in other organs of the body. Serotonin is not alone in depression, there are other neurotransmitters working in intricate ways. Ways science has still to unravel.

Most important to remember when told of the serotonin hypothesis, as if it were a scientific fact, is that there is no scientifically established correct “chemical balance” for serotonin or other neurotransmitters.

Serotonin, dopamine and other neurotransmitters in the brain do play roles in the development of anxiety and depression, but CANNOT be treated as individual chemicals on their own independent of the others.

A few quotes on the subject to illustrate the point:

A serotonin deficiency for depression has not been found.”

Psychiatrist Joseph Glenmullen, clinical instructor of psychiatry at Harvard Medical School, in Prozac Backlash: Overcoming the dangers of Prozac, Zoloft, Paxil and other antidepressants with safe, effective alternatives. New York: Simon and Schuster. 384 p.

I wrote that Prozac was no more, and perhaps less, effective in treating major depression than prior medications. I argued that the theories of brain functioning that led to the development of Prozac must be wrong or incomplete.”

Brown University psychiatrist Peter Kramer, author of Listening to Prozac, which is often credited with popularizing SSRIs, in a clarifying letter to the New York Times, July 7 2002.

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. In fact, we cannot measure brain serotonin levels in living human beings so there is no way to test this theory. Some neuroscientists would question whether the theory is even viable, since the brain does not function in this way, as a hydraulic system.”

Stanford psychiatrist David Burns, winner of the Bennett Award given by the Society for Biological Psychiatry for his research on serotonin metabolism, when asked about the scientific status of the serotonin theory in 2003.

Indeed, no abnormality of serotonin in depression has ever been demonstrated”.

Psychiatrist David Healy, former secretary of the British Association for Psychopharmacology and historian of the SSRIs, in Let Them Eat Prozac (2004): The unhealthy relationship between the pharmaceutical companies and depression. New York: New York University. 351 p.

We have hunted for big simple neurochemical explanations for psychiatric disorders and have not found them.”

Psychiatrist Kenneth Kendler the coeditor-in-chief of Psychological Medicine, in a 2005 review article: Kendler K.S. Toward a philosophical structure for psychiatry. Am J Psychiatry 162:433-440.

The subject is complex. This is the main reason science has still not understood the mechanism for depression. The facts bandied about with such frivolous confidence by well meaning doctors, are actually hypotheses and speculation. These hypotheses are taught at medical schools as facts, for lack of any substantial theories. Before Copernicus everyone in Europe thought the sun revolved around the earth every 24 hours. If everyone looks at a problem from the same perspective, they will see the same thing and draw the same conclusions.

This is not a trivial matter. A study published in Child and Adolescent Psychiatry and Mental Health 2008, 2:26, showed that youth in the United States are three times more likely to be medicated than European youth. Youth in the United States are ten times more likely to be medicated for ADHD in the United States than in most European countries.

The most complex and difficult questions facing science, and especially psychiatry and psychology, today concern the mind, the brain, their interrelationship, and their interactions with other people and the world around us. The philosophical implications have been debated for thousands of years, and we are not much closer today, as there is still no consensus on the basic presuppositions the debate rests on.

History of the Serotonin Hypothesis

So how did this serotonin idea come about. For a start serendipity has played a major role in the development of antidepressive drugs. The earlier types of tricyclic antidepressants drugs, developed in the mid 50s, were initially meant to be for the treatment of schizophrenia. Trials showed the schizophrenia got worse, but some of the patients’ depressions lifted. So the next trials were on patients with depression. Still to this day there is no clear explanation as to how these tricyclic drugs work for depression. Guesses and hypotheses, yes, but knowing - no.

The tricyclic drugs, the most popular of which are amitriptyline and imipramine, have side effects. These includes impotence, constipation, weight gain, confusion and even . . . depression. So new drugs were developed.

In In 1965, the hypothesis was suggested, that depression was due to low levels of the neurotransmitter norepinephrine, and later serotonin. The research carried out at the time on these neurotransmitters had errors in their methodology. There is to date no reliable proof that serotonin is a primary chemical in depression. There have been unsuccessful attempts to induce depression by inhibiting serotonin; unsuccessful as depression did not result. Other tests to reduce depression by increasing levels of serotonin have not given clear results, because serotonin works together with other neurotransmitters and not independently on its own . However increasing serotonin levels while taking modern selective serotonin reuptake inhibitors (SSRIs) have resulted in serotonin poisoning or serotonin syndrome.

The serotonin hypothesis has been given a long life, by the pharmaceutical giants latching on to it and designing a range of drugs called selective serotonin reuptake inhibitors (SSRIs). These drugs cost multimillions of Dollars to develop and market, and they are today a multibillion Dollar industry. These drugs like Prozac and Zoloft and theSerotonin-norepinephrine reuptake inhibitors (SNRIs) like Effexor act by inhibiting the reuptake of serotonin (and norepinephrine) after being released in synapses (gaps between brain cells).

The pharmaceutical industry is actively keeping the hypothesis alive by selectively publishing studies supporting their hypothesis, while ignoring trials indicating their drugs are not really effective.

After 20 to 40 years of touting these drugs by the pharmaceutical companies, independent research has shown they help only a minority of users. Recently researchers have tested whether they actually work, using pharmaceutical companies own results. One study found only 29 per cent of patients responded to the tricyclic antidepressants.

An antidepressant meta-analysis study on selective serotonin reuptake inhibitors (SSRIs) by scientists from the University of Hull in the United Kingdom, published in 2008, looked at the results from 47 clinical trials. These were both published and unpublished clinical trials submitted to the United States Food and Drug Administration (FDA) for the most popular SSRIs, including Prozac, Paxil, Zoloft, and Effexor. They found the antidepressants helped mainly those suffering from the most severe depression, and even then did not produce convincing evidence. For people with mild or moderate depression there was little difference to taking a dummy pill. All but one of the positive  results were published, but most of the negative results .

In another study, published in the New England Journal of Medicine, of all but one of the 38 positive studies given to the Food and Drug Administration were published, but most of the negative ones went unpublished. In a case of one negative and one positive trial, the two were made into one with a positive result. Among 74 Food and Drug Administration registered studies, 31%, were not published. There was a clear bias towards choosing which reports to publish. Scientific published reports are not always impartial and objective. Studies viewed by the FDA as having negative or questionable results were, with 3 exceptions, either not published (22 studies) or published in a way that conveyed a positive outcome (11 studies). According to the published literature, it appeared that 94% of the trials conducted were positive. By contrast, the FDA analysis showed that only 51% were positive.

How statistics are presented can turn a neutral report positive. For example, in a trial 100 patients with depression are given a placebo, and 100 patients are given the active antidepressant. The results show an improvement in 35 patients who received the placebo, and in 50 patients who received the active anti depressant pills. The report states the antidepressant was more efficacious than the placebo. But 35% were actually placebo effect, leaving only 15% of the patients being helped by the antidepressant.

A doctor reading the medical journals would think that individual antidepressants were more effective than they actually are. Doctors and patients d0 not get the full picture.

Confirmation Bias

There is a psychological phenomenon called confirmation bias. This happens when we have become convinced something is true. We look for confirmation and apparent proofs. We tend to ignore evidence not supporting our particular belief. This is why it is so difficult to change some peoples opinions.

When a generation has been taught a hypothesis, they continue teaching this to the next generation as a fact, and that generation believes it to be true.

For a doctor who is a believer in antidepressants, the response to a patient's depression not going away, is to increase the dose. If the patient suffers serious side effects, then another drug is prescribed. The thought of Cognitive Behavioural Therapy does not enter the believer’s mind.

This is why it is important, as a patient, or a patient's family, to be informed of the different treatments available, and not trust a doctor who is locked into one solution, usually medication, but choose a physician who is open to other treatments. Sometimes two treatments together are necessary.

Antidepressant Side Effects

Although SSRIs and SNRIs are supposed to have less side effects than the tricyclic antidepressants, this is not always so, as some patients feel better on tricyclics than SSRIs and SNRIs. Many patients prefer the depression to the side effects. In fact physicians are now seeing long-term side effects with selective serotonin reuptake inhibitors far in excess of what was expected from clinical trial data. Clinical trials are usually of short duration, and long term effects are therefore not known when the drugs go on the market. Nightmares, impotence, decreasing male fertility and weight gain are problems doctors do not expect, as they are not on the medications’ fact sheets.

Alternative reasoning

When starting a course of anti depressants, the biochemical effect comes on fairly soon, but the relief from symptoms usually occurs three to six weeks or more after changes in neurotransmitter levels. This suggests that the precise role of neurotransmitter levels in depressive illness is still not understood.

If a lack of serotonin is the cause of depression, then the obvious cure would be increasing serotonin levels. Since nobody has zero serotonin (they would not survive) there must be a cause of the deficiency. This point has been ignored. There is a possible rate limiting step in the biochemical process. A hydroxylase enzyme reaction could become less efficient as a result of stress or some other psychological strain. testing patients by giving them a diet supplement of the product after this step should solve the controversy once an for all. This has been actively hindered by the pharmaceutical industry.

Serotonin is produced in the body through biosynthesis and cannot directly be increased by food supplements (serotonin would be destroyed in the stomach), but can be through supplement of the immediate precursor. This is 5-HTP or 5-Hydroxytryptophan. To test this patients can be given this precursor for serotonin. This is a cheap and healthy answer, but has been strongly resisted by the pharmaceutical industry.

However, the serotonin system in our bodies is inimately connected with the dopamine system, so a natural dopamine supplement must be taken together with the 5-HTP. This is Tyrosine.

Many patients who have tried 5-HTP have had positive results, feeling a release from depression. What studies of FDA reports and serotonin research show, is that depression is extremely complex and no one-cure-fits-all answer is possible. We are all individuals, with our own psyche, and metabolism. When wide ranging results are found as in the field of depression, the obvious answer is that it is too complex to generalise. Generalising about the general population is justified, but not applying that to an individual.

(An important WARNING: Do not try 5-HTP if you are taking: Monoamine oxidase inhibitors (MAOIs), Selective serotonin reuptake inhibitors (SSRIs), Combined reuptake inhibitors and receptor blockers, Serotonin and norepinephrine reuptake inhibitors (SNRIs) or Norepinephrine and dopamine reuptake inhibitors (NDRIs) antidepressants, as this will result in SEROTONIN POISONING. First wean off the antidepressants, do not stop suddenly, and be off antidepressants for at least a month.)

Tricyclics can be taken with 5-HTP.

In his book, Blaming the Brain: The Truth About Drugs and Mental Health Professor Emeritus of Neuroscience Elliot Valenstein wrote, “Although it is often stated with great confidence that depressed people have a serotonin or norepinephrine deficiency, the evidence actually contradicts these claims.” This book reviews the evidence for the serotonin hypothesis.

Science writer John Horgan, in his critical examination of modern neuroscience, The Undiscovered Mind, wrote, “Given the ubiquity of a neurotransmitter such as serotonin and the multiplicity of its functions, it is almost as meaningless to implicate it in depression as it is to implicate blood.”

The understanding that the brain is more complex than the pharmaceutical companies want us to believe, is not new science, but the voices have been crying in the wilderness for decades. If we stop and switch off the cacophony of advertising, we might hear a voice telling us to treat the cause of depression and not suppress the symptoms.

The reasoning behind the lack of serotonin as the cause of depression, is like saying:

the cause of headaches is the lack of aspirin.

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