I’ve been just been copied in with an email to Tim Berridge at the MHRA:
Dear Mr Berridge
I’m writing because I have kindly been copied in with your recent email to Mr Fiddaman regarding Serotonin and its alleged link to the cure of depression.
I’m confused by all this, so to help me understand matters could you confirm that the MHRA’s current position is that depression is in fact a medical condition caused by a chemical imbalance and that by increasing levels of serotonin in the brain chemistry this condition can be cured.
I only ask as it seems the Royal College of Psychiatrists and the Institute of Psychiatry have accepted that depression isn’t caused by a chemical imbalance.
Also, could I ask you to consider the following statements which are directly linked to this discussion:
“Although it is often stated with great conﬁdence that depressed people have a serotonin or norepinephrine deﬁciency, the evidence actually contradicts these claims”. Professor Emeritus of Neuroscience Elliot Valenstein, in Blaming the Brain (1998), which reviews the evidence for the serotonin hypothesis.
“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”. Science writer John Horgan, in his critical examination of modern neuroscience, TheUndiscovered Mind (1999).
“A serotonin deﬁciency for depression has not been found”. Psychiatrist Joseph Glenmullen, clinical instructor of psychiatry at Harvard MedicalSchool, in Prozac Backlash (2000).
“So far, there is no clear and convincing evidence that monoamine deﬁ ciency accounts for depression; that is, there is no “real” monoamine deﬁcit”. Psychiatrist Stephen M. Stahl, in a textbook used to teach medical students about psychiatric medications, Essential Psychopharmacology (2000).
“Some have argued that depression may be due to a deﬁciency of NE [norepinephrine] or 5-HT [serotonin] because the enhancement of noradrenergic or serotonergic neurotransmission improves the symptoms of depression. However, this is akin to saying that because a rash on one’s arm improves with the use of a steroid cream, the rash must be due to a steroid deﬁciency”. Psychiatrists Pedro Delgado and Francisco Moreno, in “Role of Norepinephrine in Depression,” published in the Journal of Clinical Psychiatry in 2000.
“…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 in 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 A.E. 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).
“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.
Although SSRIs are considered “antidepressants,” they are approved treatments for eight separate psychiatric diagnoses, ranging from social anxiety disorder to obsessive-compulsive disorder to premenstrual dysphoric disorder. Some consumer advertisements (such the Paxil Web site) promote the serotonin hypothesis, not just for depression, but also for some of these other diagnostic categories.
Thus, for the serotonin hypothesis to be correct as currently presented, serotonin regulation would need to be the cause (and remedy) of each of these disorders.
I await you reply with baited breath