Serotonin and mental illness
It is doubtless that serotonin activity in the human brain is strongly connected to mental wellbeing and psychiatric disorders, and this association is confirmed by numerous studies in both animals and humans.
Not only are certain individuals more likely to develop a slew of mental illnesses because of genetic idiosyncrasies in their serotonin systems (the SS and LS genotypes in 5-HTTLPR alone are a risk factor for depression, anxiety, bipolar disorder, alcoholism, obsessive-compulsive disorder etc. (Gonda, et al., 2008), not to mention the range of serotonin receptor polymorphisms that have similar such effects), but responses to psychiatric drugs such as SSRIs and even an individual’s general affect—what some might call ‘mood’ or even, to an extent, ‘personality’—are influenced by genetic, inherited variations in his or her serotonin system. Furthering our understanding of serotonin is vital in the fight against mental illness and in better understanding the human condition.
Kramer (1993) speaks of a small but significant minority of patients who are given serotonergic antidepressants such as Prozac (fluoxetine) to alleviate depressive symptoms and report that the drugs make them feel “better than well” and wonders whether such drugs should be limited only to those with mental illnesses if they could confer benefits even on healthy individuals. He is not alone in such thoughts; Charlton (1998) attempts to examine the ethical issues this raises, suggesting that such individuals should be allowed access to such drugs otherwise reserved for the mentally ill. Unbeknownst to Kramer, his suggestion that antidepressants might have a role in the lives of healthy individuals was confirmed in a striking way by later double-blind, placebo-controlled research showing more positive emotion and better social functioning in mentally healthy individuals given SSRI antidepressants (Knutson, 1998). On a similar note, much research has been done on illicit serotonergic drug MDMA (‘Ecstasy’) and its potential psychotherapeutic use in patients suffering post-traumatic stress disorder to great success (Turner A., 2008), with some prominent psychotherapists describing the compound as “penicillin for the soul” in reference to its ability to trigger therapeutic, cathartic emotional release and create exquisite feelings of connectedness to others (Boal, 2004; Pearce, 2008).
A hugely significant scientific discovery occurred in 2006 when a French group of molecular biologists created a knockout mouse with a specific gene missing (the TREK-1 gene), and in doing so created an animal with an apparently depression-resistant phenotype (Heurteaux, et al.)—evidence, if any more was needed, that depression has clear biochemical underpinnings if not always a biochemical root cause. The significance of this finding cannot be understated: by unravelling the exact molecular mechanism of depression we can develop hugely more effective medicines and gene therapies for the disease as well as a whole host of other related mental illnesses.
This should not be seen as an endorsement of the current generation of serotonergic drugs for the purposes of ‘cosmetic psychopharmacology’ as Kramer puts it—rather, an examination of the potential for serotonin to affect our predisposition to mental illness, mental wellbeing, social interactions, personality and untold more. The genetics of serotonin will undoubtedly play a part in our future, hopefully for the better, and as this body of research expands exponentially we can hope to better understand how one’s genetics changes the very fundamental nature of oneself and those around us, to improve our ability to treat mental illnesses and to enrich the lives of healthy individuals too.
Pages: 1 2 3 4
Serotonin, disease and the future
Serotonin and mental illness
It is doubtless that serotonin activity in the human brain is strongly connected to mental wellbeing and psychiatric disorders, and this association is confirmed by numerous studies in both animals and humans.
Not only are certain individuals more likely to develop a slew of mental illnesses because of genetic idiosyncrasies in their serotonin systems (the SS and LS genotypes in 5-HTTLPR alone are a risk factor for depression, anxiety, bipolar disorder, alcoholism, obsessive-compulsive disorder etc. (Gonda, et al., 2008), not to mention the range of serotonin receptor polymorphisms that have similar such effects), but responses to psychiatric drugs such as SSRIs and even an individual’s general affect—what some might call ‘mood’ or even, to an extent, ‘personality’—are influenced by genetic, inherited variations in his or her serotonin system. Furthering our understanding of serotonin is vital in the fight against mental illness and in better understanding the human condition.
Kramer (1993) speaks of a small but significant minority of patients who are given serotonergic antidepressants such as Prozac (fluoxetine) to alleviate depressive symptoms and report that the drugs make them feel “better than well” and wonders whether such drugs should be limited only to those with mental illnesses if they could confer benefits even on healthy individuals. He is not alone in such thoughts; Charlton (1998) attempts to examine the ethical issues this raises, suggesting that such individuals should be allowed access to such drugs otherwise reserved for the mentally ill. Unbeknownst to Kramer, his suggestion that antidepressants might have a role in the lives of healthy individuals was confirmed in a striking way by later double-blind, placebo-controlled research showing more positive emotion and better social functioning in mentally healthy individuals given SSRI antidepressants (Knutson, 1998). On a similar note, much research has been done on illicit serotonergic drug MDMA (‘Ecstasy’) and its potential psychotherapeutic use in patients suffering post-traumatic stress disorder to great success (Turner A., 2008), with some prominent psychotherapists describing the compound as “penicillin for the soul” in reference to its ability to trigger therapeutic, cathartic emotional release and create exquisite feelings of connectedness to others (Boal, 2004; Pearce, 2008).
A hugely significant scientific discovery occurred in 2006 when a French group of molecular biologists created a knockout mouse with a specific gene missing (the TREK-1 gene), and in doing so created an animal with an apparently depression-resistant phenotype (Heurteaux, et al.)—evidence, if any more was needed, that depression has clear biochemical underpinnings if not always a biochemical root cause. The significance of this finding cannot be understated: by unravelling the exact molecular mechanism of depression we can develop hugely more effective medicines and gene therapies for the disease as well as a whole host of other related mental illnesses.
This should not be seen as an endorsement of the current generation of serotonergic drugs for the purposes of ‘cosmetic psychopharmacology’ as Kramer puts it—rather, an examination of the potential for serotonin to affect our predisposition to mental illness, mental wellbeing, social interactions, personality and untold more. The genetics of serotonin will undoubtedly play a part in our future, hopefully for the better, and as this body of research expands exponentially we can hope to better understand how one’s genetics changes the very fundamental nature of oneself and those around us, to improve our ability to treat mental illnesses and to enrich the lives of healthy individuals too.
Pages: 1 2 3 4