Last week’s post about Antidepressants and Autistic Spectrum Disorder came with an article attached. This article was first sent to and first turned down by BMJ Open because it contained references to a set of animal studies. BMJ Open it turns out is a human studies only journal.
The interest in the animal studies listed below is that animals conceiving and giving birth while on SSRIs do not have depression or other nervous problems but their offspring appear to have neurodevelopmental delay at a greater rate. It’s tricky to establish neurodevelopmental delay in animals but one accepted marker is asexuality and these offspring are more likely to be asexual. Asexuality features because of an assumption it points to a disturbance in social functioning.
 Polleux F, Lauder JM. Toward a developmental neurobiology of autism. Mental Retardation & Development Disabilities Research Reviews. 2004; 10:303-317.
 Maciag D, Simpson KL, Coppinger D, Lu Y, Wang Y, Lin RC, Paul IA. Neonatal antidepressant exposure has lasting effects on behaviour and serotonin circuitry. Neuropsychopharmacology. 2006a; 31(1):47-57.
 Maciag D, Coppinger D, Paul IA. Evidence that the deficit in sexual behavior in adult rats neonatally exposed to citalopram is a consequence of 5-HT1 receptor stimulation during development. Brain Research. 2006b; 3(125): 171–175.
 Rayen I, Steinbusch H, Charlier TD, Pawluski JL. Developmental fluoxetine exposure and prenatal stress alter sexual differentiation of the brain reproductive behaviour in male rat offspring. Psychoneuroendocrinology. 2013; 38:1618-1629.
 Khatri N, Simpson KL, Lin RC, Paul IA. Lasting neurobehavioural abnormalities in rats after neonatal activation of 5-HT 1A & 1B receptors: possible mechanism for 5-HT dysfunction in ASD. Psychopharmacology. 2013; 231:1191-1200.
 Vieira ML, Hamada RY, Gonzaga NI, Bacchi AD, Barbieri M, Moreira EG, Mesquita SF, Gerardin DC. Could maternal exposure to the antidepressant fluoxetine and St John’s Wort induce long-term reproductive effects on male rats? Reproductive Toxicology. 2013; 35:102-107.
There is no suggestion from this literature that asexuality in people is down to antidepressant use in pregnancy or childhood, and many of those viewing themselves as Asexual appear socially gifted rather than disadvantaged.
It’s a racing certainty that some asexual and transgender states go back centuries, maybe millennia. The key word is some.
Asexuality came on to the radar for many people with the creation of AVEN and an internet presence in 2001. It has grown rapidly since. This may reflect the emergence of the internet. The people best placed to work out what might be going on is the asexual community.
When the first cases of people becoming suicidal on SSRIs were reported a key factor that persuaded many was the ability of some of those who were put on these drugs to tell the difference between treatment induced suicidality, which was new, and the suicidality linked to depression. “Doc I’ve been suicidal before, but this was different”. A key strategy for pharmaceutical companies was to blur distinctions and deny the validity of individual observations.
The best way to nail down a possible contribution of serotonin reuptake inhibiting antidepressants to some cases of asexuality will require the asexual community to get involved in exploring variations in asexuality. This is dangerous and maybe impossible if done in a manner that threatens the identity of members of the community. But it’s difficult to celebrate difference fully and to call for its recognition without being willing to explore wherever difference leads.
The issues of asexuality and antidepressants was touched on previously. The effects of many of these psychotropic drugs on sexual functioning is profound. If they may influence the development of some asexual states, what about a possible effect on Gender Dysphoria? This will be touched on in a linked post later this week.