In neurobiology, there is a shorthand description of something that most of us will have some grasp of, even if one is not trained in biology. The formula is: 'G x E' (genes x environment). It means: a person may develop a condition due to two things:
1. Genetic susceptibility. Many disorders and diseases are somewhat 'preprogrammed', in a veiled way. Our DNA is the nuclear structure in all of our cells that carries the instructions for the making of proteins. Proteins play an enormous variety of different roles in all organism. They are also named: polypeptides, and are chains of tiny building blocks, called amino acids. There are 22 so-called standard amino acids. DNA is the blueprint for the eventual structure of proteins, it determines the exact sequence of the amino acids in a protein. Now, suppose something 'went wrong' in the DNA code. One element in it, let us call it a nucleotide, has for one reason or another been beplaced by another. This may be the cause of one amino acid in our protein being replaced by another; the 'programme' instructs the building of the protein in a slightly different way.
This replacement can have a great impact. Because important proteins in our whole body, including the brain, may have been altered a bit in their structure. Whilst this is not always threatening (it can even be an improvement in some cases), it can hamper the proper functioning of that protein.
If we consider that the molecules in the membrane (the 'wall') of our nerve cells are also proteins, we begin to understand that if these proteins are altered in structure, they are in theory also altered in their function.
A highly interesting, and replicated result in science is that a certain protein in nerve cells, called the glutamate transporter, can be altered in the way I described, and moreover, this alteration is much more often seen in patients with OCD than in healthy control subjects. The protein (or rather: set of proteins) in question have the following function: it is responsible for the transport of the amino acid glutamate back into the nerve cell. Glutamate is the neurotransmitter (messenger molecule) most present in our brain.
Now we see a connection. Suppose that in OCD patients, the transport of glutamate back into the cell is defective. This transport is important for the normal function of our brain. Moreover: if present in too high quantities (levels) outside of the nerve cells, glutamate can become damaging. It can be responsible for a degeneration of nerve cells themselves and the protecting cells around them (the so-called glia cells).
We have seen that an ever so tiny change in genetic coding, our blueprint so to speak for all of our body structures, can have a considerable consequence for the proper functioning of a certain part of our body, here that part is the brain.
To recap: there is a possible connection, called an association, between an altered protein structure, the glumate transporter (which has the posh name of SLC1A1) and the occurrence of obsessive compulsive disorder.
Research here is difficult, time consuming, pricey, and it is quite hard to find homogenous groups of patients. The latter demand is important: if I throw in checkers, hoarders, washers, and order-addicts into my experimental group, women and men, children and adults, medicated and unmedicated people, then chances are very slim that I will obtain any trustworthy result. So there is a need for a precise selection procedure.
The above problems are the reasons that research takes a lot of time. That is why we have little reliable information about the special role that serotonin (another messenger molecule) in all probability plays in OCD. We do know that serotonin reuptake inhibitors work in about half of all OCD patients. But how do they work? There is, in the serotonin system, a comparable molecule (protein) as there is in the glutamate system. Its name? You will know: the serotonin transporter. We even know that this molecule has various possibel sites for mutations within it, and there even exist 'missing parts' in the genes that code for this transporter. But there has been no consistent result in studies that try to link the serotonin transporter to OCD.
Which is puzzling.
2. Now, here is the second part of the formula 'G x E'. The 'E' means 'environment', as we saw. It was observed that not all people that carry the mutations mentioned above, or other aberrations in essential proteins in the brain, actually develop OCD. Moreover, when researchers decided to interview patients about their life history, an interesting fact presented itself: in all likelihood, dramatic life events may 'trigger' the occurrence of OCD in susceptible people. In other words: you may have a genetic disposition for OCD, but you may at the same time not develop the illness itself. Simply put: you seem to have been lucky. Other people who have the same genetic disposition may develop OCD; and then chances are that there are events in their life history that 'unpacked' the disorder. Such events may be: problems at childbirth; physical and/or sexual abuse in childhood; emotional abandonment in general; and also things of a less severe nature that particularly impact on one's private sensibilities.
Most of us will know that OCD is also called an 'anal fixation'. Funny that... Sigmund Freud developed that concept a century ago; he had an all too severe potty training in mind, that could traumatize children and would make them into all too precise, neurotic, obsessed adults in the long run, with a strong tendency towards cleanliness, collecting, checking. Psychologists used this idea throughout the last hundred years, and still do, but its use is on the wane. In fact, 'anal fixation' and 'anal personality' have become staple phrases for the lay population, and are being used in TV sitcoms and silly quizzes.
I gave the example of Freud because it is a vivid illustration of a life event that can eventually (and potentially!) be a factor in the development of a mental disorder.
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