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Friday, November 7, 2008

Smell of Schizophrenia (suggested)

Note: This is written only to promote awareness and may not be accurate.

For a while, there has been a 'vibe' in psychiatric journals (probably mostly heard of but ignored) that schizophrenics can have a certain odor at times. The suspected chemical (probably from one or 2 PubMed papers) is trans-3-methyl-2-hexenoic acid (MHA).

This would not seem to be likely a candidate substrate for the xenobiotic enzymes (at a guess) and shows how various enzymes that are not branded part of the 'general xenobiotic metabolizing enzyme group' can cause various smells if the enzyme is overloaded for some reason and the chemical(s) it breaks down is malodorous ... for instance (very mild) sweaty-feet odor syndrome (Isovaleric acidemia) and dimethylglycinuria. There are many enzymes in the human body, and if they deal with a malodorous chemical and are often saturated for some reason, it's likely the person will at times smell of that chemical(s). Once again it proves the principle that people can smell of unmetabolized compounds.

It is of particular interest because of the conclusions and results they came up with, which may be the same 'rules' (in general) that apply to all metabolic odor conditions, that are summarised in this schizophrenia news blog...

http://www.schizophrenia.com/sznews/archives/004743.html
The chemical exuded in the sweat of these patients with chronic schizophrenia causing the distinct odor is a chemical called trans-3-methyl-2-hexenoic acid (MHA). The study found that the group of patients with chronic schizophrenia could not detect that chemical odor as well as the study group without schizophrenia, nor as well as the study group with just first-episode psychosis.

Further study is needed to determine if the reduced olfactory sensitivity to the chemical (ability to smell it) is due to olfactory habituation effects (we tend to not be as sensitive to a smell which we are constantly exposed to), abnormal chemical processing or a genetic predisposition.

Other scents tried, such as some pheromones and cleaning fluid, could be detected equally by all three groups.

The team noted that:

In patients with chronic schizophrenia, reduced sensitivity to MHA correlated significantly with the severity of disorganized and negative symptoms.

"The results confirm that olfactory identification deficits... occur in the presence of relatively intact acuity for traditionally used substances," the authors conclude.

It is hoped that this chemical in the sweat, as well as the olfactory sensitivity to it may help in early diagnosis, and possibly be another direction for genetic and biological research into the understanding of this type of schizophrenia.
So what the study is saying is:
  • All in the group had normal smell sensitivity to all odor chemicals in the test apart from 'schizophrenics' towards MHA
  • The more 'schizophrenic' a person was, the less able they were to detect MHA odor
Anyone with a body odor or halitosis problem will likely recognise this pattern; because for most, usually the sufferer nor 'loved ones' can smell the sufferer. This may be very true for metabolic/systemic/bloodborne odor problems in particular.

One theory for metabolic body odors not being detected could be that the sufferers 'olfactory receptors' to those smells is always/often 'saturated', and/or needs a higher level to detect a difference. Perhaps carriers also carry these smells in their systems at undetectable levels but it means their sensitivity is reduced. But that doesn't seem to explain why those with 'classic' external BO or 'classic permanent' halitosis still 'exist'. For instance if you could smell a 'loved one' with a curable/washable 'classic external' BO problem would you not tell them? It must be assumed that for most with 'classic external' BO, neither they nor their loved ones can smell them (same as metabolic cases).

It also raises the notion that this sort of testing could be used for metabolic odor conditions. for instance, perhaps TMAU sufferers cannot detect Trimethylamine (not from themselves) as good as a normal person. And perhaps 'carriers' not as good as a 'normal' person. Perhaps even one day it could be used to let a sufferer know their current 'TMA load'. It seems worthy of investigation.

original study: http://www.ncbi.nlm.nih.gov/pubmed/17156856
pubmed search of MHA. 1st paper: 1969
Dr Warrick Brewer website : (Dr Brewer was the lead scientist in the MHA paper)

Addendum:
An interesting sidenote is that as mentioned here before, pharmacogenetics/pharmacogenomics (personalized medicine) is likely to be the sensible 'future' of patient treatment (We hope, since currently it's one blind dose for all), to which the 'medical system' is likely to be very slow in practicing (mostly due to attitudes and self-preservation). Ironically one of the first 'pharmacogenetic' tests developed was in response to the common bad reaction some (many?) have towards 'helpful' psychiatric drugs. It seems that many schizophrenics are low in a certain 'xenobiotic metabolizing enzyme' important in metabolizing psychiatric drugs (CYP2D6).
Since a lot of the CYP2D6 substrates are psychiatric drugs (antidepressant and antipsychotics, for example), the AmpliChip CYP450 has been extensively used in psychiatry.
Quote from Wikipedia Amplichip CYP450 page
As good as it is that a share-listed pharmaceutical company has come up with a DNA test for this now (Roche Amplichip CYP450 DNA test), one would think an overall assessment of all those enzymes would make more sense. Also, history may look back and decide the old routine was : patient has enzyme issue and feels depressed ... Dr prescribes a drug and makes it far worse.
In 1997, the journal Science described "personalized prescription" or "tailoring drugs to a patient’s genetic make-up" in their "six research horizons for 1998" and predicted that it will "soon" reach clinical practice. More precise estimations for the generalized used of personalized prescription have been provided: the year 2015, according to the lay journal Time and 2020, by JAMA. Because CYP2D6 metabolizes many of the psychiatric drugs, psychiatry has become the first area of medicine for the practical clinical use of pharmacogenetic testing. A recent article in a mainstream economic journal focused on "personalized medicine," presenting an example of a bipolar patient who had a complicated pharmacological treatment history. Although many psychiatrists may not be ready for "personalized prescription," their patients may be reading this article or listening to government officials promoting "personalized prescription" in the media.

http://psy.psychiatryonline.org/cgi/content/full/47/1/75


The Roche Amplichip DNA test (There are probably more extensive, cheaper versions of this test)

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