Year : 2009 | Volume
: 31 | Issue : 1 | Page : 1--2
Primary prevention in psychiatry
Asha Hospital, Hyderabad, India
M S Reddy
Asha Hospital, Hyderabad
|How to cite this article:|
Reddy M S. Primary prevention in psychiatry.Indian J Psychol Med 2009;31:1-2
|How to cite this URL:|
Reddy M S. Primary prevention in psychiatry. Indian J Psychol Med [serial online] 2009 [cited 2020 Jan 29 ];31:1-2
Available from: http://www.ijpm.info/text.asp?2009/31/1/1/53307
As on today, any discussion on primary prevention in psychiatry sounds adventurous and unrealistically grandiose. The 20 th century facilitated a fast-forward from tertiary prevention to secondary prevention of various psychiatric disorders. It is but natural to have hope kindled in our hearts that the 21 st century leads us one step forward with some light on primary prevention in psychiatry.
The saddest part of psychiatric morbidity is that almost all the major psychiatric disorders affect the patient at his or her prime age - the second and third decades - and in the most crucial phase of his or her development and maturity (educational, occupational, marital, and social identity); and in most cases, they leave a significant disability and an ugly scar on the personality. The only way this can be stopped is primary prevention. Though this sounds an impossible goal to achieve at present, there seems to be some hope with more and more evidence coming in favor of epigenetics and neuroplasticity.
Definitions of primary prevention are vague, and the evidence is not very convincing for the implementation of primary prevention programs in psychiatry. As we all know, the goal in primary prevention is preventing the occurrence of a particular illness and reducing its prevalence in the community - the kind of eradication achieved in the case of smallpox and being planned for poliomyelitis. The best results in terms of primary prevention will be in the case of infectious diseases, where the etiological factors are well defined and identified. Also, in those with noninfectious etiology, serious attempts are being made to achieve primary prevention; stopping smoking to prevent lung cancer and providing dietary supplement of iodine to prevent goiter and thyroid disease are two examples. The same is true in the case of public awareness camps on obesity and exercise , with the goal of reducing the incidence of diabetes, an area of major concern for WHO in the 21 st century.
Lack of objectivity, questionable diagnostic validity, and absence of laboratory confirmatory tools are a few significant drawbacks in the classificatory system of psychiatric disorders. Reasonable diagnostic purity is essential before we conceptualize any kind of prevention. Any plan for primary prevention should be clear about what we are planning to prevent. Among psychiatric disorders, the efforts at primary prevention should focus first, perhaps, on illnesses like bipolar disorder, schizophrenia, OCD, dementia, etc., where the boundaries are not very diffuse and biological etiology is more in acceptance. Eradicating dementias secondary to vitamin deficiencies can be an achievable practical goal. The highly discussed prevention-related findings for anxiety, depression in childhood and adolescence, suicide, substance abuse, and eating disorders are not conclusive and provide little evidence that incidence is lowered.
The vision for primary prevention in psychiatry
Universal prevention aimed at the general population - better postpone it, maybe to the last decades of the 21 st century.Selective prevention aimed at subgroups of populations at higher risk, viz., high-vulnerability and high-risk groups. This is somewhat similar to taking measures to prevent obesity in a patient who has a first-degree relative with diabetes. The aim is to identify specific precipitating factors, if any, and see how they can be nullified.Indicated prevention directed at the population not just with high risk but with minimal and detectable symptoms which do not satisfy the diagnostic criteria - the concept of early illness (early psychosis) and initiation of treatment at the earliest. This is not primary prevention strictly but more like secondary prevention bordering onto primary prevention. Newer drugs (SDA, SSRI) with much favorable side-effect profile may give us this leverage of erring on the side of starting treatment before confirmation of diagnosis. (Starting a patient on anti-Koch's treatment in some cases of pyrexia of unknown origin (PUO) is a fairly well accepted medical practice in the Indian context.) But this is highly controversial and may open a Pandora's box. The suggestion is that this should be tried only on an individual basis and should be highly selective, to start with.
There is some consensus that among the psychiatric interventions, targeted interventions (selective, indicative) are more promising. Identify and highlight preventive efforts (like seat belt, helmets in preventing injuries) and culturally sensitive approaches that do exist and Dr. M. S. Reddy appraise them. Most of my colleagues in the field of psychiatry, I am sure, agree with my observation that we encounter much less of catatonia these days in the psychiatric wards. And of late, there seem to be not many patients with hysterical aphonia in a psychiatrist's clinic. Why is it so? What could be the reasons and what are the factors? If there is some clue to these phenomena, maybe, it could be a point of kick start for primary prevention in psychiatry.