Possible, New Support of my Explanation of Schizophrenia


These represent possible, new support of my explanation of schizophrenia.  These are articles to which I have responded.  If you are reading these, you may already know my hypotheses, however, since these are responses to investigators who may not know my hypotheses, I have included my basic hypotheses.



Internaltional Clinical Psychopharmacology (Int Clin Psychopharmacol) 2006 Mar;21(2):93-98.



High prevalence of the metabolic syndrome among a Swedish cohort of patients with schizophrenia.

Hagg S, Lindblom Y, Mjorndal T, Adolfsson R.

aDivision of Clinical Pharmacology, Department of Pharmacology and Clinical Neuroscience, Umea University, Umea bDivision of Clinical Pharmacology, Department of Medicine and Care, Linkoping University, Linkoping cDepartment of Clinical Science, Section of Psychiatry, Norrland University Hospital, Umea, Sweden.

Several cardiovascular risk factors have been linked to antipsychotic treatment and cardiovascular mortality is increased in these patients compared to the general population. The full metabolic syndrome (or its components) is associated with an increased risk of cardiovascular disorders. The prevalence of the metabolic syndrome was investigated using a cross-sectional study design in a cohort of 269 patients, aged 20-69 years, with schizophrenia living in Northern Sweden, and was defined according to the criteria of the National Cholesterol Education program. The prevalence of the metabolic syndrome was 34.6% (95% CI=28.8-40.3) and highest (43%; 95% CI=32-53) for participants aged 40-49 years. Clozapine treated subjects reached the highest prevalence of the metabolic syndrome (48%; 95% CI=34-62). The prevalence was similar for men (32.8%; 95% CI=25.8-39.8) and women (38.0%; 95% CI=27.9-48.2). Men had a high prevalence of hypertension (49.2%; 95% CI=41.7-56.6) and women had high prevalence of low high-density lipoprotein cholesterol (40.2%; 95% CI=30.0-50.4) and abdominal obesity (75.0%; 95% CI=66.0-84.0). Subjects with the metabolic syndrome had significantly higher mean body mass index (BMI) (P<0.001), HbA1c (P=0.002), and fasting serum insulin (P<0.001) compared to non-metabolic syndrome subject. Subjects with the metabolic syndrome had also significantly more often a positive history of cardiovascular diseases compared to non-metabolic syndrome subjects (25.8% versus 12.5%; P=0.01). Of all study subjects 36.8% were obese (BMI>30). These results clearly show that the metabolic syndrome and its components are highly prevalent in patients with schizophrenia. Physicians treating patients with schizophrenia are recommended to monitor the components included in the metabolic syndrome.




My hypothesis regarding schizophrenia is that low dehydroepiandrosterone (DHEA) in utero and/or during the early postnatal period thereby reducing growth and development of the brain. This reduced growth is exposed later in life by cortisol (stress) and testosterone which reduce the availability of DHEA. This may explain why schizophrenia occurs following a stressful, precipitating event and occurs after puberty. DHEA begins to decline around age twenty. Therefore, schizophrenia often occurs in the late teens and early twenties. Schizophrenia is characterized by low DHEA.  As DHEA is reduced during the critical period of onset, the brain of schizophrenics is reduced in function and anatomy.

The metabolic syndrome may be due to low DHEA (Journal of the American Medical Association 2004; 292: 2243-8). Hagg, et al., report a prevalence of the metabolic syndrome in their schizophrenic population. I suggest the findings of Hagg, et al., may support my hypothesis regarding schizophrenia.