Serum cholesterol and parasuicide

Garland et al (2000) reignited the various controversies on the role of cholesterol in psychiatric disorders. The methodology used was similar to those in previous studies (Asberg et al, 1976) which did not control for the substances used in parasuicide. This may affect the levels of the chemical or metabolites being researched. Garland et al (2000) did not mention the methods used in those parasuicides and whether they would have affected serum cholesterol.

Engelberg (1992) and Block & Edwards (1987) held contrasting views on the relationship between cholesterol and serotonin uptake. The work by Heron et al (1980) used to support the hyposerotonergic function caused by low cholesterol appeared flawed. The serotonin site labelled by Heron et al (1980) is not the uptake site (Hawton et al, 1993), and therefore changes in brain serotonin content cannot be explained on the basis of their data. Furthermore, the serotonin stored within brain cells is not accumulated from blood but synthesised in situ from L-tryptophan.

Plasma cholesterol is in a dynamic state, entering the blood complexed with lipoproteins that keep it in solution and leaving the blood as tissues take up cholesterol. High-density lipoprotein (HDL)-cholesterol that transports circulating cholesterol to the liver for clearance plays a crucial role. Excess HDL can result from excess alcohol (Parkes et al, 1989). This increases the amount of cholesterol transported peripherally, causing low serum cholesterol. Alcohol, drugs and poisons are usually involved in parasuicides (Asberg et al, 1976) and low cholesterol level may therefore be due to ethanol misuse or poisoning. It is unlikely that cholesterol would provide the needed answers to parasuicide. It would only reduce this complex human behaviour to a ‘matter to mind’ paradigm.