Select Committee on Home Affairs Appendices to the Minutes of Evidence

Cannabis: some further facts—Professor Susan Greenfield: January 2002


  Despite extensive evidence reviewed by Ameri (1999 Progress in Neurobiology Vol 58, pp 315-348) concerning the effects on the neurochemistry and pathology of the brain, there is some cynicism regarding doses used experimentally, and how one can extrapolate from what is seen as a caricature laboratory situations to the "normal" human ones. In particular, Chiang and Burnett (1984 Clin Pharmacol Ther Vol 36, pp 234-238) report that hippocampal neurons in vitro treated with the same dose of THC as found in a single marijuana cigarette, is enough to kill 50 per cent of neurons within six days. A 10-fold higher concentration, 10µM, kills cells within three hours.

  Against the argument that this is an overly large dose, is the evidence that it is a receptor mediated effect (Chan et al, 1998 J Neuroscience Vol 18, pp 5322-5332) and therefore cannot be attributed to non-specific membrane damage. Moreover, the assumption that the dose given 1µM THC, is the same as that found in human plasma, is correct. This concentration is assuming a relatively low average dose of the active ingredient, THC, in a cannabis cigarette of 5-10 mgs. Concentrations of THC can be routinely higher—20 mgs, and even up to 65 per cent.

  The molecular weight of THC is 314.5, therefore 1 mg in one litre would be 3.18µM, and hence in a total plasma volume of approximately three litres, 1 mg would indeed yield 1.06µM. At a 10 times higher dose this would be approximately 10µM. The peak brain concentration is about a third of that found in the plasma, ie would be between 1-3µM, within easy range of the concentration used in the experimental situation.

  Although the exposure to this concentration in experiments may be longer, than that taken socially, we know that THC does remain in the body for a long time, and therefore such concentration would be in no way sustainable.


Cognitive deficits

  Even after abstaining from cannabis effects persist. (see Solowij N, 1998 Cannabis and Cognitive Function, Cambridge University Press and Solowij N, 1995 Life Sciences Vol 56, pp 2119-26).

Increased risk of dependence

  Abstinence symptoms following oral THC administration to humans (Haney M et al, 1999 Psychopharmacology Vol 141 pp 385-94); and Abstinence symptoms following smoked marijuana in humans (Haney M, et al, 1999 Psychopharmacology Vol 141, pp 395-404).

Increased risk of psychotic episode

  Can occur in those with no previous psychiatric history (Maguire P et al, 1994 Schizophrenia Research Vol 13, pp 161-7) and aggravated in those already with the illness (Hollister L, 1998 "Cannabis" Acta Psychiatr Scand Suppl Vol 345 pp 108-18), (Linszman D, et al, 1994 "Cannabis abuse and the course of recent-onset schizophrenic disorders" Arch Gen Psychiatry Vol 51, pp 273-9), and (Martinez-Arevelo M, et al, 1994 "Cannabis consumption as a prognostic factor in schizophrenia" Br J psychiatry Vol 161, pp 648-53).

previous page contents next page

House of Commons home page Parliament home page House of Lords home page search page enquiries index

© Parliamentary copyright 2002
Prepared 22 May 2002