Haldol – The fastest way to a smaller brain: Questions

Posted by protonmind on January 30, 2011
Posted in: Addiction, Neuroscience, Schizophrenia. Tagged: , , , , , , , , .

Continued from the fastest way to a smaller brain I

Question about Haloperidol

The main effects of Haldol is probably the blockade of the Dopamine-2 receptor (D2) Haldol is pretty effective in doing that and there is no daught about that, but in the long run Haldol up-regulates the D2 receptors (2). I can hardly imagine a stronger way to create a state of dependence than a substance that amplify the problem it is said to work against, but masking this side effect as long as you continue to take Haldol.

Nature News wrote: “Antipsychotics deflate the brain”, but they don’t write about how this medication up regulates the density of the D2 receptor and that this actually have a potential to increase the symptoms in the persons using this drug. That gives me some questions about Haldol (Haloperidol)

1 If you take a medicine to conquer a syndrome caused by high D2 activity, does the medicine cause more sickness if it up regulates the D2 receptor?

2 Is it a possibility that Haldol actually makes the consumer sicker in the long run and by the unregulated D2 density also more dependent of Haldol?

3 Some sources on the net claims that Haldol is not addictive, is it any scientific proof for that statement?

4 Since Haldol causes the fastest decrease in brain size ever recorded, how shall we interpret this result beyond the manufacturer’s rhetoric’s?

4.1 That decreases in brain size causes increased independence or

4.2. A decrease in brain size causes decreased independence and probably also an increased probability of addiction?

References and readings

(1)
Olanzapine increases in vivo dopamine and norepinephrine release in rat prefrontal cortex, nucleus accumbens and striatum
Xi-Ming Li, Kenneth W. Perry, David T. Wong and F. P. Bymaster

(2)
Psychopharmacology (Berl). 2000 Oct;152(2):174-80.
Increased dopamine D2 receptor binding after long-term treatment with antipsychotics in humans: a clinical PET study.
Silvestri S, Seeman MV, Negrete JC, Houle S, Shammi CM, Remington GJ, Kapur S, Zipursky RB, Wilson AA, Christensen BK, Seeman P.

(3)
Long-term haloperidol treatment (but not risperidone) enhances addiction-related behaviors in mice: role of dopamine D2 receptors.

(4)
Questioning an Axiom: Better Prognosis for Schizophrenia in the Developing World? Schizophrenia Bulletin, Volume34.

The CAC-Hålet theory – the etiology of Schizophrenia. The etiology of Schizophrenia here in short.