THC and altitude
Posted: Tue Jan 11, 2011 5:33 pm
There are people here who are much more intelligent than me and I am hoping this might pique their interests. It was stated on the Ritalin thread that Ritalin is a vasoconstrictor and might lead to more complications at altitude. This got me thinking about another drug that is commonly used in the mountains and the effect it might have on performance since it seems that the pot smokers of our group of climbers cope with altitude slightly better than those who don't puff. Anyone wanna discuss/explain while I go take a, uh, smoke break?
Cerebrovascular Effects:
Matthew & Wilson[xxxiv] found "In experienced marijuana smokers, marijuana smoking was accompanied by a significant bilateral increase in cerebral blood flow (CBF) especially in the frontal regions and cerebral blood velocity." Tunving et al[xxxv], studying long-term cannabis users found decreases in cerebral blood flow during the early stages of detoxification, reverting to normal after 9-60 day follow-up. Similar results were found by Lundqvist et al[xxxvi] - "Cerebral blood flow (CBF) was measured in 12 long-term cannabis users shortly after cessation of cannabis use (mean 1.6 days). The findings showed significantly lower mean hemispheric blood flow values and significantly lower frontal values in the cannabis subjects compared to normal controls" Ellis et al[xxxvii] found "Anandamide (AN) and delta 9-THC similarly induced a dose-dependent dilation (of cerebral arterioles) starting at concentrations as low as 10(-12) M. Maximum dilation for AN was 25% and that for delta 9-THC 22%. Topical coapplication of indomethacin, a cyclooxygenase inhibitor, completely blocked dilation"
Bloom et al[xxxviii] found different areas of the brain to have different blood-flow responses to THC ยท "Changes in regional cerebral blood flow were observed in 16 of the 37 areas measured." Stein et al[xxxix] in the rat, an O"Leary et al[xl] in human recreational users, also found wide variations in cerebrovascular response in different brain regions.
Strokes and Neuroprotectivity:
There are a number of case studies describing patients who have suffered strokes following or during cannabis use, some, but not all,of these cases can be explained by use of other drugs (alcohol or stimulants). Cooles & Michaud[xli] report a case history of a patient suffering a stroke following a heavy bout of cannabis smoking. Alvaro et al[xlii] reported another case history "of a young man and heavy cannabis smoker who suffered posterior cerebral artery infarction during his first episode of coital headache"In a further case history, Lawson & Rees[xliii] reported "A 22-year-old man with a five-year history of drug and alcohol abuse presented with a left hemiparesis preceded by three transient ischaemic attacks, two of which occurred whilst smoking cannabis" although in response, McCarrom & Thomas[xliv] stressed the likely role of alcohol or other drugs in the etiology of such strokes. Mouzak et al[xlv] described "Three male patients (mean age 24.6 years) who were heavy cannabis smokers presented with transient ischemic attacks (TIA) shortly after cannabis abuse... The urine analysis was positive for cannabis metabolites. There were no other abnormal findings in the rest of the meticulous and thorough study of all 3 patients, which leads to the conclusion that cannabis was the only risk factor responsible for the observed TIA, contradictory to other studies, which support that cannabis is a 'safe' drug."
However, it is clear that cannabinoids have a variety of cerebrovascular effects, increasing the blood supply to the brain[xlvi], and can protect against potentially fatal brain cell death following a stroke by reducing tumour necrosis factor, which causes self-destruction in exposed cells. The use of cannabinoids for treatment of brain damage arising from strokes is reaching an advanced stage of the licensing process, Job[xlvii] reported in 2000 "Dexanabinol is a non-psychotropic cannabinoid NMDA receptor antagonist under development by Pharmos Corp for the potential treatment of cerebral ischemia... cardiac failure, head injury and multiple sclerosis (MS)... it is in phase III trials for traumatic brain injury... Pharmos estimates that the worldwide market for dexanabinol in the treatment of severe head trauma may reach $1 billion per year" Leker et al[xlviii] investigated the effect of dexanabinol, a synthetic cannabinoid which is a NMDA antagonist, with antioxidant and anti-tumour necrosis factor alpha properties, on the levels of brain damage (infarct) following experimentally induced ischaemic strokes in rats, finding "Dexanabinol significantly decreased infarct volumes. It also significantly lowered TNFalpha levels in the ipsilateral hemisphere although not to the level of sham operated rats... In conclusion, dexanabinol may be a pluripotent cerebroprotective agent."
Cerebrovascular Effects:
Matthew & Wilson[xxxiv] found "In experienced marijuana smokers, marijuana smoking was accompanied by a significant bilateral increase in cerebral blood flow (CBF) especially in the frontal regions and cerebral blood velocity." Tunving et al[xxxv], studying long-term cannabis users found decreases in cerebral blood flow during the early stages of detoxification, reverting to normal after 9-60 day follow-up. Similar results were found by Lundqvist et al[xxxvi] - "Cerebral blood flow (CBF) was measured in 12 long-term cannabis users shortly after cessation of cannabis use (mean 1.6 days). The findings showed significantly lower mean hemispheric blood flow values and significantly lower frontal values in the cannabis subjects compared to normal controls" Ellis et al[xxxvii] found "Anandamide (AN) and delta 9-THC similarly induced a dose-dependent dilation (of cerebral arterioles) starting at concentrations as low as 10(-12) M. Maximum dilation for AN was 25% and that for delta 9-THC 22%. Topical coapplication of indomethacin, a cyclooxygenase inhibitor, completely blocked dilation"
Bloom et al[xxxviii] found different areas of the brain to have different blood-flow responses to THC ยท "Changes in regional cerebral blood flow were observed in 16 of the 37 areas measured." Stein et al[xxxix] in the rat, an O"Leary et al[xl] in human recreational users, also found wide variations in cerebrovascular response in different brain regions.
Strokes and Neuroprotectivity:
There are a number of case studies describing patients who have suffered strokes following or during cannabis use, some, but not all,of these cases can be explained by use of other drugs (alcohol or stimulants). Cooles & Michaud[xli] report a case history of a patient suffering a stroke following a heavy bout of cannabis smoking. Alvaro et al[xlii] reported another case history "of a young man and heavy cannabis smoker who suffered posterior cerebral artery infarction during his first episode of coital headache"In a further case history, Lawson & Rees[xliii] reported "A 22-year-old man with a five-year history of drug and alcohol abuse presented with a left hemiparesis preceded by three transient ischaemic attacks, two of which occurred whilst smoking cannabis" although in response, McCarrom & Thomas[xliv] stressed the likely role of alcohol or other drugs in the etiology of such strokes. Mouzak et al[xlv] described "Three male patients (mean age 24.6 years) who were heavy cannabis smokers presented with transient ischemic attacks (TIA) shortly after cannabis abuse... The urine analysis was positive for cannabis metabolites. There were no other abnormal findings in the rest of the meticulous and thorough study of all 3 patients, which leads to the conclusion that cannabis was the only risk factor responsible for the observed TIA, contradictory to other studies, which support that cannabis is a 'safe' drug."
However, it is clear that cannabinoids have a variety of cerebrovascular effects, increasing the blood supply to the brain[xlvi], and can protect against potentially fatal brain cell death following a stroke by reducing tumour necrosis factor, which causes self-destruction in exposed cells. The use of cannabinoids for treatment of brain damage arising from strokes is reaching an advanced stage of the licensing process, Job[xlvii] reported in 2000 "Dexanabinol is a non-psychotropic cannabinoid NMDA receptor antagonist under development by Pharmos Corp for the potential treatment of cerebral ischemia... cardiac failure, head injury and multiple sclerosis (MS)... it is in phase III trials for traumatic brain injury... Pharmos estimates that the worldwide market for dexanabinol in the treatment of severe head trauma may reach $1 billion per year" Leker et al[xlviii] investigated the effect of dexanabinol, a synthetic cannabinoid which is a NMDA antagonist, with antioxidant and anti-tumour necrosis factor alpha properties, on the levels of brain damage (infarct) following experimentally induced ischaemic strokes in rats, finding "Dexanabinol significantly decreased infarct volumes. It also significantly lowered TNFalpha levels in the ipsilateral hemisphere although not to the level of sham operated rats... In conclusion, dexanabinol may be a pluripotent cerebroprotective agent."