Der mangler stadig en masse forskning på området, men p.t. lader THC til at have en neuro-beskyttende effekt. Se f.eks.
Exogenous Anandamide Protects Rat Brain against Acute Neuronal Injury In Vivo.
Citat:
The CNS is highly vulnerable to ischemia. Neuronal death caused by ischemia is executed via a complex array of processes in which excitotoxicity plays a major role. In excitotoxicity, cell death is triggered by the overstimulation of excitatory amino acid receptors. This leads to cytotoxic levels of calcium and to subsequent activation of destructive pathways, involving among others caspases, calpains, and the generation of reactive oxygen species (Dirnagl et al., 1999; Doble, 1999).
Compounds that interfere with excitotoxicity may be used as neuroprotective therapeutic agents. Interestingly, the brain has various endogenous protection factors at its disposal (e.g., adenosine, melatonin, and estrogens) (Reiter, 1998; Hurn and Macrae, 2000; Picano and Abbracchio, 2000). Several reports have also revealed a connection between the endogenous lipid anandamide [N-arachidonoylethanolamine (AEA)] and neurodegenerative diseases (H. S. Hansen et al., 1998, 2000; Di Marzo et al., 2000b; Baker et al., 2001).
AEA mimics in part the actions of Delta 9-tetrahydrocannabinol (THC), the psychoactive compound in marijuana. Together with 2-arachidonoylglycerol (2-AG), AEA represents a class of lipids, termed endocannabinoids because of their ability to activate the CB1 and CB2 cannabinoid receptors. AEA is rapidly translocated into the cell via a transporter protein and is then immediately inactivated by a fatty acid amide hydrolase (FAAH) (Pertwee, 1997; Di Marzo et al., 1998).
Several lines of evidence indicate that AEA can serve to protect the brain against neuronal injury (H. S. Hansen et al., 1998, 2000): (1) AEA and its precursor N-arachidonoylphosphatidylethanolamine are normally found in low concentrations in the brain, but their levels increase in a calcium-dependent manner postmortem and with severe neuronal injury (Schmid et al., 1990; Kempe et al. 1996; Hansen et al., 1999; H. H. Hansen et al., 2000, 2001; Sugiura et al., 2000); (2) exogenous AEA protects cerebral neurons from in vitro ischemia (Sinor et al., 2000); (3) CB1-mediated closing of N- and P/Q-type calcium channels protects neurons against in vitro secondary excitotoxicity (Shen et al., 1996; Shen and Thayer, 1998); (4) we have demonstrated recently that THC can reduce neuronal damage via the CB1 receptor in an in vivo model of excitotoxicity (Van der Stelt et al., 2001); (5) WIN55.212, a synthetic cannabinoid, protected rat brains against focal and global ischemia (Nagayama et al., 1999); and (6) CB1 expression is enhanced in the cortical mantle zone in rats after ischemia (Jin et al., 2000). As yet, in vivo neuroprotection by AEA has never been reported.
(og den fortsætter...)
Det er dog stadig tvivlsomt, om det er en særlig smart ide at kaste sig ud i diverse fester blot med den forskel at man ryger hash. Med en hjernerystelse skal man holde sig fuldstændig i ro, ellers risikerer man såvidt jeg ved langvarige komplikationer.
Ting som alkohol og amf bør i særdeleshed være udelukket. Alkohol kan slå hjerneceller ihjel, bedøve dig så du ikke mærker din tilstand og gøre dig overmodig, og jeg tvivler meget på at amfetaminen med den kraftige ansporing til hård fysisk aktivitet og forhøjet blodtryk er et hak bedre.
Som jeg startede med at sige, så pas på selvom det er hash. Der er ikke forsket tilstrækkeligt i emnet til at frikende hash med sikkerhed, og det ville sgu være ærgerligt at bytte én nats utålmodig fest for måneders bivirkninger. Det bedste råd må stadig være mådehold.
Log ind
Tilmeld
OSS
Søg
ellers er jeg på røven.
