I also support vaporization, which uses a much faster method than tincture but its just as safe and more efficient than the rest.
According to the linked blog post, the benefit of the Cold Method is that the cannaboids are kept intact, whereas the benefit of the Hot Method is that the cannaboids are not kept intact (THCA converted to THC).
A friend on IRC points out an important caveat: This experiment was not anywhere close to in vivo research.
" In a 96-well plate, triplicate samples of a 20 μL solution of 23 nM Aβ, 2.30 μM HuAChE, and various concentrations of THC in 0.215 M sodium phosphate buffer, pH 8.0, were prepared. "
Is alzheimer's prevention relevant at all ages? Or do the relevant substances only build up after a certain point?
Would you still be you if the THC gets its way? In particular, I'd be wary of the effects claimed on short-term memory and overall motivation.
That's a legitimate concern; in any case, marijuana-me sounds much more like me than Alzheimer's-me.
It is noteworthy that THC is a considerably more effective inhibitor of AChE-induced [Abeta] deposition than the approved drugs for Alzheimer’s disease treatment, donepezil and tacrine, which reduced [Abeta] aggregation by only 22% and 7%, respectively, at twice the concentration used in our studies.
Waitwaitwhat? A drug was approved for the purpose of reducing AChE-induced Amyloid beta deposition, with an effect size of only 7%? That's not effective at all! How did that happen?
Donepezil was never approved as an aid to prevention of Alzheimer's or even as a treatment focused on the pathophysiology. The only thing it appears to be effective in (which is also its only FDA-approved use) is as symptomatic relief, in improving memory and cognitive symptoms in various stages of Alzheimer's. It's believed to do this by enhancing cholinergic neurotransmission in the brain (damage to these synapses is thought to be the reason for part of the cognitive damage done by Alzheimer's). I believe that the prescribing information explicitly says that there is no evidence that it delays the progression of the disease. EDIT: that is correct, see 12.1 in the prescribing info
I haven't looked in detail at tacrine, but IIRC its pharmacological rationale is the same as that of donepezil. (Also, all the regulatory information above is US-centric.)
In a post last August called Alzheimer's vs. Cryonics, I left the following comment:
23andMe recently showed that people of my genotype are more than twice as likely to develop Alzheimer's as others in my ethnic group. I have a 15% chance of getting Alzheimer's before I'm 80, up from 7%. See Patri's post about this.
An initial Googling has generated things like 'eat paleo', 'get caffeine', 'exercise', and 'use your brain'. I'm planning to do further research about decreasing Alzheimer's risk.
I really recommend that everyone do 23andMe for this precise reason.
wedrifid made an insightful response:
I wonder, how much does that single bit of information (doubling the chance) matter to those decisions? Should you have been doing those things anyway, for the Alzheimer's prevention and the other benefits? Is it the motivational factor of the formal personal certification that is important or the actual information?
wedrifid nailed it. Transhumanists have a huge interest in making the necessary lifestyle adjustments to prevent Alzheimer's. Even if cryonics were certain to work, I'd like it to be me that is resurrected when the technology is available, and I won't still be me if Alzheimer's gets its way.
So I've been keeping an eye out for relevant information. I haven't done rigorous research yet, but a friend recently sent me a study: "A molecular link between the active component of marijuana and Alzheimer's disease pathology." I've uploaded the full text of the article here.
A sample from the abstract:
Here, we demonstrate that the active component of marijuana, Delta9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid beta-peptide (Abeta) aggregation, the key pathological marker of Alzheimer's disease. [...] Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Abeta aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.
From the conclusion:
It is noteworthy that THC is a considerably more effective inhibitor of AChE-induced [Abeta] deposition than the approved drugs for Alzheimer’s disease treatment, donepezil and tacrine, which reduced [Abeta] aggregation by only 22% and 7%, respectively, at twice the concentration used in our studies.
Therefore, AChE inhibitors such as THC and its analogues may provide an improved therapeutic for Alzheimer’s disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing [Abeta] aggregation, thereby simultaneously treating both the symptoms and progression of Alzheimer’s disease.
I, for one, would like to know if smoking weed could help prevent a fate that's plausibly worse than death-and-cryonics. So for those who know more about biology than I do: how promising are these results? What else has been shown to help prevent Alzheimer's?