The endocannabinoid system seems to be the main mechanism our bodies use to naturally regulate inflammation. My understanding is that there is a growing belief among cannabinoid researchers that our cannabinoid receptors can get blocked as we get older, and so there may be a need to either supplement with phytocannabinoids and/or employ various techniques to unmethylate our CB1 receptors. There are a number of folks doing pre-clinical research on cannabinoids as potential treatments for alzheimers and other inflammatory / autoimmune diseases using various cannabinoids.
Here is a cool paper about how colorectal cancer seems to result from the CB1 receptors being knocked out:
It's possible that most cancers result from the same mechanism, although we don't really know yet. What we do know is that regular marijuana users have a 62% lower chance of head and neck cancers, and that there are an enormous amount of studies showing that cannabinoids can promote both apoptosis (cell death) in cancer cells and are anti-angiogenic, meaning they cut off the blood flow to the tumors.
If it's a receptor thing, it wouldn't only apply to phytocannibanoids, right? I'm given to understand there are a number of synthetic cannabinoid receptor agonists with much higher affinity and/or selectivity than the phytocannabinoids. Are you aware of any research into the potential differences?
I suppose it wouldn't make much difference, since as you say it only takes a tiny amount of cannabis despite THC being only a partial agonist.
In general though I think cannabis is a good example of why plant-based medicine is often more safe and effective than using synthetics. That is, when one molecule in a plant acts as a poison, then generally there will be some other molecule in the plant to counteract that poison. That's exactly what we see here, with the anti-psychotic effects of the CBD balancing out the psychotomimetic effects of the THC. And most patients seem to find the plant-based medicine to be both more tolerable and also more effective. Obviously there are many many cases where plant-based medicine is an inferior choice, as with aspirin, but in this case it seems to be winning at least so far.
Also, there is some suggestion that with plant-based medicine the body actually has the ability to pick and choose which compounds to use depending on what it's current needs are:
"Medicinal plants contain a wide array of chemical compounds. At first, this looks like chaos, but more investigation reveals a distinct order. Natural selection pressures push a plant to "try out" variations on molecules to enhance the plant's odds of surviving stressful environments. So, often, one molecule is present in the greatest amount and has the most dramatic effect in a human body -- but along with it are variations of that molecule in the same plant.
For example, for several years, I did ethnobotanical study in South America, researching native uses for coca leaf, which most of us know only as the source of the isolated, problematic, addictive drug cocaine. For Andean Indians, whole coca leaf is the number one medicinal plant. They use it to treat gastrointestinal disturbances; specifically, for both diarrhea and constipation. From the perspective of Western pharmacology, this makes no sense. Cocaine stimulates the gut, it increases bowel activity, so obviously it would be a good treatment for constipation, but what could it do for diarrhea except make it worse?
However, if you look carefully at the coca leaf's molecular array, you find 14 bioactive alkaloids, with cocaine in the greatest amount. While cocaine acts as a gut stimulant, other coca alkaloids can have precisely the opposite action, they inhibit gut activity.
This means that when you take the whole mixture into the body, the potential is there for the action to go in either direction. What decides it? The state of the body, which is a function of which receptors in the gut's tissues are available for binding. During my time in Andean Indian communities, I collected many reports about whole coca's paradoxical, normalizing effect on bowel function, and experienced it firsthand, as well."
Totally off topic, but do you happen to know anything about capsaicin?
I began eating hot peppers a few months ago and it had a dramatic impact on my condition. CF is rooted in a defect in a cell channel, the CFTR, which handles trafficking of certain molecules into and out of the cell. Capsaicin, the active ingredient in hot peppers, forces a different channel open at lower than normal temps. I asked around and got a snippet or two suggesting some indirect relationship between the types of things the two channels process but nothing conclusive. Capsaicin has worked effectively as a biohack for me, especially when combined with walking (and a zillion other things I was already doing for my condition). Yet I have turned up little in the way of solid information as to why/how.
If you like spicy things they are actually really good. It's kind of like a combination between drinking a Snapple and getting maced in the face by the cops.
Yes, it stands for cystic fibrosis. Average life expectancy in the US is currently around 36 or 37, way up from age 18 roughly 18 or 20 years ago. I was diagnosed just before my 36th birthday with a milder classification of it which is emerging and is most often called "atypical cystic fibrosis". I spent a year at death's door. It's been a long haul back from there.
It's not really a lung disease. It's a genetic disorder. All cells in the body are impacted in their function. Mucus membranes are the most obviously negatively impacted. Lungs happen to be lined with mucus. So is the gut and malabsorption and lack of adequate weight gain is another major issue which is frequently life threatening but gets less press than the high incidence of lung transplant.
re: "when one molecule in a plant acts as a poison, then generally there will be some other molecule in the plant to counteract that poison"
How does that happen? From an evolutionary point of view, it seems a bit unlikely. Unless it's part of the plant's reproductive strategy, a plant's goal is usually not to be eaten. (However, animals often evolve to counteract plants' defenses.)
Mutation 'A' has has both benefits and drawbacks, so mutation 'B' fixes some of those drawbacks. Sure, it's good for a plant to be poisonous to animals that want to eat it, but not at the expense of poisoning itself.
Then don't smoke a joint. The standard sized joints that NIDA hands out for research are 0.7 grams. The amount needed to get this anti-inflammatory effect is roughly .02 grams, in other words 1 / 35th of a joint. There are also two different ways that you can get the same health benefits without any psychoactive side effects. First, you can get high-CBD weed. CBD is a non-psychoactive cannabinoid that basically cancels out the effects of THC. Second, if you juice raw cannabis it is basically non-psychoactive, because without heating or drying it the THCA never gets decarboxylated into THC. Here are a couple articles about this:
"The standard sized joints that NIDA hands out for research are 0.7 grams."
Really? That seems like a lot. I was a sporadic recreational smoker about 15 years ago, we bought marihuana one gram at a time and that gram would last us a weekend. Maybe the difference is in THC content; I bought in the Netherlands where quality is generally high and THC concentrations relatively high in higher-end varieties, from what I understand (I don't have experience with foreign varieties to compare it with). Then again, our usage customs are different from elsewhere in the world, too; we rolled joints out of tobacco and only sprinkled on some marihuana. When I told that to Americans they'd look at me as if I was crazy.
Actually the cool thing about it is that not only does it prevent neuroinflammation, but it also promotes neurogenesis. There was a recent study that tracked IQs before and after using cannabis, and what they found was that those who took up smoking cannabis actually gained almost six IQ points. (For less than 3.5 grams per week.)
Huh— it's more than I would have guessed, but thinking about it, I buy it. Anecdotally, an eighth a week is about the point where you can see it starts to slow people down.
I can't help but feel like it's got as much to do with the fact of smoking every day as with the raw amount... I guess there aren't that many people out there who'll smoke an eighth in a day and then take a week off, though, so maybe it'd be hard to pin down.
As there is a rather large cohort of regular and past cannabis smokers entering into prime Alzheimer years we are going to see if this is true within the decade and do not even need to fund a study. If the Alzheimer rate starts to drop then this is worth further research, but if not I will begin to suspect some people are blowing some rather fragrant smoke on this issue...
The 0.7km/week for a house mouse translates to about 7.5 miles/week for a 5'8" tall man compared to a 10cm long mouse. Lots of assumptions, but 7.5 miles is way more than the average sedentary person jogs in a week. It's also very easy to reach for a recreational jogger. Lots of assumptions in there.
And animal models of disease (or aging) are much simpler than real life human biology. One big reason being that lab strains of mice (and maybe the rats in this study, too) are inbred and very homogeneous - genetically speaking. So, something which has a big effect in a lab animal might be due to some strange combination of genes that most "outbred" species (like humans) don't ever have.
As an additional benefit to exercise: cardiovascular health is closely correlated with mental health and performance, due to the maintenance (or improvement) of blood flow to the brain.
My girlfriend just told me about a study that also seemed to show that exercise can be useful in treatment of schizophrenia (by promoting hippocampal development).
This appears to be the study (she read it in Psychology Today, which didn't reference it by name):
Exercise does cause damage to your body, both structural and oxidative. Fortunately, that damage triggers repair mechanisms which make you stronger than before. See http://en.wikipedia.org/wiki/Hormesis#Physical_exercise
An aside: Reading this article made me wonder why I tasted blood after particularly hard workouts. Apparently the heart can pump with enough pressure to rupture some of the capillaries in your lungs. A tiny amount of blood leaks out and gets aerosolized. At least, so says this paper: http://abughrai.be/Vulnerability%20of%20pulmonary%20capillar...
Seriously, how can one not already realize this? You can of course work yourself to death, but you'd think people would have noticed how much healthier they feel when they have been exercising, and how quickly they deteriorate when they haven't.
The above poster is - as I understand it - pointing out that this study does not necessarily contradict the hypothesis you mentioned. A small amount of exercise is shown to be beneficial, but it is entirely possible that larger amounts of exercise are detrimental.
Do you know if any research has been done into that hypothesis? Because - failing a confirming study - it does not seem to fit with anything I've heard. I mean, maybe some organs can get overwhelmed if metabolism is pushed too high too quickly, but in general I doubt that a fast metabolism even correlates with lower life expectancy.
The HN title gives the impression that they reversed aging. They only reversed changes in memory performance in old mice that are infected with E.coli.
It would be interesting to know how they assessed memory performance - are they using spatial memory tests?
Good question. Appears that they use contextual fear conditioning to assess memory.
From the research article:
"We chose to use the immediate-shock fear conditioning paradigm (Fanselow, 1990; Rudy et al., 2002) as the learning task. Here, foot shock is delivered very quickly upon exposure to the experimental context on the fear conditioning day. However, the rats are preexposed to the context at an earlier time. The preexposures are required so that the subjects are able to form a 'conjunctive representation' of the context, so that it can be associated with the shock on the conditioning day (Rudy et al., 2002). We chose this fear conditioning paradigm because it is highly and specifically dependent on the hippocampus (Rudy et al., 2002), and we have already shown that E. coli interferes with memory of this task in aging rats (Barrientos et al., 2006)"
http://www.youtube.com/watch?v=2uVXs6CY2ps
http://www.freedomtoexhale.com/clinical.pdf
The endocannabinoid system seems to be the main mechanism our bodies use to naturally regulate inflammation. My understanding is that there is a growing belief among cannabinoid researchers that our cannabinoid receptors can get blocked as we get older, and so there may be a need to either supplement with phytocannabinoids and/or employ various techniques to unmethylate our CB1 receptors. There are a number of folks doing pre-clinical research on cannabinoids as potential treatments for alzheimers and other inflammatory / autoimmune diseases using various cannabinoids.
Here is a cool paper about how colorectal cancer seems to result from the CB1 receptors being knocked out:
http://www.drugs.com/clinical_trials/turned-off-cannabinoid-...
It's possible that most cancers result from the same mechanism, although we don't really know yet. What we do know is that regular marijuana users have a 62% lower chance of head and neck cancers, and that there are an enormous amount of studies showing that cannabinoids can promote both apoptosis (cell death) in cancer cells and are anti-angiogenic, meaning they cut off the blood flow to the tumors.