I don’t at all feel insulted; it is hard enough to communicate in person, let alone over the intertubes. I know I can’t do a data dump that includes all the background and all the chains of facts and logic that lead to my conclusions.

I do have “commercial” aims, but my real motivation is to improve people’s health. If it is correct that many of the health effects of meditation are mediated through NO (Stefano’s and Benson’s hypothesis, not mine), and that some of those same health effects can be achieved by raising NO levels other ways (Stefano’s hypothesis), and if the bacteria I am working with are natural commensal bacteria (my discovery) then raising NO levels with my bacteria (my conclusion) could be a tremendous health boon with no negative side effects (my conclusion). If the same health effects as 30 minutes of meditation could be achieved in non-meditators with a non-invasive, benign measure, the public health implications would not be small.

I think the most important public health effect would be to reduce the level of conflict among people. I think you would agree that if everyone in the world had the physiological effects of 30 minutes of meditation every day, that the world would be a very different place. That is the kind of world that I want to live in. That is my ultimate motivation, to produce that kind of world for my children and for everyone’s children to live in.

My apologies if I’ve insulted you or got the wrong impression. It seemed to me that you were saying your theories about NO were controversial (particularly because of their expansive or inclusive nature) even amongst those in the same field as you. My main point was my own lack of ability to be able to discern the validity of your theory on its own merits since I’m not qualified and that since there is controversy amidst experts there’s added problems in my trying to understand how valid your theory is considered by people who are qualified to discern such things. Thanks for being open about your own commercial aims – it’s refreshing.

Many of the neurological aspects of my ideas started from my own experiences when I raised my NO level (which were totally unexpected). I do have a low NO physiology, and have had it my entire life. I inherited it from my mother, who I am quite sure had Asperger’s. She and both her parents died with advanced Alzheimer’s, which I am sure came from their low NO physiology. I have Asperger’s, which I only recognized after it got better when I raised my NO level. I am an MIT grad, Tau Beta Pi. I have access to the MIT libraries, and am not quite hyperlexic, so I have read a great deal of the literature pertaining to NO and other aspects of physiology that relate to it. When I raised my NO level my thinking became much clearer and more creative. My ability to absorb and integrate information improved remarkably (it was never poor). My depression and anxiety improved remarkably, I lost weight, my liver enzymes improved greatly, my metabolic syndrome greatly improved, my hypertension improved. I have a lot of personal insight, due in part to being able to dissociate (and 20+ years of therapy). The changes I experienced since raising my NO level were much greater than from any prior treatments, and were unexpected.

I appreciate that that my experiences are “anecdotes”, but I am only using them as a starting point for hypothesis generation. There are well known physiological pathways described in the literature mediated by NO involved in (just about) all the things that I have experienced. For the most part I experienced them before I read about them. I appreciate that until someone understands the details it won’t seem credible and until it seems credible no one is going to try and understand the details. I don’t know how to explain it except by going into the details. That is the way I came up with them, that is the only way I know how to understand them, that is the only way I know how to explain them. I am happy to discuss my motivations in pursuing these ideas more, but that won’t help you understand them, and without knowing me and where I am coming from, hearing my motivations provides for no increased credibility.

I have talked with George Stefano, and he and I are on exactly the same page. We emphasize different things, but I don’t think there is any serious disagreement between us. He is an academic researcher who needs to keep his lab funded; I am solely interested in trying to commercialize my bacteria. He doesn’t get the respect in the NO research community that he should.

I appreciate that some aspects of the Buddha story have mythic components. One of the things that I have been trying to understand lately is what aspects of physiology have caused human myths to adopt the form of the monomyth that Joseph Campbell talks about in his “Hero with a thousand faces”. Many aspects of stress physiology involve NO, and quite a few of the transitions Campbell talks about can be partly “explained” through NO physiology. Most modern humans have never experienced the life threatening stress that was common in human evolutionary time. Unless you have experienced it, it is difficult to appreciate what it can do, and what it can invoke in people.

Part of what is compelling me to try and get my story out there is that I appreciate what low NO can do. I am quite sure that it is low NO that induces the acute psychosis of postpartum psychosis in women, and which induces the “berserker” state in men. Low basal NO makes that state easier to enter. I suspect that incidents of “road rage”, school shootings and infanticide have components related to low basal NO levels.

We know that physiology is extremely complicated. We know that virtually every aspect of physiology is regulated extremely well (even though the details are not understood). When physiology “goes bad” and results in disorders or diseases, those regulatory systems must have “gone bad” for that to happen. For the most part that regulation is feedback regulation. Each aspect of physiology that requires feedback regulation requires a setpoint and regulation around that setpoint. When that regulation “goes bad”, is it good regulation around a bad setpoint, or bad regulation around a good setpoint?

If it were bad regulation around a good setpoint we would expect to see both positive and negative deviations around the “good” setpoint. Perturbing physiology so as to improve regulation would be expected to improve regulation and improve what ever disorder has occurred.

If it were good regulation around a bad setpoint we would expect to see deviations in only one direction. The only way to fix good regulation around a bad setpoint is via shifting the bad setpoint to a good setpoint. This is an extremely important distinction. A bad setpoint is like a thermostat set too high. You can overwhelm a thermostat set too high by bringing in enough ice to overwhelm the heating system. But that causes the heating system to run at maximum heat delivery.

In all the neurodegenerative diseases it is observed that there is reduced brain metabolism. Is that reduced ATP generation and consumption due to a few pathways “gone bad” (i.e. bad regulation around a good setpoint)? Are there a few pathways that consume enough ATP that if they “went bad” sufficient reduction in ATP production and consumption would be observed? I think that if only a few pathways had “gone bad”, it would be pretty obvious which ones had gone bad because there are at most only a few pathways that can consume enough ATP to cause the observed perturbation were they to go bad. In other words, there can be at most 2 pathways that consume 50%, 3 that consume 33%, 4 that consume 25%, 5 pathways that consume 20% of ATP production.

If more than 5 or 10, or 20 pathways have to “go bad”, to cause the observed ATP reduction, the premise that these pathways have “gone bad” simultaneously becomes unlikely. It becomes more likely (in my opinion) that instead of bad regulation around a good setpoint, it is good regulation around a bad setpoint. For many pathways to go bad simultaneously that is the only credible mechanism, good regulation around a bad setpoint.

Nitric oxide is one of the few things that does affect global setpoints in many different pathways. There has to be a mechanism that keeps all of the different pathways “in sync” as organisms change their physiology to accommodate different needs. For example, NO sets the ATP setpoint via sGC and cGMP. NO is what causes mitochondria biogenesis. Low NO invokes ischemic preconditioning which reduces ATP levels and ATP consumption.

Fifi

Didn’t mean to go past your question before signing out.

Well I guess, I’m looking for a good explanation for any aside from the usual “The brain lights up…” stuff. What causes the brain to light up then? I’m looking for a more coherent, unifying causal model for brain activity. I would think if there are good (i.e., true and comprehensive) explanations, they could be presented fairly completely.

Also my point is in some ways about communicating with excessive confidence, which I suggest is not in keeping with the scientific approach. I was taking this to mean something more than “it’s in the brain” as constituting a good explanation. Something that went beyond correlations between the description of something mystical and a brain region being active. Also I don’t imagine that experiemnts have been done on all the varieties of mystical experiences, and I meant “all” to address Steven’s post in which he indicated that there is a materialist explanation for “all” that is mysticism. I understand feeling confident that we’re getting there or at least getting somewhere but not that we’re all there.