tag:blogger.com,1999:blog-3045634714760830992.post6018149857039696547..comments2023-06-05T11:51:38.383-04:00Comments on Evolutionary Psychiatry: Omega 6, Obesity, and Endocannabinoids (Again)Anonymoushttp://www.blogger.com/profile/04429177284200775781noreply@blogger.comBlogger36125tag:blogger.com,1999:blog-3045634714760830992.post-15456842761422901892013-07-04T18:44:48.449-04:002013-07-04T18:44:48.449-04:00Rimonabant was designed to block CB1 receptors in ...Rimonabant was designed to block CB1 receptors in the brain and thus treat obesity by reducing appetite, however many of the benefits are now believed to be due to the drug's effects on peripheral organs such as the liver and adipose fat tissue. There is now an abundance of published scientific literature which supports the role of the peripheral CB1 receptor in the development of the cardiometabolic problems associated with obesity including T2 diabetes and liver damage. There is also evidence that these peripheral receptors are responsible for changes in energy balance that leads to much of the weight gain - but that is more contentious. <br />Obesity is, in most cases, linked to hyperactivation of the cannabinoid system - that is increase in amounts of both the endocannabinoids and the receptors. The mechanisms are well described by which CB1 receptor in particular causes increased fat and glucose production, inflammation and cell death (apoptosis) leading to fibrosis and tissue damage in organs including the liver, heart, kidneys, pancreas and eyes. <br />It is quite probable that hyperactivation of the cannabinoid system may be induced by high ratios of omega 6/omega 3 fatty acids in the diet, but this may not relate directly to the amount of arachidonic acid-containing phopholipids in cell membranes. It is possible that it is the production of reactive oxygen species during the metaboolism of different fats and sugars that is the determining factor. It is also known that high amounts of fructose and alcohol as well as hepatitis C virus can have similar effects - all resulting in similar liver pathology mediated by the CB1 receptor.<br />Unfortunately, it seems likely that, following the withdrawal of rimonabant, the Pharma industry will be too nervous to revisit the CB1 area, even though the development of drugs which do not enter the brain should be possible. So sadly the real value of such a drug for so many people in the 21st century will probably never be realised. Anonymoushttps://www.blogger.com/profile/17280845315167269509noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-5838846909388666022013-03-25T05:58:09.618-04:002013-03-25T05:58:09.618-04:00Look at this:
The rise and fall of CB1 receptor a...Look at this:<br /><br />The rise and fall of CB1 receptor antagonists: possible future perspectives<br />György Bagdy<br />Department of Pharmacodynamics, Semmelweis University, 1089 Budapest,<br />Hungary<br />E-mail: bag13638@iif.hu<br />BMC Pharmacology 2011, 11(Suppl 2):A55<br /><br />Abstract: Cannabinoid type-1 (CB1) receptor antagonists were among the most promising drug targets in the last decade. <br />They have been explored and found to be effective as therapeutic agents for OBESITY and related cardiometabolic problems, including e.g. dyslipidaemias, diabetes, and metabolic syndrome. However, the use of rimonabant, the first marketed CB1 receptor antagonist, has been suspended due to its anxiogenic and depressogenic side effects, which were present in about 20–30% of the patients, i.e. a 2.5–3-fold increase compared to placebo.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-56046872748973480452012-12-14T08:55:41.889-05:002012-12-14T08:55:41.889-05:00I found this longitudinal study on depression and ...I found this longitudinal study on depression and dietary patterns interesting...<br />http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0051593 <br /><br />"The highest quartile of low-fat, western, high snack and high fat-sweet diets in men and low-fat and high snack diets in women were associated with higher likelihood of depressive symptoms.."<br />"Conversely, the highest quartile of traditional diet (characterized by fish and fruit consumption) was associated with a lower likelihood of depressive symptoms in women compared to the lowest quartile,... as the healthy pattern (characterized by vegetables consumption) ... in men and women, respectively. However, there was probably a reverse causality effect for the healthy pattern.<br /><br /> Roy Nelsonhttps://www.blogger.com/profile/17742330742531093952noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-70530720526801114132012-10-16T15:53:46.940-04:002012-10-16T15:53:46.940-04:00Just thinking; early cannabis use stops young peop...Just thinking; early cannabis use stops young people from learning to their full capacity;<br />Omega 3 is a treatment for attention deficit disorder;<br />Is attention deficit disorder a result of high anandamide levels?<br /><br />http://www.neurology.org/content/72/17/1526.short<br />Dysfunction of the dopamine (DA) system has been proposed to explain some of the clinical manifestations of attention-deficit/hyperactivity disorder (ADHD), a diagnostic concept describing children with inattention, impulsivity, and hyperactivity.1<br /><br />A complex interaction between DA and the endocannabinoid system (ECS) has been found experimentally,2 and the ECS has already been implicated in a number of DA-related disorders, such as schizophrenia, Parkinson disease, Huntington disease, and drug addiction.3 Of note, the association between ADHD and drug abuse has been described, as well as that between ADHD and abnormal activity of reward-related brain areas. These findings further suggest that the DA system and DA/ECS interaction might be altered in this disorder.1 Based on these premises, we investigated the possible alterations of anandamide (AEA) metabolism in ADHD. Notably, the endocannabinoid AEA reduces the activity of the DA transporter,4 and might therefore be implicated in the dysfunction of DA uptake mechanisms involved in ADHD pathophysiology.1<br /><br />Of course, dopamine disregulation also relates to food reward.<br />And ritalin and amphetamines are dopamine agonists.<br />Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-39551260482936246692012-10-10T22:16:30.657-04:002012-10-10T22:16:30.657-04:00As for the conspiracy theory
1) all businesses are...As for the conspiracy theory<br />1) all businesses are conspiracies. That's how capitalism works; people conspire to take money from others within the law.<br />2) linoleate was imposed on fast-food manufacturers in the US by the Center for Science in the Public Interest lobby group. The fast food restaurant chains did not think of it themselves; this has been an unintended consequence of the war on saturated fat. Without "Health" experts jumping the gun before the facts were known (we probably needed more omega 3s, if anything, not less SAFAs plus more linoleate) there would not be the juxtaposition of oil and fructose in MacDonalds today.<br />It should have been a wonderful conspiracy, but it has the history of being a massive balls-up instead.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-89371161139531450582012-10-08T10:07:31.547-04:002012-10-08T10:07:31.547-04:00can someone help me to discover more details about...can someone help me to discover more details about how to find a way to having a great Flaxseed oil vegetarian with omega nutrition dishes ?<br /><br />i want to make a wonderful healthy food to my gest,<br />in most cases they not much like organic food to say the list ,<br />so please i need your help<br />make me pursues them that health diner can go with the phrase "wonderfully lovely satisfy diner"<br /><br /><br /><br /><a href="http://flax-seed-benefits.com" rel="nofollow">flax seed benefits</a> the guyhttps://www.blogger.com/profile/02210395960418186329noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-81523443718468924852012-10-07T18:13:01.724-04:002012-10-07T18:13:01.724-04:00The "food reward" paradox might be that ...The "food reward" paradox might be that no food is intrinsically over-rewarding, but that some nutrients, eaten for a long time, and not especially "rewarding" in themselves, can prime us to find other nutrients "rewarding" to an extent that over-rides appetite.<br />This makes sense in an evolutionary way; fructose and linoleate are "windfall" nutrients and an animal that responded to their abundance by eating more, fattening, and slowing its metabolism would be ready for winter.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-40342016216999068422012-10-07T10:55:51.346-04:002012-10-07T10:55:51.346-04:00I read my post again, and maybe (obviously) what I...I read my post again, and maybe (obviously) what I said could be taken the wrong way, and for that I must apologize. I really like the points you were making, and the relationship to cannabis is a fascinating concept. I agree that the "food reward" business plan could exist, but I do not think that is the whole answer. Vegetable oil consumption to the exclusion of animal fats, combined with wheat consumption, is entirely in line with "official" dietary recommendations that are still in use. <br /><br />The nature of the problem is that somewhere along the way people got most of the dietary facts almost entirely backward.<br /><br />Guyenet seemed to propose, as I understood from his many posts, that people got fat because the food was "rewarding" to them. It wasn't just palatable, it was something more...something ineffable, perhaps. You on the other hand in your practice consider a specific group, binge eaters, with an addiction problem regarding food. So yes, clearly that group would have something going on in addiction centers of the brain. Maybe that really is food reward. But that is not what Guyenet was talking about, and I read many of his posts on the topic. <br /><br />Your post seemed to indicate that one likely cause of obesity was the interference of the omega 6 with the various feedback signals to stop eating, much as caused by the munchies. It is difficult for me to see how that impaired signaling could be characterized as a reward. And I do not think that is what you were trying to say. Of course, the term reward is not essential to the concept, but it was not chosen at random.<br /><br />The problem with the munchies is that nothing really makes you stop eating, except perhaps the dawning awareness that you are mindlessly eating. And eating caused by the munchies does not really satisfy. It is all a product of the satiety signaling systems not working properly. That is not a reward, and more like the opposite of a reward. The urge to eat when the system has been impaired is essentially involuntary and the feelings of hunger are real. How could we better describe the mindless over-consumption of the high fat and wheat food items you describe.<br /><br />What you were describing in you post, as I understood it, had far more to do with generalized population obesity than a small group of people addicted to food. I think the research you describe is important to understanding what is going on with obesity. Of course, it may also apply in some ways to the binge eaters you describe. What is disturbing is the stealth aspect of the vegetable oil consumption: what if people were told on the bottle (or package) that their cannabis receptors and satiety signaling systems were being influenced by the vegetable oil? <br /><br />Thank you for your posts on this topic.Richardhttps://www.blogger.com/profile/13579689230767618822noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-46346638136052423452012-10-07T09:28:19.184-04:002012-10-07T09:28:19.184-04:00Her website was hacked twice, but it is fixed now....Her website was hacked twice, but it is fixed now.Anonymoushttps://www.blogger.com/profile/04429177284200775781noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-17801901758209044602012-10-07T09:27:09.684-04:002012-10-07T09:27:09.684-04:00There's a difference between the questions I a...There's a difference between the questions I ask and statements I make on this blog, and what I do personally in life. I think it is utterly reasonable to most processed food most of the time. <br /><br />My research into food reward has been more along the lines of binge eating, which is not synonymous with obesity by any account, but is quite common in the populations I treat. In binge eating, there are small but clear randomized controlled trials showing that binge eaters have similar brain activation to those who are addicted to alcohol and drugs, for example, an excess of activation in reward areas in anticipation of eating certain foods and decrease in actual satisfaction compared to those without bingeing when eating the foods. Combine that and the "using" dreams people often have when starting a clean diet, and that's pretty interesting information.<br /><br />Is there a conspiracy to create and manufacture high reward food? Not a conspiracy, it's just business sense to make food that people will want to consume and buy more of. That omega 6 oils, cheap salt, and high fructose corn syrup make sugary-fat and salty foods cheap is just a bonus, and certainly trans fats interfering with omega 3 absorption and an excess of omega 6 could be especially disastrous. <br /><br />Anonymoushttps://www.blogger.com/profile/04429177284200775781noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-64609396206183899052012-10-07T00:38:49.182-04:002012-10-07T00:38:49.182-04:00I had that same issue at one point. Not today.I had that same issue at one point. Not today.Richardhttps://www.blogger.com/profile/13579689230767618822noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-51575116221865481562012-10-07T00:37:17.522-04:002012-10-07T00:37:17.522-04:00I read this and your other posts on the subject, a...I read this and your other posts on the subject, and it seems to me, jargon aside, that what you seem to be saying is that food reward (a misleading term) is related to the omega 6/vegetable oils which, combining with the lack of satiety provided by grain consumption, leads to obesity. It doesn't have to be a large effect and easily proved, because the daily effect could be quite small. What would matter would be the cumulative effect. And most of us see that every day.<br /><br />Thus the "food reward" is not necessarily some scheme by evil corporations (although it might be) but instead could an unfortunate circumstance related to several changes in modern diet. We could propose that although wheat is a much less desirable food than some others, people might not eat so much wheat that it makes them obese were it not for the "munchies" related to the omega 6 consumption. So it isn't the carbs themselves, exactly, but rather the massively excessive consumption of vegetable oils leading to excessive consumption of carbs. (This would be a pernicious effect of people also being told to go on a low saturated fat diet. This leads of course to fewer animal fat calories and protein and more grains, etc.) When people stop eating the omega 6 fats to excess (and eat more sardines?) the system for signaling of satiety is restored to its proper functioning state. Maybe that is all we need to do? No need to go primal, etc., in terms of obesity?<br /><br />As someone amused by concepts of truth, I sometimes wonder at the hesitancy to take a risk with causality. You have pretty much investigated the matter and come to some interesting ideas. Is it proof? Concepts like proof and causality and truth are related, and are sort of ultimate and final terms, signaling the end of some quest and a statement of the stated facts matching "reality." (Whatever "reality" is, as opposed to human constructed systems, etc.) In this grail-like quest people are extremely cautious because they don't want to get it wrong. Correlation is not causation, the double blind "gold standard" etc. But a cautious statement regarding causality is justifiable at some point in this discussion. It would even be helpful.<br /><br />S. Guyenet went wrong in his statements about food reward, and became a cautionary tale, when he started to suggest that the food, or eating the food, by itself was "rewarding" and somehow made people happy. The proposal you seem to be advancing is that obesity is an unintended consequence of excessive omega 6 consumption that gives people the unthinking, hidden, desire to eat, and eat more, by interfering with satiety signaling. Neither the eating nor the food "rewards" the individual or makes them happy. If anything, such an unthinking, unknown desire is the conceptual opposite of a reward.<br /><br />It is one thing to smoke a joint and know you have done it, and know you will get the munchies, compared to consuming an omega 6 oil and not knowing you have eaten a food with certain chemical properties that make you feel hungry by interfering with proper satiety signals. Does that prove that omega 6 oils make you fat? No, but it is a link in chain of events.<br /><br /><br /><br />Richardhttps://www.blogger.com/profile/13579689230767618822noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-9889298419183029722012-10-05T18:07:07.850-04:002012-10-05T18:07:07.850-04:00The fact that some cannabinoids are anti-psychotic...The fact that some cannabinoids are anti-psychotic while others, like delta-9 THC are pro-psychotic should warn us against seeing natural cannabinoids as all having similar effects on food reward. The EPA anandamide analogue may have oppositional effects.<br /><br />Does NAC make LA-plus-fructose less addictive?Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-14240533510760717292012-10-05T18:00:11.461-04:002012-10-05T18:00:11.461-04:00Hi, Emily,
I don't know if this is happening ...Hi, Emily,<br /><br />I don't know if this is happening to anyone else who has recently tried to access your blog, but Google Chrome is blocking access because it says your site has been infected, or may infect others who visit, because of judytsafrirmd.com being a known malware distributor. <br /><br />FYIMs.Pearlhttps://www.blogger.com/profile/06972564003247318170noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-90630501138950761902012-10-04T20:36:11.398-04:002012-10-04T20:36:11.398-04:00Note that a sufficiency of EPA would reduce phosph...Note that a sufficiency of EPA would reduce phospholipidase activity on AA, making less available for anandamide. There may be an EPA analogue of anandamide.<br />Yes, there is:<br />"In addition to anandamide (arachidonyl ethanolamide) perhaps the<br />Eicosapentaenoyl ethanolamide should be tested."<br />http://www.bio.net/bionet/mm/neur-sci/1996-June/024277.htmlPuddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-70997692058385561292012-10-04T20:31:39.312-04:002012-10-04T20:31:39.312-04:00It might be that AA produced from LA concentrates,...It might be that AA produced from LA concentrates, at least at first, in different cell partitions from dietary AA and that they have somewhat different localised effects. Also, LA>AA competes with ALA>EPA, while AA would not, but would still compete with EPA going into and out of membranes.<br /><br />LA> anandamide mimics cannabis in its effect on appetite. omega 3 protects against this.<br />Cannabis increases propensity to develop psychosis. Omega 3 reduces incidence of psychotic episodes.<br />Does omega 3 reduce cannabis munchies?<br /><br />http://bjp.rcpsych.org/content/194/4/371.full<br /><br />@Chris, the absence of FADS mutations in Native Americans backs Paleo claims that these were originally highly carnivorous populations.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-80929105728387846632012-10-04T16:30:22.954-04:002012-10-04T16:30:22.954-04:00Yes, I think you do need to get a considerable amo...Yes, I think you do need to get a considerable amount of fish oil (2 grams seems reasonable) on a high omega 6 diet…RDA is more like 400mg thoughAnonymoushttps://www.blogger.com/profile/04429177284200775781noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-44200886522852277632012-10-04T16:29:21.174-04:002012-10-04T16:29:21.174-04:00Meant omega 3, not omega 6 in my reply, of courseMeant omega 3, not omega 6 in my reply, of courseAnonymoushttps://www.blogger.com/profile/04429177284200775781noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-47391638025061035492012-10-04T07:23:50.562-04:002012-10-04T07:23:50.562-04:00Ok I am running across papers that discuss d5d and...Ok I am running across papers that discuss d5d and d6d being upregulated in the presence of insulin, and that the presence of insulin is a factor in the creation of eicanosands. This again supports my budding theory that dietary AA == good & necessary & preferred vs AA synthesized in the body via the d5d pathway which appears to be costly. Interestingly, in my cite [1] in my original post above, the authors expressed the same hypothesis of such being costly (having a genetically upregulated d5d/d6d), since those polymorphisms were actually a mutation that swept near completely (homozygously) through africa but didn't take complete hold beyond africa where the ancestral alleles held on quite well - it must have been evolutionarily costly. The map of the globe showing presence in populations elsewhere is fascinating (note, the native Americas show a complete absence of this mutation - where are they getting their AA/EPA/DHA?).<br /><br />George, I agree with you that we may actually start seeing a unification of all of these hypotheses of obesity via the pufa metabolism.<br /><br />@Emily and George, One more thought: could the "addictive" endocannabinoid's actually be nature's way of driving people to consume LA in order to produce necessary AA even if such comes at a cost? It may be what the body really wants is dietary AA, but will settle for producing its own more "costly" form.Anonymoushttps://www.blogger.com/profile/06571125588778516777noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-90512654172890677442012-10-04T00:17:07.399-04:002012-10-04T00:17:07.399-04:00Your #3 paper conflicts with #2, however #3 reflec...Your #3 paper conflicts with #2, however #3 reflects a healthy group whereas #2 appears not to be(can't access that paper to confirm). However, in both cases, the cascade was impaired at the d5d, which meant buildups of GLA/DGLA not getting converted to AA.<br /><br />It was the AA that was protective to the Koreans, who were healthy and had high AA/DGLA ratios; and while not stated in the paper, that AA is presumably obtained from the diet.<br /><br />While on the other hand, if one is NOT getting sufficient AA from the diet, a strong d6d (acting at the end of the cascade as well as the beginning) mentioned in your cite #2 abstract may be depleting dietary AA away. I would love to get at that paper to see what the AA levels were for those in the study.<br /><br />I am really beginning to think AA is not a bad thing, its a good thing, and one either needs a strong d5d (thanks to FADS1 genetics) or needs AA supplied in the diet (and that latter might be the preferred). A strong d5d also means getting EPA (and eventually DHA) from dietary ALA to balance it out - for those fortunate enough to have a good FADS1 gene.<br /><br />Anonymoushttps://www.blogger.com/profile/06571125588778516777noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-40858936128930706912012-10-03T20:27:09.773-04:002012-10-03T20:27:09.773-04:00@ Blissful, a second-hand copy of The Zone Diet wi...@ Blissful, a second-hand copy of The Zone Diet will tell you all you need to know about GLA. It's good as a one-off fix, but not for longer use, in my experience.<br /><br />Thanks Chris, I've read that the opposite applies to Pima peoples too. It shouldn't affect the influence of diet on the ratios, but it would make animal sources of AA, EPA and DHA more or less important for different alleles.<br />This helps to explain differentials in obesity and disease epidemiology between races in the US.<br /><br />Your ref 1: short-term clinical trials don't answer the effect of LA accumulation. It wouldn't happen till membranes were saturated, which might take 6 months or years in humans.<br />Also, it is the inhibition of DHA synthesis as well as increase of AA that matters.<br />Some people might be more or less resistant to the effect; which helps explain why not everyone gets food-addicted by eating fast food, and why it happens sooner or later with different people.<br />Let's look and see if these genes are associated with obesity in a high-LA food environment.<br /><br />FADS gene polymorphisms in Koreans: association with _6 polyunsaturated fatty acids in serum phospholipids, lipid peroxides, and coronary artery disease<br />http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=272536<br /><br />Recent insights into the relation of Δ5 desaturase and Δ6 desaturase activity to the development of type 2 diabetes<br />http://journals.lww.com/co-lipidology/Abstract/2012/02000/Recent_insights_into_the_relation_of__5_desaturase.3.aspx<br /><br />Fatty acid desaturase (FADS) gene polymorphisms and insulin resistance in association with serum phospholipid polyunsaturated fatty acid composition in healthy Korean men: cross-sectional study<br />http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3111337/Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-35746485445800144162012-10-03T07:30:47.707-04:002012-10-03T07:30:47.707-04:00George, please read my cite above - a study publis...George, please read my cite above - a study published just recently shows it really is a matter of genetics, particularly for Africans - Africans tend to be near homozygous for alleles in FADS1+2 genes the encode for the most efficient conversion of LA/ALA to AA/EPA. Those genes are not as well entrenched elsewhere in the world as shown in the study.<br /><br />[3] Mathias RA, Fu W, Akey JM, Ainsworth HC, Torgerson DG, et al. (2012) Adaptive Evolution of the FADS Gene Cluster within Africa. PLoS ONE 7(9): e44926. doi:10.1371/journal.pone.0044926 Anonymoushttps://www.blogger.com/profile/06571125588778516777noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-3534997155369019882012-10-03T00:24:08.206-04:002012-10-03T00:24:08.206-04:00What are your thoughts on consuming chicken skin? ...What are your thoughts on consuming chicken skin? Healthy or unhealthy? From a Paleo perspective, it seems that our paleo ancestors would have eaten the skins.<br /><br />Also what about GLA gamma-linolenic acid which is an omega-6? Good or no good? I've seen it as a supplement for reducing inflammation? Which is confusing because omega-6 is inflammatory.Anonymoushttps://www.blogger.com/profile/15787417321539228927noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-46822737777455941692012-10-02T18:44:08.303-04:002012-10-02T18:44:08.303-04:00(6:3 ratio of 144:1 in first reference; I can see ...(6:3 ratio of 144:1 in first reference; I can see that's the wrong way round. But 144:1 - yikes!)<br />I think many of the questions raised around whether this research applies to humans can be answered by Susan Allport's book on omega-3, "The Queen of Fats".<br />She's not up to anandamide (the book's from 2006), but it's obvious that, as the 6:3 ratio increases, conversion of LA to ARA increases step-wise, because inhibition from ALA is lost.<br />So whether humans "can" convert LA to ARA, or ALA to DHA, is probably a matter of ratios, more than genetics. Elongase, desuratase and phosphlipidase are not optional enzymes; they are non-specific but somewhat prefer ALA as a substrate.<br />Many interesting details in the book; leafy greens can be an important dietary source of ALA omega 3. The highest 3:6 ratio was found in Africans eating lots of greens and cooking with palm oil, yet eating little fish.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-5114836553775603952012-10-01T23:22:43.786-04:002012-10-01T23:22:43.786-04:00I'm aware 2 of corroborating finds
1) in NASH,...I'm aware 2 of corroborating finds<br />1) in NASH, 3:6 ratio may be as great as 144:1<br />http://www.kenes.com/easl2010/posters/Abstract221.htm<br /><br />2) obesity in the US correlates with a high gamma- to alpha-tocpherol ratio, showing high intakes of corn or soy oil which have this unusual tocopherol ratio.<br />"gamma-Tocopherol levels were significantly higher in obese individuals (P < .05), whereas alpha-tocopherol levels did not differ among BMI subgroups."<br />http://www.ncbi.nlm.nih.gov/pubmed/20534324<br />also, it may takes a lifetime, and have some gender bias:<br /> "In older women gamma-tocopherol and gamma-tocopherol:alpha-tocopherol ratios were directly related to indices of obesity. In young men alpha- and gamma-tocopherols were directly correlated with obesity, but gamma-tocopherol:alpha-tocopherol ratio was not."<br />http://www.ncbi.nlm.nih.gov/pubmed/15230997<br /><br />Conversion of LA to AA and anandamide may be stepped up after many years exposure, and of course there is more genomic variation in humans (and between races and genders) than in mice. Not everyone fattens on this diet (and some will die of other diseases first) but of those who do fatten, a substantial proportion may indeed fatten for this reason.<br />What I really like about this hypothesis is that it suggests a way to reconcile FRH, CIH, CICO, and food toxins into one united theory of obesity.<br />Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.com