tag:blogger.com,1999:blog-1629175743855013102.post6016323656596864161..comments2024-02-25T02:24:14.972-08:00Comments on Whole Health Source: Is it Time to Re-write the Textbooks on Insulin and Obesity?Stephan Guyenethttp://www.blogger.com/profile/09218114625524777250noreply@blogger.comBlogger65125tag:blogger.com,1999:blog-1629175743855013102.post-15773850327420589962012-12-24T20:26:27.181-08:002012-12-24T20:26:27.181-08:00This comment has been removed by the author.Roseanna Smithhttps://www.blogger.com/profile/15130626011982018586noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-9534817759879591732012-12-19T15:50:08.093-08:002012-12-19T15:50:08.093-08:00Hi, good job. Thanks for sharing the information o...Hi, good job. Thanks for sharing the information on Health. This information is very useful for the people. Please keep try posting.Fat Loss Factor Reviewhttps://www.blogger.com/profile/18422105158175494257noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-25732480355949562172012-12-15T19:23:09.245-08:002012-12-15T19:23:09.245-08:00Thanks for nice post, i like your post and i wan&#...Thanks for nice post, i like your post and i wan't to share with my friends. please than visit-<br /><a href="http://www.socialmediabar.com/settingclearintentions" rel="nofollow">A Complicated Online Marketing World.</a><br />Anonymoushttps://www.blogger.com/profile/00436499764430990763noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-68527235362686152622012-12-15T01:55:09.861-08:002012-12-15T01:55:09.861-08:00“The molecular basis for the effects of dietary sa...<i>“The molecular basis for the effects of dietary saturated fat on plasma LDL cholesterol levels is well understood. Saturated fat influences the LDL receptor activity of liver cells as described by Brown and Goldstein, dietary saturated fat suppresses messanger RNA synthesis for the LDL receptor. This decreases hepatic LDL receptor activity and slows the removal of LDL from the blood, thus increasing the concentration of LDL cholesterol in the blood. Dietary cholesterol augments the effects of saturated fat further suppressing the hepatic LDL receptor activity and raising the plasma LDL cholesterol levels”</i>.<br /><br />–Heart Disease, Environment, Stress and Gender [proceedings of the NATO Advanced Research Workshop on Increase in Coronary Heart Disease in Central and Western Europe: Stress and Gender Related Factors, 20-24 May, 2000, Budapest, Hungary]<br /><br /><i>"Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. <b>First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels.</b> Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies". </i><br /><br />--Brown & GoldsteinPeterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-14257739597514269222012-12-15T01:49:39.176-08:002012-12-15T01:49:39.176-08:00This comment has been removed by the author.Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-14065285800878643672012-12-14T10:16:51.699-08:002012-12-14T10:16:51.699-08:00"I give my support to Stephen's newfound ..."I give my support to Stephen's newfound plant-based, high-carb fare"<br /><br />Good one bro<br /><br /><br /><br />Why don't you go and post all this stuff on chris masterjohn's blog, i'm sure he would be up for a debate.Tomhttps://www.blogger.com/profile/03527380079206830955noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-5616181970930081602012-12-14T09:42:54.596-08:002012-12-14T09:42:54.596-08:00@Chris,
ok, I'll do an exception just for yo...@Chris, <br /><br />ok, I'll do an exception just for you. The world has learned about oxLDL pretty much from Daniel Steinberg. Steinberg advocates a low-fat diet that result in very low LDL-C levels. The discordance between LDL-P and LDL-C is pretty much seen only with people who have metabolic syndrome. Again, skeptics miss the overall picture, which scientists like Daniel Steinberg try to convey;<br /><br /><b>Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia</b><br /><br /><i>"One important line of evidence comes from a consideration of the Japanese experience. In 1952, mortality from CHD among Japanese men 55 to 64 years of age was <10% of what it was in the United States.15,16 Their total cholesterol levels at the time averaged ≈160 mg/dL (estimated LDL, ≈80 mg/dL). It is noteworthy that the Japanese enjoyed this relative immunity to CHD despite the fact that the prevalence of one of the major risk factors—cigarette smoking—was much higher in Japan than in Western countries,17 and another—-hypertension—was just as high.18 Even the diabetic population in Japan fares better than the diabetic population in Western countries. In 1985, almost 30% of British male diabetics but only ≈15% of the Japanese male diabetics had CHD.19 The implication is that if blood cholesterol levels are sufficiently low, the other dominant risk factors, including cigarette smoking, hypertension, and diabetes mellitus, constitute much less of a threat"</i>.<br /><a rel="nofollow">http://circ.ahajournals.org/content/118/6/672.full</a> <br /><br /><b>Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists</b> (2011)<br /><br /><i>“All lipoprotein particles in the LDL fraction are atherogenic, independent of size”</i><br /><br />http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf<br /><br />LDL-P, oxLDL, etc are abused in online by the cholesterol confusionist in order to make the big picture very blurry and confused. This is what merchants of doubt do. To trick lay people, they aim to sabotage, confuse and distort an issue where scientific consensus is exceptionally strong:<br /><br />The Cause of Atheroclerosis (W. Roberts, editor-in-chieg, American Journal of Cardiology)<br /><br /><i>"In summary, the connection between cholesterol elevation and atherosclerotic plaques is clear and well established. Atherosclerosis is a cholesterol problem! If one has elevated cholesterol, has an elevated blood pressure, smokes cigarettes, or has an elevated blood sugar, these additional factors serve to amplify the cholesterol damage but they by themselves do not produce atherosclerotic plaques! Societies with a high frequency of systemic hypertension or a high frequency of cigarette smoking but low cholesterol levels rarely get atherosclerosis"</i>. <br /><br /><i><b>Thus, although not clearly established at this time, to prevent atherosclerotic plaques, the serum LDL cholesterol must be <70 mg/dL, the serum total cholesterol certainly <150 mg/dL, and the high-density lipoprotein (HDL) cholesterol >20 mg/dL. The latter—surely a surprise to most readers—is in patients with a serum total cholesterol level about 130 mg/dL and a LDL cholesterol level of about 60 mg/dL.</b> Exactly what HDL cholesterol level is required to prevent plaques is unclear at this time, but clearly if the LDL cholesterol is very low (eg, 50 mg/dL), then a low HDL cholesterol—as long as it is >20 mg/dL—appears not to be dangerous. Ideal may be equal serum HDL and LDL cholesterol levels or an HDL cholesterol > LDL cholesterol.<b>In summary, the recommended guideline numbers—particularly those for primary prevention—are intended for decreasing the risk of atherosclerosis events, not for preventing formation of atherosclerotic plaques"</b></i><br /><a rel="nofollow">http://ncp.sagepub.com/content/23/5/464.full </a>Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-71310967150665867162012-12-14T06:18:32.612-08:002012-12-14T06:18:32.612-08:00Peter, for all the dancing around you've done-...Peter, for all the dancing around you've done-- reiterating how many times you've "demonstrated" your theory by copious block-quoting of your preferred sources -- you still haven't convincingly made your case. Of course, now you've "demonstrated" that LDL-C is the be-all/end-all, you get to refer to everything else, including criticisms undermining central tenants of that theory, as "denialism". Elsewhere, you make statements about "those laypeople new to obesity research" as though you yourself have some professional qualifications in this area. <br /><br />Pray tell, what is your professional involvement with biomedical research? In particular, what gives you the professional insider knowledge to dismiss a high-profile researcher like Ron Krauss out of hand? <br /><br />BTW, your quoting of Steinberg is interesting, because he himself seems to be saying that modified LDL is what is taken up to initiate foam cell formation. The self-aggregation referred to was induced by mechanical treatment in vitro (not in vivo), and therefore still counts as modification in my book. <br /><br />Look, I agree that LDL-P is important, because it is the substrate for various modifications that can initiate foam cell formation. Less substrate (within reason) = less foam cell formation (probably). But this is obviously mediated by many pathways, and is contingent on the size/integrity of the LDL particle. <br /><br />I'm not a researcher in this field, nor am I a genius, but it doesn't take rocket science to figure out that the relative magnitude of these other processes, and variability within LDL, could easily outweigh the simple mass measurement of LDL-C in terms of determining risk. From the papers I've seen, inflammation, antioxidant-status, and so on, are considered by *main-stream* researchers to be important aspects of the atherosclerotic process. I suggest that you are persistently misrepresenting this aspect of the field. <br /><br />As you say <br />"buddies, unfortunately I cannot no longer participate in the discussion." But as Blake said, "opposition is true friendship", so I thank you for stimulating me to look deeper into this area to see if I've missed something. <br /><br />Chris Chris Wilsonhttps://www.blogger.com/profile/07791413012165238990noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-22514261399336462792012-12-14T03:57:36.144-08:002012-12-14T03:57:36.144-08:00Denialism: what is it and how should scientists re...<b>Denialism: what is it and how should scientists respond?</b><br /><br /><i>"The third characteristic is selectivity, drawing on isolated papers that challenge the dominant consensus or highlighting the flaws in the weakest papers among those that support it as a means of discrediting the entire field. An example of the former is the much-cited Lancet paper describing intestinal abnormalities in 12 children with autism, which merely suggested a possible link with immunization against measles, mumps and rubella.19 This has been used extensively by campaigners against immunization, even though 10 of the paper's 13 authors subsequently retracted the suggestion of an association.20 Fortunately, the work of the Cochrane Collaboration in promoting systematic reviews has made selective citation easier to detect.</i><br /><br /><i>Another is a paper published by the British Medical Journal in 2003,21 later shown to suffer from major flaws, including a failure to report competing interests,22 that concluded that exposure to tobacco smoke does not increase the risk of lung cancer and heart disease. This paper has been cited extensively by those who deny that passive smoking has any health effects, with the company Japan Tobacco International still quoting it as justification for rejecting ‘the claim that ETS is a cause of lung cancer, heart disease and chronic pulmonary diseases in non-smokers’ as late as the end of 2008.23</i><br /><br /><i>Denialists are usually not deterred by the extreme isolation of their theories, but rather see it as the indication of their intellectual courage against the dominant orthodoxy and the accompanying political correctness, often comparing themselves to Galileo".</i> <br /><a rel="nofollow">http://eurpub.oxfordjournals.org/content/19/1/2.full</a>Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-69862198104061205552012-12-14T03:56:56.877-08:002012-12-14T03:56:56.877-08:00In the end,
buddies, unfortunately I cannot no lo...In the end,<br /><br />buddies, unfortunately I cannot no longer participate in the discussion. Meanwhile, I want people to understand that in order to demonstrate the causal relationship of LDL-C cholesterol to CHD (defined as a composite of cardiovascular death, nonfatal myocardial infarction, or coronary revascularization as adopted by the CARDIoGRAM consortium) I've covered animal experiments, double-blinded, placebo controlled statin trials, surgical studies to lower LDL-C and thus CHD events through bypass of the intestine. I've covered bile-acid sequestrants, I've shown that the so-called "pleitrophic effects" of statins are plain nonsense in terms that these extra-effects are simply integral part of lipid-lowering itself. I've referred to mendelian randomized controlled trials with over million genotypes, and covered a meta-regression curve accumulated from 108 randomized controlled trials of various medical and dietary based lipid modifying interventions has established that lowering LDL cholesterol significantly decreases the risk of coronary heart disease and all-cause mortality, independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific drugs. Furthermore, I've covered epidemiology in this Guyenet's post:<br /><br /><a rel="nofollow">http://www.blogger.com/comment.g?blogID=1629175743855013102&postID=1812759267991016155</a><br /><br />I am sure there are tons of interesting deviation or something that looks like deviation in the hands of cholesterol confusionists. However, the take home message is quality over quantity, science is not a democracy, 1 study can be more important that 100 other studies because methodological superiority. Sydney trial is absolutely nothing next to REVERSAL trial, f.ex . <br /><br />Whenever you see nonsense posted by Colpo, Masterjohn and other flat earth society members keep in mind the that science is about preponderance of evidence. The cholesterol confusionist will try to use gimmick in order to sabotage and twist the truth in order to make it seem that LDL-C cholesterol +200% above to what is biologically normal is not dangerous itself. Just like the flat earth society: they try to toss every imaginable argument to confuse those who are willing to listen. In order to rationalize their appeal-to-nature fallacy and sell a diet heavy in SFA and dietary cholesterol they remain in denial about the pathophysiology of CHD. Everything goes as long as it does not include excess LDL cholesterol stucking in the intima: it's the oxLDL, it's the inflammation, it's wheat, it's the sugar, it's the obesity, it's the veggie oils, etc. <br /><br />Remember this article by Diethelm (2009):Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-85002103447090866332012-12-14T02:34:25.335-08:002012-12-14T02:34:25.335-08:00Passwater:, Is it accurate to say that only oxidiz...<b><i>Passwater:</i></b>, Is it accurate to say that only oxidized-LDL starts the plaque process? <br /><br /><i><b>Steinberg: No</b>, it seems to me very likely that other modified forms of LDL are involved in plaque formation. What we know so far is that the use of antioxidants can decrease the rate of progression of lesions by 50-80%. That would speak to a major involvement of oxidation, but other things can also lead to foam cell formation. Studies by Dr. <b>John C. Khoo in my laboratory have shown that aggregation of LDL with itself markedly increases the rate of uptake by macrophages. [15] The uptake in that case occurs by way of the native LDL receptor, not the acetyl LDL receptor or oxidized LDL receptor</b></i>. <br /><br /><i>Studies by Drs. J. S. Frank and A. M. Fogelman at UCLA have demonstrated the generation LDL aggregates in the subendothelial space. [16] <b>Aggregation does not depend upon prior oxidative modification. So here is a quite distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.</b></i> <br /><br /><i>Studies by Dr. Joseph L. Witztum and others in our laboratory have shown that minor modifications in the structure of LDL can render it immunogenic. Autoantibodies against oxidized LDL have been demonstrated in rabbits and in humans as well. Therefore, a complex of a modified LDL particle and an antibody against it can be taken up into macrophages by way of a completely different receptor, the receptor for immunoglobulins (the FC receptor).</i> <br /><br /><i>So, there are at least two or three alternative modifications of LDL that could account for foam cell formation. These have not yet been studied in vivo as intensively as oxidative modification, and so we are not in a position to say with any confidence how important they may be.</i> <br /><a rel="nofollow">http://www.healthy.net/scr/interview.aspx?Id=197</a>Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-75198295718054691632012-12-14T02:30:47.233-08:002012-12-14T02:30:47.233-08:00In my view 2 single facts speak against the "...In my view 2 single facts speak against the "pleitrophic effects" of statins:<br /><br />a) There exist ridiculously linear relationship between LDL-C lowering and the decrease of cardiovascular events observed in 5-year statin therapy initiated at mean age of 63. 15% reduction in LDL-C = 15% reduction in events, 45% reduction in LDL-C = 45% reduction in events, and so forth.<br /><br />b ) A meta-analysis on mendelian randomized controlled trials with over 1,000,000 genotypes have shown that people with inherited LDL-C lowering mutations in the statin targeted HMG-CoA gene showed no heterogeneity between other studied SNPs with regard to the decrease in CHD risk per unit of LDL reduction, which suggests that the effects of statin to the risk of CHD is mediated largely or entirely through effect on circulating levels of LDL, rather than through some other pleiotropic effect.<br /><br />@Tom<br /><br />the Colpo nonsense about fish oil and LDL-C has already refuted long time ago by PrimitiveNutrition. Your premises simply don't hold water, fish oil increases LDL-C only on patients with very high triglycerides (the second video all about oxLDL):<br /><br />RaCCG4: Fish Oil<br /><a rel="nofollow">http://www.youtube.com/watch?v=hpJTZAbr80k&list=PLDBBB98ACA18EF67C&index=16</a><br /><br />Primitive Nutrition 45: Anything but LDL, Part III.<br /><a rel="nofollow">http://www.youtube.com/watch?v=GSUJupCkV-s&list=PLCC2CA9893F2503B5&index=45</a><br /><br />Herbivore mammalians do get atherosclerosis to some degree in their wild habitat, and elevated cholesterol has been associated as the main correlate for this increased risk. Elevated LDL-C (LDL-C >70mg/dl) in free-ranging primates eating only foods in their natutal habitat is strongly associated with atherosclerosis in these primates. Wild primates typically have their LDL-C in the 40 to 70 range. Atherosclerosis is a disease of herbivores. <br /><br />"<i>Lower, the better</i>" has been repeatedly proven in randomized, placebo-controlled double-blinded trials together with mendelian randomized controlled trials. The story is ended. <br /><br />Just like Sydney trials showed corn oil may promote strokes (not necessarily atherosclerosis), there's also preliminary evidence that vegetable oils may cause damage to the endothelium, however this does not really refute the lipid theory, which dictates that elevated cholesterol CAUSES heart disease. The only vegetable oil I personally use very sparingly is canola oil (only 6% saturated fat content). Similarly, there's preliminary evidence that dietary cholesterol CAUSES damage to arteries independent of its effect to serum cholesterol levels. Again, this does not refute the lipid theory. Elevated serum cholesterol is associated with increase risk for atherosclerosis in every single mammalian specimen in the face of this planet (includes birds and insects). <br /><br />The inflammation theory behind CHD does not have any evidence from mechanism studies and neither from studies on humans. Inflammation is a downstream, not a causal factor; people with inherited high levels of CRP do not have increased risk for atherosclerosis (correlation does not equal causation):<br /><br />The Tsinamese have horrible amount of inflammation but low LDL-C cholesterol, hence no atherosclerosis. <br /><br /><b>Inflammation and Infection Do Not Promote Arterial Aging and Cardiovascular Disease Risk Factors among Lean Horticulturalists</b> <br />http://www.plosone.org/article/info:doi/10.1371/journal.pone.0006590<br /><br /><b>Take-Home Message:</b>keep your lipid-profile in check, special attention LDL-C status (all free-ranging mammalians have very low LDL-C) eat antioxidant rich plants, cut highly refined foods low in fiber (including carbohydrates and fats). <br /><br />I give my support to Stephen's newfound plant-based, high-carb fare. <br /><br />BTW elevated cholesterol levels in young people and in midlife has not only been associated with risk of CHD but also with Alzheimer, prostate cancer and impotence also in high-risk Western cohorts where LDL-C levels +200% above to what is biologically normal is the norm, thus weakening the statistical power.<br /><br />Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-48357822256510512012-12-13T22:29:08.814-08:002012-12-13T22:29:08.814-08:00Hi,
Thanks for sharing the information on Health. ...Hi,<br />Thanks for sharing the information on Health. This information is very useful for the people. Please keep try posting..<a href="http://www.johnsonmedicalassociates.com" rel="nofollow">Alternative Medicine Services</a>jsmedicalhttps://www.blogger.com/profile/07495089099305378044noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-53756177869558606022012-12-13T21:33:36.930-08:002012-12-13T21:33:36.930-08:00@Peter,
atherosclerosis is NOT the same as CHD.
...@Peter,<br />atherosclerosis is NOT the same as CHD. <br /><br />Atherosclerosis occurs naturally in many bird and mammal species including strict herbivores such as cattle.<br /><br />The only mammals that develop CHD (as distinct from atherosclerosis) are higher primates (including humans) and guinea pigs fed on poor quality diets. CHD does not occur in wild primates, "wild" humans or wild guinea pigs.blogbloghttps://www.blogger.com/profile/18029519906193388609noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-80832144873001051522012-12-13T09:38:24.567-08:002012-12-13T09:38:24.567-08:00"LDL is not the end all be all of heart disea..."LDL is not the end all be all of heart disease." (be all & end all)<br /><br />Otherwise: A necessary but not SUFFICIENT condition - in mathematical theorem proving terminology.<br />LeonRoverhttps://www.blogger.com/profile/07219165631035107225noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-76260202442714786162012-12-13T05:30:40.889-08:002012-12-13T05:30:40.889-08:00Peter,
If LDL is the end all be all of heart dise...Peter,<br /><br />If LDL is the end all be all of heart disease then how do you explain the fact that omega 3 supplementation reduces heart attack incidence even though it raises LDL levels (1)(2)(3)(4)<br /><br />"DHA supplementation from algal oil, a marine source of (n-3) fatty acids not extracted from fish, may reduce serum TG and increase HDL-C and LDL-C in persons without coronary heart disease"<br /><br />Hmmm, isn't saturated fat demonized for the same effects on HDL, triglycerides and LDL ?<br /><br />The lyon diet heart study was the most successful of it's kind, it reduced heart attack incidence by 70%. Their were no differecnes in total blood cholesterol between the control and intervention group (5) although the intervention group had higher blood levels of antioxidants and omega 3's.<br /><br />You like animal studies don't you peter ? So here's one especially for you.<br /><br />BHT reduces athersclerosis in rabbits even though it raises LDL levels (6)<br /><br />Did you also know that linoleic acid significantly reduces LDL cholesterol levels ?<br /><br />Therefore according to your statemnt that "No matter what mechanism is used, lowering LDL cholesterol will results in lower rate of cardiovascular events" we should expect to see reduced cardivascular events when we replace saturated fats with omega linoleic acid. What do we see ?<br /><br />A two fold increase in incidents in the sydney heart study and four fold increase in the rose corn oil trial (7) Whoooops. Oh yeah and cholesterol levels were reduced in both trials<br /><br />Atherosclerotic plaque contains an unusually high amount of linoleic acid and the linoleic acid content of plaque correlates well with dietary intake (8)<br /><br />"These findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered"<br /><br />This was almost 20 years ago ...<br /><br />Did you know that carotid plaque contains high levels of oxdized LDL and there is no correlation between oxidized LDL levels and total LDL levels ? (9)<br /><br />Did you know that higher levles of oxidized LDL are correlated with greater heart attack risk regardless of total LDL levels (10)<br /><br />"A potential causative role in atherosclerosis and heart disease<br />has indeed been detected for oxidized LDL, but this form of LDL<br />shows no correlation with serum levels of native LDL. Rather,<br />individual antioxidant status appears to be a ke factor influencing<br />serum concentrations of oxidized LDL" (11)<br /><br /><br />Heres an idea peter/richard (whatever the hell your name is)<br /><br />Maybe it's not saturated fat and cholesterol thats causing heart disease. Maybe it's the overconsumption of linoleic acid and the underconsumption of long chain omega 3's, a sedentary lifestyle, stress, smoking, a lack of antioxidants, vitamins and minerlas, sleep deprivation, excess adiposity, refined carbohydrates, high temperature cooking etc etc etc.<br /><br />It's clear from the above evidence that LDL is not the end all be all of heart disease. <br /><br /><br /><br /><br /><br /><br /><br /><br />1. http://www.ncbi.nlm.nih.gov/pubmed/16825676<br /><br />2. http://jn.nutrition.org/content/early/2011/11/22/jn.111.148973<br /><br />3. http://www.ncbi.nlm.nih.gov/pubmed/10189324<br /><br />4. http://www.ncbi.nlm.nih.gov/pubmed/11997274<br /><br />5. http://www.ncbi.nlm.nih.gov/pubmed/7911176<br /><br />6.http://atvb.ahajournals.org/content/11/1/15.short<br /><br />7. http://www.ncbi.nlm.nih.gov/pubmed/21118617<br /><br />8.http://www.ncbi.nlm.nih.gov/pubmed/7934543<br /><br />9. http://www.ncbi.nlm.nih.gov/pubmed/12377744<br /><br />10. http://diabetes.diabetesjournals.org/content/53/4/1068.short<br /><br />11.http://www.jpands.org/vol10no3/colpo.pdf<br /><br /><br /><br />Tomhttps://www.blogger.com/profile/03527380079206830955noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-19921979328047879352012-12-13T01:06:35.300-08:002012-12-13T01:06:35.300-08:00@Peter:
the current literature (2010-2012) strongl...@Peter:<br />the current literature (2010-2012) strongly argues that a diet high in processed food alters the gut microbiota. This in turn induces a whole body inflammatory state. according to this hypothesis CHD, cancers, obesity and diabetes are simply symptoms of systemic inflammation. <br /> <br />for example:<br /><br /><b>J Intern Med. 2010 Oct;268(4):320-8. doi: 10.1111/j.1365-2796.2010.02270.x.<br /><br />Effects of gut microbiota on obesity and atherosclerosis via modulation of inflammation and lipid metabolism.<br />Caesar R, Fåk F, Bäckhed F.<br /><br /><br />Abstract<br /><br />Recent studies have revealed a close relationship between inflammatory and metabolic pathways, and inflammation is now recognized to have a major role in obesity and metabolic diseases such as insulin resistance and atherosclerosis. The human body is home to a large number of distinct microbial communities, with the densest population in the distal gut (the gut microbiota). Bacteria have long been known to activate inflammatory pathways, and recent data demonstrate that the gut microbiota may affect lipid metabolism and function as an environmental factor that influences the development of obesity and related diseases. Here, we review how the gut microbiota may affect metabolic diseases by activating the innate immune system.</b><br />blogbloghttps://www.blogger.com/profile/18029519906193388609noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-68011174315727401612012-12-13T00:42:31.406-08:002012-12-13T00:42:31.406-08:00@ George Hendersen,
a few "radical" nutr...@ George Hendersen,<br />a few "radical" nutrition researchers have now decided that we should use animals with a similar digestive system to humans eg pigs and dogs. <br /><br />Mice are arguably one of the worst possible mamalian models for human nutrition studies.blogbloghttps://www.blogger.com/profile/18029519906193388609noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-61597584345738150062012-12-12T15:31:03.367-08:002012-12-12T15:31:03.367-08:00Arguing with a vegan online: not even once. Arguing with a vegan online: not even once. Travis Culphttps://www.blogger.com/profile/02611059005476928227noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-90892043085227303302012-12-11T14:03:00.348-08:002012-12-11T14:03:00.348-08:00"pop a pill", Huh?
You know, Pete, you ..."pop a pill", Huh?<br /><br />You know, Pete, you are one arrogant son-of-bitch.<br /><br />As I pointed out when commenting on this topic on Primal Don's blog:<br /><br />I pay no attention to "the Heiss and Tyroler criteria of causality", as they do not meet mine - which are "pro hac vice"LeonRoverhttps://www.blogger.com/profile/07219165631035107225noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-22978161157840995782012-12-11T08:52:11.322-08:002012-12-11T08:52:11.322-08:00This comment has been removed by the author.LeonRoverhttps://www.blogger.com/profile/07219165631035107225noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-80956991032450222782012-12-11T08:43:07.894-08:002012-12-11T08:43:07.894-08:00@Leon
The framingham algorithm is antique, and gi...@Leon<br /><br />The framingham algorithm is antique, and gives totally flawed risk profile, especially for young people. High SFA consumption is known to render HDL pro-inflamatory. <br /><br />LDL-C = Causal Factor influencing CHD<br /><br />HLD-C = Not causally related to CHD <br /><br /><b>Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease: A mendelian Randomization Analysis</b><br /><br /><i><b>"Background</b> LDL-C is causally related to the risk of CHD. However, the association between long-term exposure to lower LDL-C beginning early in life and the risk of CHD has not been reliably quantified" </i><br /><br /><i><b>Conclusions</b> Prolonged exposure to lower LDL-C beginning early in life is associated with a substantially greater reduction in the risk of CHD than the current practice of lowering LDL-C beginning later in life.</i><br /><br /><a rel="nofollow">http://content.onlinejacc.org/article.aspx?articleid=1379036</a><br /><br /><b>Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study</b><br /><br /><i><b>Background:</b> High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease processes, mendelian randomisation can be used to test the hypothesis that the association of a plasma biomarker with disease is causal </i>.<br /><br /><i><b>Interpretation:</b> Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.</i><br /><br />http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/abstract<br /><br />Pop your pills or go to see Esselstyn: <br /><br />http://www.youtube.com/watch?feature=player_embedded&v=SlIBGG8V8P4<br /><br /><b>Prevention of heart disease: LDL reduction is the outcome of choice? Absolutely yes.</b><br /> <br /><i><b>"There is only one well-established relationship between blood cholesterol lipid fraction and coronary artery disease (CAD) That meets all the Heiss and Tyroler criteria of causality. While there are a number of blood lipid fraction, only LDL cholesterol satisfies These criteria"</b></i><br /><br />http://www.ncbi.nlm.nih.gov/pubmed/16674358Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-69754220004741058182012-12-11T08:11:02.370-08:002012-12-11T08:11:02.370-08:00Gina Kolata'a NYT article has the following qu... Gina Kolata'a NYT article has the following quote:<br /> "First the investigators looked at variations in a well-known gene, endothelial lipase, that affects only HDL. About 2.6 percent of the population has a variation in that gene that raises their HDL levels by about 6 points."<br /><br /> "6 points" is approximately 0.155 mmol/L.<br /><br /> When one examines the Framingham data, it is clear that Risk Ratios are significantly lower at HDL levels >= 100 "points" i.e 2.6 mmol/L.<br /><br /> High HDL is a MARKER of Low Risk, it is not a Factor.<br /><br /> Whenever my physician suggests that I "should take a statin", "as your LDL is 3(mmol/L)", I point out the following:<br /> i) my HDL is 3 mmol/L, my TG is 0.5 mmol/L - thus my TG/HDL is in the lowest RR quintile<br /> ii) my HsCRP is 0.7 - thus the current clinical inflammation marker is also low<br /> iii) The NNT for statins 250 persons<br /> iv) I have no intention of laying myself open to "muscle weakness"<br /> v) I have no intention of interfering with my mevalonate production pathway - I could easily end up with liver damage.LeonRoverhttps://www.blogger.com/profile/07219165631035107225noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-51859190526271152182012-12-11T08:08:23.749-08:002012-12-11T08:08:23.749-08:00This comment has been removed by the author.LeonRoverhttps://www.blogger.com/profile/07219165631035107225noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-48303723169709603552012-12-10T21:52:49.933-08:002012-12-10T21:52:49.933-08:00@Karl,
I don't know even where to begin with...@Karl, <br /><br />I don't know even where to begin with you. I am seriously puzzled. What has Look Ahead trial to do with the lipid-theory? <br /><br />Other drugs besides statins work, and that's why resins (a bile acid sequestrant) were being used. In fact even bypass of the intestine has been used to decrease CAD events. A meta-regression curve accumulated from 108 randomized controlled trials of various medical and dietary based lipid modifying interventions has established that lowering LDL cholesterol significantly decreases the risk of coronary heart disease and all-cause mortality, independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific drugs<br /><a rel="nofollow">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/</a><br /><br />Most people who smoke do not get lung cancer, yet cigarette's are the causal factor in lung cancer. So, I have really hard time to understand your level of argumentation. Most drunk drivers never crash, it's just that so many do.<br /><br />Sucrose actually opens up the arteries in animal experiments (monkey). And probably does the same on humans. The sugar-CHD link is very weak. Traditionally cultures in Cuba, Costa Rica, Equador, etc have shown very high sugar consumption, and nevertheless low CHD rates, atleast compared to US.<br /><br />An update version of the lipid theory is nicely captured in this New York Times article from last May (2012):<br /><br />Doubt Cast on the ‘Good’ in ‘Good Cholesterol’<br /><br /><i>For purposes of comparison, the researchers also examined inherited variations in 13 genes that determine levels of LDL, the so-called bad cholesterol. It is well known and widely accepted that lowering LDL levels by any means — diet and exercise, statin drugs — reduces risk. Clinical trials with statins established with certainty that reducing LDL levels is protective. So, the researchers asked, did people who inherited gene variations that affected their LDL levels, have correspondingly higher or lower heart disease risk?<br /><br />The study found, as expected, that gene variations that raise LDL increase risk and those that lower LDL decrease risk. The gene effects often were tiny, altering LDL levels by only a few percent. But the data, involving tens of thousands of people, clearly showed effects on risk.<br /><br /><b>“That speaks to how powerful LDL is,” Dr. Kathiresan said.</b><br /><br />But the HDL story was very different" </i>.<br /><br /><a rel="nofollow">http://www.nytimes.com/2012/05/17/health/research/hdl-good-cholesterol-found-not-to-cut-heart-risk.html?_r=0</a><br /><br />Whether some benefit financially from a theory x is completely irrelevant whether that theory is valid or not. The causal link of elevated cholesterol to CHD was widely established already at the time when statin industry was non-existent.Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.com