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Hi Lulu, I see you keep removing negative content from this page - is there any particular reason why we shouldn't cover the reaction to Demasi's recent Catalyst show? 220.127.116.11 (talk) 08:42, 21 November 2013 (UTC)
- Lulu can you please point out your reasons for reverting here so we can discuss the merits of your edits?18.104.22.168 (talk) 23:40, 21 November 2013 (UTC)
If this page is any representation of standard practice here, it's frankly scary what passes for neutrality on Wikipedia - and with shockingly little research or critical thought into the actual issues that are being contested by this person's work - or what it might really mean that Marianne's work has been criticized and attacked. Marianne Demasi's review of the cholesterol hypothesis actually provided opportunity for rebuttal from those physicians and industry groups still in hock to the notion that cholesterol and/or saturated fat really is the 'villain' in cardiovascular disease. Industry spokespersons also had a chance for rebuttal but declined to participate. The fact of the matter is that big Pharma has systematically distorted the evidence base for and against the notion that lowering LDL cholesterol necessarily lowers risks for heart disease. The pushback against her video emerged mostly from people who were thoroughly in hock to statin manufacturers, or to the associated doctrine that saturated fat causes heart disease – despite the recent emergence of enormous evidence against those linked hypotheses, and also despite the evidence that statins really are minimally protective against heart disease with a few exceptions. So the notion that this biography page provides a balanced assessment of her contributions is itself biased. I have to wonder if those committed to posting negative reviews of her work are also industry spokespersons, receiving money from big Pharma, or otherwise financially motivated or otherwise invested in discrediting her work for reasons that they may be embarrassed or otherwise reluctant to disclose.
As someone who has written multiple textbook chapters on this subject (the relationship between inflammation and the diseases of aging) and taught at two Boston area medical schools, I thought Marianne Demasi did a quite credible job of introducing the public to the evidence against what has been presented for decades as scientific fact that in fact is simply an entrenched doctrine with a shockingly minimal evidence base – that cholesterol is the cause of heart disease. Cholesterol does not cause heart disease, inflammation and oxidative stress on the other hand look much closer to its core etiologic mechanisms. Oxidized cholesterol is the primary trigger for vessel irritation, subsequent invasion by macrophages, and a whole cascade of negative effects from there. Minus oxidation of LDL and minus any subsequent inflammatory stimulus, coronary artery disease simply doesn't happen, and the research base behind this more inflammatory view of coronary artery disease is now far more compelling than any prior notion of passive sludging of arteries from cholesterol. The passive sludging notion of heart disease is in fact dead in the water.
It's really a shame when people don't do their homework, simply don't know the basic science, and therefore really can't evaluate whether someone's work is credible or not, and also therefore whether her critics are credible. The problem frankly is that Wikipedia reviews oftentimes don't discriminate between good research and popular but unsupported assumption. 22.214.171.124 (talk) 19:36, 18 December 2013 (UTC)
- You are more than welcome to help improve this article by providing reliable sources where Demasi's work was defended. --NeilN talk to me 20:39, 18 December 2013 (UTC)
here's just a sampling of material on this:
Adv Nutr. 2013 May 1;4(3):294-302. doi: 10.3945/an.113.003657. Dietary fats and health: dietary recommendations in the context of scientific evidence. Lawrence GD. Author information Abstract
Although early studies showed that saturated fat diets with very low levels of PUFAs increase serum cholesterol, whereas other studies showed high serum cholesterol increased the risk of coronary artery disease (CAD), the evidence of dietary saturated fats increasing CAD or causing premature death was weak. Over the years, data revealed that dietary saturated fatty acids (SFAs) are not associated with CAD and other adverse health effects or at worst are weakly associated in some analyses when other contributing factors may be overlooked. Several recent analyses indicate that SFAs, particularly in dairy products and coconut oil, can improve health. The evidence of ω6 polyunsaturated fatty acids (PUFAs) promoting inflammation and augmenting many diseases continues to grow, whereas ω3 PUFAs seem to counter these adverse effects. The replacement of saturated fats in the diet with carbohydrates, especially sugars, has resulted in increased obesity and its associated health complications. Well-established mechanisms have been proposed for the adverse health effects of some alternative or replacement nutrients, such as simple carbohydrates and PUFAs. The focus on dietary manipulation of serum cholesterol may be moot in view of numerous other factors that increase the risk of heart disease. The adverse health effects that have been associated with saturated fats in the past are most likely due to factors other than SFAs, which are discussed here. This review calls for a rational reevaluation of existing dietary recommendations that focus on minimizing dietary SFAs, for which mechanisms for adverse health effects are lacking.
Clin Sci (Lond). 2013 Sep;125(5):221-35. doi: 10.1042/CS20120576. Immunological aspects of atherosclerosis. Woollard KJ. Author information Abstract
Cardiovascular disease is the leading cause of death in several countries. The underlying process is atherosclerosis, a slowly progressing chronic disorder that can lead to intravascular thrombosis. There is overwhelming evidence for the underlying importance of our immune system in atherosclerosis. Monocytes, which comprise part of the innate immune system, can be recruited to inflamed endothelium and this recruitment has been shown to be proportional to the extent of atherosclerotic disease. Monocytes undergo migration into the vasculature, they differentiate into macrophage phenotypes, which are highly phagocytic and can scavenge modified lipids, leading to foam cell formation and development of the lipid-rich atheroma core. This increased influx leads to a highly inflammatory environment and along with other immune cells can increase the risk in the development of the unstable atherosclerotic plaque phenotype. The present review provides an overview and description of the immunological aspect of innate and adaptive immune cell subsets in atherosclerosis, by defining their interaction with the vascular environment, modified lipids and other cellular exchanges. There is a particular focus on monocytes and macrophages, but shorter descriptions of dendritic cells, lymphocyte populations, neutrophils, mast cells and platelets are also included.
So I have to conclude (after reading much of this literature and summarizing some of it in a recent textbook chapter) that the pushback against Demasi is in part political (coming from threatened vested interests and associated financial motives), and in part coming from the intrinsic resistance to the changing of well-entrenched doctrines. The weight of evidence, which is really the only standard in science, is in favor of what she described. Although she was harshly criticized for hyperbole, one could have made far harsher statements than she offered about the destructive effects of well-entrenched myths defended by powerful special interests.
- Please see WP:SYNTH and WP:OR (which your speculations are). Again I ask, do you have any sources directly and specifically defending Demasi? --NeilN talk to me 03:34, 19 December 2013 (UTC)
You are not listening. This is not original research. This is simply reporting the findings of other researchers. It also is not a 'speculation' (as you dismissively term it) at this point to suggest that coronary artery disease is directly related to auto-inflammatory processes. I think this discussion is truly pointless. If you want to check this out, perhaps a brief tour of Medline/PubMed using key words 'inflammation' and 'heart disease' or 'CAD' would be instructive and educational for you, if you are interested in learning about it. Since you don't want to listen to me, perhaps you'll listen to someone else. You are clearly not in the biological sciences, and therefore (I have to believe) don't really understand how science works. It's not a question of whether original sources DEFEND Damasi's work in some explicit fashion. You really have it upside down. It's a question as to whether emerging work and the vast, confusing body of material about CAD from hundreds of original sources are - IN TOTO - more consistent with her summary or whether they are not. Original sources don't ever reference or address TV programs(!). It's astonishing that you would think that. Clearly, the difference here is between someone who "does Wiki" and someone who does serious science. These are not the same skill set, or mind set, or even way of writing about material.
- Couple things. "So I have to conclude (after reading much of this literature and summarizing some of it in a recent textbook chapter) that the pushback against Demasi is in part political (coming from threatened vested interests and associated financial motives), and in part coming from the intrinsic resistance to the changing of well-entrenched doctrines." is speculation. And I did not ask for "original sources", I asked for reliable sources. These can be media interviews with experts or statements from well-known organizations defending Demasi's position. --NeilN talk to me 18:17, 19 December 2013 (UTC)