tag:blogger.com,1999:blog-1629175743855013102.post1978777472386475770..comments2024-02-25T02:24:14.972-08:00Comments on Whole Health Source: Does Dietary Saturated Fat Increase Blood Cholesterol? An Informal Review of Observational StudiesStephan Guyenethttp://www.blogger.com/profile/09218114625524777250noreply@blogger.comBlogger116125tag:blogger.com,1999:blog-1629175743855013102.post-85242224550662559392017-02-28T17:04:55.828-08:002017-02-28T17:04:55.828-08:00This comment has been removed by the author.John Bedsonhttps://www.blogger.com/profile/14918934323959110083noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-89207902687920355072015-10-23T13:00:05.081-07:002015-10-23T13:00:05.081-07:00I relied heavily on articles such as this reportin...I relied heavily on articles such as this reporting on studies that found no association between saturated fat and cholesterol. I also thought the low carb, low insulin route was the way to go.<br /><br />I went three years on a very low carb, very high saturated fat diet. <br />LDL went from 105 to 305. Particle size tests were not great either. I repeated the test to be sure and got a similar result, I went on a very low fat diet for a month and my LDL dropped to 105. In both tests my insulin, sugar, triglycerides were low<br /><br />I was told by some low carb/palio authorities that in about a third of the people saturated fat will stimulate cholesterol production and by some that very low carb is not good; some insulin may play a role in cholesterol metabolism. Another low carb doc says that high cholesterol in the absence of insulin resistance is meaningless; its all about low insulin<br /><br />I just switched to a balanced diet, real food only and have not rechecked.<br /><br />Does it make a difference why you cholesterol is high? For instance, someone who has high cholesterol even on a low fat diet, because they can't metabolize it vs someone who has high cholesterol because they eat tons of fat?Anonymoushttps://www.blogger.com/profile/13362844163150469159noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-37438090385541137312015-01-29T18:20:03.968-08:002015-01-29T18:20:03.968-08:00This comment has been removed by the author.ELhttps://www.blogger.com/profile/13708894314922796037noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-33242603868147136342014-12-29T11:35:31.345-08:002014-12-29T11:35:31.345-08:00Great article Stephan. Could you please reply to t...Great article Stephan. Could you please reply to the comments about E4 and E2 genotypes? As I don't know my genotype, and I haven't seen a response, these comments worry me somewhat. Thank you.Daniel Steven Lewishttps://www.blogger.com/profile/16151550476340916710noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-75192186812652475592014-04-17T22:15:26.809-07:002014-04-17T22:15:26.809-07:00My comment is quite late, but I'm trying to ta...My comment is quite late, but I'm trying to talk to my md sister about butter and couldn't resist reacting to the study done in Japan, Hawaii, and California. I lived in Hawaii as a child in the late 50s/early 60s, and fresh food was actually quite unusual -- everything was shipped in except lettuce, since pineapple and sugar cane were the primary industries (at that time, tourism came in third). California was lush with fresh fruits and vegetables. I think a follow-up on overall dietary habits of the three locations would reveal a lot.<br /><br />Thank you for this blog.Kes Sparhawkhttps://www.blogger.com/profile/09703821947759171981noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-51759986859761242842013-11-07T00:30:29.026-08:002013-11-07T00:30:29.026-08:00Aneurysms, herniated discs, hemorrhoids, high chol...Aneurysms, herniated discs, hemorrhoids, high cholesterol, and emphysema are among the most destructive, painful, and numerous diseases in our society. Slipped or herniated discs are estimated to cost 200 billion dollars directly and indirectly each year in the USA alone ]. Four to six of 100 Americans autopsied died of a ruptured aneurysm. 3.6 to 6 percent of those examined had non ruptured brain aneurysms [Renkel]. Each year, 16,000 Americans die due to a ruptured aortic aneurysm. Of the 200,000 strokes that occur each year in the USA, 20% are aneurysms in the brain. I suspect that copper deficiency status is the most important parameter affecting them. For instance, aneurysms are produced in turkeys by depleting copper [Guenther]. Copper deficiency causes blood vessels to become weak and is probably the chief cause of hemorrhoids and varicose veins. Restoring copper during those diseases is imperative.<br /> That copper is below optimum in a large number of people is virtually certain from current evidence. Keep in mind that the MDR is designated too low to start with, as is the RDR. Young adult American women average 1.16 mg per day [Murphy] and men about 1.5. The difference between the sexes is no doubt primarily due to women eating less food than men. People in Belgium average 1.5 +/- 0.4 mg per day ]. Adolescent males, both incarcerated and free, are below the RDA [Gans] which has been set at 2.0 but should be at least 3.0. Porto Rican school lunches are below the federal RDR [Preston]. Hemodialysis patients have low copper and zinc serum levels [Komindr]. Even so, a full blown copper deficiency takes several months to develop in people with an injured digestive system, much longer than for zinc . This is because the liver stores large amounts of copper Emphysema [Soskel], premature gray hair [Wu], blood clotting [Milne 1896], slow healing bone breaks [Dolwet], diabetes enhancement [Cohen 1982] and anemia are such symptoms. The median layer of the blood vessel (where the elastin is) is thinner from a deficiency but its elastin copper content is the same as normal men. The overall thickness is not different [Senapati, et al]. Elastin is about as flexible as a rubber band and can stretch to two times its length [Carnes 1977]. The 39 or more different kinds of collagen are about 1000 times stiffer. A healthy artery requires about 1000 mm of mercury or 10 times the normal mean blood pressure in order to rupture [Shadwick]. Therefore keeping strength of arteries up would seem to be even more important than keeping blood pressure down although not necessarily so far as kidney glomeruli are concerned. However a copper deficiency coupled with high sodium (or high chloride?) causes disruption of the glomeruli basement membrane resulting in acute kidney failure [Moore].<br /> Copper nutrition is very important in herniated discs, hemorrhoids and aneurisms because copper is essential for lysyl oxidase, which enzyme cross links the elastin tissue. Cross linking is especially crucial for elastin tissue because elastin gets all of its strength from cross linking. The strength of collagen is not as badly affected because of the long length of collagen molecules. However inadequately cross linked collagen is subject to creep. <br /> The articles starting at; http://charles_w.tripod.com/copper.html would be useful to you, especially copper from food in http://charles_w.tripod.com/copper3.html <br /> A copper deficiency also produces high cholesterol [Klevay 1978] [Reiser]. Copper supplements would be infinitely superior to and safer than statin drugs for lowering cholesterol or eating low cholesterol food [Couzin]. However adding copper without zinc can actually make that situation worse [Festa]. Copper is also essential for an adequate immune system [Prohaska 1981] [Percival]. Premature babies can have too little copper. However babies should be supplemented with extreme care because they can not excrete copper, which is excreted with the bile in adults. This care includes not making formula out of water from copper pipes.<br />Anonymoushttps://www.blogger.com/profile/05069711348500228292noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-42118506273573211792013-04-25T17:51:51.647-07:002013-04-25T17:51:51.647-07:00Good to see this blog still valid after 2 years.
I...Good to see this blog still valid after 2 years.<br />I am interestes to find out more on the fake SFA'a used in experiments designed to make SFA's the preferred culprit re ill health.<br />There are some links in the responses but none of them open for me. Maybe some updates resources?<br />It's important to be able to show people how their opinions have been manipulated.<br />Currently here in OZ a university etc funded blog called "The Conversation" is discussing fats etc. so it's worth reading.<br />Anonymoushttps://www.blogger.com/profile/11230034602554254081noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-19543062629798412392013-04-08T14:51:07.006-07:002013-04-08T14:51:07.006-07:00Hi Steven,
Yes, I do not dispute the results of s...Hi Steven,<br /><br />Yes, I do not dispute the results of short-term trials, although the trials have not always supported the SFA-blood cholesterol link. See for example this large controlled study (LIPIGENE) that showed that large differences in SFA intake had no impact on LDL in overweight people:<br /><br />www.ncbi.nlm.nih.gov/pubmed/20938439<br /><br />My rationale for not including short-term trials in this discussion is that they're short term. I don't dispute the fact that SFA can impact blood cholesterol in the short term, but the question I'm asking is "does this effect persist in the long term"? Hence my interest in observational studies that look at the relationship between SFA intake and cholesterol over several years. Stephan Guyenethttps://www.blogger.com/profile/09218114625524777250noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-36631379596268928252013-04-05T15:10:59.753-07:002013-04-05T15:10:59.753-07:00Dr., if you get aroudn to following this up - here...Dr., if you get aroudn to following this up - here is a review of control trials:<br />http://www.ncbi.nlm.nih.gov/pubmed/12716665<br /><br />Perhaps you'd include your rationale to exclude these results - 12-91 day feeding trials. Anonymoushttps://www.blogger.com/profile/11100863479518981035noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-25057628941660620612012-08-05T09:51:48.894-07:002012-08-05T09:51:48.894-07:00Hi Steven,
Thanks for your great summary. I have ...Hi Steven,<br />Thanks for your great summary. I have to agree with Davide Palmer. I'd love to see a reanalysis based on APOE4 genotype because of its role in cholesterol transport. It may also be important to look at APOE2 as well. <br /><br />There may also be other important interactions, perhaps gender, age other genes or lifestyle factors that need to be more thoroughly examined. The problem is most epidemilogical studies is that sample sizes are often not large enough to support the variety possible interactions that can occur.Anonymoushttps://www.blogger.com/profile/11208984188387296302noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-27879990877953054592012-07-25T08:16:54.431-07:002012-07-25T08:16:54.431-07:00The study stephen points to in 2010 in footnote # ...The study stephen points to in 2010 in footnote # 3 regarding saturated fat not leading to heart disease did not take into account if the group(s) of people studied were on statin drugs or not. one of its authors Krauss has had money support from the Atkins diet group & the meat industry. That study therefore is null. Scientists & the medical community at large acknowledge saturated fat does cause a increase in ldl.Of course if diet involves a lot of fibre(fruits,vegetables,whole grains like oatmeal,legumes) a lot of ldl can be absorbed in the intestinal track should one eat large amounts of sat. fat & thus eliminated away as waste when you go to the washroom.Love those carbs !kalbertinihttps://www.blogger.com/profile/01960273722074893772noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-49645720799317989362012-03-12T15:11:11.518-07:002012-03-12T15:11:11.518-07:00I believe the basis for the idea that saturated fa...I believe the basis for the idea that saturated fat increases blood cholesterol is the role bile acids play in fat catabolism. Though cholesterol catabolism is mediated largely through the bile acid pathway, it is theorized that when there is excess triglyceride consumption, cholesterol is overproduced by the liver, overshooting the amount of cholesterol that will be degraded to form bile acids to catabolize (or really transport and make soluble for catabolism) these aforementioned triglycerides.<br />I'm writing a series on avoiding atherosclerosis and this is actually one of the questions I encountered in my research.Cys Leu Glyhttps://www.blogger.com/profile/07694553037727054977noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-83937020236293700242012-03-04T23:56:47.231-08:002012-03-04T23:56:47.231-08:00Just came across this study, thought you might fin...Just came across this <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2753.2011.01767.x/full" rel="nofollow">study</a>, thought you might find it interesting.<br /><br />"Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study"<br /><br />Petursson, Sigurdsson, Bengtsson, Nilsen, Getz<br /><br />Journal of Evaluation in Clinical Practice, Volume 18, Issue 1, pages 159–168, February 2012<br /><br />Another link <a href="http://www.ncbi.nlm.nih.gov/pubmed/21951982" rel="nofollow">PubMed</a><br /><br />Seems to indicate that for women, there's no such thing as too much total cholesterol for all-cause mortality and overall cardiovascular disease (which I think they are using to include strokes), and only slight ischaemic heart disease detrimental effects from even very high total cholesterol. Even for men, it seems the best range is between 195 and 230 mg/dl.<br /><br />The U-shaped graphs seemed different than the red-yellow-green table, however, so I am not sure I am interpreting the study correctly, since the table seems to indicate that men, too, have the best outcomes for any total cholesterol over 214 mg/dl (5.5 mmol in their chart), while the graphs seemed to indicate men had an upper limit beyond which their risk increased.stephershttps://www.blogger.com/profile/04753415893464809905noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-60444535130975406412011-10-28T16:55:56.398-07:002011-10-28T16:55:56.398-07:00It's clear that cholesterol, HDL mostly, does ...It's clear that cholesterol, HDL mostly, does some protective things. There is some evidence that bacteria and viruses damage or infect the cells in the walls of the artery. Combine that with a high-inflammation, highly-oxidizing American diet and you have the perfect storm.Dave Jameshttps://www.blogger.com/profile/14598132711777814936noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-56731679559470405822011-10-27T16:38:43.877-07:002011-10-27T16:38:43.877-07:00Hi I've not posted before, but following up on...Hi I've not posted before, but following up on cholesterol being protective.. perhaps we are ingesting chemicals/foods our body has not evolved with and so does not cope with well. To protect the lining of our arteries it produces and lays down cholesteral as a protective mechanism. Too much of this ends up restricting arteries and casugin a problems. So the cause is the foods/chemicals our body does not want (varied and related to genotype), the defense and eventual symptom is excessive colesterol production??Alisonhttps://www.blogger.com/profile/10878137777999289318noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-86993047455700423142011-07-16T22:05:06.283-07:002011-07-16T22:05:06.283-07:00Hello, I am 51. I have 2 stents. My first in 2003....Hello, I am 51. I have 2 stents. My first in 2003. I didn't want to believe it was SATFATS, so I found comfort in WAPF and Anthony Colpo. But, here I am, 2011 and I just had another stent put in after a mild MI.<br /><br />Sure, I ate the butter and steaks BUT and here is where I went wrong since 2003. I ate the white flour, sugar and plant oils.<br /><br />I am currently following Dr. Esselstyn's program for reversing heart disease. Plants, fruits and whole grains. No oils of any kind. No nuts. No meat. No dairy.<br /><br />The book says that if I follow this I will CURE my CVD and maybe even reverse some of it.<br /><br />So far, (1 month) I have lost 15 lbs. I am taking a statin and the usual heart meds.<br /><br />I miss eating meat. Trust me. I am not doing this because I am against meat and satfats. But, Dr. E makes a great case against satfats and its effects on the endothelium. Damage it enough and the the beginnings of plaques will appear.<br /><br />I dunno. I am at a loss. I WISH I had not ignored the warnings of PLANT OILS and FLOUR. if I had not consumed those since my first stent, then maybe I would have an argument against satfats in meat.<br /><br />So here I am a reluctant vegan afraid to eat meat of any kind. What do you folks think? Am I needlessly avoiding meat? Can you recommend I consume meat at this point?<br /><br />DaveDave Jameshttps://www.blogger.com/profile/14598132711777814936noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-42892726481019207102011-05-31T18:02:42.504-07:002011-05-31T18:02:42.504-07:00Here's Dr. Martijn Katan's conflict of int...Here's Dr. Martijn Katan's conflict of interest statement from a 2007 paper:<br /><br />The author has three projects funded by the Wageningen Centre for Food Sciences, an alliance of major Dutch food industries, research institutes, and the Dutch government. None was involved in this editorial. In the past 25 years he has received funding or research materials from Unilever, Nestlé, the Netherlands Dairy Organization, Campina BV, Friesland Foods, the European coffee industry, and the olive oil council, and he has spoken at expenses-paid meetings of these industries, as well as the tea council and the chocolate industry. He sometimes gives unpaid informal advice to colleagues in the food industry. He does not consult or testify for industries, accepts no money or gifts beyond a bottle of wine or book token, and has no stocks or other financial interests in food or beverage companies.<br />(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1761050/)<br /><br />Do I discount his research because he's worked extensively with industry? No. I just note it in the back of my mind and consider his papers on their own merit.Stephan Guyenethttps://www.blogger.com/profile/09218114625524777250noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-35802055006567881892011-05-31T14:09:50.354-07:002011-05-31T14:09:50.354-07:00Hi T,
I object to your suggestion that Dr. Krauss...Hi T,<br /><br />I object to your suggestion that Dr. Krauss is biased due to his (former) ties to the dairy industry. That is a totally unfounded and unprofessional personal smear that Krauss handily dismissed in his response to Dr. Katan. Did you know that Katan receives funding from Unilever, Nestle, the Olive oil council and other commercial sources with a vested interest in promoting plant oils? Unilever has been a major funding source for Katan. Who represents the "industry influenced model", Krauss or Katan? If you want to criticize people for their industry ties, you have to do it consistently rather than pick and choose, and Katan is certainly more in bed with them than Krauss. I wasn't going to bring it up because I don't think it's that relevant, but people who live in glass houses shouldn't throw stones...<br /><br />I find it disturbing that you continue to cite the Health Professionals follow-up study to support your position despite the fact that there was no statistically significant association between SFA intake and any measure of CHD after maximum adjustment. If there were really a relationship between the two factors, you wouldn't have to cite non-significant findings to support your position.<br /><br />The Nurses health study paper you cited is interesting, but they didn't look at SFA. We're talking about SFA here.<br /><br />What Krauss (and others) have found in their meta-analyses is that SFA consumption isn't associated with CHD risk, but refined carbohydrate is. Others have used mathematical models (which frankly I find questionable since they're purely hypothetical and rest on some big assumptions) to hypothesize that replacing SFA with PUFA would reduce risk. But that makes no sense. If your true goal is to reduce risk, why would you replace something that's statistically harmless (SFA) rather than something that's statistically harmful in the same studies (refined carbohydrate)? Why do they keep focusing on a SFA-PUFA swap when their own models predict that a carb-PUFA swap would be more effective? Answer: because they are desperately wedded to the idea that SFA are harmful, and they will try their best to implicate it even in the absence of evidence to support that position.<br /><br />I just read the review paper that you lauded at the end of your comment. I can't say it's quite as supportive of your position as you make it out to be. You like good measurement methods, so let's focus on the two studies that did 7-day weighed food records, the Bankers study and the Caerphilly study. The first found no association between animal fat intake and serum cholesterol across a several-fold variation in intake. The second found a significant but extremely weak association between SFA intake and serum cholesterol. "The percentage of variance in the plasma lipid concentrations which could be explained solely by the dietary variables was very small, ranging from 1 to 7 per cent". That sounds quite consistent with the conclusions of my post.<br /><br />However, there were a few studies in the review article you cited that I missed in my post. I'm going to have to look these up and read them in detail. I may end up re-writing this post if I feel it needs it.Stephan Guyenethttps://www.blogger.com/profile/09218114625524777250noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-87055908212525266062011-05-29T09:01:58.400-07:002011-05-29T09:01:58.400-07:00Saturated fatty acids (SFA) are associated with ex...Saturated fatty acids (SFA) are associated with excess coronary heart disease (CHD) mortality regardless of whether one uses Krauss’s industry influenced model where the SFA-CHD relationship is intentionally attenuated by comparing SFA primarily to refined carbohydrates, including invalidated dietary measurement methods and adjustments for dietary and serum lipids, or the model of isocaloric substitution with PUFA in the pooled analysis of validated prospective studies. <a href="http://www.ajcn.org/content/91/3/497.full" rel="nofollow">1</a> <a href="http://www.ajcn.org/content/early/2009/02/11/ajcn.2008.27124.full.pdf" rel="nofollow">2</a><br /><br />It is clear beyond reasonable doubt that a lower intake of any caloric source including SFA implies an increased intake of some other source of calories in order to maintain caloric balance, and that different substitutions for SFA have different effects on CHD risk. Therefore the SFA-CHD relationship can only be appropriately examined by comparing SFA with specific caloric sources, including PUFA and complex carbohydrates. Your claims that there exists such a thing as an independent effect of SFA or PUFA are flawed, and your reviews of epidemiological studies comparing SFA to a baseline diet characterized by processed junk food fails to be very informative.<br /><br />I consider the paper from the Nurses Health Study the most informative study in regards to the relationship between diet and CHD risk because other studies only focused on substituting macronutrients, whereas this study showed the effect of substituting one serving of food for another and the risk of CHD which is influenced by multiple simultaneous changes of both macronutrients and micronutrients. Although the results of this study cannot show a causal relationship between individual nutrients and CHD, it does indicate an association between, as I worded it “foods rich in” certain nutrients (including SFA) and CHD risk.<br /><br />The focus of the paper from the Health Professional Follow-up study was the relationship between dietary fat and CHD risk, not the use of a well standardized method to assess the relationship between diet and serum cholesterol. In this study the top vs lowest fifth intake of SFA (a difference of only 16 gm) and dietary cholesterol was associated with a 72% and 25% increased risk of fatal CHD respectively. Also replacing SFA with PUFA was significantly associated with a lower risk of CHD mortality in the longer follow-up of this study included in the pooled analysis.<br /><br />The primary source of MUFA in Norfolk is undoubtedly meat and dairy (apposed to vegetable oils used in dietary experiments), and therefore MUFA would have strongly correlated with SFA intake and therefore with LDL-C in the Norfolk study. It is notoriously difficult for researchers to compare MUFA with other sources of calories in observational studies due to this limitation, and is indicated as a likely reason why MUFA was associated with an excess risk of CHD in the pooled analysis.<br /><br />You mentioned virtually nothing about the limited ability to evaluate the validity of dietary data on free-living people, or the high intraindividual variability that results from single measurements of diet and blood cholesterol concentration. Half of the studies you cited used an invalid single 24 hour recall to measure diet, yet you failed to mention this as a possible limitation. Furthermore numerous studies within the two meta-analyses of dietary interventions I previously cited supporting the association between SFA and serum cholesterol were long term lasting up to several years.<br /> <br />A significantly more in depth review of epidemiological studies clearly challenges the content of your post, including a far greater number of studies, and describes the limitations and strengths of various types of studies. It also included studies showing an association between decreases of SFA intake with significant decreases in serum cholesterol and CHD at a population level.<br /><a href="http://www.ajcn.org/content/65/5/1597S.full.pdf" rel="nofollow">3</a>Thttps://www.blogger.com/profile/17751695901424716714noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-44066300922932757232011-05-16T12:09:21.131-07:002011-05-16T12:09:21.131-07:00Hi T,
I just looked at the Nurse's health stu...Hi T,<br /><br />I just looked at the Nurse's health study paper you referenced in support of the hypothesis that SFA contributes to CHD, calling it "probably the most informative paper to date". That paper did not even examine the association between SFA and CHD. <br /><br />Contrary to what you said, the Blue Mountain Eye study did not find any association whatsoever between SFA intake and TC/LDL. What they found was an association between TC/LDL and a CHANGE in SFA intake over time. That result is difficult to interpret due to the fact that in the same study, people who consistently ate more SFA didn't have higher TC/LDL than those who consistently ate less. <br /><br />You seem to have a tendency to misrepresent findings to support your position. I want to be clear with you, I will not tolerate that on this blog.<br /><br />The Framingham Offspring study paper you cited appears to support your position. They did find an association between SFA intake and TC/LDL. I'll add that to my post in an update. It's curious that the original Framingham study didn't see that.Stephan Guyenethttps://www.blogger.com/profile/09218114625524777250noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-52831979926967898592011-05-16T11:12:21.568-07:002011-05-16T11:12:21.568-07:00Hi T,
Let me put this plainly: I have reviewed th...Hi T,<br /><br />Let me put this plainly: I have reviewed the observational studies in detail, and you would have to be totally out of your mind to think that overall, they support a SFA-CHD association. Nearly every single one found no association whatsoever. The meta-analysis by Krauss's group only confirmed what was obvious to anyone who had even casually glanced at the studies-- which is a small minority of people.<br /><br />They way people who have a vested interest in the SFA-CHD story try to get around the lack of association is by moving the goalposts: instead, we'll measure the Keys dietary score, calculate SFA/PUFA ratios, or we'll run mathematical models where we hypothetically substitute one nutrient for another. Here's the logic: since PUFA intake is inversely associated with CHD in many studies, if we make a ratio with SFA, we'll get a significant result that will allow us to indict SFA! Even though the significance comes entirely from the PUFA side of the model and has nothing to do with SFA.<br /><br />I'm sorry, but that's baloney and it's misleading. That's not how epidemiology works. What you do is you examine if people who eat more SFA have more heart attacks than people who eat less, while controlling for other variables-- and the studies have nearly all found no association. That's how epi works in other disciplines. Moving the goalposts to Keys score, SFA/PUFA ratios and using fancy math to model nutrient substitutions will only fool people who don't know any better or are desperate to believe that there's an association. <br /><br />The point of my post was to point out that there is no good evidence for a long-term association between SFA intake and serum cholesterol. There was nothing in your comment that challenged that. The meta-analysis you cited in support of the idea that SFA increases serum cholesterol was done using studies with a median length of one month! That's exactly the point of this post-- you can't extrapolate from one month to ten years. <br /><br />I hadn't seen the EPIC Norfolk data so thanks for pointing that out. They did find a SFA-LDL association, although it was weak. They also found that MUFA intake is associated with higher LDL. Do you believe that MUFA increases LDL?<br /><br />Your characterization of the health professionals follow-up study is incorrect. After maximum adjustment, there was no association between SFA intake, CHD, fatal CHD or any other CHD-related outcome. This makes it consistent with virtually every other study conducted on the matter. See table 1 for the association between SFA and serum cholesterol (hint: there is none):<br /><br />http://www.bmj.com/content/313/7049/84.fullStephan Guyenethttps://www.blogger.com/profile/09218114625524777250noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-1660476559215493932011-05-14T12:01:30.492-07:002011-05-14T12:01:30.492-07:00Excellent article, Stephan. I wish the most outsp...Excellent article, Stephan. I wish the most outspoken doctors who support the lipid hypothesis would admit to the public that no one has a complete understanding of the mechanisms behind the progression of coronary artery disease . To do so would require a complete understanding of human cellular metabolism.<br /><br />There is far too much dogma in medicine, rather than sceince. I applaud Dr. Ravnskov for questioning this.<br /><br /><br />Excellent point , Jenny above :)<br /><br /><br />Take care,<br /><br />RazAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-37021781832686036212011-05-14T00:07:53.108-07:002011-05-14T00:07:53.108-07:00A 1997 meta-analysis included numerous additional ...A 1997 meta-analysis included numerous additional observational studies and national statistics publications in regards to the relationship between saturated fat and serum cholesterol that are not mentioned in Stephan’s analysis.(5)<br />Many of these studies found that either SFA, the SFA/PUFA ratio, Keys score or dietary cholesterol were significantly associated with serum cholesterol, including the Scottish Heart Health Study (8,000+ participants), Caerphilly Prospective Study (653 men), Costa Rica Study (202 M, 174 F), CARDIA Study (depending on age, sex and ethnicity, 4000+ participants), Puerto Rica Study (5803 participants), Ireland-Boston Diet-Heart Study (1001 participants), and the Framingham study (of which a significant amount of information has been published).(5)<br />The authors discuss the significant limitations of the use of observational studies, concluding that accurate valid and well-standardized methods are required to assess both diet and serum lipids, and single measurements of either diet or serum lipids significantly reduces the true association. Stephan cited several studies that used invalidated dietary measurement methods such as single 24-hour dietary recalls, which poorly measure habitual dietary intake and tend to fail to find a relationship between any nutrient and serum lipids.(5) Nevertheless it appears Stephan favors such studies over dietary experiments conducted under controlled conditions, precisely measuring dietary intake. A meta-analysis of 395 such dietary experiments found a significant relationship between SFA and unfavorable changes to LDL/HDL ratio compared to unsaturated fats.(6)<br /><br />In regards to the Western Electric Study, there was a non-significant positive relationship between SFA and CHD after adjusting for serum cholesterol (11% increase), indicating the likelihood of a significant relationship in unadjusted results. Also a 200mg/1000kcal decreased intake of dietary cholesterol was associated with a 34% lower risk of all cause mortality.(7)<br /><br />In the study on Japanese in Japan, Hawaii and California (Ni-Hon-San Study), studied as a group the average cholesterol was 181, 218, and 228 mg/dl for men living in Japan, Hawaii and California, respectively. CHD mortality was 1.7 times higher in Hawaii and 2.8 times higher in California than in Japan, and was associated with an increased intake of SFA.(5)<br /><br />The Health Professional Follow-up Study does not seem to provide any information in regards to participants SFA intake and serum cholesterol levels, and is definitely not the most recent study. The researchers found a significant relationship between saturated fat and a borderline significant relationship for dietary cholesterol and fatal CHD after maximum adjustment.<br /><br />A 2007 paper from the EPIC Norfolk Study with 22,915 participants is perhaps the largest observational study examining diet and serum cholesterol, and found a significant relationship between SFA and serum cholesterol.(8) Other studies that have found a positive relationship between SFA and serum cholesterol include the Blue Mountain Eye Study and the Framingham Offspring Study.(9,10)<br /><br />A new paper published in April from the Whitehall II Study including 4,469 participants found a significant inverse relationship between the PUFA/SFA ratio and LDL cholesterol.(11)<br /><br />A 2007 review including 10 dietary intervention studies not designed for weight loss and with a minimum follow up of 3 months found a significant relationship between a decreased SFA intake and lower serum cholesterol.(12)<br /><br />5. http://www.ajcn.org/content/65/5/1597S.full.pdf<br />6. http://www.bmj.com/content/314/7074/112.abstract<br />7. http://www.ncbi.nlm.nih.gov/pubmed/3052353<br />8. http://eurheartj.oxfordjournals.org/content/28/23/2930.full.pdf<br />9. http://jn.nutrition.org/content/140/1/88.full.pdf<br />10. http://www.ncbi.nlm.nih.gov/pubmed/8656227 <br />11. http://heart.bmj.com/content/early/2011/04/12/hrt.2010.216309.full.pdf<br />12. http://www.cfah.org/hbns/archives/viewSupportDoc.cfm?supportingDocID=468Thttps://www.blogger.com/profile/17751695901424716714noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-15058219315569813412011-05-13T23:53:04.300-07:002011-05-13T23:53:04.300-07:00Top researchers have criticised the meta-analysis ...Top researchers have criticised the meta-analysis of prospective studies cited by Stephan showing the relationship between saturated fat acids (SFA) and coronary heart disease (CHD) due to serious flaws and omissions.(1-3) As Katan MB correctly pointed out, “the notion that there exists such a thing as ‘the effect of saturated fat’ is flawed. A lower intake of saturated fat implies an increased intake of some other source of calories to maintain caloric balance. Different substitutions for saturated fat have different effects on risk of coronary heart disease and need to be discussed separately.”(2)<br /><br />Two of the original authors (Sun Q, Hu FB) have since admitted that the conclusions of this meta-analysis were flawed, stating that “in this meta-analysis saturated fat was compared with other calorie sources, primarily refined carbohydrates, and high intake of refined carbohydrates has been associated with a high risk of CHD.”(3) It would only be expected that a significant association would not be found when replacing SFA with other calorie sources that also have unfavorable effect on serum lipids and associated with an increased risk of CHD. The authors failed to disclose this critical information, just as the senior researcher Krauss RM failed to disclose receiving grants from the National Dairy Council, the National Cattleman’s Beef Association, and the Robert C. and Veronica Atkins Foundation.(2)<br /><br />This meta-analysis actually included adjustments for serum and dietary lipids, including serum (blood) cholesterol and dietary cholesterol, clear over-adjustments making Stephan’s remarks clearly unfounded in regards as to whether this study supports the relationship between SFA and higher serum cholesterol, and therefore a higher risk of CHD. As Stamler J pointed out in the editorial to this meta-analysis, “Of 15 studies that unequivocally concern the SFA-CHD relation, 4 did not include other dietary lipids or serum lipids among covariates. Their CHD relative risks (RRs) ranged from 1.22 to 2.77—ie, >1.07, which was the estimated CHD RR in the meta-analysis”.(1)<br /><br />Katan MB pointed out that “About half of the studies used 1 d dietary assessments or some other unvalidated method”.(2) These studies inaccurately measured habitual dietary intake and attenuated the SFA-CHD relationship found in the meta-analysis. Such studies can certainly not be classed as being “high quality”, and as Stamler J stated, “Five [studies] used dietary history or multiday food record; the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids”(1)<br /><br />Very importantly, saturated fat was associated with an overall 32% increased risk of fatal heart disease despite adjusting for dietary and serum lipids, suggesting that other factors beyond serum lipids may also promote the SFA-CHD relationship.(1)<br /><br />A pooled analysis of 11 cohort studies showed the relationship of replacing SFA with other macronutrients on the risk of CHD while using consistent adjustments, and limited the inclusion of studies only to those with “availability of usual dietary intake, and a validation or repeatability study of the diet-assessment method used”.(4)<br />This pooled analysis of actual high quality studies found a significant decreased risk of total and especially fatal heart disease when saturated fat was replaced with polyunsaturated fat, despite adjusting for dietary cholesterol.<br /><br />Probably the most informative paper to date is from the 26 year follow-up of 84,136 nurses, the only major study to show the effect of substituting actual food (containing both macro and micronutrients) and the risk of CHD. This study is inline with the literature and the recommendation to replace foods rich in SFA and cholesterol with unprocessed foods rich in unsaturated fats, fiber and antioxidants.(3)<br /><br />1. http://www.ajcn.org/content/91/3/497.full<br />2. http://www.lbs.co.il/showpost.php?p=233292&postcount=7<br />3. http://circ.ahajournals.org/cgi/reprint/122/9/876.pdf<br />4. http://www.ajcn.org/content/early/2009/02/11/ajcn.2008.27124.full.pdfThttps://www.blogger.com/profile/17751695901424716714noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-81814409558303594102011-03-19T22:21:09.758-07:002011-03-19T22:21:09.758-07:00PS - good predictor of heart disease is waist to h...PS - good predictor of heart disease is waist to hip circumference ratio. -Eat an apple a day to keep the apple waistline away - as well as the doctor. Add a carrot and keep the cancer surgeon away. Both very good foods for building healthy glyoccalyx.Anonymoushttps://www.blogger.com/profile/13365960633971341081noreply@blogger.com