tag:blogger.com,1999:blog-1629175743855013102.post6539853924424640555..comments2024-03-28T11:29:46.845-07:00Comments on Whole Health Source: The Diet-Heart Hypothesis: Stuck at the Starting Gate?Stephan Guyenethttp://www.blogger.com/profile/09218114625524777250noreply@blogger.comBlogger90125tag:blogger.com,1999:blog-1629175743855013102.post-79279755702084371402015-09-26T06:33:54.092-07:002015-09-26T06:33:54.092-07:00That's true Anne. It's the carbo not the ...That's true Anne. It's the carbo not the fats. <br />I was exercising, running minimum of 3k 4-5x a week without losing significant weight loss, but apparent weight loss was not tough after changing my diet to a high-meat, high-fat diet and low in carbo. I even almost stop running as before. Marcelhttps://www.blogger.com/profile/15451122565286355541noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-32519349632083526102015-04-06T00:26:14.408-07:002015-04-06T00:26:14.408-07:00Bris said:
"American Diabetes Association (2...Bris said:<br /><br />"American Diabetes Association (2008). "Nutrition Recommendations and Interventions for Diabetes". Diabetes Care 31 suppl: S61–78. doi:10.2337/dc08-S061. PMID 18165339.<br />http://care.diabetesjournals.org/cgi/content/full/31/Supplement_1/S61.<br /><br />They suggest an upper limit of 130g cabs/day. With a 65g protein intake this requires a 73% fat intake for a 2500/Cal diet. This sounds just like the Atkins "maintenance phase" to me! "<br />------<br /><br />The ADA didn't suggest an upper limit of 130 g/d of carbs. The ADA stated the RDA value of 130 g/d as a minimum amount of carbs needed to provide sufficient glucose for nervous system operation without having to rely on dietary protein and fat for glucose. It's clear from the rest of the paper that the ADA was not recommending a high-fat diet. The ADA also recommended limiting dietary saturated fat to less than 7% of total calories.<br /><br />Excerpts from the paper:<br /><br />"The recommended dietary allowance (RDA) for digestible carbohydrate is 130 g/day and is based on providing adequate glucose as the required fuel for the central nervous system without reliance on glucose production from ingested protein or fat (22). Although brain fuel needs can be met on lower-carbohydrate diets, long-term metabolic effects of very-low-carbohydrate diets are unclear, and such diets eliminate many foods that are important sources of energy, fiber, vitamins, and minerals and are important in dietary palatability (22).Anonymoushttps://www.blogger.com/profile/02151097017284865549noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-7650751765693518942014-01-05T18:41:33.197-08:002014-01-05T18:41:33.197-08:00I wouldn't use the Massai, who are pastoralist...I wouldn't use the Massai, who are pastoralists, or hunter/gatherers as examples of how, despite being on high fat/low carb diets have low cholesterol levels. The one thing you do not address is parasitic infestations. All h/g groups have them and our Paleo ancestors most certainly would have. This has the effect of lowering cholesterol levels. Why is this never mentioned? <br /><br />Saturated fat most definitely raises cholesterol levels. I can raise my cholesterol levels quite easily simply by increasing my intake of saturated fat. <br /><br />Early on in this thread someone mentioned that they had chest pains after a high-fat meal and other commenters suggested it was wheat or refined buns that accompanied the meal. Are you serious? Its the fat, not the damned muffins/buns/bread etc. <br /><br />When I was experimenting with a LCHF (Atkins) diet I eventually got to the point where I got chest pains and what I can only describe as a tingling sensation in my neck, hands, arms after a high fat meal. A typical breakfast was 3 eggs, bacon and some other meat plus some non-starchy vegetables like broccoli or green peppers plus a coffee with cream. <br /><br />I never got such a sensation (chest pains, tingling in the extremities, etc., from high carb meals. In fact, adopting a low-fat/high carb whole foods diet got rid of all those disturbing events permanently.Roberthttps://www.blogger.com/profile/10298704816309216145noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-37925074968161562242013-02-09T12:27:37.971-08:002013-02-09T12:27:37.971-08:00Certainly.
1) This person is conflating the effe...Certainly. <br /><br />1) This person is conflating the effect of PUFA with the effect of SFA. The long-term trials cited in which circulating cholesterol were durably reduced either involved a large increase in linoleic acid intake, or multiple dietary changes besides SFA. There are several long-term trials including the Women's Health Initiative and MRFIT where the expected long-term reduction in circulating cholesterol with SFA reduction was either absent or very small in the absence of a large increase in PUFA (0-3% reduction in TC or LDL).<br /><br />2) This person refers to the meta-analysis of Siri-Tiriano as "misleading". The reality is that the meta-analysis is the same thing anyone would conclude if they read the primary literature, since very few prospective studies have found a direct association between SFA intake and heart attack risk. The counterargument usually offered for the Siri-Tarino meta-analysis is that some of the studies it was based on adjusted for circulating cholesterol ("overadjustment"). However, Siri-Tarino responded to this critique by re-analyzing the data only including the studies that did not adjust for cholesterol, and found the exact same result (which is what one would expect, considering that little or no association is found between diet and circulating cholesterol in these studies). It is a fact that the best observational studies ever conducted have almost all reported no association between SFA intake and heart attack risk. This is frequently muddled by making PUFA-to-SFA ratios and the like, but I find this sort of argument unconvincing.<br /><br />3) This person cites the Health Professionals Follow-Up Study as if it supports the diet-heart hypothesis. Here is one of the key findings of the study:<br /><br />"The results of mutivariate analyses, with or without correction for measurement errors, however, indicated that intake of fiber is more strongly related to risk of coronary disease than intake of saturated fat or cholesterol, and that this largely accounts for the observed association with saturated fat"<br /><br />"Benefits of reducing intakes of saturated fat and cholesterol are likely to be modest unless accompanied by an increased consumption of foods rich in fiber"<br /><br />In other words, when you correct for fiber intake, the effect of SFA on heart attack risk basically disappears. Their words, not mine.<br /><br />They analyzed the data in various ways, and after maximum adjustment, they found that SFA intake was not associated with overall heart attack risk or fatal heart attack, and in fact some of the trends were inverse (which would have suggested a protective association if it had been significant). Rather than acknowledge these findings, this person focuses on one single number, which is the barely significant elevated risk of fatal MI in the highest quintile of SFA intake. However, the association between the two variables was not significant overall (p = 0.09). It is therefore not correct to suggest that this paper supports the idea that SFA is associated with heart attack risk, when nearly all of the data it contains do not support this conclusion.<br /><br />That's all I want to write about it for now.Stephan Guyenethttps://www.blogger.com/profile/09218114625524777250noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-42518642723486412442013-02-08T19:52:03.955-08:002013-02-08T19:52:03.955-08:00I was wondering if you could provide a rebuttal to...I was wondering if you could provide a rebuttal to this blogger who has criticized your articles on Diet-Heart:<br /><br />http://healthylongevity.blogspot.com/Anonymoushttps://www.blogger.com/profile/06207547237502514943noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-42196915549718203922011-04-02T17:53:12.066-07:002011-04-02T17:53:12.066-07:00Dr. Guyenet,
I just started reading your blog and...Dr. Guyenet,<br /><br />I just started reading your blog and it's addictive to say the least! Quick question: if PUFA drops LDL but increases the chances of it being oxidized, what percent of the calories do you suggest for it (little as possible?) Thanks in advance!<br /><br />JoshJosh Dalehttps://www.blogger.com/profile/00515465079744495469noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-75669140089040355322010-04-02T08:06:41.083-07:002010-04-02T08:06:41.083-07:00Greatly reducing my carbs doubled my HDL and decim...Greatly reducing my carbs doubled my HDL and decimated my trigs. It had little effect on my LDL. Well it increased slightly. but adding more saturated fat brought my HDL from 46.8 to 54.6 and reduced by LDL from 105.3 back to 93.6<br /><br />Doesn't matter how many papers claim this cannot happen, since this kind of change is common in the Real World (and many people do it much better than me)<br /><br />"“The deleterious effects of fat have been measured in the presence of high carbohydrate. A high fat diet in the presence of high carbohydrate is different than a high fat diet in the presence of low carbohydrate.” Richard Feinman, PhD "<br /><br />I think that's the nub of the problem - most dietary research is carried out on the basis that carbs are beneficial or at worst neutral, and they concentrate on the macronutrient changes they *think* are important while ignoring the changes that may actually be having the effect they are studying.<br /><br />Finally we're seeing papers like Mente<br /><br />http://www.natap.org/2009/HIV/042209_01.htm<br /><br />and a couple with Ron Krauss and Frank Hu<br /><br />http://www.ajcn.org/cgi/content/abstract/ajcn.2009.27725v1<br /><br />http://www.ajcn.org/cgi/content/abstract/91/3/502<br /><br />not to mention a whole bunch now looking at the connection between carbohydrate intake, glycemic index and HbA1c vs. cardiovascular diseaseAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-52266967025835502812009-11-10T22:10:55.180-08:002009-11-10T22:10:55.180-08:00To Bris, I just read the ADAs diet recommendations...To Bris, I just read the ADAs diet recommendations. They do not state that the 130 gram carb is an upper limit. It says "not less than 130 grams". Quite a different meaning. There is no upper limit. As a Type 1, I know that 130 is way to high to have normal BS control. Please re read the recomm. The ADA is still way off.Andrebocohttps://www.blogger.com/profile/10397879487399886462noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-38027540338483117762009-08-07T09:04:04.564-07:002009-08-07T09:04:04.564-07:00@Ashu
"What causes that pain is quite clearl...@Ashu<br /><br />"What causes that pain is quite clearly the amount of grease on the food"<br /><br />Why exactly is that so clear?Davehttps://www.blogger.com/profile/18290594860469294453noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-58067811857893046412009-08-06T16:42:26.056-07:002009-08-06T16:42:26.056-07:00@Jim
What causes that pain is quite clearly the a...@Jim<br /><br />What causes that pain is quite clearly the amount of grease on the food, wasn't it proved that greasy foods are metabolized differently/slower than regular, non greasy foodstuffs.<br /><br />All that grease is just going to cause that pain, steaks don't have grease and grilled chicken breasts don't neither.<br /><br />I highly doubt it's related to the bun, surely you've eaten wheat products without toast and they haven't had nearly the same effect on your body.Costanzahttps://www.blogger.com/profile/01740119812629648860noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-11133286758841499392009-07-29T12:31:31.609-07:002009-07-29T12:31:31.609-07:00LeenaS
Thanks for the clarification.LeenaS<br /><br />Thanks for the clarification.Robert Andrew Brownhttps://www.blogger.com/profile/05181027811602620374noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-85892622055420077762009-07-27T22:28:41.344-07:002009-07-27T22:28:41.344-07:00Dear Robert,
Sorry, I was inaccurate in my words....Dear Robert, <br />Sorry, I was inaccurate in my words. I was referring to one Stephan's response to Dave in this long line of comments, not his general SFA-chol hypothesis: <br /><br />Stephan wrote: "There is one mechanism whereby saturated fat might increase the amount of LDL oxidation in blood: massively increasing LDL concentration. When you feed rabbits or hamsters cholesterol and saturated fat (I don't know how well it works without the sat fat, maybe just as well), their LDL increases by some 10-fold, and oxLDL increases in parallel."<br />... and I do doubt that SFA-cholesterol connection in eatable amounts. <br /><br />The study he here refers to, is pretty awkward, even for rabbits: The rabbits were fed up to 5% of their food as chemical cholesterol dissolved in Wessen oil, which is mostly linoleic acid /ref: peters hyperlipid/. So there was the synthetic cholesterol, worth nearly 100 eggs a day for a human. And there was the processed fat from the Dood old days, with lots of LA, trans fats and dihydro-K...LeenaShttps://www.blogger.com/profile/09565398001624904475noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-42372168622447535362009-07-27T15:42:53.829-07:002009-07-27T15:42:53.829-07:00LlenaS
What is Stephans SFA-cholesterol-hypothesi...LlenaS<br /><br />What is Stephans SFA-cholesterol-hypothesis.<br /><br />Could you please expand your comment.<br /><br />Do the Masai not support Stephan's contentions?<br /><br />ThanksRobert Andrew Brownhttps://www.blogger.com/profile/05181027811602620374noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-91758391079797773632009-07-27T12:07:24.519-07:002009-07-27T12:07:24.519-07:00Dave said:
"The evolutionary diet of rodents ...Dave said:<br />"The evolutionary diet of rodents is, as far as I know, pretty low fat. It would not surprise if large quantities of fat caused a rat's LDL to go berserk, as they would not have evolved regulatory mechanisms to deal with this case."<br /><br />Actually, there is rather strong evidence that rodents go for fat, too, if the choice is given to them. See study on wild type (i.e. not lab bred) mice in this peter's post. Given the freew choice the wild mice gorged on saturated fat. And stayed ok.<br />http://high-fat-nutrition.blogspot.com/2008/09/physiological-insulin-resistance-wild.html<br /><br />The study above is one of the reasons, why I really don't buy Stephans SFA-cholesterol-hypothesis either. The other big reason is the maasai. And the third is Kwasniewski's OD, which is literally based on continuous, rich supply of SFA's and cholesterol. And which seems to be working very, very nicely, too.LeenaShttps://www.blogger.com/profile/09565398001624904475noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-51157223563052888952009-07-27T08:17:26.363-07:002009-07-27T08:17:26.363-07:00@Stephan
Agreed.
Let's consider some of the ...@Stephan<br /><br />Agreed.<br /><br />Let's consider some of the hypotheses discussed above in the context of overall metabolic regulation. One hypothesis seems to be the following:<br /><br />"Saturated fatty acids (SFA) reduce expression of the LDL receptor AND increase susceptibility of LDL to oxidation."<br /><br />The other would be<br /><br />"Polyunsaturated fatty acids (PUFA) increase expression of the LDL receptor AND increase susceptibility of LDL to oxidation."<br /><br />We have many examples where the body attempts to minimize oxidative stress. The PUFA hypothesis is in line with this: PUFA is prone to oxidation, so in response to increased dietary PUFA, the body responds by expressing more LDL receptors to clear LDL before it oxidizes. If SFA did indeed make LDL more susceptible to oxidation, in the SFA hypothesis we'd have the strange situation where the body's response to dietary SFA increases oxidative stress.<br /><br />SFA has been on the human (and proto-human) menu for a long time. PUFA probably has too, if nothing else from brains. Similar to the situation with glucose, it would appear we've evolved mechanisms to reap the benefits of the PUFA's found in foods while mitigating potential damamge.<br /><br />The evolutionary diet of rodents is, as far as I know, pretty low fat. It would not surprise if large quantities of fat caused a rat's LDL to go berserk, as they would not have evolved regulatory mechanisms to deal with this case.Davehttps://www.blogger.com/profile/18290594860469294453noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-18520929562549532412009-07-27T08:02:18.314-07:002009-07-27T08:02:18.314-07:00@Jim Purdy
You might try giving up the bread on y...@Jim Purdy<br /><br />You might try giving up the bread on your double bacon cheeseburgers.Davehttps://www.blogger.com/profile/18290594860469294453noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-33830964893209296732009-07-27T07:59:39.874-07:002009-07-27T07:59:39.874-07:00@Pinoy White Metal,
My fault - looks like I lost ...@Pinoy White Metal,<br /><br />My fault - looks like I lost track of the thread (though it probably is better to have scientific evidence if you're going to comment on somebody's food choices, at least beyond the effect on their breath :-)Davehttps://www.blogger.com/profile/18290594860469294453noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-49613713487834348042009-07-27T05:29:39.752-07:002009-07-27T05:29:39.752-07:00I hope Pinoy empathizes with my having to give up ...I hope Pinoy empathizes with my having to give up double bacon greaseburgers.jimpurdy1943@yahoo.comhttps://www.blogger.com/profile/12974301744118775363noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-23866796995838612452009-07-27T02:17:10.241-07:002009-07-27T02:17:10.241-07:00"While I empathize with the loss of your fath..."<i>While I empathize with the loss of your father, I'm afraid your loss, while tragic, doesn't provide any scientifically valid evidence for this discussion.</i> - Dave<br /><br />I'm sorry, I merely replied originally on Jim Purdy's comment about how double cheeseburgers affect him. <br /><br />I never claimed anything other than he might be harming himself by eating double cheeseburgers.<br /><br />Do you mean to say I cannot comment on Jim Purdy's choice of food unless I have scientific evidence? <br /><br />Anyway, I find Stephan's post very informative.Pinoy White Metalhttps://www.blogger.com/profile/07209368541344722152noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-58407297524088323772009-07-26T18:18:22.097-07:002009-07-26T18:18:22.097-07:00Dave,
There is one mechanism whereby saturated fa...Dave,<br /><br />There is one mechanism whereby saturated fat might increase the amount of LDL oxidation in blood: massively increasing LDL concentration. When you feed rabbits or hamsters cholesterol and saturated fat (I don't know how well it works without the sat fat, maybe just as well), their LDL increases by some 10-fold, and oxLDL increases in parallel. <br /><br />Obviously that bears little resemblance to the human situation, but it does show that if you have enough LDL floating around, it's one way to influence the total amount of serum oxLDL. oxLDL can go up in this way even if the particles themselves are more resistant to oxidation.Stephan Guyenethttps://www.blogger.com/profile/09218114625524777250noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-30675605351229791722009-07-26T16:59:42.932-07:002009-07-26T16:59:42.932-07:00@Pinoy White Metal,
While I empathize with the lo...@Pinoy White Metal,<br /><br />While I empathize with the loss of your father, I'm afraid your loss, while tragic, doesn't provide any scientifically valid evidence for this discussion.Davehttps://www.blogger.com/profile/18290594860469294453noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-22260978101671447742009-07-26T15:52:01.021-07:002009-07-26T15:52:01.021-07:00"Do you have any evidence to support this cla..."<i>Do you have any evidence to support this claim?</i> - Bris<br /><br><br /><br />Yes. I got buried evidence. My father died from a stroke a few years back.Pinoy White Metalhttps://www.blogger.com/profile/07209368541344722152noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-11501629544594231742009-07-25T13:57:28.205-07:002009-07-25T13:57:28.205-07:00Nice, discussion, though I think it highlights the...Nice, discussion, though I think it highlights the over-emphasis on a measurement (LDL) vs. searching for root cause (all the worse in the LDL case, since it often isn't directly measured). Type II diabetes provides an analogous example. You can easily measure fasting blood glucose, but chronically elevated blood glucose is not the cause of Type II diabetes, but a symptom. Idiot doctors treat it as if it were the disease, giving hyperinsulinemic Type II diabetics more insulin, which generally has no effect.<br /><br />The discussion of observations of in vitro oxidation of LDL highlight a similar hyper-focus on individual measurements, rather than a consideration of all available information. Fundamentally, saturated fat is less-easily oxidized than unsaturated. If presence of saturated fatty acids somehow increase the potential for LDL to be oxidized, one needs to propose a mechanism. It follows from basic and extremely well-established chemistry that presence of PUFA would promote oxidation of LDL: once a free radical is formed, it has the ability to oxidize other molecules. What is the mechanism by which SFA increases LDL susceptibility to oxidize?<br /><br />It is often said that absence of evidence does not imply evidence of absence, but this adage is often used in an empty context by those clinging to a hypothesis for which the evidence is absent. Rational reasoning demands that the hypothesis with greater evidence receive greater weight. You don't throw out knowledge of basic chemistry because an observation supports some other theory. That's backwards reasoning.<br /><br />We can throw evolution in the pot as well. The body has evolved to manufacture and store saturated fat. It would be absolutely bizarre to suppose that we evolved a mechanism that would increase oxidative stress, given the considerable effort organisms expend to minimize damage from oxidation. I don't think anyone is going to hypothesize that the chain length of SFA somehow affects the oxidation of LDL (any takers?).Davehttps://www.blogger.com/profile/18290594860469294453noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-20390773752184376042009-07-24T05:38:27.824-07:002009-07-24T05:38:27.824-07:00Edwin K
Jim, eating greasy bacon double cheeseburg...Edwin K<br /><i>Jim, eating greasy bacon double cheeseburgers especially if you do it on a regular basis means you are piling up on low-density lipoprotein. And from a layman's point of view, I guess you have to go easy on those kind of food or you'll find yourself in some hospital room later on down the road.</i><br /><br />Do you have any evidence to support this claim?<br /><br />Saturated fat prevents coronary artery disease? An American paradox.<br /><br />Robert H Knopp and Barbara M Retzlaff<br />American Journal of Clinical Nutrition, Vol. 80, No. 5, 1102-1103, November 2004Brishttps://www.blogger.com/profile/05771534538377496202noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-83533285716335868832009-07-23T14:59:31.345-07:002009-07-23T14:59:31.345-07:00Rahmin
You can reduce something in the blood str...Rahmin<br /><br /><br />You can reduce something in the blood stream by making more of something or using less of it.<br /><br />Healthy people make less LDL.<br /><br />Omega 6 eaters use more LDL so lowering blood LDL <br /><br />Omega 6 encourages the body to take LDL up more quickly.<br /><br />Omega 6 increases oxidisation of LDL in the blood and LDL once trapped in the vascular membrane. I suspect Omega 6 also increases the inflammatory processes in the macrophages.<br /><br />Because more LDL is taken up I guess Omega 6 eaters get higher levels of LDL trapped in the vascular structure, and higher level of oxidation and damage, so no benefit from increased Omega 6 intake in vascular disease terms which explains the stats.<br /><br />I suspect healthy people have low LDL because they make less not use more.Robert Andrew Brownhttps://www.blogger.com/profile/05181027811602620374noreply@blogger.com