Will the Popularity of LCHF Trigger a New Epidemic of Heart Disease?

Diets low in carbohydrate and high in fat (LCHF) have become increasingly popular lately. Many experts in the field of epidemiology and cardiovascular disease have expressed grave concern and warned that this change in dietary pattern may increase the risk of heart disease. Some have argued that LCHF poses a threat to public health in many countries around the globe.

Will the Popularity of LCHF Trigger a New Epidemic of Heart Disease?

A recent increase in butter consumption may reflect the magnitude of the problem and is by many considered alarming. Butter consumption hit a 44-year high in 2012, according to US government data, while margarine is at a 70-year low. In Germany today, butter outsells margarine by a three-to-one margin, and the gap is widening. A similar increase in butter consumption is reported in Scandinavia and many other European countries.

Although butter fits well with an LCHF lifestyle, choosing butter may also reflect the fact that people are changing their perception of food and searching for healthier alternatives. They’re moving away from highly processed foods and artificial ingredients.

The question whether LCHF is harmful or not touches the core of our understanding of the causes of heart disease and the reasons for the so-called coronary heart disease (CHD) epidemic. That’s why this debate is both important and challenging. Let me tell you why so many specialists believe LCHF may be harmful. Then, maybe you can have your say on the issue.

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The Coronary Heart Disease Epidemic

For the past 60 years, CHD has been a major health concern. Although initially most prominent in high income countries, today over 80% of the world’s deaths from cardiovascular disease occur in low and middle-income countries. An estimated 17.3 million people died from cardiovascular diseases in 2008, representing 30% of all global deaths. Of these deaths, an estimated 7.3 million were due to CHD and 6.2 million were due to stroke.

The clinical presentation of CHD varies greatly. Sometimes it is a silent chronic disease that progresses slowly. In other cases it is sudden, unexpected and unpredictable. Through the decades, CHD has brought to an end the lives of many people in their prime. It has robbed wives of their husbands and husbands of their wives. It has tragically, without warning, robbed young children and adolescents of their parents.

The most malignant form of CHD, acute heart attack (acute myocardial infarction) was relatively unknown in the beginning of the 20th century. Then came the epidemic. In the 1950s acute myocardial infarction was recognized as one of the most common causes of death in the industrialized world.

The symptoms were often dramatic and devastating. A previously healthy person was suddenly hit by severe chest pain, commonly associated with serious irregularities of heart rhythm, often resulting in sudden death. The survivors often had to deal with the consequences of damage to large parts of their heart muscle, sometimes resulting in heart failure, severely compromised quality of life and a shortened life span.

Although still an important cause of death around the world, the death rate from CHD has declined in the USA, CanadaAustralia, New Zealand and all European countries. It is in the countries with the highest incidence that the greatest decline has occurred. Studies have reported up to 80 percent decline in mortality from CHD in the last 30 – 40 years in countries like the UK, Slovakia, Poland, Netherlands, Ireland, Finland, Iceland and Sweden. A recent Swedish study indicates that CHD deaths are still falling, both among the old and the young.

It is a bit unclear how much of the decline in death rate from CHD is due to a reduction of the incidence of the disease and how much is due to improved survival of those affected. Obviously prognosis has improved and some studies have reported declining incidence of CHD.

Another question is whether the decreasing trend in CHD mortality is due to changes in major cardiovascular risk factors, better medical and surgical treatment, neither of these or both.

Many investigators have used the so-called IMPACT model to analyze the role of preventive measures versus treatment measures on the death rate from CHD. All these studies report that more than half of the mortality decline is attributable to reductions in major risk factors.

The Role of Diet

Although there are some differences, the interpretation of the data from countries where the IMPACT model has been used follows a common path. Lowering of blood cholesterol appears to be an important contributor to the decline in mortality from CHD in many of these studies. Therefore, dietary measures aimed at lowering blood cholesterol are usually highlighted by investigators. The Icelandic experience is a good example.

Icelandic investigators reported an 80% decline in death rate from CHD between 1981 and 2006. Based on the IMPACT model approximately 73% of the mortality decrease was attributable to risk factor reductions. Among these, a reduction in blood cholesterol played the biggest role, and appeared more important than reduction in smoking, lower blood pressure and less physical inactivity. Importantly, adverse trends were seen for obesity and diabetes, increasing mortality by 4% and 5% respectively”

The investigators concluded that:

“The large fall in cholesterol between 1981 and 2006 reflects major changes in the Icelandic diet following the issue of Dietary Goals for Icelanders”.

These goals are very similar to the dietary goals for the U.S and most European countries. Let me quote the Icelandic paper again:

The National policy is based in the dietary goals where the reduction of saturated fat, mainly from milk and dairy products, lamb and margarine, is greatly emphasized. The food policy and the dietary goals have greatly influenced nutrition education and awareness in the country”.

“Icelandic food supply data clearly demonstrate the subsequent changes. In the 1970s, the diet was characterized by high consumption of whole milk and dairy products, margarine, butter, lamb, mutton and fish. However, between 1981 and 2006 there was a 73% drop in whole milk and dairy consumption, and the supply of lamb and mutton decreased by 50%”. 

“From the 1990s, the consumption of total fat in percent energy has decreased from 40% to 36%. But more importantly, the composition of fat has also changed from more saturated and trans-fatty acids to cis-unsaturated”.

Will the Popularity of LCHF Trigger a New Epidemic of Heart Disease?
Sheep grazing on green grass in South Iceland

Interestingly, while these changes occurred, the consumption  of refined sugars increased (sugared beverages in particular) and fish consumption decreased. So, although less total and saturated fat may have contributed to lowering of blood cholesterol among the Icelanders, it is obvious that many of the alterations in dietary habits between 1981 and 2006 were of negative nature. This is also reflected by the fact that overweight and obesity more than doubled during the same time period.  

So, finally, here’s the point: If the decreased consumption of whole milk, dairy, lamb and mutton played such an important role in lowering cholesterol and reducing the death from CHD among the Icelandic people, LCHF must certainly pose a threat, but….

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Saturated Fat –  The Villain or a Red Herring 

So, once again it all comes down to saturated fat; dairy, butter and red meat. However, keep in mind that no food product contains only saturated fat and no other types of fat. Pure saturated fats or pure unsaturated fats are never consumed. For example, beef contains a high proportion of monounsaturated fat in addition to saturated fat. Dairy (milk, cream, cheese and butter) is the only food class where the proportion of saturated fat is much higher than the proportion of other types of fat.

Through the years we have been led to believe that saturated fatty acids (SFA) elevate blood cholesterol. We have also been told that high cholesterol will increase the risk of heart disease. Therefore, it’s easy to assume that consuming SFA will increase the risk of heart disease. However, the problem is that the effects of SFA on cholesterol and different lipoproteins have been oversimplified. Furthermore, the epidemiological evidence linking saturated fats with CHD was weak from the beginning.

Will the Popularity of LCH Trigger a New Epidemic of Heart Disease?
Saturated Fat – The villain or a red herring

Although SFA may elevate total cholesterol and LDL-cholesterol, they appear to elevate HDL-cholesterol as well. Therefore, the availability of atherogenic lipoproteins doesn’t necessarily increase. Furthermore, SFA lower small dense LDL particles and raise large buoyant LDL particles. Large particles generally impose less risk than small particles. So, stating that saturated fats adversely affect blood lipids is misleading.

Although carbohydrates are less likely to elevate total and LDL-cholesterol, they often elevate triglycerides and lower HDL-cholesterol. These lipid changes may harbor negative cardiometabolic effects.

One of the first papers that advised decreased intake of SFA was published in 1961 by The American heart Association. Some of the support for this came from observational studies, including Ancel Keys Seven-Countries Study, which suggested a relationship between SFA intake and the risk of death from CHD.

Later, in the Nurses’ Health Study a greater ratio of polyunsaturated fatty acids (PUFA) to SFA was associated with lower risk of CHD. The Finnish Mental Hospital Study published 1979 found fewer deaths from CHD and lower rates of heart attacks in a hospital that administered dairy products in which SFA’s were replaced with PUFA’s, compared with regular SFA-containing dairy products. On the other hand, the intervention component of the Minnesota Coronary Survey did not show that increasing the amount of PUFA at the expense of SFA did result in less risk of CHD.

Intake of different types of fatty acid in relation to the risk of CHD was studied in the large Nurses’ Health Study. When carbohydrates were used for comparison, trans-fats were most strongly related to the risk of CHD. SFA intake was not significantly related to increased risk of CHD when compared with carbohydrates. So, replacing SFA with carbohydrates was a wash. In fact, a pooled analysis of large cohort studies indicated that there was a significantly greater relative risk for CHD with carbohydrates compared with SFA. However, MUFA’s and PUFA’s were associated with lower risk compared with carbohydrates.

A systematic review of of the evidence supporting a causal link between various dietary factors and coronary heart disease was published in 2009. The pooled analysis from 43 randomized clinical trials showed that increased consumption of marine omega-3 fatty acids  and a Mediterranean diet pattern were each associated with a significantly lower risk of CHD. Higher intake of polyunsaturated fatty acids or total fats were not significantly associated with CHD, and the link between saturated fats and CHD appeared weak.

For the last five years, a number of reports (1, 2, 3, 4, 5) have cast doubt on the association between the consumption of SFA or major foods that contain SFA (meat and milk) and the risk of CHD. These studied can’t be neglected when analyzing the current evidence for the association between SFA and heart disease.

Will the Popularity of LCH Trigger a New Epidemic of Heart Disease?

Trans-fats are the only type of fats that seem to impose more risk for CHD than carbohydrates. There’s no evidence that replacing other types of fats with carbohydrates will reduce risk. So, reducing carbohydrates and increasing fat consumption should not increase the risk of heart disease, unless carbohydrates are replaced by trans-fats. Therefore it is unlikely that the declining death rate from heart disease may be explained by decreased consumption of saturated fat. Furthermore, if trans fats are avoided there is no reason to believe that the popularity of LCHF will trigger a new epidemic of heart disease. 

It’s now 2014 and the death rate from CHD continues to decline, despite LCHF being around for quite many years now. If there comes a day when we will see a slowing of the decline or an increase in death rate, I guess many experts will blame changed dietary habits associated with the popularity of LCHF. In fact, a reversal of the decline in population cholesterol levels was recently reported in Sweden, where the popularity of LCHF is very high. However, as of today this has not been reflected in a reversal of the decline in mortality from CHD.

In most countries where the death rate from heart disease has fallen, overweight, obesity and type 2 diabetes have increased. Because obesity is strongly linked to cardiovascular risk, many experts are surprised that the incidence and death rate from CHD continue to decline. Most likely, there is a time lag between the increased incidence of obesity and death rate from CHD. Ultimately, if obesity trends are not reversed, it is unlikely that the decline in CHD mortality will continue.

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charles grashow
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charles grashow

https://fpim.org/articles/heart-health/ldl-cholesterol-sometimes-the-simple-questions-are-the-most-revealing/ “Our cells however do not need the cholesterol contained in LDL particles; nonetheless, most of us believe they use it. This belief is untrue. LDL-C is actually not utilized to any significant degree by any organ systems in human beings. Other animals may use some of it here and there, but not us. We just don’t need it. In fact, the goal of LDL particles is to get to the liver ASAP for disposal. Otherwise, these particles tend to land in places where we do not want or need them, our blood vessel walls to be more specific. You… Read more »

George
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George

The many cells that express LDL receptors presumably have some use for cholesterol or other contents of LDL. Although the liver takes up the largest proportion, this may just be typical of the combination of prodigality and parsimony in the body’s nutrient homeostasis systems; once back in the liver, the cholesterol from LDL will be recycled into bile acids, another arm of the cholesterol cycle, and most of it will be resorbed from the gut, so a traced cholesterol molecule might re-appear in serum LDL several times before being excreted. The only reason that cells may not need lipids from… Read more »

pronutritionist
Guest

Doc, do you happen to know if mobile phones, urbanisation (habitation nearer to hospitals), better in-ambulance care and peri-infarction treatments have a clear role in the reduction of CHD mortality? I guess it’s much faster to get some form of medical care nowadays compared to 30-50 years ago.

In Finland, CHD mortality has decreased some 80% since 1960s but absolute number of CHD cases/100 000 has not declined. CHD is shifted more and more to older people and to females.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

The most dramatic improvement in the treatment of acute heart attack (ST elevation acute myocardial infarction) during the last 15 years involves acute PCI. This approach has significantly lowered mortality in the countries where it is practiced. Acute PCI is taking the patient directly to the cath lab and perform an angiography and thereafter open the artery and place a stent. The sooner you’re able to do this, the better the prognosis of the patients. In that respect, better ambulance care and habitation near hospitals is important, and mobile phones probably are to. Also, a large part of those who… Read more »

RichardOrnishForLife
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RichardOrnishForLife

Doc, so basically nothing new under the sun. You throw us the basic diet-heart denialism wrapped in some kind of attempt to appear neutral. In your review about SFA you manage to leave out autopsy studies, research into LDL receptors, genetic studies, highly controlled feeding studies from broad range of different mammalian specimen, including over 12 sub-human primate species and global epidemiology. Instead, you want us to believe that one-sided epidemiology coming entirely from homogenous Western population is the key to understand the diet-heart. I cannot say but, this is rather weak. Well, I am glad you at least covered… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Richard. We should all try our best to keep up to date; this paper is straight out of the oven https://annals.org/article.aspx?articleid=1846638

RichardOrnishForLife
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RichardOrnishForLife

Sure,

let’s wait for the comments by other scholars. Let say, I’m quite skeptical that this paper is able us to forget 100 years of progressive research into diet-heart.

Mie
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Mie

Did you read comments on Medscape?

https://www.medscape.com/viewarticle/822092

The authors chose not to consider fat modification/exchange properly and also decided to analyze n-3 and n-6 fatty acid intake separately. If you’ve read the full text, could you explain the rationale behind this? E.g. Ramsden et al 2010 showed that mixed n-3 and n-6 diets had beneficial effects on CHD end points.

Stew
Guest
Stew

You don’t address the fact that there is a significant minority of low carbers whose LDL particle count goes much higher, even while they have a small proportion of small particles. As Dr. Dayspring points out, it is now well accepted that when there is a high LDL particle number, the size of particles is virtually meaningless. So isn’t it a bit misleading to characterize the development of large fluffy LDL particles as beneficial, when in many low carbers, it is at the expense of a big, ominous increase in particle number?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Stew. You’re right about the importance of particle number, I’ve actually written some articles addressing the issue:
https://www.docsopinion.com/health-and-nutrition/lipids/ldl-p/
https://www.docsopinion.com/2012/11/21/the-difference-between-ldl-c-and-ldl-p/

It’s possible that particle number is the most important issue as you suggest, I’m aware of that. However there are studies showing that particle size may also play a role so I’m not ready to seep that under the rug.
Thanks for the comment.

James
Guest
James

Particle size can be a determinant of risk in a subset of people. Once adjusted for particle number, the size is irrelevant. This puts the particle size argument in context.

For the majority of people LDL-c is concordant with LDL-p, therefore LDL lowering is the most sensible strategy. It’s hard to believe a responsible doctor would be oppose this strategy that has been proven beneficial in hundreds of studies over the last 50 years.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

James. I never said that lowering LDL-C is unimportant. However, it’s not the only thing that counts. In fact, Non HDL-C is probably a better marker of risk because it better reflects cholesterol within all atherogenic lipoproteins, not only in LDL.

Mie
Guest
Mie

Axel, c’mon: “Although SFA may elevate total cholesterol and LDL-cholesterol, they appear to elevate HDL-cholesterol as well. Therefore, the availability of atherogenic lipoproteins doesn’t necessarily increase. Furthermore, SFA lower small dense LDL particles and raise large buoyant LDL particles. Large particles generally impose less risk than small particles. So, stating that saturated fats adversely affect blood lipids is misleading.” First of all, check out e.g. Mensk et al (2003) meta-analysis of metabolic ward studies. Foods higher in safa don’t have the same kind of beneficial effect on total chol.:HDL ratio as foods higher in unsaturated fatty acids. Therefore stating that… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Mie. It has been claimed for many years that the effects of SFA on blood lipids are all negative which as you know is not true. Of course I’ll be the first to admit that if you need to lower LDL-cholesterol per se, choose PUFA’s rather than SFA. However there are individuals where LDL-cholesterol is not the main issue, for example those with the metabolic syndrome. In our previous discussion on LDL particle size I cited Dr. Ronald M. Krauss. His research indicates the main effect of SFAs is on larger particles, which are in his opinion (based on research)… Read more »

charles grashow
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charles grashow

So – if we’re not sure whether or not it’s LDL-P or the LDL particle size doesn’t it make sense to err on the side of caution and lower BOTH small and large particles?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Yes Charles. Do you know how to do it? 🙂

charles grashow
Guest
charles grashow

Have you read Track Your Plaque by Dr William Davis?

RichardOrnishForLife
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RichardOrnishForLife

Doc, one of the most prominent actors shaping the new Nordic dietary guidelines referred the meta-analysis by S-T with a term “fiasco” in a private email communication with me. She told me that prominent actors advised the publish the paper. This is how papers with R. Krauss name on it are referred to, as fiasco’s. Krauss receives grants from eggs center, pork board, Cattlemen’s beef association, Atkins Foundation, etc. Certainly it might be that this does not influence his approach, and he is not like other merchant of doubts spreading confusion, but it is just good to bear in mind.… Read more »

Mie
Guest
Mie

Now Richard, you’re resorting to bullshit again. Your idea of Krauss’ work is misguided. FYI, Krauss advocates less safa and more unsaturated fats & minimally processed carbs.

Richard
Guest
Richard

Mie, stop being naive. Ronald Krauss is a bullet-proof, industry sponsored, merchant of doubt: https://www.amazon.com/Merchants-Doubt-Handful-Scientists-Obscured/dp/1608193942/ref=sr_1_1?ie=UTF8&qid=1395144687&sr=8-1&keywords=Merchant+of+doubt Ofcourse Krauss knows that SFAs are highly problematic and saying anything to the opposite would make him the but-end of a riducule among his peers. Ofcourse he is against high intakes of SFAs. That’s not the issue here, the scientists who worked for cigarette industry knew the drill, they were not hired for putting up outward lies or completely deny the harmfull effects of cigarettes, they were hired to make the audience confused. Krauss who is hired by the Egg center, Pork board and Dairy… Read more »

Mie
Guest
Mie

So … Even though Krauss

a) has published studies showing that low car diets high on red meat have non-beneficial effects on blood lipids (that is, showing that high red meat intake has adverse effects!)

and

b) recommends less safa and more unsaturated fats & minimally processed carbs

he is not to be trusted? Because … Naomi Oreskes has published a book which doesn’t deal with Krauss, his studies or the matter (different effects of different types of dietary fats on risk factors and/or CVD end points)??

I’ve gotta to admit: you lost me here. Totally.

FrankG
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FrankG

“… industry sponsored, merchant of doubt…”

And who were the group who drew up the NCEP ATP III guidelines being paid by?!?

Seventy two financial conflicts of interest, among 8 of the 9 self-appointed committee…

https://www.nhlbi.nih.gov/guidelines/cholesterol/atp3upd04_disclose.htm

“… [those] who worked for cigarette industry knew the drill, they were not hired for putting up outward lies or completely deny the [harmful] effects of cigarettes, they were hired to make the audience confused.”

Sounds kinda like your job description… eh Richard?

Mie
Guest
Mie

“Of course I’ll be the first to admit that if you need to lower LDL-cholesterol per se, choose PUFA’s rather than SFA. However there are individuals where LDL-cholesterol is not the main issue, for example those with the metabolic syndrome.” Fair enough. “In our previous discussion on LDL particle size I cited Dr. Ronald M. Krauss.” And I responded. FYI, Krauss’ recent contributions have shown that low carb in the context of higher red meat intake has adverse effects on particle size. Want a link? “His research indicates the main effect of SFAs is on larger particles, which are in… Read more »

Axel F Sigurdsson
Guest

Mie. Although you seem believe otherwise, a recent publication in the European Heart Journal confirms that there still are some scientists who believe that LDL-particle diameter may be of importance. https://eurheartj.oxfordjournals.org/content/early/2014/02/24/eurheartj.ehu055.abstract

I think the jury’s still out there 🙂

Mie
Guest
Mie

I can’t access the full text, so a few comments on the basis of the abstract: 1) I’m sure you noticed that larger LDL was associated with BIGGER risk of CVD death than sdLDL? How does that fit in with your take on sdLDL being the relevant predictor of the risk? 2) Of course, the whole issue is made more difficult to dissect due to the definitions for sdLDL and larger LDL: 16,8 nm. As far as I know, there are no set definitions for what precisely is the particle size for given subtype, but generally sdLDL is defined being… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Mie. I’ve often admired your mental sharpness, so this is a surprise. I don’t have “a take on” anything specific concerning particle size. You know as well as I do that there are studies indicating an association between particle size and risk. In my article I only cited these studies. It’s not “my take”. I cited many other studies as well. My intention by drawing your attention to the European Heart Journal study was to make you realize that LDL particle size may play a role. At least that possibility has not been abandoned by everybody. I’m glad I succeeded.… Read more »

Mie
Guest
Mie

Axel, as much as I enjoy your sarcasm (really, I do: in fact, you should do it more often – it brings a nice bite to your texts), I’ve gotta to say that I’m not impressed with this answer. You wrote (and I quote) “Furthermore, SFA lower small dense LDL particles and raise large buoyant LDL particles. Large particles generally impose less risk than small particles. So, stating that saturated fats adversely affect blood lipids is misleading.” and gave a link to a 1998 paper discussing sdLDL/larger LDL. Now, why would you use that as a reference when stating that… Read more »

charles grashow
Guest
charles grashow

From the abstract

“Both large and small LDL diameters are independently associated with increased risk of mortality from all causes and, more so, due to cardiovascular causes compared with LDL of intermediate size.”

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Mie. Saying that saturated fat adversely affects blood lipids is misleading because it doesn’t tell the whole story. That’s my “take” and the reason I referred to the particle size issue and the HDL issue.

Mie
Guest
Mie

Axel, notice that I referred to this before by stating:

“therefore stating that safa has an adverse effect on lipids compared to unsaturated fats is not misleading.”

I reckon you can spot the key part. Of course, when compared to e.g. sugar or trans fats, the story’s different. However, I think the comparison should be made to what’s relevant & recommendable.

Teitur Guðmundsson, MD
Guest

Seems to prove the point that nobody really knows for sure and possibly no specific diet exists as the ultimate one. Balance probably needs to be the key factor between nutrition, exercise and risk factors should be taken into account for every individual. But the TURF war will go on and is exciting to follow here as well as elsewhere. Good writing by the way !

VeryLowLDL36
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VeryLowLDL36

What about the Dean Ornish diet and the other eponymous Esselstyn diet that seem to indicate a cure for CHD from no oils at all as well as no meat or fish? Their studies indicate a way to even reverse heart disease. Why isn’t there more attention given to these diets to see if they do in fact work?

RichardOrnishForLife
Guest
RichardOrnishForLife

Excellent point, Dean Ornish drug free (even Aspirin free) program results in 40% drop in LDL cholesterol on an average patient in 12-weeks. This is comparable to Atorvastatin therapy. A meta-analyses of clinical trials have found that low-carbohydrate diets elevate LDL cholesterol and impair endothelial function https://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8976486 Unfortunately, I need to clarify myself because of horrible typing conducted in the early hours. I meant to say that many prominent shcolars adviced the journal that published the notorious S-T meta-analysis (2010) to not to publish it, and it didn’t pass the peer review either. Nevertheless, the journal decided to publish the… Read more »

charles grashow
Guest
charles grashow

The question I have with regard to the Esselstyn study is that all of the patients were placed on statins at the start of the study. Were the people ever taken OFF of the statins at any point ??

RichardOrnishForLife
Guest
RichardOrnishForLife

Charles, Esselstyn’s patients were on very low-dose Lovastatins, such low-potency statins have never shown to actually cause regression of heart disease. Moreover, Esselstyns most dramatic case was his own colleague who did not take any drugs, he showed practically 100% regression of his artery disease at least judged by angiograms. He managed to lower his LDL to 38mg/dl. Besides, it’s very easy for us accept the success of Esselstyn’s approach. In one experiment Armstrong and colleagues induced severe atherosclerosis in rhesus monkeys by feeding a diet with 40% of calories from egg yolks for 17 months. The egg yolks were… Read more »

FrankG
Guest
FrankG

((yawn)) In order to make a convincing argument first you need to show that you are capable of being a credible source… “Esselstyn’s patients were on very low-dose Lovastatins, such low-potency statins have never shown to actually cause regression of heart disease.” What utter nonsense.. why on earth bother with them if they do nothing? But wait.. there’s more..! Each participant also received an individualized prescription for a cholesterol-lowering drug. The most frequent regimen included cholestyramine, 4 g twice daily, and [Lovastatin], 40 mg to 60 mg daily. “ https://www.heartattackproof.com/study02_methods.htm “Lovastatin is used for: Lowering high cholesterol in certain patients.… Read more »

VeryLowLDL36
Guest
VeryLowLDL36

I can tell you that after following Esselstyn’s strict diet WITH NO STATINS my LDL went from 110 to 36MG/DL. Total Cholesterol went from 176 to 91. Unfortunately Triglycerides and HDL haven’t improved (169 and 21) but I feel much better than ever before. I’m now at 170lbs with a BMI of 26 whereas prior to Esselstyn I was at 200lbs. Not sure how it’s affecting my heart but based on the way I feel I’ll be sticking with it.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

I agree with you completely. Stick with the diet that you feel best with. There is no diet that fits everybody. Your numbers are a bonus and certainly indicate that you have improved your risk profile. Congrats.

charles grashow
Guest
charles grashow

Have you had your ApoB measured? LDL-P, small LDL-P?

High trigs might be problematical.

VeryLowLDL36
Guest
VeryLowLDL36

I plan to have my LDL-P checked but at such low LDL-C levels would it even matter? Total cholesterol is quite low as well. I’ll respond once I have the results.

charles grashow
Guest
charles grashow

With your higher triglycerides the particles could be predominately small and dense – SO the question then becomes this – if you have a small number of small particles are you in any kind of danger?

charles grashow
Guest
charles grashow

https://www.heartattackproof.com/study02_methods.htm
Each participant also received an individualized prescription for a cholesterol-lowering drug. The most frequent regimen included cholestyramine, 4 g twice daily, and lovastarin, 40 mg to 60 mg daily. Time-release niacin was prescribed for a short while but was discontinued when many patients reported nausea, vomiting, and swollen ankles.

My question still remains – How long were the patients on the statin drug?

As to plaque regression on low dose statins
https://www.summitmd.com/pdf/pdf/081010_1.pdf

fifek2000fifek
Guest

As far I can see that everybody, as well supporters of low fat diet, as of high fat-low carb diet will find many strong medical papers with meta-analyses confirming their rights. I just think that the best way is to eat everything natural: meat, fish, vegetables, fruits, cream, eggs, butter etc. Just food who our healthy grandparents ate: some of them ate only potatoes with sour milk, and others pork fat with red pepper or fat sausages with wine. No right recipe, until natural food and moderate physical effort. And no stress. That’s all.

charles grashow
Guest
charles grashow

https://annals.org/article.aspx?articleid=1846638&resultClick=3 Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis “Data Synthesis: There were 32 observational studies (530 525 participants) of fatty acids from dietary intake; 17 observational studies (25 721 participants) of fatty acid biomarkers; and 27 randomized, controlled trials (103 052 participants) of fatty acid supplementation. In observational studies, relative risks for coronary disease were 1.02 (95% CI, 0.97 to 1.07) for saturated, 0.99 (CI, 0.89 to 1.09) for monounsaturated, 0.93 (CI, 0.84 to 1.02) for long-chain ω-3 polyunsaturated, 1.01 (CI, 0.96 to 1.07) for ω-6 polyunsaturated, and 1.16 (CI, 1.06… Read more »

RichardOrnishForLife
Guest
RichardOrnishForLife

It’s already on; medscape covers the fuss:

“But the meta-analysis has already been questioned. In an email exchange with heartwire , Dr Eric B Rimm (Harvard School of Public Health, Boston, MA) said, “My colleagues were quite surprised at the findings. We uncovered a serious mistake in their review of PUFA that likely will change the results substantially.” And the parts of the meta-analysis focusing on PUFA didn’t summarize the relevant studies correctly, according to Rimm, who added that “the results are in serious question.”

https://www.medscape.com/viewarticle/822092

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Richard. Don’t you think it’s fair to also report the authors response to the claims.

“Regarding assertions of errors in the report, Di Angelantonio said, “We recently spotted some minor mistakes in some of the data that will not in any way affect the main results of the study.” He confirmed that another group contacted him and his coauthors about “some other minor mistake,” adding, “We are making an erratum that will be sent to [Annals of Internal Medicine] in the next 24 hours, so there will be an updated version. But it’s unlikely that the main conclusions will change.””

charles grashow
Guest
charles grashow

https://www.medscape.com/viewarticle/822092 CV Risk and Saturated Fats: The Debate Roils On https://www.medscape.com/viewarticle/804400 Dietary Saturated Fat Has Undeserved Bad Reputation, Says Review “The influence of dietary fats on serum cholesterol has been overstated,” concludes a review in an American Society for Nutrition publication that, in its words, “calls for a rational reevaluation of existing dietary recommendations that focus on minimizing dietary SFAs [saturated fatty acids], for which mechanisms for adverse health effects are lacking” [1]. Indeed, argues the author, Dr Glen D Lawrence (Long Island University, Brooklyn, NY), it is likely other factors, such as oxidized polyunsaturated fatty acids (PUFAs) or preservatives… Read more »

RichieProOrnish
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RichieProOrnish

@VeryLowLDL36, LDL of 36 without drugs, that’s amazing. Your are not just improved for your risk-profile but most likely all the existing atheroma plaques have started to regress. In experimental models, lowering LDL to very low levels is simple enough for disease regression. Don’t worry about HDL-C nor Triglycerides, these markers are risk-predictors in a population that consume high SFA and high dietary cholesterol fare, these markers are not causally related to CHD. Modulating these markers from the baseline does nothing for heart disease. Third World societies which are virtually immune to coronary disease so long as they persist in… Read more »

FrankG
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FrankG

“What is metabolic syndrome? Metabolic syndrome is a cluster of metabolic risk factors. When a patient presents with these risk factors together, the chances for future cardiovascular problems are greater than any one factor presenting alone.” https://www.heart.org/HEARTORG/Conditions/More/MetabolicSyndrome/About-Metabolic-Syndrome_UCM_301920_Article.jsp “How is metabolic syndrome diagnosed? To diagnose metabolic syndrome, most doctors look for the presence of three or more of these components: * Central or abdominal obesity (measured by waist circumference): >> Men – Greater than 40 inches >> Women – Greater than 35 inches * Fasting blood triglycerides greater than or equal to 150 milligrams per deciliter of blood (mg/dL) * Blood… Read more »

Mie
Guest
Mie

Frank, the above paper states very clearly why LDL and HDL can be considered causative risk modifying factors. Notice that this doesn’t mean that LDL is the one, single cause for CAD. Of course, if you disagree, it’d be appropriate to explain why in more detail.

In addition: in my opinion, there’s one clear problem in discussing HDL & interventional evidence. “Richard” knows this/should know this as I’ve explained it before. Don’t know if he’s a still an HDL denialist, though.

FrankG
Guest
FrankG

Mie I can certainly agree that it is not as simple as just “LDL”… this is where I take issue with Richard’s (or whatever he calls himself next time) persistence that only “LDL” counts. Plus his further disinformation drawing on the tenuous lines of association between SFAs, Lipids, Atherosclerosis and Mortality.. as if eating SFAs inevitably leads to death. For example above he boldly states “Not a single death from atherosclerosis verified in these people.” Is atherosclerosis ever listed as a cause of death? Indeed I recall reading recently about how atherosclerosis is widespread in the Maasai and yet does… Read more »

Mie
Guest
Mie

I agree with you on many issues, a couple of comments however: “So until that is taken into consideration I am not willing to accept that “atherosclerosis = death”… no matter how many times Richard implies it is so.” Until what is taken into consideration? Hard to say anything about the case which you’re referring to (based on hearsay), but remember we’re talking about a disease which has multifactorial etiology which means that it’s not all about LDL. And which doesn’t mean that LDL doesn’t matter. “Meantime we have populations (such as the French — at least traditionally) eating diets… Read more »

charles grashow
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charles grashow

So – does it matter how LDL is lowered – drugs, diet or a combination of the two?

Get your LDL <70, get your TC <150 and you're heart attack proof – correct?

Since my TC is 126 and my LDL is 71 I should have nothing to worry about.

BUT – I eat meat, full fat dairy and eggs as part of my diet!

What are your thoughts RichieProOrnish??

Mie
Guest
Mie

As long as the key factors are in order, I’d say you can feel pretty confident about your cardiovascular health. That’s what matters in the end, not your diet.

P.S. I think you and everyone else here already know “Richard”s thought on that. 🙂

VeryLowLDL36
Guest
VeryLowLDL36

I’ll post my LDL-P results once I have them. What confuses me however are occasional articles that seem to indicate a good proportion of individuals arriving at the ER with angina and CHD along with low LDL-C levels. However this study seems to indicate that LDL-C < 70 is required for high risk individuals https://www.health.harvard.edu/fhg/updates/update1104b.shtml. Nonetheless I've seen other studies indicating low LDL-C isn't sufficient https://www.thedoctorwillseeyounow.com/content/heart/art2561.html. Who the hell knows!

davebrown9
Guest

A recent New York Times article featured 99-year-old biochemist Fred Kummerow. Quote: “In the past two years, he (Kummerow) has published four papers in peer-reviewed scientific journals, two of them devoted to another major culprit he has singled out as responsible for atherosclerosis, or the hardening of the arteries: an excess of polyunsaturated vegetable oils like soybean, corn and sunflower — exactly the types of fats Americans have been urged to consume for the past several decades.” https://www.nytimes.com/2013/12/17/health/a-lifelong-fight-against-trans-fat.html Experts who attended a meeting of the International Society for the Study of Fatty Acids and Lipids (ISSFAL), in May 2010 seemed… Read more »

Mie
Guest
Mie

“Biochemistry research suggests that high omega-6 intake is problematic.”

However, the intake levels required are in real life & with recommended diets impossible. E.g. Med.diet, paleo, low carb, DASH etc. etc. No need to worry.

davebrown9
Guest

Not sure I understand what you said there. At least a few aware scientists are concerned about the excessive amount of omega-6 in the food supply. Most aren’t paying attention. Excerpt from the May 2010 meeting of the International Society for the Study of Fatty Acids and Lipids (ISSFAL): “The debate concluded with agreement by all that we need a randomized controlled trial to compare the effect of low and high intakes of LA. The trial should have typical US intakes of omega-3 PUFAs, with 7.5% energy from LA (the current US intake) in one group and 2.0% LA (historical… Read more »

Mie
Guest
Mie

Dave,

According to NHANES 2009-10, an average American gets 6,5% of tot. E from pufa, so I SERIOUSLY doubt that they’re getting get more than that of linoleic acid alone. If you read the article you’re citing, you must have noticed that it doesn’t give a reference to the “7,5%E LA” claim.

RichardOrnishForLife
Guest
RichardOrnishForLife

Mie, you conveniently changed to topic from HDL-C to HDL and insisted I that I am a denialist, LOL, well done. Yes, HDL is causative factor in heart disease. HDL-C is not. People who’ve lived their whole life with very low HDL-C levels due to genes are not at higher risk of CHD. Besides, unlike with LDL, no one seems to know how to modulate HDL in order change the prognosis of an individual patient. There’s no existing therapies. In experimental models Probucol seems to work by boosting HDL metabolism. It also decreases HDL-concentrations. So maybe in the future, pharmacologic… Read more »

RichardProOrnish
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RichardProOrnish

Charles wrote: “Since my TC is 126 and my LDL is 71 I should have nothing to worry about. BUT – I eat meat, full fat dairy and eggs as part of my diet! What are your thoughts RichieProOrnish??” My thoughts. According to prospective cohort studies, dietary cholesterol influences CHD over and above its effects on serum lipids (Stamler 2010). I recall, you mentioned that you take Lipitor (Atorvastatin). That’s good, everyone consuming eggs and meat as part of their regular diet need to be on a high-potency statin. Your LDL is low and if you have not been diagnosed… Read more »

charles grashow
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charles grashow

@RichardProOrnish 10mgs/day of Atorvastatin (generic Lipitor) is not “a high-potency statin’! The dosage range of LIPITOR is 10 to 80 mg once daily so I’m on the LOWEST dose for the drug. As to eggs please show me studies that prove that ONE egg/day is harmful. You also said “in clinical trials LDL <75 is the threshold, and once we go under this, the plaques start to regress. This does not mean that person becomes immune to CHD; smaller and more stable plaques can still erupt and cause MI's and strokes on people with existing CHD. Frankly, LDL of 70… Read more »

Mie
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Mie

Richard:

“That’s good, everyone consuming eggs and meat as part of their regular diet need to be on a high-potency statin.”

Yet again, a blanket statement and as such, BS. You’ve GOT to learn to understand the difference between population level strategies and individuals. Otherwise you’re JUST LIKE an average cholesterol denialist or a tobacco advocate with their stories about “a relative” who had LDL >500 and/or smoked – and yet lived to be be 100 years old.

RichieProOrnish
Guest
RichieProOrnish

Doc, I wanted to tell you that, your colleague from the East, professor Timo Standberg, who was largely responsible for shaping the national guidelines for treating dyslipidemia published an article in Finnish medical journal called “LDL cholesterol is only causal factor in artery disease”. Its basically the message that is identical to the message spread by the UT Southwestern medical center in Dallas -crew. In fact he has close ties to William Roberts and Brown & Goldstein. In his article, which is just an, though, he recited to Esselstyns, although express his skepticism whether such solutions will be for the… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Richard We had this discussion a concerning PCSK9 a few months back. Then I drew your attention to a study by Cohen and coworkers published 2006. In that study PCSK9 mutation was associated with lower levels of LDL cholesterol and lower risk of coronary heart disease. However, coronary artery disease was found among individuals with the mutation. Despite a very low plasma level of LDL cholesterol (53 mg per deciliter [1.4 mmol per liter]), one patient died at the age of 68 years, within 24 hours after his first myocardial infarction. Thus, patients with very low LDL cholesterol can have… Read more »

RichardOrnishForLife
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RichardOrnishForLife

Axel, this individual patient that you refer to did NOT have the heterozygous form of the knock-out mutation. Instead he had some kind of a gene that inactivated PCSKY9 only modestly, yielding about 15% lower LDL since birth compared to Western norm. Those with heterozygot form of the mutation have their life-long LDL around 50-70s (1,3-1,8mmol/). Almost (if not all) of these people black, African-Americans. We haven’t identified anyone with atherosclerosis among these people. despite plethora of risk factors in these people. Darren McGuire who mentioned this in AHA meeting actually work with these patients and operates in the same… Read more »

Mie
Guest
Mie

This isn’t a matter of opinion, Richard. Confusing population level and individual level & claiming something as stupid as you just did is an unforgivable mistake, one that shows that the person uttering such nonsense has no role in commenting on these things.

As far as your reading comprehension skills are concerned (let’s leave the issue that Roberts ignores the only dietary intervention that has shown CVD mortality benefits & which isn’t vegan): what do you think the word “most” in the quotation means? Hmm?

RichardOrnishForLife
Guest
RichardOrnishForLife

Mie, this is certainly a touchy subject to you, I must say 🙂 Let’s leave he aggressive outbursts, and instead focus on the topic. There’s nothing wrong with my comprehension skills. In fact, being very well acquainted with Roberts ideas, I can tell with utmost certainty that the “most” in Roberts phrase means literally “all”. It’s just a polite way to put it, you know. You demonstrate many similarities with the cranks in physics. If you are unable understand something, the top-experts must have it wrong. You have it all correct by default. The idea that Robert’s as an experienced… Read more »

Mie
Guest
Mie

“In fact, being very well acquainted with Roberts ideas, I can tell with utmost certainty that the “most” in Roberts phrase means literally “all”. It’s just a polite way to put it, you know.” And we have … your word for it? I’m afraid that doesn’t suffice at all, as you have no credibility nor expertise on these matters. “If you are unable understand something, the top-experts must have it wrong.” Yet again, your reading comprehension fails you. My point was about your interpretation, not any given expert’s opinion. As I’m sure you’ll keep on trolling here in the future… Read more »

charles grashow
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charles grashow

@RichardOrnishForLife

There are no studies to show that the method by which you reach TC<150 and LDL<80 is important. That is – that diet is better than drugs or vice-versa.

As Roberts said – the goal is the important thing.

If you have links to papers that show lipid goals achieved via diet are somehow better than the same goals achieved via drugs (statins) and supplements than please post them as I have not been able to find any.

charles grashow
Guest
charles grashow

Do you have a link to the full paper

https://www.ncbi.nlm.nih.gov/pubmed/19406281

David Brown
Guest

In all of this discussion about LCHF diets there has been no mention of resistant starch and gut microbes. Dr. Sigurdsson, I suggest you look into the matter. The LCHF approach has helped many and harmed some depending on biochemical make up. Where fat loss is concerned, I’m guessing resistant starch would be the answer for many of those who cannot tolerate high fat intake. I subscribe to several feed publications because feed researchers seem to have a better grasp of certain aspects of nutritional biochemistry than most weight loss experts. To maximize efficiency, those who raise livestock need to… Read more »

RichardOrnishForLife
Guest
RichardOrnishForLife

Low Carb Diets and Coronary Blood Flow
Blood flow within the hearts of those eating low carb diets was compared to those eating plant-based diets.

https://nutritionfacts.org/video/low-carb-diets-and-coronary-blood-flow/

Birgir
Guest
Birgir

What is your opinion on studies showing low-carb(not sure if they are high fat or high protein etc. in the studies) diets impair flow-mediated dilatation(there are a few ones and a meta-analysis of them)?

https://www.nmsociety.org/docs/LowCarbDiet/lowcarbvascular.pdf .. is this saying the adverse effect is only while adapting to the LC diet?

FrankG
Guest
FrankG

In the study you linked, the low carb diet is high fat “…restricted in carbohydrate (percentage of carbohydrate-fat-protein = 12:59:28) The “adverse” effect was only temporary for the low-carb diet. Despite the initial promise of the low-fat diet, it ended up doing worse in this regard… “After 12 weeks, peak flow mediated dilation at 3 hours increased from 5.1% to 6.5% in the [low-carbohydrate] group and decreased from 7.9% to 5.2% in the [low-fat diet] group (P = .004). These findings show that a 12-week low-carbohydrate diet improves postprandial vascular function more than a [low-fat diet] in individuals with atherogenic… Read more »

RichardOrnishForLife
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RichardOrnishForLife

People, Michel Greger MD refers to some amazing material, y’all must see the video. This video answers directly to Doc’s originally question about LCHF being harmfull. Dr Fleming, a nuclear cardiologist, measured the impact of LCHF diet directly to the coronary arteries. You may just forget all the risk markers, this is the real thing. He had 26 patients who were advised to go on a healthy, high carb vegetarian diet. After a year some of the patients went along the LCHF bandwagon. Those who sticked with vegetarian diet showed improved blood flow to their coronary arteries, those who ate… Read more »

FrankG
Guest
FrankG

R O F L …maybe we should just let your initials speak for themselves.

Or to put it “politely” I think that most of your comments are BS 😛

How you can possibly think that anything to you post can be taken as credible is incredible… you must have nothing but contempt for people and the truth.

charles grashow
Guest
charles grashow

Esselstyn had one patient who triglycerides was well above 300 (they came down from the 700mg/dl range prior he started the therapy) and stayed persistently in the 300s range, and yet even this patient showed regression of his artery disease.

https://www.heartattackproof.com/reversal01.htm

At the 12 year mark multiple patients had LDL > 70. Why would there be regression?

RichardOrnishForLife
Guest
RichardOrnishForLife

Frankie,

the study you refer to is not the one I referred to. The study you speak about was done by Jeff Volek himself who is of course bullet-proof man of the Atkins foundation. These people make a living by writing low-carb books, they also do studies where they utilize the typical Atkins gimmicks. See if they reported the fiber intake for the “low-fat” -group.

FrankG
Guest
FrankG

Oh right… kinda like… we should be wary of any research where there is a potential conflict of interest? Ties to a drug (or other) company that could benefit financially (and reward the researchers) from a favourable outcome? Selling books, TV shows, or movies? Drug companies and major food manufacturers funding research labs in Universities? Leveraging those “donations” into deciding what gets studied and how? People who are motivated by ideological agendas, rather than following the data in an unbiased method? What about researchers who are otherwise squeaky clean but clearly still desire to get their articles published, to keep… Read more »

FrankG
Guest
FrankG

@ RichieProOrnish

“the study you refer to is not the one I referred to…” maybe because I was not replying to you, Dick..!

For someone who claims not to have a reading comprehension issue, you sure seem to have a reading comprehension issue 😛

Biggi
Guest
Biggi

The study I linked to showed the reduced flow-mediated dilatation is temporary, but what about the studies the Greger video points out. Aren’t those long term diets?

The video does seem to have somewhat of a confirmation bias and pick out the negative from the studies does it not? A study shows higher mortality rate but no increase in CVD, but another shows reduced FMD but some other factors improve, and yet it’s edited that so that the message is low carb = heart attack?

Biggi
Guest
Biggi

I´m not sure how relevant the FMD is and if it’s on long term diets or short term or if it’s long term effects or only post prandial. Hopefully the Doctor can give his opinion on these studies and the meta-analysis..

Mark Buster
Guest

Interesting arguments by all, but it seems everyone looks at only one or two things and short term effects. You are not looking for the overall effects long term. I was taking lipitor and and eating pescatarian. My TC was 120, LDL 42, HDL 43, hbA1c 8.8, and my doctor was bragging about how great my Cholesterol tests were and said nothing of BG tests. What is more important? There are arguments by experts both ways on the cholesterol influences of CHD, CAD, overall mortality etc. Aren’t the dangers of high blood sugar undeniable with the exception of at what… Read more »

VeryLowLDL36
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VeryLowLDL36

“Ornish’s regimen included a diet that was very low in fat and completely vegetarian. It also emphasized moderate exercise, stress-reduction techniques, and quitting smoking (if applicable). The diameter of the coronary artery was measured at the beginning of the study and again at the end of the study one year later. For people following the usual recommendations for coronary patients, the average percentage of narrowing was 42.7% at the beginning of the study and increased to 46.1% at the end of the study. For patients on Ornish’s plan, the average percentage of constriction was reduced 2.2% during the period of… Read more »

fifek2000fifek
Guest

But, in fact, what is Low Carb Diet? How much of carbs should I eat in this diet? Less than 100 g a day or 10% of day energy demand. Is it somewhere determined? What about proteins and fats then? How much of them. I assume that eating 50 g of carbs a day and the same amount of fat and proteins is totally different while I would eat 50 g of carbs and 200 g of fats and 100 g of proteins. I mean: the same amount of carbs is not crucial (ok, less than 100 g), but rather… Read more »

Cherry
Guest
Cherry

Very amusing comments – didn’t learn much about your opinions on LCHF or the affects of saturated fat when keto adapted, However I thought some of the comedians among you might enjoy this ‘Low cholesterol levels associated with higher death rates in critically ill patients’ https://www.ncbi.nlm.nih.gov/pubmed/24727873 and Charles, just enjoy your egg!

charles grashow
Guest
charles grashow

@Cherry

Was the low cholesterol due to the patients being critically ill OR were they critically ill because of their low cholesterol??

Yes – I enjoy my hard boiled egg in my morning smoothie.

Andrés
Guest
Andrés

@charles grashow:

[IRONY]It is a pity that ethical thing about not killing on purpose and stopping a trial because of it[/IRONY]: Effect of statin therapy on mortality in patients with ventilator-associated pneumonia: a randomized clinical trial (via David Evans).

Paul Jaminet has written extensively about the role of lipoproteins on the immune system.

Judit Victor
Guest

Hi Doc, I think I am the ONLY person with Heterozygous Familial Hypercholesterolemia in the UNIVERSE who opted for total Keto dieting on 1 February 2012. Within few weeks my numbers came down from 13 to 6 for the first time in my life. Troublre is, no-one of my ilk wants to do the diet. I didn’t care if I died or not – i HAD to try this diet since none of my family tolerates statins at all. We WILL die from those pills – we get kidney failure very quickly (from rhabdomyolises). I can NEVER go off this… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

@ Judit Vicor.
Thanks for the comment. It’s very interesting to see how well your lipid numbers have responded to a ketogenic diet. It shows very well how differently we respond to different diets. I’m sorry to hear about your son and I really hope he’s doing well.

Max_Headroom
Guest

Hi, Judit, found your comment by chance and I need to comment: Nope, you’re NOT the only one! I’m having heterozygous FH type IIa and I’ve tried a ketogenic diet in 2013 for 8 weeks. Same results: Fantastic LDL (below 60) TG and blood glucose doing nicely, tested after 4 and 8 weeks. But my physician didn’t believe those benefits and tested for elevated CRP – result: everything in working order, 3.6! But since it was too hard to follow this diet long-term I’ve switched no to a more “mild” form of LCHF. I’m limiting saturated fats but include much… Read more »

charles grashow
Guest
charles grashow

@Andres

Your point being?

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