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.
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.
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, Canada, Australia, 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”.
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….
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.
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.
106 thoughts on “Will the Popularity of LCHF Trigger a New Epidemic of Heart Disease?”
“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 know how that story goes – plaque forms; plaque ruptures; heart attacks or strokes ensue…”
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 LDL is that they will usually have already received them shortly before, when it was a VLDL or IDL particle.
As it only takes a few seconds for blood from anywhere in the body to reach the liver, our blood could easily be kept almost completely clear of LDL if this was in fact part of the design.
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.
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 die from CHD, die before they reach hospital, most commonly due to arrhythmia. Most of these deaths can also be prevented if the patient reaches hospital before the arrhythmia occurs.
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 the IMPACT models.
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
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.
Did you read comments on Medscape?
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.
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?
Stew. You’re right about the importance of particle number, I’ve actually written some articles addressing the issue:
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.
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.
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.
“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 safa has an adverse effect on lipids compared to unsaturated fats is not misleading. The effect MAY be inconsequential in some, especially if your lipid levels are fine.
Second of all, large LDL particles are virtually just as atherogenic as the smaller ones when compared PARTICLE BY PARTICLE. In a previous conversation I referred to e.g. MESA study which clearly showed that once you sort the particle numbers, ANY kind of LDL is clearly atherogenic in large quantities. Just like “Stew” pointed out. In addition, if increasing safa decreased the risk by increasing particle size (which, consequently, would have to matter), this would be seen in both epidemiological studies and RCTs?? However, there is no evidence suggesting that increased safa intake – after adjusting for confounders – is beneficial. Or if you have some, please do show it.
Of course, the evidence from cohort studies and RCTs points out that focusing MERELY on safa/fat intake is not warranted for a variety of reasons (it’s often accompanied by decreasing fat intake & rising carb intake which isn’t ideal; changes in diet are too minor to make a difference in risk factors etc.etc.). This, however, does not mean what some people interpret it to mean.
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) less strongly associated with CHD than small particles. Thus, he has suggested that SFA induced increases in LDL-cholesterol may not signify a proportional increase in CVD risk. However carbohydrates (especially sugars) have a major influence on smaller particles. Since smaller particles have less cholesterol per particle, their levels can increase with higher carb intake without a proportional increase in LDL cholesterol. “So, stating that saturated fats adversely affect blood lipids is misleading.”
Of course it is possible that particle number is the main issue, although everybody doesn’t agree on that. It is possible that the association between small LDL and heart disease reflects an increased number of LDL particles in patients with small particles.
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?
Yes Charles. Do you know how to do it? 🙂
Have you read Track Your Plaque by Dr William Davis?
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. To me, it does not appear that the view of this scientists are not taken too seriously by anyone else apart from those in denial.
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.
stop being naive. Ronald Krauss is a bullet-proof, industry sponsored, 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 counsil does what he is paid to do, spray confusion. And unfortunately it’s working, just look at Doc. Doc cites Krauss material and thinks SFAs are a red herring. You never see Krauss claiming that he has been outwardly misunderstood even though his material forms the basic staple of every diet-heart denialist.
In addition, Krauss hold several patients in regards to LDL phenotype techology, which probably explains why he is so keen making things more complicated than they are: as noted by Stamler in regards to Krauss ideas.
“As to item 10, the concern (1) about influences of dietary composition on triglycerides, HDL cholesterol, glycemia/diabetes, and “metabolic dyslipidemia” is also one-sided. The evidence is overwhelming that the main “driver” of these traits is caloric imbalance producing overweight/obesity (10). These metabolic traits all respond favorably to even modest weight reduction with diets of varied nutrient composition, including heart-healthy fare (see below) (11, 12)”.
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!)
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.
“… 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…
“… [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?
“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.”
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 his opinion (based on research) less strongly associated with CHD than small particles.”
Which is not the case when you look at the issue particle by particle (EPIC, MESA, two mention a couple of recent contributions in the field) and which applies – for the most part – to people with metabolic syndrome. You need to put Krauss’ work into context. Science has a tendency to progress. 🙂
“Thus, he has suggested that SFA induced increases in LDL-cholesterol may not signify a proportional increase in CVD risk.”
On healthy people, if the increase is minor and the context is othewise ok. However, the same goes for carbs: there’s no evidence to suggest that. Not even in the case of sugars – minor increase and the context. Thus, if you choose to highlight the dangers of one and not the other, aren’t you … Well, cherry-picking?
“Of course it is possible that particle number is the main issue, although everybody doesn’t agree on that.”
To state that one particular aspect of LDL is the “main issues” is, in my opinion, misleading. The best option is to have both low LDL-C and LDL-P.
“It is possible that the association between small LDL and heart disease reflects an increased number of LDL particles in patients with small particles.”
Not just possible but the current valid scientific opinion.
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 🙂
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 <20 nm. That would mean that the whole research was conducted in sdLDL region. But that doesn't change the main issue: why would larger particles be more atherogenic, if particle size was the main problem?
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. The results of the study are unimportant in this context.
In fact the study showed that both large and small particles were independently associated with risk, but intermediate size particles less so. These are just the results of a scientific study. Whether they fit into “my take” or not is irrelevant. You know I change my mind all the time. That’s the prize you have to pay for believing in science.
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 it’s “misleading” to say that safa adversely affects blood lipids unless you yourself believed so? Or was it just a case of missing “According to some scientists”? 🙂
Personally, I don’t care what your “take” is or whether you even have on. It’s okay to disagree. I just find your stance a bit confusing in this case.
In addition, did the recent paper you cite above even adjust for particle numbers?
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.”
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.
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.
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 !
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?
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
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 meta-analysis but included a chief editorial that tore down the whole paper and made it look ridiculous. I have never seen indication that Doc has bothered to actually read nor consider the message in the editorial by Stamler (2010). In an article from the 1977 Stamler presents the evidence against SFA in attempt to answer whether the AHA have been wrong about SFA and dietary cholesterol all the years.
Moreover, I meant to say that Doc shouldn’t be to confident about the message sprayed by Ronald Krauss, because the people that matter have referred some of his material as “fiasco”. In other words, highly influencial people do not take his work seriously. Stamler expressed his deep skepticism for Krauss idea’s as well. In addition, I think Doc should not put high hopes for the new paper published in annals of internal medicine either. Among other things, Stamler (2010) noted that stronger the methodology of the study, stronger the association of SFA and CHD even when serum lipids are adjusted. Many observational studies using the 24-hour dietary recall could not even show association of dietary intake of SFA and serum cholesterol levels. Moreover, the bulk of observarstudies that looked at SFA intake and CHD in the past adjusted for serum lipids.
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 ??
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 then removed from the monkeys diet and replaced with a cholesterol-free diet with either 40% of calories from corn oil or low-fat chow with 77% calories from sugar for three years, resulting in a reduction of serum cholesterol to <140 mg/dl and a marked regression of atherosclerosis.
In experimental models maintaining elevated LDL is all that it takes to induce atherosclerosis and sudden cardiac death. Global epidemiology shows that populations that are plagued by nearly all risk markers but having low LDL are virtually immune to CHD (The Japanese f.ex who had very high blood pressure, low HDL, moderately elevated triglycerides in the 1960s and nearly all of the men smoked, yet they showed 1/37 of the level CHD mortality compared to Finland at the time)
“The molecular basis for the effects of dietary saturated fat on plasma LDL cholesterol levels is well understood. Saturated fat influences the LDL receptor activity of liver cells as described by Brown and Goldstein, dietary saturated fat suppresses messanger RNA synthesis for the LDL receptor. This decreases hepatic LDL receptor activity and slows the removal of LDL from the blood, thus increasing the concentration of LDL cholesterol in the blood. Dietary cholesterol augments the effects of saturated fat further suppressing the hepatic LDL receptor activity and raising the plasma LDL cholesterol levels”.
–Heart Disease, Environment, Stress and Gender [proceedings of the NATO Advanced Research Workshop on Increase in Coronary Heart Disease in Central and Western Europe: Stress and Gender Related Factors, 20-24 May, 2000, Budapest, Hungary]
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. “
“Lovastatin is used for:
Lowering high cholesterol in certain patients. It is used along with an appropriate diet. It is used in certain patients to reduce the risk of heart attack and chest pain caused by angina. It is also used to slow blood vessel blockage and to reduce the need for medical procedures to open blocked heart blood vessels. It may also be used for other conditions as determined by your doctor.”
“Usual Adult Dose for Hyperlipidemia
Initial: 20 mg orally once a day with the evening meal.
Maintenance: 10 to 80 mg/day in 1 or 2 divided doses.
Lower doses are utilized for patients requiring a smaller reduction in cholesterol level.”
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.
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.
Have you had your ApoB measured? LDL-P, small LDL-P?
High trigs might be problematical.
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.
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?
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
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.
Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis
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 to 1.27) for trans fatty acids when the top and bottom thirds of baseline dietary fatty acid intake were compared. Corresponding estimates for circulating fatty acids were 1.06 (CI, 0.86 to 1.30), 1.06 (CI, 0.97 to 1.17), 0.84 (CI, 0.63 to 1.11), 0.94 (CI, 0.84 to 1.06), and 1.05 (CI, 0.76 to 1.44), respectively. There was heterogeneity of the associations among individual circulating fatty acids and coronary disease. In randomized, controlled trials, relative risks for coronary disease were 0.97 (CI, 0.69 to 1.36) for α-linolenic, 0.94 (CI, 0.86 to 1.03) for long-chain ω-3 polyunsaturated, and 0.89 (CI, 0.71 to 1.12) for ω-6 polyunsaturated fatty acid supplementations.”
Potential biases from preferential publication and selective reporting.
Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”
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.”
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.””
CV Risk and Saturated Fats: The Debate Roils On
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” .
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 in processed meats, that are also present in high-SFA foods that lead to adverse health effects typically associated with high SFA intake.
“The meager effect that saturated fats have on serum cholesterol levels when modest but adequate amounts of polyunsaturated oils are included in the diet, and the lack of any clear evidence that saturated fats are promoting any of the conditions that can be attributed to PUFA, makes one wonder how saturated fats got such a bad reputation in the health literature,” Lawrence writes in the review published May 1, 2013 in the journal Advances in Nutrition.”
Dietary Saturated Fat Has Undeserved Bad Reputation, Says Review
“The adverse health effects that have been associated with saturated fats in the past are most likely due to factors other than SFAs,” the article concludes. “Consequently, the dietary recommendations to restrict saturated fats in the diet should be revised to reflect differences in handling before consumption . . . It is time to reevaluate the dietary recommendations that focus on lowering serum cholesterol and to use a more holistic approach to dietary policy.”
Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence
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 their traditional very-low-fat diets; in Ornish’s celebrated study, a moderate rise in triglycerides coincided with a marked reduction in coronary events. However, it must pointed out that at later stages, also the triglycerides came down on Ornish’s patients. Atherosclerosis is simply LDL disease, and frankly, nothing else. No matter how fat you are, no matter how many fags you smoke per day, no matter your diabetes status, if your LDL has been very low for a long period of time, you are doing to die in CHD. This fact is verified not only in experimental animal models but also in thousands of African-Americans with hetorozygot PCSK-9 knock-out mutation. Not a single death from atherosclerosis verified in these people. As top-snotch atherosclerosis researcher Evan Stein concluded:
“There is only one well-established relationship between blood cholesterol lipid fractions and coronary artery disease (CAD) that meets all the Heiss and Tyroler criteria of causality. While there are a number of blood lipid fractions, only LDL cholesterol satisfies these criteria”
3/4 of the existing world was on low-fat starch-based diet still couple decades ago, so this is pretty much a good solution to every single person out there, set aside individual food allergies. Look for the blue zones.
you are NOT going to die in CHD, that is.
“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.”
“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 HDL cholesterol:
>> Men – Less than 40 mg/dL
>> Women – Less than 50 mg/dL
* Blood pressure greater than or equal to 130/85 millimeters of mercury (mmHg)
* Fasting glucose greater than or equal to 100 mg/dL”
“These criteria were proposed by the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) and are the most current and widely used.”
And because I already brought attention to the potential conflicts of interest in the NCEP panel… I’ll point out that: similarly the WHO diagnostic criteria for Metabolic Syndrome fails to make any mention of LDL but DOES put an emphasis on Triglycerides and HDL.
Maybe they don’t have any “top-[notch] atherosclerosis researcher[s]” working for them.. do ya think???
As for causality I don’t think ANY has yet been established.. all we have so far is association… just like the almost 100% association between firefighters and house-fires.. do we assume they cause them?
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.
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 not lead to increased early mortality… I also recall during basic naval medical training how we heard about the widespread atherosclerosis seen in the young USA men and boys being operated on in war-torn Vietnam. It came as a surprise to the surgeons, as it did not fit into the general ideas about CVD, current then and to a large extent still around today.. 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.
Too many of the studies he quotes (intermixed with his own opinionated commentary) from his always world-leading, authoritative, top-notch researchers (while anyone who thinks differently is a charlatan, quack, denier etc…) stop well short of mortality and rely on oh so scary conclusions based on atherosclerosis or just “LDL” numbers. Leaving readers to draw their, own inevitable conclusions GASP! Meantime we have populations (such as the French — at least traditionally) eating diets high in SFAs and living to a ripe old age.
For an anonymous commenter who seems to haunt many blogs — and seems unable to even keep track of his own name — to categorically promise “…you are NOT going to die in CHD…” is downright barmy and in my view unsafe. He repeatedly shows that he cannot be counted as a credible source.
“LDL” is not a single homogenous, unified topic.. it has many subtleties and nuances — as you rightly say, it needs to be considered alongside many other risk factors.
Heck we still have MDs who talk about cholesterol blocking arteries like the sludge building up in plumbing pipes for cripes sake… I think it is time we moved on with a more rational discussion.
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 high in SFAs and living to a ripe old age.”
The French paradox is old news, I’m afraid. Not a real paradox.
“LDL” is not a single homogenous, unified topic.. it has many subtleties and nuances — as you rightly say, it needs to be considered alongside many other risk factors.”
Of course. LDL per se isn’t bad. It’s just that abnormal levels of it are clearly a risk factor. Now, of course not EVERYONE who has high LDL-C or LDL-P will be in problems. Nonetheless, on population level (and often on individual level too), it’s best to keep them in check. Heck, with weight management and proper diet, that’s not even a biggie.
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??
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. 🙂
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!
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 to think it important to ascertain the impact of omega-6 linoleic acid restriction on heart disease morbidity and mortality. Excerpt:
“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 intake) in the other. It would study cardiac endpoints and continue for about 5 years.” https://www.karger.com/Article/Pdf/324749
In October, 2010 J. Bruce German and Cora J. Dillard published another analysis of the saturated fat controversy.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950926/ They said, in part, “Lipids and their simplest structural elements, the fatty acids, provide myriad functions at all levels of cellular life. Nutritional scientists are still wrestling to develop a rudimentary understanding of the roles that dietary lipids exert.”
Personally, I’m delighted that the anti-saturated fat campaign is losing traction. I’m still concerned about the lack of interest in question of whether high omega-6 intake is healthy or harmful. Biochemistry research suggests that high omega-6 intake is problematic. Excerpt from Page 191 of The Modern Nutritional Diseases: and How to Prevent Them by Fred and Alice Ottoboni:
“BIOCHEMICAL LESSON: The significant point is that good health depends on regulating the D5D enzyme. High insulin levels due to dietary sugar and starch and high dietary omega-6 to omega-3 ratios, stimulate the D5D enzyme, and move the biochemical set point from normal toward inflammation. On the other hand, control of dietary sugar and starch, reduction of LA in the diet, and a daily supplement of fish oil to provide EPA will inhibit the D5D enzyme so that the appropriate amounts of both proinflammatory and anti-inflammatory eicosanoids are produced. Keep in mind that all of the eicosanoids, both the so-called good and bad, are important. The body is designed to use eicosanoids with opposing effects to control vital functions. In a state of optimum health, the good and the bad eicosanoids balance one another.”
While researchers are finally taking note of added sugars and refined carbohydrates, they are, more or less, still ignoring the omega-6 hazard. Meanwhile, the edible oils industry, through selective breeding, is quietly reducing the omega-6 content of soybean, canola, corn, and sunflower oils. Fro example:
When these seed oils have more or less fully replaced the current oils, there should be a noticeable reduction in chronic inflammatory disease and depression.
“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.
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 intake) in the other. It would study cardiac endpoints and continue for about 5 years.” https://www.karger.com/Article/Pdf/324749
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.
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 agents also lower HDL-C in humans by tackling impaired HDL metabolism, who knows. In Western epidemiology, those with high HDL-C have other protective elements in their HDL cholesterol due to genes and/or lifestyle or those that have low HDL-C suffer from plethora of conditions that influence their risk, and the low HDL-C in these people is just some kind of red flag, a passive bystander. This is what explains the association, not aggregate HDL-C.
don’t be confused because of blog post. Just listen to the real experts.
“The dramatic success of cholesterol-lowering therapy might suggest that low cholesterol levels would be all that is required to prevent the development of atherosclerotic disease or halt or reverse established disease. This might be true if plasma cholesterol concentration could be reduced to very low levels long before the usual time of development of clinical disease”
“Experimental studies directly support the central role of LDL in atherogenesis. Current concepts suggest that higher plasma levels of LDL lead to increased transport into the intima, where LDL becomes bound to proteoglycans, greatly prolonging its residence time. This makes LDL susceptible to a variety of modifications, including oxidation, enzymatic modification, nonenzymatic glycation, aggregation, and immune complex formation. All of these lead to enhanced macrophage uptake, foam cell formation, and initiation of the cascade of events resulting in progression of the atherosclerotic lesion”.
Yes, you are right, 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 is good for a people in their 20s and 30s but nothing to cheer for in people who have existing disease, in these people the LDL must be lowered literally close to zero unless they are on a low-fat whole-food vegan diet. Esselstyn and Ornish fare seems to make people immune to CHD even though many of these people don't show perfect LDL levels. I don't what explains this. Anyways, there are on-going trials on PCSKY-9 trials that test whether lowering LDL-C to the levels unheard before will show benefit to the background statin therapy, all the scientific leads indicate that these trials will be highly successful.
“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 with CHD, I think you can be rather calm with your risk profile. If you have been diagnosed with CHD you need to quee for the injections targeting PCSK9 to get your LDL down to 20s. Although, you could improve your diet a bit. Eggs are completely unnecessary. I understand that beef is culturally important food for many, but eggs, please.
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 is good for a people in their 20s and 30s but nothing to cheer for in people who have existing disease, in these people the LDL must be lowered literally close to zero unless they are on a low-fat whole-food vegan diet. Esselstyn and Ornish fare seems to make people immune to CHD even though many of these people don't show perfect LDL levels. I don't what explains this"
Esselstyn stated tha with TC<150 and LDL-C<80 you are HEART ATTACK PROOF even if you smoke, drink, etc!
Twenty questions on atherosclerosis
Of the various atherosclerotic risk factors, which one is an absolute prerequisite for development of atherosclerosis?
If the LDL cholesterol level is <100— and possibly it needs to be <80 mg/dL—the other previously mentioned risk factors in and of themselves are not associated with atherosclerosis. In other words, if the serum total cholesterol is 90 to 140 mg/dL, there is no evidence that cigarette smoking, systemic hypertension, diabetes mellitus, inactivity, or obesity produces atherosclerotic plaques.
BTW – on the last last blood work my HDL-C was 48, Triglycerides were 36 and ApoB was 64
I've taken new blood work recently (NMR, hsCRP, etc )as well as a CT scan to determine CAC score and a carotid artery ultra sound. Will see my cardiologist next week – will post results soon after
Per my scan in 12/2007 my CAC score was 30 SO plaque should start to stabilize and regress
“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.
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 majority. This is the first time I see Nordic scholars taking lifestyle measures seriously. I repeat that the undisputed fact is that there’s not a single individual with heterozygot PCSKY9 mutation who died in MI. Yet, most of the African-American individuals have all the other risk factors present in them, high glucose, elevated blood pressure, overweight, etc.
Roberts WC. It’s the cholesterol, stupid! Am J Cardiol 2010;106:1364-6.
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 a heart attack.
Cohen and coworkers concluded that the reduced risk of coronary artery disease among those with the PCSK9 mutation was most likely related to their low levels of LDL-C. However, they did not exclude the possibility that PCSK9 may also have direct atherogenic effects that are independent of plasma levels of LDL cholesterol.
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 department as Hobbes and Cohen. Pay attention also to the baseline date of Japan from the 7CS.
Yes, the patient had very low LDL, but we don’t his life-long cumulative exposure. Morever, as the Swedish scholars pointed out, LDL levels drop temporarily after MI.
Mie, you’ve probably misunderstood something, but I actually don’t have the tendency to spray my own ideas. I continue to rely on real, top experts.
Evaluating lipid-lowering trials in the twenty-first century.
“…Only pure vegetarians for practical purposes do not need statins, most of the rest of us do”
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?
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 scholar has figured out this more thoroughly than you have just simply doesn’t occur to you.
Yes, Mediterranean diet added to the background statin therapy with diuretics, aspirins, blood-clotting medication thrown in has indeed shown to be beneficial in terms of CHD protection next to controls eating even poorer diet. However, these trials do not support the idea that Mediterranean diet alone in a drug-free context is able to provide physiologically normal cholesterol levels for most of the adult population. And, that was pretty much the point Roberts tried to make.
“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 so I’ll leave you to it. But you’ll have to keep it up by yourself from now on.
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.
Do you have a link to the full paper
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 be concerned about comfort level, appetite control, body composition, and energy expenditure. When the gut bugs get what they need, the host body gets what it needs maintain health.
Feed researchers don’t want growing hogs to get restless between feedings. To keep the animals comfortable they add resistant starch to the diet. Here’s a recent AllAboutFeed article:
Feeding pigs more fibre may lead to less aggression and improve gut health while maintaining performance. However, type of fibre and feeding level are important factors influencing these effects.
According to Wageningen UR researcher Carol Souza da Silva “Fibre gives restricted-fed pigs more satiety, whereas ad libitum-fed growing pigs compensate the lower energy in fibrous diets by increasing intake.”
Souza da Silva tested different types of fibre in her research, but found that feeding fermentable fibres was best for pigs. “Such as cassava roots or raw potatoes.” The aim of her research was to determine how and which types of fibres influence satiety, to prevent pigs from becoming hungry between meals, thereby improving their welfare. In her research she noticed that pigs fed resistant starch maintained a ‘full’ feeling for up to more than seven hours after their meal. “The pigs were less hungry, which was also reflected in their behaviour. Moreover, resistant starch was found to change gene expression patterns and microbiotica composition in the hind gut, reflecting improved gut health and stabilized glucose levels.”
Feeding more fibre to sows prevents them feeling hungry, avoiding behavioural problems. More fibre in the ration is also good for fattening pigs, according to the researcher. “Their energy system can, to a large extent, adapt to this reduced energy ration. They compensate this by increasing their intake, consequently growth is then similar to fibre-free rations . In future our research will focus on the body composition after slaughter, which is influenced by fibrous diets.”
During her research Souza da Silva collaborated with human nutrition researchers. “They have similar questions about satiating effects of fibre and the role in prevention of overweight and obesity. The digestive physiology of pigs and humans is very similar”, she adds. “We supply each other with information and results.”
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.
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?
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 dyslipidemia.”
Let’s wait to see what incredible ad hoc explanation Dickie-Poo can come up with to dismiss this 😛
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 the LCHF cuisine showed remarkably worsen arteries, even compared to baseline scans. Now, I don’t have the paper, so I don’t know what people actually ate, but probably nothing remotely different from that espoused by popular low-carb books. You know, those books which start by addressing how Keys cherry picked the seven countries. Diets high in saturated fat are not fed to people enrolling to trials paid by the Atkins foundation. But somehow people reading about these trials get the impression that SFA and dietary cholesterol are both red herrings when, in fact, the Atkins group is put to a starvation diet and guided to ditch animal fats in favor of plant fats. Obviously this doesn’t happen when free-living people get to self learn about the low-carb diets.
in regards to nonsense about high triglycerides having an impact on VeryLow36 health, in the context of whole-food vegan diet, 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.
An elevation of triglycerides reflecting decreased triglyceride clearance may not be pathogenic — relevance to high-carbohydrate diets.
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.
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.
At the 12 year mark multiple patients had LDL > 70. Why would there be regression?
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.
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 their positions, or hopefully even be granted tenure? To be invited (and paid) to speak as a domain expert? etc… etc…
Yes… yes… I do see what you mean — perhaps you ARE finally making some sense after all 😛
“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 😛
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?
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..
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 point damage occurs? With 50%+ with heart disease having normal lipid panels and 50%- with heart disease with higher than normal lipid panels, I chose going VLCHF because I see no advantage to continuing my use of statins or to be scared of SFA’s.
Dr. Sigurdsson, I do appreciate your views and acknowledgement of arguments from both sides. I tend to believe in your main points that there is nothing really definitive proving any one of the lipids is good or bad. I don’t know how others can be so one sided knowing there is contradictory evidence out there that is ignored to try to prove their point.
“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 the study, from 40.0% to 37.8%. For the patients with the most constriction, the difference was even greater.
Since the 1990 study, Ornish and various coauthors have continued to research how lifestyle changes alone can positively affect heart disease in both the long- and short-term. In 2007, he published a study in the Journal of the Society of Behavioral Medicine that found reductions in the risk factors of coronary heart disease in just three months.”
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 proportions. Am I right? What do you think?
Therefore, different results of low each carb diet can be obtained, assuming constant (low) amount of carbs, but different ratios of fats/carbs/proteins.
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!
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.
[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.
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 diet again. Sorry about all the cap locks but I need to tell this. My trigs came down from 3 to 0.7. I just wish I could find a cardiologist here in South Africa who would look at what happened to me but of course, such do not exist. But i DID impress my GP. My sons however, also have the disease and thus far are not on the LCHF diet. I cannot force them. My eldest (34) has just had quintuple bypasss surgery. My heart is broken by this, but they have to decide themselves.
@ 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.
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 rapeseed-, olive- and lineseed-oils. I’ve eliminated bread, grains, potato and noodles and stick to lot of greens but also dairy products. I’m under 50 g carbs a day.
I’m on statins (atorvastatin) and want now to get rid of ezetimibe if the results (next testing is in April) are still that great!
It’s astonishing; my whole life I was pushed by “official recommendations” to a carb-rich diet (60%) and now I’m learning: it’s the insulin, stupid!
I hope, I can drop off the last 10 kg and head on for a while…BTW, ultrasonic sound checking of major neck arteries gave no hint for artheroclerotic plaques so far…and I’m in the mid-40s!
Keep on going!
Your point being?
@charles grashow: Bringing down cholesterol of critically ill patients seems quite a bad idea. I think the answer to “were they critically ill because of their low cholesterol??” is yes. From Papazian et alter: “In statin-naive patients, day-28 mortality was 21.5% (95% CI, 15.4% to 29.1%) with simvastatin and 13.8% (95% CI, 8.8% to 21.0%) with placebo (P = .054)”.
I am not sure it is a good idea bringing it down on healthy people either. I am acting as it is not while waiting to see convincing evidence about all cause mortality. I don’t like all that focusing on cardiovascular disease only. I don’t like the oversimplification of cholesterol role in the human body.
The study you linked to was on mortality in patients with ventilator-associated pneumonia. Not valid IMHO
I don’t uderstand the whole discussion, meta-analyses, cohort studies etc. Biochemistry is science, as physics, mathematics, chemistry. There are no sucspicions, opinions, alternatives. There are just facts. And the fact is one – no insulin – no atherosclerosis. No matter what lipids concentrations in blood are found. Of course, unfavorable proportions of lipids follow from wrong diet, which cause insulin secretion.
But as well as in Low Carb High Fat Diet, as in Montignac, Dukan, Ornish and each and every diet where there are no simple carbohydrates or their intake is very low, causing slow insulin secretion, there are no atherosclerosis. The problem is just metabolism of glucose in arthery walls (pentose or hexose paths, which depends on insuline secretion). Nothing more.
I have been on a LCHF diet for 4 months. I have also been doing some walking. I have lost 40 lbs. My HDL has gone done from 165 to 105. My BP has gone down from 145/90 to 128/70. I showing low blood protein before… still don’t know what that actually means, but now I’m not. Actually, my doctor was thrilled/ surprised/ impressed when he read the blood work – I had improved in nearly every category – and this was a full blood work up. He asked what have I been doing? When I told him he looked confused! But he said to KEEP DOING IT because it’s working. I’m not a doctor (obviously) but I do know this is the only thing that has ever worked for me. Only medication I take is synthroid… so it has all been diet and light exercise. The reason I wanted to do a LCHF diet is I am obese and my health was declining. I had tried every diet and exercise program I could find and nothing worked for me. When I read about LCHF… the idea of eating things that are natural really resonated with me. I mean – do I really need to eat things with ingredients I can’t pronounce? And well… the line fat doesn’t make you fat, sugar makes you fat – that really got me. I don’t know if I’m doing the right thing (I’m sure others will say I am not), but it’s working for me – I feel great, have more energy than I’ve had in years, I’m losing weight and my blood work shows much improved in many areas. And my BP is lower. So who’s to criticize? Would you rather obese patients keep gaining weight and being unhealthy? Or if they find something that works… shouldn’t they go for it?
Well done, I live a LCHF lifestyle and after a year have never felt happier or healthier. I was also obese and have had improvements in my blood chemistry. Its is great to be able to eat until you are satisfied and enjoy good food. Best of all it doesn’t take constant will power to achieve your health goals.
Why has my blood pressure normalized since eating 70 percent fat and the rest protein , trying to ignore carbs….my cholesterol and triglycerides have also normalized and I have lost weight have more energy?……why is it that until the introduction of carbs in the native North American population was diabetes, and obesity non existent?…..argue all u want….I have seen the results!
I have been reading these messages with interest. I am not qualified in anyway to comment but thought I would share my experience of LCHF.
Lost three inches from waist and obviously loads of Kgs.
Blood pressure lower.
Energy levels up.
“Normal” LDL and good HDL,lower CRP and triglycerides; according to Doctor.
So accordingly to many I will not live as long but hey I feel so much better on LCHF and my quality of life has increased considerably.
Also my 88 year old father has been LCHF for over two years, I now never see him, he is gardening virtually everyday and has incredible levels of energy. Unbelievable transformation for someone who is 88!
Incidental perhaps but…
Let the derision begin.
Voleks work seems to indicate that increased sat fat intake leads to decrease blood sat fat content in context of vlc
The other feinman : https://feinmantheother.com/2012/02/22/saturated-fat-on-your-plate-or-in-your-blood/
What year is this? We were hearing this way back when the medical establishment was getting going on the obesity epidemic.
To me the whole cholesterol-hypothesis seems to be seriously flawed. It is much more probable that an unfavorable lipoprotein-profile represents a marker of the disease rather than the disease itself. For example, why do we see a massive drop in the rates of stroke and coronary artery disease in Japan during the last decades that coincide with rising cholesterol levels in that population? This, and so much more, is pointed out in dr Malcolm Kendrick’s book, “The Great Cholesterol Con”. For me, his alternative hypothesis, a HPA-axis dysfunction, comes much closer to harmonising our current understanding of basic biochemistry and physiology with the known cardiovascular risk factors.
Very interesting article. Also, you have a picture of meat on a bone. What meat is that?