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Atherosclerosis is the most common underlying cause of cardiovascular disease (CVD. It is caused by a complex interplay between lipoproteins, white blood cells, the immune system and the normal elements of the arterial wall.
Atherosclerosis can affect all arteries in the body but seems to have a strong affinity for the coronary arteries. The resulting thickening of the arterial wall and the building of plaques may lead to blockages and blood clotting causing damage to the heart muscle. The result is coronary heart disease, the most common cause of death in most countries around the world.
Lipids and lipoproteins appear to play a role in the development of atherosclerosis. Lipoproteins are the particles that transport cholesterol and triglycerides in the blood stream. It is possible to measure a number of different lipoproteins in blood as well as they amount of fat carried by specific lipoproteins.
According to the experts, blood levels of cholesterol transported in low-density lipoprotein cholesterol (LDL cholesterol) are strongly associated with the risk of developing coronary heart disease while cholesterol transported by high-density lipoprotein cholesterol (HDL cholesterol) is associated with low risk.
In other words, LDL cholesterol is atherogenic while HDL cholesterol is not.
Consequently, food that raises LDL cholesterol may be considered atherogenic and should be avoided while food that lowers LDL cholesterol should be preferred. This is the foundation of the diet-heart hypothesis, the cornerstone of public health advice on diet and health.
Apolipoprotein B (apoB) is another example. High blood levels of apoB are associated with increased risk of heart disease. On the other hand, apoA1 is associated with low risk. Studies suggest that the apoB:apoA1 ratio is more effective at predicting heart attack risk, than either the apoB or apoA1 alone. So, a high apoB:apoA1 ratio is atherogenic while a low ratio is not.
Health authorities in most countries recommend restricting saturated fats because of their adverse effects on blood lipids. Instead, monounsaturated and polyunsaturated fats are recommended.
Thus, because of its high content of saturated fat, the intake of regular fat cheese should be restricted, and replacement of high-fat dairy products with low-fat alternatives is recommended.
Red meat is also regarded as a major contributor to saturated fat intake. Therefore, limited intake is recommended by most health authorities.
On the other hand, fiber and complex carbohydrates are recommended because they tend not to lower LDL cholesterol and are therefore not considered atherogenic.
But, can we rely on these public health recommendations? Should we avoid food because of the simple fact that it contains saturated fat? Is it possible that specific saturated fatty acids may affect blood lipids differently? Furthermore, could the effects of saturated fats on blood lipids depend on other nutrients in the food matrix?
Recently these issues were addressed in an interesting scientific paper by Danish investigators at the Department of Nutrition, Exercise and Sports at The University of Copenhagen. The results were published online in the American Journal of Clinical Nutrition and can be assessed here.
Which is Most Atherogenic, High-Fat Cheese, High-Fat Meat or Carbs?
The Danish investigators compared the effects of three different diets on blood lipids and lipoproteins. Two of these diets had a high content of saturated fat in the food matrix of either cheese or meat. All three diets contained the same amount of calories.
The CHEESE diet contained high amounts of dairy fat while the MEAT diet had a high content of high-fat processed and unprocessed meat containing similar amounts of saturated fat.
The third diet had a high-carbohydrate content. The energy from cheese fat and protein in the CHEESE diet was replaced by carbohydrates and lean meat creating a low-fat, high-carbohydrate diet (CARB).
The main carbohydrate-rich foods used to replace cheese in the CARB diet were fruit, white bread, pasta and rice, marmalade, and cake, sweetened biscuits, and chocolate.
In the CHEESE and MEAT diets, 35% of energy came from fat, and 50% from carbohydrate, whereas in the CARB diet 25% of energy came from fat and 60% from carbohydrates. The protein content was the same (15%) in all three diets. In the CHEESE and MEAT diets, 15% of energy was from saturated fat.
Fourteen overweight postmenopausal women were randomized to three full-diet periods of two weeks duration separated by washout periods of no less than two weeks. A cross-over design was used, Hence, the participants tested all three diets but the sequence of the diets was randomized.
Results
The CHEESE diet caused a 5% higher HDL cholesterol, and 8% higher apoA1 concentration, and a 5% lower apoB:apoA1 ratio than the CARB diet.
The MEAT diet caused an 8% higher HDL cholesterol, and a 4% higher apoA1 concentration than the CARB diet.
There were no differences between the CHEESE and MEAT diets in HDL cholesterol and apoA1 concentrations.
There were no significant differences between diets in total cholesterol, LDL cholesterol, triglycerides, and apoB concentrations.
Furthermore, there were no differences in fasting glucose, insulin concentration or insulin resistance (HOMA-IR) between the three diets.
Conclusions
The authors of the paper conclude that cheese consumption of 2-3 times the average intake in Danish adults did not have detrimental effects on blood lipids and lipoprotein concentration.
They write, “Danish dietary guidelines recommend reducing the intake of saturated fat to reduce CVD risk. However, our trial and others studies suggested that the choice of nutrients or foods as a replacement for saturated fatty acids is highly important with respect to CVD risk. Recent meta-analyses on dietary fatty acids and risk of coronary outcomes did not suggest monounsaturated or polyunsaturated fatty acids to be preferable replacements for saturated fatty acids (1,2).”
Furthermore, the authors conclude that the fact that total cholesterol and LDL cholesterol were similar with the CHEESE, MEAT, and CARB diets may be explained by the relatively high content of monounsaturated fats in the CHEESE and MEAT diets. Studies suggest that monounsaturated fats may reduce LDL cholesterol and raise HDL cholesterol significantly.
And, the paper’s final words:
Diets with cheese and meat as primary sources of saturated fatty acids cause higher HDL cholesterol and apoA1 concentrations and therefore, appear to be less atherogenic than a low-fat, high-carbohydrate diet.
The Bottom Line
The Danish paper suggests that based on lipid and lipoprotein measurements in overweight postmenopausal women, a low-fat, high-carbohydrate diet is more atherogenic than a high-fat diet rich in cheese or meat.
It is highly likely that other macro or micronutrients in food will affect the effect of specific fatty acids on blood lipid and lipoproteins. Hence, the general recommendation to restrict saturated fat intake appears pretty senseless.
But, can atherogenicity be based solely on simple lipid measurements?
Well, so far we have believed so, and it certainly is one of the reasons health authorities came to the conclusion that saturated fats are bad and carbs, and mono and polyunsaturated fats are good.
But, let us remember that there is scientific data suggesting that the effects of diet on cardiovascular health are mediated through many other biologic pathways, including oxidative stress, low-grade inflammation, insulin sensitivity, endothelial dysfunction and blood clotting mechanisms.
Would the results of the study be different if the participants were younger or not overweight?
Possibly. We don’t know the answer. But the question illustrates the fact that dietary recommendations have to be tailored to the individual. A normal-weight person may respond differently to a certain diet than someone with overweight and insulin resistance.
The Danish paper adds further evidence to the belief that the widespread recommendation to restrict the intake of saturated fat is misleading, if not absurd, and should be omitted.
I already know that taking Red Yeast Rice (a plant based Lovastatin) can lower Cholesterol by as much as 60 points in one week and Triglycerides by 150 and have records to prove it. The reason I do the one week challenge is to see how RYR performs WITHOUT any dietary change. If this fails, I move to detox the liver.
Now I am investigating Niacin (Endur-acin) 1500 to see if it can transform a bad LDL profile to a good one. Studies say yes. I will know in a few more weeks. This product (at least for me seems tolerable with flushing).
BTW, fats are not the enemy for most, it’s the refined carbs. The liver was never meant to process to many refined foods in combination with a sedentary lifestyle. We have all gone against our original design to always be I motion and eating only when energy is required. Now we rarely move and eat more for the experience.
What’s the difference between taking Red Yeast Rice or a statin itself??
Plant based (organic) vs chemicals. Plus the side effects are far less. Last but not least, a two month supply at any vitamin store or Amazon is $15.00. With an option like this and if it works this well, why bother with Big Pharma. Read what Mayo Clinic says about RYR.
Cost of atotvastatin thru Walamrt.
I use 20 mgs QED – 30@20mgs = 60days. Cost is $10.90 for 2 months. So far – no side effects at all
If you’re going the supplement route why not try Pantethine?
Here are two studies you might find of interest – BTW I use this in addition to the atorvastatin
https://kgksynergize.com/wp-content/uploads/2013/11/2011-CVD-Rumberger-et-al.pdf
Pantethine, a derivative of vitamin B5 used as a nutritional supplement,
favorably alters low-density lipoprotein cholesterol metabolism in low– to
moderate–cardiovascular risk North American subjects: a triple-blinded
placebo and diet-controlled investigation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942300/
Pantethine, a derivative of vitamin B5, favorably alters total, LDL and non-HDL cholesterol in low to moderate cardiovascular risk subjects eligible for statin therapy: a triple-blinded placebo and diet-controlled investigation
I also use Bergamot as well
https://www.thegoodlifeletter.com/pdf/Bergamia-Risso-Study.pdf
Hypolipemic and hypoglycaemic activity of bergamot polyphenols: From
animal models to human studies
https://www.statinanswers.com/types.htm
One way to classify statins is by how they are manufactured. Some are derived from micro-organisms through biotechnology. These are called fermentation-derived or Type 1.
Others are made through chemical synthesis (no living organisms involved). These are synthetic, or Type 2 statins. It is common for pharmaceuticals to be made through fermentation or through chemical synthesis.
I’ve tried most everything in the alternative world. RYR is safest best bang for the buck. Niacin has the ability to alter a bad LDL profile. I will never understand why the public is so accepting of medication with so many side effects no matter what the cost. Might as well just put the top ten drugs in the water supply as long as Americans can’t seem to live without the local pharmacy.
have you tried Bergamot and/or Pantethine?
Did you read the studies I linked to?
More potent statins lower LDL more –> better option. Unless you’re among those who get side effects (more potent statins at bigger doses tend to be more likely to cause those).
The whole “organic vs chemicals” thing is nonsense.
Im so disappointed that there are so many out there like you that don’t even know the difference. I’ve seen so many patients on LOW dose statins that suffer from myalgia, arthralgia, dysglycemias and now possibly dementia. All from these wonder drugs. So by all means take a drug for every symptom you have and never stop. Big Pharma really appreciates your ignorance of what harm they do. One one thing; you do know (although I now wonder) that people die of heart attacks every day while being on statins. And while your at it, drink as much diet pop as you can. That’s safe right?
There’s no difference, apart from what I stated. Chemohobia is just plain silliness. In addition, I didn’t claim that low dose statins don’t cause side effects, did I? It’s a known fact, however, that more potent statins are more likely to cause them.
And no one’s forcing you to take any kind of medication. Just keep on poppin’ them “natural” alternatives of yours. Hug a tree, too, while you’re at it.
Great post, as usual. Thank you.
To your point about individual differences…did the study show the results for individual subjects? With some crossover tests, I’ve seen researchers pay a great deal of attention to variations among the average results, and too little attention to the variations among individuals. (I don’t have access to the full study.)
For example, if I were a subject of this study and I did much better or worse on one of the diets, it would make no sense for me to adopt the diet that had the best average result. The obvious recommendation would be for me to eat what was best for me.
Thanks again,
Richard
Thanks Richard.
I do agree with you. I think it would be useful to look at individual differences instead of means. However, these numbers aren’t provided in the paper. Table 4 only provides mean values for laboratory measures before and after the dietary intervention.
I agree guys I have said before what works for me might not work for u…So u just cant say with certainty that one way is best or the only way.
From the study
Author Notes
↵1 Supported 50% by the Danish Dairy Research Foundation and the Danish Agriculture and Food Council (Denmark) and 50% by the Dairy Research Institute (United States), the Dairy Farmers of Canada (Canada), the Centre National Interprofessionel de l’Economie Laitière (France), Dairy Australia (Australia), and the Nederlandse Zuivel Organisatie (Netherlands).
SO – the study was 100% funded by the dairy industry – any thoughts on that?
A cynical person might conclude this study was clearly designed to make cheese look “heart healthy” – and the only way to that is to compare cheese to something even worse – refined junk carbs like cake, sweetened biscuits, marmalade, white bread. I mean, is this a joke?! They should have just compared cheese to candy bars. Oh wait, they did – “chocolate”. I can’t see the whole paper, so perhaps their point is something like, we know that a high-carb diet made up of whole grains, leafy veg, whole real foods, plant-predominate, that diet sends LDL crashing through the floor and literally clean out arteries, reversing atherosclerosis. But we want to study junk carbs, how most people eat… I guess that’s interesting.
But I certainly don’t think this study says anything about the absolute value of saturated fat in the diet. We don’t even know what happened to their total LDL levels. The conclusion I draw is that yes, one can create a diet *even worse* than high-fat.
Wouldn’t a better headline for this post be “Which is more atherogenic, high-fat cheese, high-fat meat, or processed carbs?” We can do better than all three of these lousy choices.
Max,
I get your cynicism. I know that the research seems contradictory to what we’ve heard for decades, but that’s precisely its value. It’s limited of course, as all studies must be, but it adds a little more to what we think we know.
For years, researchers lamented that they couldn’t get studies about fats and saturated fats funded, because everyone thought they already knew the answers. But over the past 10 years or so, more and more studies have been done,with findings that are similar to this one.
Recent research is also showing that LDL (aka LDL-C) is a very poor indicator of risk. Putting it on the floor doesn’t help many people. (For example, 40% of heart attacks in the US each year happen to people who have “normal” LDL levels.)
I respectfully suggest that you review research from the last ten years or so. You’ll find many, many studies that support everything said in Axel’s post.
Richard, thanks for your response. I guess what I’m saying is that one can design a study to get the results one desires, and this is a perfect example. If the best that can be said of the cheese is that it moved HDL 5%, this is from 40 to 42… not so impressive to me.
I personally do eat cheese occasionally, quite enjoy it, and would be delighted to be convinced it’s a heart-healthy food. This study hasn’t convinced me. Has it convinced you?
That 40% of heart attacks happen to people with normal LDL levels could mean that LDL is worthless as a predictor… or, it could mean that what we call “normal” (150) is actually too high (for those predisposed). Most everyone in the field considers an LDL under 75 “heart-attack proof”. But the only way to get there *without drugs* is through diet, really minimizing animal foods.
There’s plenty of evidence that Ornish/Esselstyn diet reverse atherosclerosis and prevent repeat cardiac events. Doesn’t mean it’s the only way. I would love to see one study, just one, that shows the equivalent for a high-fat diet. Show me it reverses disease in folks who have it and I’d be the first on board!
Nice reply. Thanks.
There are many studies supporting low-carb, high-fat diets, even those with saturated fats. Some of them increase LDL but improve other parameters. Too many to list them all. Here are a few:
https://www.nytimes.com/2014/09/02/health/low-carb-vs-low-fat-diet.html?_r=1
https://www.ncbi.nlm.nih.gov/pubmed/2007164
Axel has referred to many studies on this site. You can Google “westman pubmed ketogenic diet” to find Dr. Eric Westman’s research. He cures patients in his Duke clinic every day with ketogenic diets.
And there’s this study, that includes the Ornish diet:
https://jama.jamanetwork.com/article.aspx?articleid=205916
There’s one area where perhaps we all agree, which is that we are different and we respond differently to different diets. That’s why I asked Axel about the crossover design of this study. Often the research will expose those differences. The implication is that there is no such thing a one right diet for everyone.
Thanks again,
Richard
Thanks Richard. I do agree that we each respond differently to diets, and this is why personal experimentation is so important. I’ve known people who have responded wonderfully and horribly on both low-carb and low-fat.
I looked at the links you sent. One immediate thing stood out. All of the studies including the NYT review (Mozzafarian) and Westman’s studies (except the JAMA), compare a “low-fat” diet which is defined as less than 30% of calories from fat. Again, a cynical person might say, hang on, that’s not low-fat! Ornish/Esselstyn/etc call for no more than 10% calories from fat. This might seem nit-picky but come on, this is a life or death thing for people, and they’re using a strawman for low-fat – bring on the cake and “sweetened biscuits”!
I couldn’t find any Westman pubmed studies using a ketogenic diet to reverse coronary artery disease. He looks at risk-factors. It’s an intriguing idea. Westman uses it to good effect for blood sugar and obesity, as does another famous diabetologist, Dr Richard Bernstein. Is it opening arteries and preventing future events? Doesn’t seem his pubmed studies address that, from what I briefly scanned.
So I compare that to this:
https://www.ncbi.nlm.nih.gov/pubmed/25198208
https://www.jfponline.com/fileadmin/qhi/jfp/pdfs/6307/JFP_06307_Article1.pdf
Check out the before/after images of totally-clogged arteries fully opened and flowing again. Are you gonna believe the dairy council or your lyin’ eyes? 🙂
One of the major knocks on the Ornish/Esselstyn approach is how “extreme” it is, who would really comply. I think a ketogenic diet would deserve a similar critique for being quite difficult for most people.
Anyway, I love the topic and hope exploration continues on all fronts. Thanks
Good points. However…
Such a study, to satisfy both parties, might not exist. (Extremely low-fat vs. extremely low-carb, or ketogenic, diets.) The A to Z study might be the best currently available. I’ve heard that it is getting a follow-up; perhaps it will cover the range you want.
And how exactly would someone prove they were reducing future events? They can’t. All they can do is suggest it by implication, from epidemiological studies or by extrapolation from RCTs.
(I don’t think Ornish or anyone else has done a study where he knows for sure that deaths were prevented. Has he? If so, how? I suspect his test outcomes were all based on improved risk factors. Many, many studies for low-carb diets also show that they improve risk factors.)
I don’t think there are any epidemiological studies that include significant numbers of people on ketogenic diets for sustained periods of time (unless one uses the Inuit or other isolated cultures). And I believe the same goes for people on extremely. low-fat diets, like the one you suggest.
Also, I think the low-fat argument is missing a huge issue, namely metabolic syndrome. The evidence for it and insulin resistance as risk factors is overwhelming. So is the evidence (from Westman and many others) that low-carb diets improve and even cure insulin resistance, metabolic syndrome, obesity and T2 diabetes. And of course, ALL of those problems are very highly correlated with heart disease.
(It should also be noted that LDL is not included in the metabolic syndrome assessment. I believe that’s because it lacks statistical and clinical significance for it. Other factors are far more important than LDL.)
In short, there’s the huge condition called metabolic syndrome that the low-fat hypothesis doesn’t have a good answer for. Most doctors and researchers see it a major contributor for T2 diabetes and heart disease. (I don’t know how many cases of heart disease are linked to metabolic syndrome, but I think it’s a very high percentage, especially when smoking is excluded as a factor.)
Obviously, you and I won’t settle this debate now. But I agree with Axel’s assessment. This study, along with other evidence, suggests that fats and saturated fats are not the villains we once thought they were.
I’m making the distinction between risk factors (lipids, a1c, etc) and actually examining the arteries of each participant before and after. This is what Ornish and Esselstyn do. Is the disease progressing or regressing? Of course they track the blood markers too, as well as number of future events. In the study I linked to, of 177 compliant patients there was 1 event, a 0.6% rate. In the ones non-compliant but receiving “the best” of standard care, meds, etc, 62% had an adverse event. I know which group I’d want to be in!
I would be very interested to see a similar study (by necessity, small scale) using the ketogenic intervention.
To your point on large-scale epidemiological studies, this is how Ornish etc got started – they stole their ideas (received inspiration, shall we say) from the diets many non-Western cultures that had/have extremely, shockingly low rates of heart disease, diabetes… most of Africa, all of East Asia, including China and Japan. These guys ate 90% carbs with no CVD or type 2 diabetes. All of the “Blue Zones” diets (longevity) follow the same pattern. And when those Japanese emigrated to Hawaii, yep, they started dropping dead of heart attacks just like white Americans. So they figured out it’s the diet, not the genes.
Totally agreed about metabolic syndrome… but again… this is where the low-fat WFPB (whole food plant based) diet really shines. I used to think, of course it’s the carbs, because carbs=sugar and diabetes=high blood sugar. But the low-fat approach works stunningly well for reversing metabolic syndrome and t2 d. If you want the details, watch “Forks over Knives” and read Barnard’s book, or at least the Amazon comments:
https://www.amazon.com/Neal-Barnards-Program-Reversing-Diabetes/dp/1594868107/ref=sr_1_1?ie=UTF8&qid=1437933469&sr=8-1&keywords=neal+barnard
I know low-carb seems like an effective approach for this, but low-fat absolutely works as well, apparently addressing the root cause of fatty liver.
Max – One last question. Do you have any idea what the calorie level was for the subjects in the study you mentioned?
No fish, meat, or dairy. No added oils. No avocados, nuts or added salt. No sugar, sugary foods or processed carbohydrates. No fruit juices.
In other words, that HAD to be a very low calorie diet, on average. Using a normal (unaltered diet) as a control group wouldn’t make a lot of sense in that case, would it? It would make more sense to compare such a low-calorie plant-based diet to other very low-calorie diets.
In other words, the reduced calorie level of the diet could be a big confounder. (It would be stunning it if were not.) Perhaps many low-calorie diets would be as effective, with a variety of different macronutrients.
I wonder how much weight the subjects lost, and how many of them stayed on the diet when the study was over.
(That’s a big challenge with nutrition studies, of course, it’s almost impossible to control for just one variable.)
Thanks again (to you and Axel) for the conversation.
I don’t know the average calorie intake per participant. But you are pointing to one of the major benefits of this method of eschewing calorie-rich foods (oil being the ultimate example of “empty but dense calories” for so-called nutrient-dense foods. I do know that there is no portion-limitation on the allowed foods – eat as much whole grains, beans, veggie and fruit to your heart’s content – truly to satiety.
Since this diet needs to be continued indefinitely to keep the benefits, it would be unrealistic to expect people to literally be hungry for the rest of their lives.
So in a way, this likely offers some of the benefits of calorie restriction but without counting calories or restricting portions at all. It is true that usually excess weight melts away, but it’s important to note that some with CAD are not overweight. The doctor I worked with said most people get to the weight they were when they graduated high school (unless one was fat in high school).
Esselstyn’s patients, especially his early ones, were really the sickest of the sick: multiple failed stents and bypasses, literally told to go home and die. The study began before statins.
I believe this study is as good proof-of-concept as we are going to get. If I were given the choice of a bypass or strict diet like this, for me at least it’s a no-brainer.
One other possibly confounding factor is role of the lead doctor. Esselstyn is a zealous proponent of the diet and closely followed each patient, to the point of reviewing their food logs in person, weekly, and then monthly. He also has followed the diet himself since 1985, along with his family, stating that he won’t ask his patients to do something he wouldn’t do. The inspiration and confidence a patient gets from this personal care from the doctor probably can’t be overstated, in terms of compliance. His TED talk gives a good sense of his charisma and integrity.. now in his mid 80s and healthy as a horse!
And yes, thanks. I enjoyed the discussion too!
The only problem I have with this study is that no before/after lipids were peublished.
Some food for thought on the “30% isn’t really low fat”
argument, as well as the studies you
cited:
– The mechanisms by which a fat-centric metabolism
(AKA lowish carb, high-healthy –fat diet) promotes overall health are
increasingly well-understood and I am not aware of any of them that would
likely reverse on a lower fat diet. For example:
– For most people, the body will tend to shift its fuel preference based on diet, and a lower fat diet will further down-regulate preference for fat as a fuel source. There is lots of discussion about the science behind this under the topics of “fat adaptation” and “metabolic flexibility”. This leads to a whole host of bad things like increasing difficulty in losing body fat, increased hunger due to inability to preferentially draw on body fat stores for fuel, leptin/ghrelin
issues, and others. In my personal experience, I did ok, not great,
at around 20-30% fat, but my health went off a cliff when I went lower fat than
that. Conversely when I went high fat, my hunger declined dramatically, and it
became much easier to lose body fat.
– Exchanging fat for (non-fiber) carbs, which is
what lower fat by definition produces, will generally provoke a higher insulin
response and increase the degree to which the body relies on its version of
sugar for fuel at the cellular level, neither of which are associated with good
outcomes.
– If one is reducing seed oils (AKA vegetable
oils) then that would likely provide net benefit at a lower fat level, however
the evidence against these oils, especially soybean and corn oil seems strong
enough that they should never be allowed in any diet.
The ornish crowd is famous for changing very valid variables (e.g. smoking, exercise, nutrient quality in the overall diet) and then highlighting a very dubious variable (e.g. animal sources) and that
appears to have happened here. From what I know of the rest of the science looking at association, mechanism and evidence,
the whole improvement in CAD risk likely comes down to this sentence in the
second study: “Patients were also asked to avoid sugary foods (sucrose,
fructose, and drinks containing them, refined carbohydrates, fruit juices,
syrups, and molasses). Subsequently, we also excluded caffeine and fructose.
Exercise was encouraged but not required.”
Speaking of animal sources, the ornish crowd also
lumps all animal sources together. There are some valid arguments to limit
consumption of muscle meats, especially industrially produced ones. The issue with the methionine/glycine ratio, and to a lesser extend the effect of
grain on the fat in the meat seem like valid issues (although likely a weak
affect given the lack of strong association with bad outcomes) however most
diets suffer from poor nutrient quality and eliminating egg yolks and liver
seems counter-productive for most people. And I am not aware of any study or mechanism which equates fish (except for smoked fish) with anything but
improved outcomes while there is lots of evidence linking unfermented grains,
especially whole grains, with bad outcomes for many people.
Finally, to be sustainable, a healthy diet should lead to lack of cravings, minimal hunger unless nutrients or energy are
truly needed, and an ability to go for extended periods (up to 24 hours for example) without eating. Any signs of
lowered thyroid function or metabolic rate (AKA “starvation mode” ) have their
own set of bad consequences. Lowering
fat and increasing carbs generally leads to increased hunger and cravings due to the reasons stated above, so even if that is one way to improve CAD risk, it will likely not be the best way if it leads many people to being ”hungry and miserable”. It would be interesting to
see statistics on the drop-out rate for the low-fat studies, and from what I
vaguely remember, they are fairly high and the implication is that the
participants are at fault for being
weak-willed rather than considering whether the diet itself made the
participants who were not on the naturally thin end of the spectrum more hungry due to the increased reliance on sugar as a fuel source, and the resulting increase in hunger.
Hi Gabriel,
Thanks for the food for thought.
I think you may be confusing/conflating Ornish and Esselstyn (whose paper I cited). Ornish did indeed intervene using multiple variables (exercise, meditation, etc. in additional to a plant-based diet – he allows a bit of fish now, I believe). Esselstyn, who incidentally began his research before Ornish (though published after) focuses exclusively on diet. Of course, it would likely be unethical to prevent participants from exercising, quitting smoking etc. but those encouragements are constants among both cohorts.
Regarding drop-out rates, 89% in Esselstyn’s study were adherent (177 out of 189). Again, this is a very low drop-out rate likely due to the doctor’s close personal supervision of patients. But also, these are people who have already suffered at least one heart attack. They are highly motivated, especially if they see for themselves the diet is improving their health (elimination of angina, etc)
I find it helpful to remember that Ornish and Esselstyn are not “vegan vigilantes” on an ideological crusade, dreaming up studies to justify their points of view. They are medical doctors caring for patients who are at the edge of what Western medical intervention can offer and want to find out what works. They prefer to use the phrase “plant-based” to vegan because frankly, vegan does not equal healthful – ie. it’s not hard to construct a crappy vegan diet (french fries, anyone?) and it seems the key to reversing CAD from their work is really the symphony of massive phytonutrients from the right plants while eliminating endothelial antagonists foods like most meat, dairy and oils.
You write “From what I know of the rest of the science…the whole improvement in CAD risk likely comes down to this sentence in the
second study: “Patients were also asked to avoid sugary foods (sucrose,
fructose, and drinks containing them, refined carbohydrates, fruit juices,
syrups, and molasses)…”
The science underpinning the rationale for considering meat, dairy, and oils both atherogenic and carcinogenic is not really new or controversial as far as I can tell, probably best laid out in Campbell’s The China Study. Esselstyn’s book is also good, as are books by McDougall, Fuhrman, Pritikin, Barnard, etc.
In a more fun, digestible format:
Denise Minger’s “Lessons from the Vegans”
https://www.youtube.com/watch?v=KFfK27B_qZY&feature=youtu.be
Making heart attacks history: Esselstyn at TED
https://www.youtube.com/watch?v=EqKNfyUPzoU
this small but fascinating gem of a study from 1955:
ANGINA PECTORIS INDUCED BY FAT INGESTION IN PATIENTS WITH CORONARY ARTERY DISEASE: BALLISTOCARDIOGRAPHIC AND ELECTROCARDIOGRAPHIC FINDINGS
https://jama.jamanetwork.com/article.aspx?articleid=301511
(this study is referenced and explained in Minger’s presentation above)
If you are attributing the stunning 99.4% effectiveness of the longest-running plant-based (in this case, fully vegan) intervention as having nothing to do with the lack of meat/dairy/oils and *solely* to the reduction in refined carbs, well, that strikes me as an unlikely explanation of the success. Junk carbs have no place in any healthful diet, for sure. But you know their diets were 80%+ carbs, right? Plenty of those dreaded whole grains…
And the intervention didn’t just reduce risk and improve numbers, it literally stopped and reversed the disease, cleaning out their arteries. Before this work, atherosclerosis was considered irreversible – a view now totally discredited. I’d truly love to see evidence for a high-fat intervention does the same.
That every patient with diseased arteries is not at least given the dietary treatment evidence, which is low-cost, low-risk, and has numerous other health benefits, is in my opinion, unconscionable. If there were a high-fat intervention with similarly stellar results, those should be shared as well.
I’m curious to know how you understand the population-based support for such plant-based diets…. Africa, Asia, the so-called Blue Zones… where coronary artery disease, diabetes, obesity don’t need to be reversed because they simply don’t exist like they do for us. These folks are not “fat-adapted”… and they are not fat, but quite slim, as anyone who has traveled in these places can attest. I doubt whole societies walk around hungry or have “cravings” as you mention. They are not vegan either, it must be said, but seem much closer to that on the spectrum. Okinawan diet, for example, is 80% carb (a lot of sweet potatoes) and 98% plant-based, which works out to a small serving of meat once a month.
On a personal note: about 10 years ago I tried to purchase a blood glucose meter in Japan. No problem, right- they are ubiquitous in all US drugstores. Well, I had to go to 5 different pharmacies before they could locate one, since diabetes is (was) so rare – pharmacies simply didn’t stock them.
“But the only way to get there *without drugs* is through diet, really minimizing animal foods.”
I use 20mgs atorvastatin QED plus other supplements. I eat meat, eggs, full fat diary plus nuts, seeds, fruits, veggies, etc.
Last blood test
5/11/15
TC – 129
Direct LDL – 67
HDL – 54
TG – 36
LDL-P 873
ApoA1 – 137
ApoB – 56
ApoB/A1 Ratio – .41
Omega-6/Omega-3 Ratio – 3.3
EPA/Arachidonic Acid Ratio – 5.0
Wow, impressive numbers. Do you have a sense of the effect of the statin/other supplements vs diet alone. It’s hard to compare diets like this, but when I ate eggs and whole-fat dairy daily and meat pretty often, my LDL was 199. HDL was 95 but, still…
When I was doing LCHF my TC was was 299, LDL was 199 and LDL-P was 1500. Since I’m only using 20 mgs every other day the combination of the statin and the supplements appears to be a very good combination
Max.
You have a point here and I did have similar thoughts.
To cast more light on the issue I can tell you that chocolate was included in all three diets but was there was obviously most of it in the CARB diet.
“The main carbohydrate-rich foods used to replace cheese in the carb diet were fruit (84g), pasta and rice (58g), marmalade (20g), and cake, sweetened biscuits and chocolate (13g).”
Table 2 provides some data;
Sugar as a percent of total energy consumption was 7.5% on the CHEESE diet, 6.9% on the MEAT diet, and 8.9% on the CARB diet.
Dietary fiber (g/d) was 35.8 on the CHEESE diet, 36.6 in the MEAT group and 37.0 on the CARB diet.
Thank you for the additional info.
Fiber intakes sound pretty high. Lots of fruit and veggies in all diets?
“The Danish paper adds further evidence to the belief that the widespread recommendation to restrict the intake of saturated fat is misleading, if not absurd, and should be omitted.”
Err, no, it really doesn’t. The point was (and is) favouring unsaturated fatty acids over saturated ones. And a short-term risk marker study doesn’t really cut it in terms of calling anything “absurd”.
But hey, whatever gives you the chance to continue diving deeper into the “safa-whitewash” bandwagon …
That is indeed an important point. The study per se is interesting, but if one tries to use it as evidence against the dietary guidelines (in the Nordic countries, at least), it’s time to actually read the guidelines. They recommend exchanging saturated fats with unsaturated fats, not carbs, chocolate and cakes. Other trials has shown that an overall healthy diet based on the Nordic nutrient recommendations can lower the ApoB:A1 ratio, independently on total fat intake (see https://onlinelibrary.wiley.com/store/10.1111/j.1365-2796.2010.02290.x/asset/j.1365-2796.2010.02290.x.pdf;jsessionid=41ABE70826C64A8B2D1DA2E77B62E1C0.f03t02) and other risk factors as well (as Astrup himself showed here: https://ajcn.nutrition.org/content/99/1/35.long).
The main carbohydrate-rich foods used to replace cheese in the CARB diet were fruit, white bread, pasta and rice, marmalade, and cake, sweetened biscuits, and chocolate.
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Yeah, that’s a real fair comparison of what should be included in a low fat, high carb diet.
I’m sure Dean Ornish recommends this to all of his patients.
Seriously, you generally have some good posts. This is not one of them.
Will,
I’m just writing about a recent paper published in a respected scientific journal.
I didn’t design the study. So, I guess blaming me is unfair if you don’t like the study design or the results.
Sorry for the harshness of the tone, it’s just that this study looks like an attempt to vindicate high sat. fat diets versus a high carb diet but the high carb portion looks like a load of processed rubbish for the most part, doesn’t seem like a fair comparison to me.
Indeed. Dose and context.
The problem I see is that what keeps being called high fat diets are not high fat. Is there not a study in regards to CVD/CAD using a truly high fat (75%+) diet?
Also does it really matter what your lipid numbers are if there are no inflammation markers?
Yes Will. You’ve got a point there. Appreciate your input.
Exactly. This paper is being quote a lot by paleo/low-carber right now but their bias is obvious, either that or they did not read the paper. The high-carb diet was nothing else but a junk carb diet. Also, most of the test did not reach statistical significance (see table 4). The study was either underpowered or the group too homogenous. Useless study.
So, when will we see a study looking a high-fat, high animal diet vs beans, oats, quinoa, vegetable and fruits?
was the meat and cheese consumed from grass fed cows or ? Just wondered how this would play into the equation
Previous research by Tholstrup (the first author in this new study) and collegues actually found no improvement on risk factors with grass fed compared with conventional butter…
Excerpts from a paper I read about in a book back in the early 1980s: “There are big differences in the incidence of ischaemic heart disease between South Indians and North Indians (Padmavati, 1962; Malhotra, 1967a). Among railway employees in the trade of sweeper the disease is 15 times more common in men from South India as compared with those from North India…Dietary Factors. The results of the dietary survey of the two groups are summarized in Table I. The mean consumption of fats in our Udaipur (Northern) group was 75 g., against 7 g. in our Madras (Southern) group. The fats in our Udaipur group were derived from milk, ghee, and fermented milk products, which are saturated and of animal origin. In contrast to this, the fats in the diets of our Madras group were derived from seed oils, mostly ground-nut or sesame oil, which have a preponderance of unsaturated fatty acids.” https://heart.bmj.com/content/30/3/303.full.pdf
Contemporary research – excerpt: “Interestingly, despite widespread recommendations for consumers to avoid high fat foods (including whole fat dairy products), previous studies in humans have demonstrated that whole fat dairy consumption is associated with multiple health benefits, including lower risks of insulin resistance, metabolic syndrome, and type 2 diabetes.” https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0132117
While it’s true that certain chain lengths of saturated fat raise LDL cholesterol, the effect may be beneficial. For example, “Riechman and colleagues examined 52 adults from ages to 60 to 69 who were in generally good health but not physically active, and none of them were participating in a training program. The study showed that after fairly vigorous workouts, participants who had gained the most muscle mass also had the highest levels of LDL (bad) cholesterol, ‘a very unexpected result and one that surprised us.'” https://www.eurekalert.org/pub_releases/2011-05/tau-cn050511.php
The amazing thing about the saturated fat/heart disease debate is that most scientists continue to ignore alternative explanations. Here’s the latest on that front: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0132672
Hi, my cholesterol levels are as follows: 6 reading, LDL=3.4, HDL=1.9, TRIGL=NORMAL. On the banting diet at the moment for nearly a month. I’m small frame, 69,2kgs 60yrs, with underactive chronic thyroid and menopausal. Any advise welcomed. Thanks
Beatrice Golomb, MD, PhD, is a (some say “the”) leading expert worldwide on the adverse effects of statins. I provide some links below. For the record, Dr. Golomb is no slacker. She graduated with honors from Harvard in physics by the age of 19. In the next 5 years, she finished her MD and PhD (biology) degrees.
The largest ever meta-analysis on the adverse effects of statins reviewing 891 studies and trials on the adverse effects of statins. Title: Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849981/ It’s a long paper, but worth the work to slog through. Conclusions are quite clear.
The UCSD Statin Study group where you can share your experiences, thus contributing to a very large international database on reported effects – https://www.statineffects.com/info/
For fun, a brief video primer, which still has plenty of good info, on who benefits from and who is detrimented by statin use:
https://www.youtube.com/watch?v=Q_miCHrRvPg