The story of saturated fats and their proposed association with coronary heart disease is bewildering. Although it illustrates the great power of public health authorities and the food industry, it tragically exposes the frailty of governmental handling of health issues.
When dietary and lifestyle recommendations don’t rely on solid scientific evidence, the outcome may be disastrous. Further damage may result from the fact that as soon as contradictory evidence becomes available, authorities will tend to sweep it under the carpet. That’s human nature. You will want to defend your position for as long as you can.
Although most public health authorities still stick with their recommendations about saturated fat, recently an important clinical support resource called UpToDate changed their stands regarding the issue.
UpToDate is an evidence-based clinical decision support system authored by physicians to help clinicians make the right decisions at the point of care. It is highly respected and used by medical professionals and universities worldwide. UpToDate is probably the most trusted clinical decision support resource in the world.
Saturated Fats and Coronary Heart Disease
For decades, doctors, dietitians and other medical professionals have recommended that we limit the intake of saturated fats in order to reduce the risk of coronary heart disease.
When it comes to dietary advice, avoiding animal and dairy fats has frequently been top of the list among the experts. Red meat, whole-fat milk, cheese, cream, butter and eggs should be avoided as much as possible.
Slowly but securely this has become ingrained into our way of thinking. Having eggs and bacon for breakfast is associated with a feeling of guilt. We can almost vision the fat plugging our arteries. So strong is the power of education.
Health officials have urged us to avoid saturated fats as much as possible, saying it should be replaced with polyunsaturated fats like that found in nuts, fish, seeds and vegetable oils.
In an article updated September 24, 2014 the recommendations of the American Heart Association are very clear:
Eating foods that contain saturated fats raises the level of cholesterol in your blood. High levels of LDL cholesterol in your blood increase your risk of heart disease and stroke.
Eating foods that contain saturated fats raises the level of cholesterol in your blood. Be aware, too, that many foods high in saturated fats can be high in calories too.
The American Heart Association recommends aiming for a dietary pattern that achieves 5% to 6% of calories from saturated fat. That means, for example, if you need about 2,000 calories a day, no more than 120 of them should come from saturated fats. That’s about 13 grams of saturated fats a day.
One of the main reasons saturated fats have a bad reputation is that they increase LDL-cholesterol, a type of cholesterol associated with risk of heart attacks.
However, the effects of saturated fats on blood lipids are much more complex than that.
For example saturated fats also increase HDL-cholesterol, the so-called good cholesterol. Furthermore, intake of saturated fats appears to increase the size of LDL-particles. In theory, this could help reduce risk.
So the association with blood lipids is hardly reason enough to advise against the intake of saturated fats. Then, what is?
During the last ten years, a substantial amount of evidence has emerged suggesting that the association between saturated fats and coronary heart disease is either very weak or may not exist at all. Nonetheless, public health authorities have stood firmly by their earlier recommendations.
Recently a large meta-analysis of observational studies found no relationship between the intake of saturated fats and coronary artery disease.
Although many experts did criticize this paper, it certainly doesn’t add any support to the conclusion that eating saturated fats is associated with increased risk.
UpToDate’s recent revision indicates their experts have taken these recent data very seriously:
Although it is known that there is a continuous graded relationship between serum cholesterol concentration and coronary heart disease (CHD), and that dietary intake of saturated fats raises total serum cholesterol, a 2014 meta-analysis of prospective observational studies found no association between intake of saturated fat and risk for CHD.
The meta-analysis also found no relationship between monounsaturated fat intake and CHD, but suggested a reduction in CHD with higher intake of omega-3 polyunsaturated fats; a benefit with omega-6 polyunsaturated fats remains uncertain.
Given these results, we no longer suggest avoiding saturated fats per se, although many foods high in saturated fats are less healthy than foods containing lower levels.
The Bottom Line
In 1977 senator George McGovern’s Select Committee on Nutrition and Human Needs published its famous report, “Dietary goals for the United States”, highlighting the importance of limiting the intake of saturated fats.
Following the publication, Doctor D.M. Hegsted, professor of nutrition at Harvard School of Public Health, who assisted in the preparation of the report said: “The question to be asked, therefore, is not why should we change our diet but why not. What are the risks associated with eating less meat, less fat, less saturated fat, less cholesterol, less sugar, less salt and more fruits, vegetables, unsaturated fat and cereal products – especially whole grain cereals? There are none that can be identified, and important benefits can be expected.”
In my opinion, these words reflect the unscientific approach of the committee.
Certainly Hegsted had developed the so-called “Hegsted equation” showing that cholesterol and saturated fats raised blood levels of LDL-cholesterol while monounsaturated fats had little effect and polyunsaturated fats appeared to lower the levels.
However, at that time there was no evidence that the effect on LDL-cholesterol was a measure of a heart healthy diet. It was only a hypothesis, yet to be tested.
Today, blaming the rising incidence of coronary heart disease 40-50 years ago on the intake of red meat, whole-fat milk, cheese, cream, butter and eggs appears naive at best.
To condemn one macronutrient and suggest it be replaced with another, without having any scientific evidence that such and intervention is helpful, would today be considered careless and irresponsible.
Sticking with the same conclusion for 40 years, despite abundant contradictory evidence is shocking and hard to understand. Hopefully, UpToDate’s recent reconsideration of the issue is a sign that the tide is turning.
Of course, there’s no reason to promote high consumption of saturated fats and surely there will often be healthier options. However, it’s time we stop telling people that avoiding saturated fats may protect them from heart disease. Why should we say such a thing if it’s not supported by evidence?
It will be interesting to see how public authorities such as the American Heart Association will react to recent scientific evidence on the proposed link between saturated fats and coronary artery disease. Will we see a change in the forthcoming 2015 version of The Dietary Guidelines for Americans?
Will their approach be evidence-based or not? Will they accept that red meat, whole-fat milk, cheese, cream, butter and eggs can be a part of a healthy diet? Will they reconsider their recommendations like UpToDate now has officially done? Only time will tell.
The evidence that the lipid hypothesis is a dying dinosaur is overwhelming. Returning to the diets of of our distant ancestors for me is a no brainer. However, to expect the huge vested interests of scientific grants, pharmaceuticals, agriculture, lobbyists etc etc to roll over any time soon is at best naive.
However, this is the age of the internet and access to information unparallelled in the history of the world. Therefore I see change coming from bottom up rather than top down. It will be interesting to see what route the vested interests take when the incoming tide becomes a tsunami!
You’re either confusing lipid hypothesis with diet-heart hypothesis or in denial. There’s no doubt whatsoever that blood lipids have an important role in CVD.
Thanks for the passive aggressive lesson in semantics Mie – somewhat undermined by you understanding completely my meaning.
https://en.wikipedia.org/wiki/Lipid_hypothesis
“There’s no doubt whatsoever that blood lipids have an important role in CVD”
There is a big step (with probably many intervening steps) from “important role” to “causative”.
“The meta-analysis also found no relationship between monounsaturated fat intake and CHD, but suggested a reduction in CHD with higher intake of omega-3 polyunsaturated fats; a benefit with omega-6 polyunsaturated fats remains uncertain.”
Uncertain is it? Not from a biochemical/physiological stand point. Intakes of omega-6 exceeding 1 to 2 percent of total caloric intake are problematic. Since there are no RCTs of any length wherein researchers had subjects reduce their omega-6 intake to pre industrial levels, there is no evidence from epidemiology to corroborate what we know from biochemistry. Comment excerpted from an August 25, 2014 message from Fred and Alice Ottoboni and posted her with permission from the authors:
“The paper appended below is new, hard to understand, and elicits the true cause of obesity. It is a break-through paper.
What it says is that humans have a system called the endocannabinoid system. It is primarily in the brain and simply described as a system that makes you feel good when you do the right thing and not feel good when you deserve no praise. This the way it controls diet when one is normal.
The big finding in this paper, using mice, is that the modern American diet includes an average of about 8% of calories from linoleic acid, the main fatty acid in vegetable oils. A healthy diet should contain only about 1% of calories from linoleic acid. This has been known for a long time by some of us.
This study showed that dietary excess of linoleic acid at 8% of calories, distorts the endocannabinoid system so that it rewards the victim for overeating and also somehow brings about uncontrollable obesity despite the best efforts of the victim. Importantly, the authors of this study are of top quality. Note JR Hibbeln is among them.
We are just starting to study the biochemical processes involved and will keep you informed. The clear recommendation here is to do everything possible to remove linoleic acid from your diet. This is difficult because labels do not include linoleic acid content in anything. Here is what we have come up with.
Stop the following:
vegetable fats and oils
everything that may contain vegetable fats and oils
avocados
peanuts and peanut oil
nuts of all kinds (except Macadamian)
all deep fried foods”
https://link.springer.com/article/10.1007%2Fs11745-013-3842-y
As for the physiological effects, take a look at this: https://blogs.babycenter.com/mom_stories/does-dha-in-maternal-body-fat-10-01-2014-boost-babies-brains/
Excerpt:
So evolution designed women’s bodies to supply the DHA, and it looks as though most comes directly from the fat stores around our hips, thighs, and buttocks – the so-called “gluteofemoral deposits.” It’s fat the female body is loathe to part with, except during the last trimester of pregnancy and lactation. Then it becomes baby food. When researchers traced the fats found in breast milk, they found that 80% of the milk’s healthful omega-3 fatty acids (including DHA) were derived from body fat, not from a woman’s current diet. Should we have new respect for feminine fat? Perhaps. But there are also important nutritional implications for kids. For instance, consider what happens when a girl approaches adolescence. Her body starts accumulating gluteofemoral fat and storing up DHA for her future offspring. But she also has a growing brain and needs DHA for her own, immediate use. As a result, she may require extra DHA. This could be especially true if her diet is high in omega-6 fatty acids, such as linoleic acid (found in safflower, sunflower, soy and corn oils) and arachidonic acid (found in meat, eggs, and dairy products). As I noted in a previous post, high levels of omega-6 fatty acids can interfere with the body’s ability to synthesize its own DHA from non-marine plant foods.
For nearly 40 years the American Heart Association, the Harvard School of Public Health, and the United States Department of Agriculture have advised Americans to replace saturated (animal) fats with polyunsaturated (seed) oils rich in omega-6 linoleic acid. Has the public complied? https://newsroom.heart.org/news/trans-fats-still-weighing-americans-down
Axel,
“Of course, there’s no reason to promote high consumption of saturated fats and surely there will often be healthier options. However, it’s time we stop telling people and patients that avoiding saturated fats may protect them from heart disease. Why should we say such a thing if it’s not supported by evidence?”
Err, because a) the statement “Avoid safa & get no heart disease” is a straw man (the focus has always been in excessive use of safa in Western context, just as you yourself stated) on a general level whereas b) especially in high risk individuals this remains ONE of the many relevant cornerstones of a healthy diet?
Seriously, this much ado about safa is comical. In both “camps”. Focus on actual diets, please.
Mie,
Appreciate your comment.
This article was meant to highlight UpToDate’s new recommendations regarding saturated fats. I don’t see what’s comical about that.
I’m not sure the focus has always been on excessive use – if you look at the AHA recommendations it’s now 13 g/day. That’s a small bite of cheese.
As you mention excessive consumption I wonder; Is there evidence that “excessive” consumption of SFA increases the risk of coronary artery disease?
“Is there evidence that “excessive” consumption of SFA increases the risk of coronary artery disease?”
In 1971 Roger J. Williams, PhD wrote, “No discussion of heart disease would be complete without mention of the question of saturated fats. It has come to be almost an orthodox position that if one wishes to protect oneself against heart disease, one should avoid eating saturated (animal) fats. While this idea may not be entirely in error, it is misleading in its emphasis. The evidence shows that high fat consumption, when accompanied by plenty of the essential nutrients which all the cells need, does not cause atherosclerosis or heart disease. https://nutritionscienceanalyst.blogspot.com/2008/02/nutrition-against-disease.html
Twenty Six years later, in correspondence published in the European Heart Journal, Dr. Laura Corr noted, “Ask almost any member of the general public about a diet which would reduce their chance of heart disease and the reply is the same: “a low fat diet”. On closer questioning, this means a diet with a reduction in cholesterol and saturated ‘animal’ fats, i.e. less meat, butter, milk and cheese. Most national and international recommendations for the prevention of heart disease, whether for primary prevention of or for patients who have developed the clinical manifestations of coronary heart disease, have made dietary restriction of total and saturated fats and of cholesterol the primary advice and often the sine qua non in relation to all other forms of management. To this extent they are to be congratulated that the message seems to be so universally accepted. Unfortunately, the available trials provide little support for such recommendations and it may be that far more valuable messages for the dietary and non-dietary prevention of coronary heart disease are getting lost in the immoderate support of the low fat diet”
In the 17 years since no further evidence connecting high saturated fat intake with heart disease has accumulated.
As Dr. Williams pointed out, the problem should not be defined in terms of excessive intake of saturated fat but in terms of unbalanced intake of all the nutrients required for healthy cellular metabolism.
That’s interesting Dave. Thanks.
This excellent post made my wholegrain biscuit with French full fat Brie taste even better. Thank you! 🙂
Nyt oikeesti Mie, tule pois huutelemasta sieltä. Nolottaa tommonen….
Saario, use English if you want to bitch about something.
Or better not: don’t bitch. Contribute.
“This article was meant to highlight UpToDate’s new recommendations regarding saturated fats. I don’t see what’s comical about that.”
Now Axel, I’m sure you read my message and can therefore see what I consider comical.
I”’m not sure the focus has always been on excessive use – if you look at the AHA recommendations it’s now 13 g/day. That’s a small bite of cheese.”
Or then not. For instance, the 5-6 % limit by AHA is one of these examples. These kind of limits in isolation mean nothing.
Or vice versa: using quotation marks with “excessive”. Like you do:
“As you mention excessive consumption I wonder; Is there evidence that “excessive” consumption of SFA increases the risk of coronary artery disease?”
I’m also sure you’re aware of the role of fatty acids in inflammation and blood lipis and what happens when SFA –> PUFA. What more would you like to know?
Nice to see that one more important resource is updating their opinion on this matter. In Finland, so called “experts” are not even close in updating their opinion. Actually, if one is claiming that saturated ain’t that dangerous after all, he is immediately considered almost as lunatic.
I totally agree what UpToDate is saying about, diary products. Recent studies have repeatedly shown positive effects of fatty diary products rather than negative.
Once again I would really hope that scientists would now go forward. We can’t say for ever that we need more and more similar studies. If saturated fat and it’s effect on heart disease has not been studied enough, then what is ?
Future studies, should not categorize foods just based on their saturated fat content, I think it’s pretty clear now that, not all products containing saturated fat are equally heart healthy.
Lipid hypothesis is another question, and of course better not to mix it up with diet heart hypothesis.
I often wonder if young people feel the same way about fats as older people do. Having been brought up in the 80’s I tend to have that ‘fat is bad’ mentality ingrained into me. Not that I think that now but I understand how someone can fear fats. With all this change going around us, Atkins etc, I wonder what young people of today think about fats. Not enlightened young people but the general populace. Because that would let us know if all this pro fat work is actually having an effect.
@Someone,
Here is some evidence that at least a few scientists in Finland are reconsidering SFA (click my link above).
But notice that mixed PUFA at around 5%E seems protective in that study – but the effect is the same if it replaces carbohydrate, trans fats, or MUFA. No additional benefit from lower SFA.
Holy cow! I’m afraid of “fat” and I’m afraid of “non fat” these days. So hard to determine what is right. I feel like saturated fat is (full fat dairy, eggs, etc) is the right way to go..then my blood work comes back high LDL…but also high HDL and very low triglycerides and large buoyant particles (Subclass A I think it’s called)…What to do? what to eat? I think I will just give up eating as every time I turn around I am putting the wrong thing in my mouth. Help!
Doc,
you asked if there is evidence of excessive SFA intake and the risk of CHD, yes, there is. In the seven country study the intake of SFA explained 89% of the differences in the mean serum cholesterol levels across the 16 different cohort studies. This is a study where differences between SFA intake were 10-fold at highest. We cannot even dream of getting similar differences in the intake within homogenous populations.
I think a more legitimate question would be whether SFA intake influences the risk of CHD in a context of population that has high SFA diet at the baseline. In other word, does SFA tinkering merit benefits in the context of Western diet that is already high in animal fat. Moreover, a legitimate question is to ask whether something was done improperly back in the time. Most of cohort used utilized 24-hour dietary recall. As elaborated by Katan et al:
“A major weakness of the meta-analysis is the imprecision of dietary assessment methods used in the underlying studies. About half of the studies used 1-d dietary assessments or some other unvalidated method. Food intake varies from day to day, and there is a substantial literature showing that a single 24-h recall provides a poor estimation of the usual dietary intake of an individual (5). Such methods cannot reliably rank individuals by their long-term intake, especially within populations with a uniformly high saturated fat intake. Such imprecision in the assessment of disease determinants systematically reduces the strength of association of determinants with the disease. This is referred to as attenuation (6) or regression dilution bias (7). Observational studies that used such dietary assessment methods failed to show an association between diet and serum cholesterol concentrations (6). This shows the shortcomings of such dietary methods, because the effect of diet on serum cholesterol concentrations has been well established in randomized controlled trials (2, 8). Thus, the lack of a significant association between saturated fat intake and CHD may well reflect the consequences of regression dilution bias”
https://ajcn.nutrition.org/content/92/2/459.2.long
Now, Doc, tell me, what is the evidence showing that modulating HDL from the baseline is beneficial. We know that higher HDL level is important risk predictor for CHD but we have no data showing that CHD risk is altered when the HDL-C is modulated. People are not changing their diets in these cohorts. Risk predictor is not a synonym with causal factors. Populations that have been virtually immune in the past show consistently very low serum cholesterol levels that are mediated via low-SFA diets. This is a powerful natural experiment.
Richard
You wrote:
“Now, Doc, tell me, what is the evidence showing that modulating HDL from the baseline is beneficial. We know that higher HDL level is important risk predictor for CHD but we have no data showing that CHD risk is altered when the HDL-C is modulated
I think you’re right. We don’t have data proving that modulating HDL-cholesterol will reduce risk.
I also agree that “risk factor is not synonym with causal factors”. But that is true for LDL-cholesterol as well.
Large intervention trials have not proved that lowering LDL cholesterol by reducing the intake of fat will lower the risk of heart disease.
The Women’s Health Initiative Randomized Controlled Dietary Modification Trial is a good example. MR-FIT is another example of such a trial. Both very large intervention trials.
“risk factor is not synonym with causal factors”
…and yet we see so many houses-of-cards constructed using nothing more than this misunderstood (or deliberately misconstrued) principle
I am with you Grace. I insisted my husband have a cholesterol test after his younger brother had a heart attack and was found to have very high cholesterol. I have always frowned on my husband frying bacon and eggs…drinking wine and generally what I considered to be an unhealthy diet. I on the other hand boasted about my low fat diet.. daily jog and no alcohol.
I had the test at the same time and my husband had perfect readings for blood pressure and cholesterol while I was mortified that my results were high on both counts. My doctor gave me a prescription for Statins straight away. I read the guidelines in the box and felt very uncomfortable about taking them and spent hours on the Internet reading about all things cholesterol.
I told the doctor I wasn’t going to take them before I had the chance to look at my diet etc so that is where I am at the moment.
Of course I have to put up with my husbands smirking face every time he fries his bacon!!
Dee, I hear what you are saying and it is a very interesting point. When I got married some twelve years ago I came straight out of a public health job and background, so I ate low fat. I was one that joined others in public health advising diabetes type II patients to eat low fat (and more carb). My husband on the other hand ate his eggs and bacon and full fat milk and steak with the fat on and even sausages. I used to drool with hunger but stuck to my guns. No cheese for me, or full fat milk, and only the leanest meat and salads etc. Now, whose the one with high cholesterol (total 6) and high blood pressure (considered hypertensive)? ME. I’m at a loss. We both partake of the same exercise mind you, and also, he has a resting heart rate of 60 while mine is around 80bpm. Some fascinating research opportunities I feel between couples with the same otherwise lifestyles. OK so I’m 50 and well into menopause and not HRTing, but still, all that missing out on yummy food, for what. The heart foundation led me up the garden path I feel. Just wonder if the experts out there could agree on anything please so I can eat without worrying about dying of a stroke or not knowing who to believe. The heart foundation used to provide our resources by the way. I asked for evidence for their diet hear hypothesis recently and the referred me to a patient information leaflet.
One error: “increase LDL-cholesterol, a type of cholesterol associated with risk of heart attacks” should at best be “increase LDL-cholesterol, cholesterol contained in the lipoprotein associated with risk of heart attacks”. The cholesterol in LDL is the same as that in HDL, VLDL, chylomicra etc. Lipidologists have gone further and determined that the risk is from the amount of LDL particles, not the total amount of cholesterol contained in all the LDL particles.
Good point Yossi. But I don’t think it’s an error.
I’m aware of the role of particles but here I was in fact talking about LDL cholesterol (the amount of cholesterol carried by LDL particles). That’s still the test that is most often used to assess risk and it’s a measure that has been associated with increased risk of coronary artery disease in observational trials.
You may be right that cholesterol itself could be a surrogate marker and that it’s the lipoproteins themselves that are more important.
I’ve actually written a lot on my blog about the role of LDL particles, particle count, particle size etc.
Yossi, And to the layman, that is what is so confusing. Since leaning more to a full fat diet…mainly to eat less refined foods, more in their natural state…my LDL went way up but my particals are large…so do I worry or not??
Dee, I feel your pain…but in the reverse…my husband eats more of the low fat (yet not really healthy :0) Diet and looses weight and has better blood work…I eat healthy and have high LDL and part of me knows it is ok because of the large particles, but the other part of me has been scared of “fat” for so many years. My doc wanted to do the same thing and I told him exactly the same thing. I will not go on statins! I know I can reverse this with diet…but am I doign the right thing cutting out eggs, going back to low or non fat?! ARGH!!! Have a great day and stay healthy…whatever that means!! :0)
“Although it is known that there is a continuous graded relationship between serum cholesterol concentration and coronary heart disease (CHD), and that dietary intake of saturated fats raises total serum cholesterol, a 2014 meta-analysis of prospective observational studies found no association between intake of saturated fat and risk for CHD.”
So what does the scientific method say to do when the observations don’t fit what is “known”?
Frank
Obviously there is correlation between serum cholesterol and coronary heart disease (CHD). However, that doesn’t prove a causative relationship. In other words it doesn’t prove that cholesterol causes CHD.
According to the 2014 meta-analysis there is no association between saturated fat intake and the risk of CHD. This might also imply that the elevation of serum cholesterol associated the intake of saturated fats does not increase the risk of CHD
Once again it’s about the difference between correlation and causation.
I agree entirely Dr Sigurdsson.
But it does seem that this principle constantly needs to be stated, to dispel misrepresentations by those who seem to revel in, or otherwise benefit from the inherent confusion.
Doc wrote:
“This might also imply that the elevation of serum cholesterol associated the intake of saturated fats does not increase the risk of CHD”
No, it just implies that it’s different to track an association within a homogenous group that is uniformly exposed to the variable, high SFA intake, that is. Nevertheless, all modern epidemiological studies show association between SFA and CHD. The studies that do no show this association is of sub-standard methodology. Very simple.
Moveover, it’s also very difficult to clinically show that very modest difference of dietary intake between in the intervention arm would yield significant changes given that that the whole population shows cumulative exposure high SFA diet since birth. The average duration of these trials is just few years. For the same reason, all the major trials studying the effects of smoking to lugn cancer risk have failed.
There exists a hefty body of experimental studies that demonstrate that elevated LDL cholesterol is harmful independent of the mechanism used. In addition, there are literally housands of animal studies showing that saturated fat and dietary cholesterol accelerates atherosclerosis across virtually every type of vertebrate, and that they are the sine qua nons for the dietary modification of experimental atherosclerosis. This includes mammalian, avian and fish species- herbivores, omnivores and carnivores, and over one dozen different species of nonhuman primates. Again this cannot be attributed to the way that the animal was raised as when taking into consideration the amount of antioxidants and carotenoids as well as the lack of cholesterol, tropical plant fats high in lauric, myristic and palmitic acids will also accelerate atherosclerosis in animals to a similar degree as saturated animal fats.
As concluded by Jeremiah Stamler:
“To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case”.
https://ajcn.nutrition.org/content/91/3/497.full
Richard.
You wrote:
“Nevertheless, all modern epidemiological studies show association between SFA and CHD. The studies that do no show this association is of sub-standard methodology. Very simple.”
If I understand you correctly you are implying that all studies that have yielded results that don’t agree with your own opinion are unreliable and useless.
Hmm… I think a further dialogue between us on this matter will be useless.
Thanks for commenting.
Axel,
“This might also imply that the elevation of serum cholesterol associated the intake of saturated fats does not increase the risk of CHD”
You’re oversimplifying things here. These meta-analyses haven’t really specified HOW MUCH the relevant risk markers have changed. Simple “SFA –> something else” exchange isn’t necessarily going to change things that much – might even change things for the worse.
Don’t mistake this with the role of elevated LDL in the etiology of CHD.
Mie… “You’re oversimplifying things here.” …in the same way that you risk overstating things here?
Applying the scientific method rarely, if ever, allows one to talk in absolutes: as if the questions have all been answered and the discussion is over.
I read Dr Sigurdsson’s “This might also imply that…” to, at least, accept the possibility that alternate interpretations still exist and still need to be explored, rather than dismissed out of hand.
Death rates from heart attack have fallen but the incidence of heart attack remains as high as ever despite the lower cholesterol levels in developed countries.
I would point out that the lowest point on the total cholesterol/mortality curve lies on that part of the curve that is considered dangerously high. Last time my total cholesterol level was measured it was 201 mg/dL which made me quite happy.
Excerpt: This graph has been obtained through a nonlinear analysis, and I think it provides a better picture of the relationship between total cholesterol (TC) and mortality. Based on this graph, the best range of TC that one can be at is somewhere between 210, where cardiovascular disease mortality is minimized; and 220, where total mortality is minimized.
https://healthcorrelator.blogspot.com/2009/12/total-cholesterol-and-cardiovascular.html
Thanks Dave
These are important points.
You’re absolutely right. Mortality from coronary hart disease has fallen quite dramatically in most western countries in the last 30 years.
It’s more difficult to obtain numbers regarding incidence, particularly in the US.
However, it’s clear that incidence has fallen in most European countries. That’s true for the UK and the Scandinavian countries.
Of course this is due to many factors, better treatment and better risk factor profile.
In fact this has been analyzed in many countries by the so-called IMPACT model.
According to the studies less smoking, lower cholesterol levels and less hypertension have played a substantial role.
This study analyzed factors explaining the declining incidence of myocardial infarction in the UK.
In many countries these good results have partly been offset by the increasing incidence of obesity and type 2 diabetes.
I agree that Jakobsen et al.’s pooled metaanalysis is superior to the recent one by Chowdhury et al. (or Siri-Tarino et al.’s from 2010). If UpToDate based their advice on Chowdhury et al., that would be unfortunate since that is a metaanalysis on studies that are not able to answer the question whether a SFA intake according to the recommendations is beneficial. The recommendation is not only to eat less SFA, but to replace more with unsaturated fats.
When you want to investigate the effects of one type of fatty acid, it’s important that you control for other fats, because of high colinearity. Most of the studies in Chowdhury et al’s analysis failed to do that. Few of them looked at intake of trans-fats, so it’s possible that those who ate the least SFA ate more trans-fats (which was shown in the ATBC study). Relationships between diet and health are always multivariate, i.e. the intake of one component must be seen in relation to other components. When those other components are prone to measurement error, it is no surprise that correlations with disease will become statistically non-significant.
Some of the studies in Chowdhury et al. had a follow-up period of 20 years, while the dietary data was assessed only at baseline. To quote Willett and Stampfer in Willett’s Nutritional Epidemiology (2012 ed.):
Only two of the studies in Chowdhury et al. had multiple diet assessments, the Nurses’ Health and Health Professionals’ Follow-Up study. In Nurses’ Health Study, the mean SFA intake fell from 15,6 E% in 1980 to 9,4 E% in 1994.
The most important problem is however the small variations in SFA intake within the cohorts. When there is little variation in one dietary component within a population, you would expect *not* to see a correlation between that component and disease.
As Geoffrey Rose explained 30 years ago, to identify a causal factor, the exposure must be heterogenously distributed in the population: «The hardest cause to identify is the one that is universally present, for then it has no influence on the distribution of disease.»
Thanks for your input Erik. These are important points. Appreciate it.
I do regularly read the articles on your Norwegian website. Appreciate your scientific, analytical and unbiased approach.
I do agree with you that there’s lot of evidence suggesting that replacing SFA’s with PUFA’s may be beneficial. However, what does it mean and how should it be implemented?
There are many different types of PUFA’s and for example the omega 3 vs. omega 6 issue is still highly debated. Are all PUFA’s better than SFA’s? Probably not. Where does monounsaturated fat fit into the picture?
There are also many types of SFA’s, not all of them raise cholesterol.
Although discussing macronutrients and different types of fat (instead of food) may be problematic, one has to wonder why saturated fats (along with trans-fats of course) have been demonized (because I think they have).
I think the cholesterol issue has in fact played a huge role. If we believe in the lipid hypothesis, how can we ever recommend something that raises LDL-cholesterol?
But today most of us know that it’s not only about cholesterol, or LDL-cholesterol for that matter. Believing that the effect on cholesterol is what defines a healthy food is an oversimplification and has in many aspects landed us on the wrong track.
Thank you. These are of course important questions, too. I agree that we shouldn’t judge a nutrient only because of its effects on cholesterol. I think a fruitful approach will be to look at different food sources of saturated fats, as some groups already have started to do.
Regarding PUFA, there sure are som inconstancies. On that note, this was just published in Circulation:
Dietary Linoleic Acid and Risk of Coronary Heart Disease: A Systematic Review and Meta-Analysis of Prospective Cohort Studies (https://circ.ahajournals.org/content/130/18/1568.abstract)
The authors conclude that
This review also included unpublished and updated cohort studies. For instance, data from ATBC was reanalyzed. All studies except for two adjusted for other fats, which is a strength, but they of course have some of the same limitations as other dietary cohort studies.
They say that a 5 % exchange in energy from SFA to linoleic acid was associated with a 9 % lower risk of total CHD, which is constitent with the metaanalysis by Jakobsen et al. (2009) and Mozaffarian et al from 2010 (of RCTs). Further, they claim that “Recommendations to reduce LA in the diet are based on minimal direct evidence.”
An interesting comment from Harries and Shearer was also published: Omega-6 Fatty Acids and Cardiovascular Disease: Friend, Not Foe? (https://circ.ahajournals.org/content/130/18/1562.extract)
Quote from above comment:
“They say that a 5 % exchange in energy from SFA to linoleic acid was associated with a 9 % lower risk of total CHD, which is consistent with the meta analysis by Jakobsen et al. (2009) and Mozaffarian et al from 2010 (of RCTs).”
It is assumed that lowering LDL cholesterol automatically lowers risk. But is it really that simple? Excerpt:
“Increases in plasma cholesterol are associated with progressive increases in the risk of atherosclerotic cardiovascular disease. In humans plasma cholesterol is contained primarily in apolipoprotein B-based low density lipoprotein (LDL). Cells stop making the high-affinity receptor responsible for LDL removal as they become cholesterol replete; this slows removal of LDL from plasma and elevates plasma LDL. As a result of this delayed uptake, hypercholesterolemic individuals not only have more LDL but have significantly older LDL. Oxidative modification of LDL enhances their atherogenicity…But why should elevation of plasma LDL concentration accelerate its oxidative modification? Investigations of dietary factors that influence plasma LDL-cholesterol, the “lipid theory,” show that consumption of saturated fat increases LDL levels, whereas consumption of polyunsaturated fat decreases LDL levels and, concomitantly, disease risk (8-14). Yet the chemical composition of LDL-containing polyunsaturated fats should render them more susceptible to oxidative damage. The seeming inconsistencies between the findings of these two distinct research areas could be due to the confounding effects of variable lipoprotein age.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC41359/
Quoting the remainder of the paragraph:
“Further, they claim that ‘Recommendations to reduce LA in the diet are based on minimal direct evidence.’”
I wonder what they mean by direct evidence. Are they referring to RCTs, biochemical experiments, or both? If RCTs are the only consideration, then, yes, there are no RCTs in which linoleic acid is reduced to pre-industrial levels. Excerpt from the ISSFAL 2010 Dinner Debate: Healthy Fats for Healthy Hearts:
“Prof. Uauy noted an unsettled issue of great importance: the need for data comparing the effects of omega-3 PUFAs at varying backgrounds of omega-6 PUFAs. Until there are new data to sort this out, we should be cautious in defining recommendations, he stated. There was also a suggestion from the floor that AHA withdraw its advisory statement, to which Prof. Harris responded that he was all for more data, but in his opinion AHA would be unlikely to withdraw the statement. 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
Actually, not everyone agreed on the need for a RCT involving high and low intakes of linoleic acid. Earlier this year I wrote to one of the scientists who attended the debate. His response:
“I must confess that while I participated enthusiastically in the debate I did not agree with the statement that ‘we need a randomized controlled trial to compare the effect of low and high intakes of LA. In my opinion this will simply delay any action on a true solution and is frankly only going to profit the investigators who conduct such a massive and costly trial. The truth is profoundly obvious to any who read the literature comprehensively. Humans differ in their lipid metabolism and response to diet to such an extent that population wide recommendations are impossible. The future has to include personal measurements of lipid metabolic status and individualized solutions.”
Dave. The last part is a key issue;
“Humans differ in their lipid metabolism and response to diet to such an extent that population wide recommendations are impossible. The future has to include personal measurements of lipid metabolic status and individualized solutions”.
That’s painting with too big a brush. Of course there’s individual variation, but would you REALLY argue that e.g. population-wide recommendations to e.g. reduce the intake of sugar and TFA are “impossible”? Or that e.g. sky-high LDL-C/LDL-P are meaningless on a population level?
Or did I just misundestand you?
Yes Mie. Misunderstanding is the right word.
Ok, glad to hear it. Perhaps you could be more careful with the wording next time. 🙂
Erik: “The recommendation is not only to eat less SFA, but to replace more with unsaturated fats.”
Chowdhury et al. probably based their conclusion on all the data in their analysis including trials where SFA was replaced by PUFA. Hence, they did take this into consideration also. Observationally, they found possible benefits for dairy fat and marine fatty acids, but the latter was not supported by their trial analysis.
I haven’t seen any convincing arguments for replacing SFA with unsaturated fats.
Chowdhury did not include any trials, and no, they did not assess substitution effects, i.e. what people who ate less saturated fat ate instead (as David Katz pointed out in an article, this may just imply that saturated fat is as unhealthy as sugar: https://www.huffingtonpost.com/david-katz-md/study-saturated-fat-as-ba_b_5507184.html).
The recommendation to replace some of the SFA with unsaturated fats has several arguments. Some of it comes from dietary trials with multifactorial interventions (where not only saturated fats were replaced, such as trials with the Mediterranean diet).
Ursula Scwhab and colleagues recently did a systematic review on dietary fats/fatty acids and the effect on different end-points. They found “convincing evidence” that exchanging SFA with unsaturated fat reduced CVD risk (especially in men), while they did not find a direct effect from SFA per se.
Erik: “Chowdhury did not include any trials”
Huh, have you read the full study? Chowdhury et al. also included trial analyses that evaluated replacing safa with pufa, among others.
They did include trials, but these were on supplemental n-3 or n-6 fatty acids – not whole dietary interventions. Four studies on ALA supplementation, 17 on n-3 PUFA and 8 on n-6 PUFA. As the athors say: “No data were available on interventions related to saturated or monounsaturated fatty acids.”
That’s probably because you don’t consider anything that doesn’t support your notions “convincing”? The SFA –> PUFA exchange has been shown to be moderately beneficial in virtually all meta-analyses of RCT’s, despite the fact that several issues have attenuated the benefits (including the modest reductions, overemphasis on n-6 fatty acids on exchange trials, the inevitable problems introduced by heterogenous trials etc. etc.). Now, Chowdhury et al. didn’t discuss the effects of this exchange in their paper so your “probably” is simply speculation.
Of course, all of this is secondary in terms of actual diets. No matter whether you go for Mediterranean, low fat, paleo, low carb etc. etc, you’re gonna end up with a diet lower on e.g. SFA and sugar and higher on e.g. unsaturated fats & dietary fiber than the present Western diet. And as long as the basic outlines are in order, that’s what matters. A diet higher on e.g. SFA or sugar can be healthier than another diet as long as the big picture’s in order.
… which is why I consider this much ado about SFA comical. Dose and context.
Mie: “The SFA –> PUFA exchange has been shown to be moderately beneficial in virtually all meta-analyses of RCT’s”
I do not call small and sometimes non-significant reductions in soft endpoints a “benefit”. To come to the conclusion that you do you have to ignore a lot of considerations and data.
Mie: ” Now, Chowdhury et al. didn’t discuss the effects of this exchange in their paper so your “probably” is simply speculation.”
Are you claiming that they didn’t take into consideration the trial evidence involving this exchange even though their own analysis involved trials with this exchange? They did refer to the trial analysis as “replacement of saturated fat with omega-6 polyunsaturated fatty acid” in the correspondence section of their paper, so they are aware that the trials were not simply an increase in PUFA but an exchange of safa with pufa. This consideration probably went into their conclusion:
“Third, we considered 27 randomized controlled trials of fatty acid supplementation or replacement (105,085 participants, 6229 CHD cases). In aggregate, these trials have not suggested clear benefits after supplementation with alpha-linolenic acid (relative risk: 0.97, 0.69-1.36) or with long-chain omega-3 fatty acid (0.94, 0.86-1.03), or replacement of saturated fat with omega-6 polyunsaturated fatty acid (0.86, 0.69-1.07)” – https://annals.org/article.aspx?articleid=1846638
Their conclusion naturally follows from this: “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”
Z.M.
“I do not call small and sometimes non-significant reductions in soft endpoints a “benefit”.”
You do realize that I was talking about meta-analysis of studies of hard endpoints? E.g. Skeaff and Miller etc. etc.?
BTW, you “happened” to ignore the points I made concerning the reasons why the benefits of this exchange are likely to have been (significantly?) attenuated in the meta-analysis …
“Are you claiming that they didn’t take into consideration the trial evidence involving this exchange even though their own analysis involved trials with this exchange?”
Where do they indicate specifically what kind of change in endpoints results from the replacement of X% of tot.energy from SFA with PUFA and/or MUFA (cf. the abovementioned Skeaff & Miller)? Why do they differentiate with n-3 and n-6 PUFA – cf. e.g. Ramsden et al 2010 which showed that exchange of SFA for both n-3 and n-6 showed a clear benefit in CVD endpoints (pooled non-fatal MI and CHD death)?
Reductionism, that’s what it is.
Mie: “BTW, you “happened” to ignore the points I made concerning the reasons why the benefits of this exchange are likely to have been (significantly?) attenuated in the meta-analysis …”
There is a big difference between possible explanations as to why a trial failed (or speculating that benefits may be attenuated) and well-controlled trials showing positive evidence of benefit. You have to show the latter, not the former. Also, bias can go both ways, and you have to take into consideration both.
Mie: “Where do they indicate specifically what kind of change in endpoints results from the replacement of X% of tot.energy from SFA with PUFA and/or MUFA (cf. the abovementioned Skeaff & Miller)?”
In the correspondence section as I quoted above: “In aggregate, these trials have not suggested clear benefits after supplementation with alpha-linolenic acid (relative risk: 0.97, 0.69-1.36) or with long-chain omega-3 fatty acid (0.94, 0.86-1.03), or replacement of saturated fat with omega-6 polyunsaturated fatty acid (0.86, 0.69-1.07)”. It’s a trial analysis, so I’m not sure how X% of energy comes into it, and the endpoint was coronary outcomes.
They defined omega-6 as mixed polyunsaturated intervention with linoleic acid as the primary fatty acid. Ramsden et al. would no doubt disagree with this labeling but Chowdhury et al. is surely aware since one of their own subgroup analyses separated specific and mixed PUFA and found similar results to Ramsden. However, neither Ramsden nor Chowdhury over-interpreted the results. For example, Ramsden et al. is aware of the considerable confounding in Oslo, possible trans-fat differences in many trials, and believes that the benefits may be due to omega-3 specifically (particularly marine fatty acids), because there was hardly any benefit in the two better controlled “mixed” PUFA trials where ALA was used. Chowdhury basically wanted to include the entirety of the evidence but also thinks that some of the smaller trials are more bias prone (hence their additional analysis of trials with at least 100 events), and takes the position that more research is needed before any conclusion is made.
The best argument can be made for omega-3, but the data is mixed. Nevertheless, I agree that the focus should not be on individual nutrients as some argue (https://www.ncbi.nlm.nih.gov/pubmed/23312372), but the problem is that some people make claims about specific nutrients, which requires specific evidence.
Z.M.
“There is a big difference between possible explanations as to why a trial failed (or speculating that benefits may be attenuated) and well-controlled trials showing positive evidence of benefit. You have to show the latter, not the former. Also, bias can go both ways, and you have to take into consideration both.”
… and again you fail to actually comment on the points I made, most noticeably the problems in meta-analyses of RCT’s investigating SFA-PUFA exchange. Also, notice that I wasn’t talking about failed trials per se.
“Nevertheless, I agree that the focus should not be on individual nutrients as some argue”
When talking about benefits of a given diet, they’re hardly reduced to a single factor, yes. Of course, that doesn’t mean that a single factor as ONE constituent among others doesn’t matter: take away one tree at a time and soon there’ll be no forest. Virtually all diets showing benefits in CVD either in hard end-points (Mediterranean) or relevant risk markers (add rational forms of low-carb, paleo, DASH, vegan etc. etc.) have certain key factors in common, including the abovementioned fat ratio: less SFA than in e.g. Western diet, more unsaturated fats. And this is a more or less natural follow-up of the diet itself, not something that’s a result of a huge struggle to eat less SFA.
I was too hasty with sending the reply:
“It’s a trial analysis, so I’m not sure how X% of energy comes into it, and the endpoint was coronary outcomes.”
Did you not read what Eric wrote above?
“Chowdhury did not include any trials, and no, they did not assess substitution effects, i.e. what people who ate less saturated fat ate instead”
Nor read the Schwab et al meta-analysis?
“However, neither Ramsden nor Chowdhury over-interpreted the results.”
… which goes to show that the problems evident in these meta-analyses (direct result of what went on in the trials) should indeed be born in mind.
Add to that what we know about the role of excessive SFA in lipid levels and inflammation, and you’ve got the rationale behind the SFA –> PUFA exchange as PART of a healthy diet.
In addition, notice that no one’s arguing it’s the only thing that needs to be warranted. Nor that it would be enough in controlling the prevalence of CVD. Just like no one’s arguing that e.g. more fiber, more n-3 fatty acids in relation to n-6 fatty acids, moderate alcohol consumption, more vitamin D etc. etc. considered in isolation are the only things that need to be warranted. Would you therefore argue that any single one of these can be discarded since its role in isolation in hugely heterogenous studies (and the meta-analyses carried out on these) is more or less insignificant?
There is no reply button on your last post, so I’m answering here.
Mie: “positive effects due to BOTH n-3 & n-6 replacement of SFA”
You’re not being fair. IF “mixed” PUFA is beneficial it does not necessary follow that both n-6 and n-3 are beneficial, as you seem to be implying. Claiming that is in your words, speculation. It may be that only n-3 PUFA is beneficial or even that n-6 PUFA is attenuating the benefits of n-3 PUFA (as many researchers would argue). Ramsden’s position is more consistent with the evidence, and they make a more compelling argument than the other side in my view.
Your position essentially hinges on Oslo (without Oslo the result would be no effect), which employed so many interventions that it’s impossible to properly test the effects of replacing SFA with PUFA. I’m sure you know that Ramsden et al. listed the numerous confounders in Oslo, and it’s unfortunate that they included it in their analysis given this knowledge. Nevertheless, it should be noted that neither CHD death nor total mortality were significantly reduced despite the inclusion of Oslo. Hooper et al. 2012 did the right thing and excluded Oslo in sensitivity analyses and labeled it a trial at high-risk of bias.
The better controlled trials (dietary changes largely restricted to fat) were Rose, MCS, SDHS, MRC, and LA Veterans. Were these trials perfect? No, and in fact it can be argued that the control groups in many of these trials were disadvantaged by certain factors, but the fact that no clear benefits were seen in any of these despite this, should have killed the SFA/PUFA exchange idea long ago.
Now, if you want to specifically claim that n-3 fatty acids are beneficial (particularly marine fatty acids), you’ll have a much better argument that is more consistent with the evidence.
Mie: “Now, do I recall correctly you mentioning something about having to stick to what the trials show instead of “speculating” on why they show what they show?”
I can’t remember the point I was trying to make, but I do recall that you misunderstood it.
BTW this is my last reply, so take the last word if you desire 🙂
Don’t say that Grace…..I have just started to eat eggs again after not having them for ages plus I bought Almonds, Walnuts and Brazil nuts for snacks and just read in an earlier message not to eat any nuts.
The whole thing is mind boggling!
Dee!
Believe me, I am not giving up my eggs anytime soon. We even went as far as getting backyard chickens to have healthy eggs. I will give up my full fat yogurt and nuts before my eggs :0) However, I am curious why one of the commenters above said only Macadamia nuts are ok? Does this all boil down to moderation or is that crazy talk now days also?!
Grace….yes the nut comment was a new entry into what not to eat! I am travelling to Australia next week knowing my Doctor wants me to take Statins so the trip has been clouded with thinking i might have a heart
attack so far from home. plus, like losing your no claims bonus after a car accident my travel insurance has shot up with the mention of high cholesterol
More and even more evidence that there is no need to fear saturated fats. I am a diabetic type 2. diagnosed 3 years ago and my A1C is very good as well as the lipids. No medicine and hold on to a lowcarb diet including saturated fats. I have no education in medicine, but have read a lot about various diets and found lots of convincing anecdotes and studies that the fear of fats has no scientific reliability.
There is an ongoing debate on this issues here in Sweden and it looks like a paradigm shift is at hand. I suppose you know about that being Icelandic. Interesting blog to read and found a link to this blog from a member of a Diabetes forum where i am active.
Thanks Hans.
I do follow the debate in Sweden. In fact I consider Sweden to be my second home country. I lived there for many years and did most of my training in cardiology in Göteborg. Defended my thesis at the University of Göteborg 20 years ago 🙂
Yes, Göteborg. When studying I went down there from my hometown Östersund and worked there one summer as an assistant, mainly “vak” i,e supervising patients in intensive care at Sahlgrenska. A very responsible duty.Really liked the city and the special kind of witty humour among the inhabitants. Now I am retired living down south in Skåne along the Öresund strait.
When it comes to blogs/forums I follow Kostdoktorn “Diet doctor” and especially the international site “Diabetes Forum”, where you get a lot of support from diabetics around the globe and also keeps updated in findings concerning health and diets for diabetics. If I was diagnosed let us say 20 years ago I should probably have been in a worse condition, but exchanging views on the net helps a lot. Just like this blog.
Dee,
Go enjoy yourself! The stress of worrying about it will also cause a heart attack! Nice chatting with you on a very interesting and mind boggling subjec!
Grace…..Thanks. I do have the pleasure of another cholesterol test before I leave and I don’t know if that is good or bad. Ignorance might be bliss in this case before I leave.
I believe a lot people discount the role of stress in heart disease. I am a good example of what stress can do. I have been going to a cardiologist for over 20 years because of irregular heartbeat. I would get a heart scan every few years. I had one in 2004 and it was OK. I opened a very stressful business in 2005. In 2008 I had to have 5 bypasses from blockage. Nothing changed in my life but the stress. In 2010 I downsized the business to get the stress off of me and have been OK since.
Good point Gary.
Stress is important. Here is an overview I wrote last year on the issue. It covers most of the main scientific evidence.
You know?… sometimes it’s just a matter of faith. I went over to the dark side about 7-8 years ago when I was diagnosed with T2 diabetes.
I had pretty much always eaten “well” and ended up obese and with diabetes so to continue eating the way I had eaten for most of my life didn’t make much sense. At that point the high fat diet did make sense as it was natural and traditional.
I cut all seed oils and went out of my way to eat animal fat… I thought, you only live once, and that’s not forever… I’d rather die quick of a heart attack than one limb at a time.
I eat butter by the spoonful, lamb dripping, cook in beef fat and have a spoonful of coconut oil daily as a tonic, but I would rather go hungry than eat food that has been anywhere near canola oil, sunflower oil, soy “anything” or any other modern oil. Olive oil I will only eat cold as in a salad.
I lost 24 kg and have never and I mean never enjoyed my food more… I am 57 years old, still a diabetic, but am not on medication, I eat a low carb high fat diet… I cook my chips and fish in beef dripping just like they did in the 1970s.
As you can see I still eat carbs (chips) but I stay away from processed food. My HbA1c is usually in the low 7’s and that is the figure they aim for with meds. (All other blood work is also good)
Saturated fat is NOT the enemy, and even animal fat is not ever 100% saturated, it is always a mix of the three. (pork fat for instance is mostly mono-unsaturated, coconut oil is the highest % saturated fat)
I will never change now, and it would not surprise me if I lived longer, happier and healthier than most of you. BTW for those that mentioned it? Eggs are great!
For those that don’t know, rising cholesterol in the blood is caused by inflammation, the inflammation is caused by seed oils, don’t eat the seed oils– the inflammation goes away and so does the high cholesterol… try it…
Absolutely agree. Diagnosed at the age of 63 3 years ago A1C 7.5. ( corresponds to latest international standard 58 ). Got a brochure from the Swedish health authorities how to handle the diabetes. Started to doubt the recommendations and found lots of anecdotes and findings on the net, which pointed in another direction, so after just two weeks an immediate change to a lowcarb diet. Butter instead of margarine and most important quite drastically reducing the intake of carbs.
The result: lost 7 kg the first month and 6 months after diagnosis I had lost 20 kg. Eating without being hungry. No more Metformin and latest HbA1C 5.2. Like a non diabetic. Very good lipids as I mentioned in my first post. Just can’t get into my mind how the health authorities recommend a large amount of carbs for diabetics. In Swedish the old term was Sockersjuka “sugar disease”. That’s what it´s all about. Diabetics can’t stand sugar, no matter if it is refined or carbs in grains like bread. Just the same.
The parity of the carbon chain in SAFA is meaningful. And it seems those (saturated) fats, that are generated by liver from sugars and carbohydrates, are the worst, at least according to this study:
“Results were consistent across the eight countries and in sensitivity analyses. When dietary correlates were assessed, odd-chain SFAs were associated most strongly with dairy products, as expected. Even-chain SFAs correlated more strongly with drivers of de-novo lipogenesis, including alcohol, soft drinks, and potatoes, than with direct dietary sources such as meat, butter, or cheese.”
All SAFA is not created equal.
https://www.thelancet.com/journals/landia/article/PIIS2213-8587%2814%2970166-4/fulltext
Erik: “They did include trials, but these were on supplemental n-3 or n-6 fatty acids – not whole dietary interventions…As the athors say: “No data were available on interventions related to saturated or monounsaturated fatty acids.”
Erik, it seems that there is a problem of semantics here. All the trials included involved replacing safa with pufa, which is why they are often referred to as such. Is Mozaffarian’s 2010 analysis (which you seem to accept) an analysis of the SFA/PUFA exchange?
Erik: “not whole dietary interventions”
This does not make any sense. If you claim specifically that replacing safa with pufa is beneficial then you have to look for studies that isolated this change as best as possible i.e. not whole dietary interventions. BTW, some trials in Chowdhury did employ whole dietary interventions, which should have been excluded, although one of their objectives was to include as much of the evidence as possible.
Vepa A Murari
October 28, 2014
I am a 79 yo Vegetarian from India,who took up a LC HF Diet from 1st Jan 2014. Carbs less than 50gms/day, Fats (Saturated) above 65 gms/day), Protein about 60gms/day. I added an egg with yolk daily to my diet within these limits.
With a 55 year long Cardiac History and Diabetic 43 year History, to reduce both risks. Because I had developed Diabetic Neuropathy Complication. The Neuropath wanted I control my sugar better. I lost 15kg within the first 4 months, without exercise, my SUGAR CONTROL IS VERY GOOD like a non- diabetic, with simple medication Dianorm 80+Metformin 1275 mg with no bother whether Carb is 50 or 150(occasionally) gms/day My Neuropathy pains cramps of over 10 years are gone.
To assuage my Cardiologist fears, taking up the Anti AHA Diet of so much Sat Fat, based on these various websites,EVEN BEFORE starting Diet, I had the blood tests done to provide results the normal way and also the new Lipoprotein tests.
WHILE THE CONVENTIONAL INDICATED a Cholestorol risk, the Lipoprotein tests INDICATED I was no risk. As the diet progressed, Hb1Ac has improved, and Lipoprotein tests indicates I continue no risk.
I underwent yesterday a Senior Citzen Geriatric Check by a leading Hospital with special emphasis on Cardiac LINKED WITH Diabetes risk. The doctor, who does not know my previous history opined I was better than many younger people. I was not outside any single parameter EVEN THE OLD WAY to be a risk. On hearing my history, the doctor was amazed, and opined there was nothing to indicate the LCHF diet had harmed me in any way, although as doctors they cannot recommend diets outside officially approved guidelines.
The new lipid tests, though still not officially accepted, are available in most major towns of India. And in my view they assess Cardiac risk better – whether or not Diabetes is an added risk, by reducing the emphasis on Cholestorol per se.
Doc,
did you see that the NLA published their own treat-to-LDL-targets guidelines. The president of NLA argues that LDL concept is simple, the theoretical underpinning behind it is sound, it works and the patients have easy time to grasp it. He also fears that the new guidelines espoused by AHA/ACC will bring more confusion and will take an important metric away from the patients. The LDL metric empowers people and in best cases it motivates to change according to him.
https://www.medpagetoday.com/Cardiology/Dyslipidemia/48126
Doc, do you continue treat to target, or have you embraced fully the new guidelines set by the AHA/ACC, if I may ask?
BTW, a new randomized mendelian trial was just released. A cumulative exposure to high LDL since birth most likely causally related to arterial stenosis, whereas HDL-C and triglycerides are not.
https://jama.jamanetwork.com/article.aspx?articleid=1919440
Again, the researchers looked at various polymorphism that elevate LDL with a differing mechanism; no heterogeneity with the results. This confirms that elevated LDL is harmful independent of mechanism used.
“A cumulative exposure to high LDL since birth most likely causally related to arterial stenosis, whereas HDL-C and triglycerides are not.”
Excerpts from the JAMA article referred to above:
“Low-density lipoprotein cholesterol may promote calcification in these early lesions, via the formation of cholesterol microcrystals that act as nidi ( A point or place at which something originates, accumulates, or develops.) for initial calcification, and also via oxidized LDL, a potent proinflammatory and pro-oxidant mediator that is known to strongly induce an osteogenic phenotype in valvular cells…our results suggest that early lipid lowering, prior to the development of even mild forms of aortic stenosis, may be required to prevent aortic valve disease; this hypothesis remains to be tested in a randomized trial.”
The fats in oxidized LDL are polyunsaturated. Saturated fats are chemically stable.
Mie: “Did you not read what Eric wrote above?
Eric is wrong, as I said before. Again:
“Third, we considered 27 randomized controlled trials of fatty acid supplementation or replacement (105,085 participants, 6229 CHD cases). In aggregate, these trials have not suggested clear benefits after supplementation with alpha-linolenic acid (relative risk: 0.97, 0.69-1.36) or with long-chain omega-3 fatty acid (0.94, 0.86-1.03), or replacement of saturated fat with omega-6 polyunsaturated fatty acid (0.86, 0.69-1.07)” – https://annals.org/article.aspx?articleid=1846638
In other words, they DID analyze trials where SFA was replaced by PUFA, which they called “replacement of saturated fat with omega-6 polyunsaturated fatty acid” here. Even if they never mentioned it, anyone familiar with the trials included would know this. If this is not what you mean, then you would have to clarify.
Mie: “which goes to show that the problems evident in these meta-analyses (direct result of what went on in the trials) should indeed be born in mind. ”
Exactly, but one of the main problems in most analyses is inclusion of trials with inappropriate designs (FMHS), or blatant confounders (Oslo, STARS), or incomplete analyses (no cause-specific data for the SDHS prior to 2013). Most trials are also inadequately blinded or had differences in care. The fact that no clear reductions in events and no reduction in mortality are seen despite this, is even more reason to think that the SFA/PUFA exchange is useless.
Mie: “Add to that what we know about the role of excessive SFA in lipid levels and inflammation”
As we know from the past, I do not agree with this, so I’m not going over this again.
Mie: “In addition, notice that no one’s arguing it’s the only thing that needs to be warranted.”
A specific claim is being made i.e. replacing SFA with PUFA is beneficial. Therefore, specific evidence of this is required. Trying to change the topic to diet patterns doesn’t address the specific claim, since using trials that clearly employed multiple interventions (e.g Lyon, Oslo-1) cannot be used as evidence for a single intervention. It is especially illogical to attribute results in these trials to specific factors (e.g. SFA reduction) which have already failed in numerous other better controlled trials. Hence, if you look at ALL trials, what separates the more successful trials (consistent large reductions across most or all endpoints including total mortality) from the failed ones is not changes in saturated fat, but
rather omega-3 specifically. This is partly supported by trials with omega-3 as the only intervention (e.g. GISSI-P). Hence, I can get with the idea that omega-3 is beneficial (but only in certain populations it appears), and this does not necessarily entail modifying saturated fat.
Yes I know, you would probably reply that I misunderstood or failed to understand some point, but I feel the same way about your replies. It would be so much easier if you sat down with me in person 🙂
What the hell’s wrong with WordPress, by the way? Why do the replies end up all over place?
Anyhow:
“In other words, they DID analyze trials where SFA was replaced by PUFA, which they called “replacement of saturated fat with omega-6 polyunsaturated fatty acid” here.”
… but just like Eric pointed out, a) did also include SUPPLEMENTATION trials (you do know the difference between “exchange” and “supplementation”, right?) and b) did not indicate the results in “X% of SFA –> PUFA) as e.g. Skeaff and Miller, thus rendering any meaningful comparison of exchange meaningless (as you really have to standardize the size of the exchange to be able to compare the effects in a meaningful way). And add the artificial separation of n-3 and n-6 fatty acids. Thus, there’s simply nothing useful in Chowdbury et al.
“Exactly, but one of the main problems in most analyses is inclusion of trials with inappropriate designs (FMHS), or blatant confounders (Oslo, STARS), or incomplete analyses (no cause-specific data for the SDHS prior to 2013).”
… and if you’d read these meta-analyses, you’d have realized that e.g. FHMS tends to carry an insignificant “weight” (%) due to the trial’s size and thus doesn’t really contribute to the possible confounding – whereas e.g. WHI (which biases the results due to a) fat reduction and b) replacement of SFA with mostly refined carbs) confounds the results considerably due to its size. As for Oslo being confounding (the difference in smokers, right?), you could say the same thing of e.g. Rose Corn Oil where most important factors (e.g. appliance) where nowhere to be found in the original paper.
However, virtually all meta-analyses prior to this one have shown benefits in fat exchange – despite there being clear reasons why the exchange (when carried out in especially high risk population) would be beneficial if and when executed along the current guidelines. In addition, we have clear evidence from metabolic ward studies indicating that the mechanism via which SFA in larger quantities is inferior to unsaturated fat (impairment of LDL receptors) when it come to lipids as well as studies investigating inflammatory effects of fats (SFA being in par with carbs whereas PUFA is somewhat anti-inflammatory).
Therefore, even if you wanted to be cautious, you’d have to state that there’s at the VERY least evidence hinting that fat exchange is beneficial. Now, you’re doing just about everything to go out of the way to claim otherwise.
“As we know from the past, I do not agree with this, so I’m not going over this again.”
Yes, I know your denialist background when it comes to lipids and their role in CVD. No need to go there again.
“A specific claim is being made i.e. replacing SFA with PUFA is beneficial. Therefore, specific evidence of this is required.”
Well then: see above.
However, once again, you failed to address the “no-forest-just-trees” approach which you obviously are trying to go for – and which I commented on already.
“It is especially illogical to attribute results in these trials to specific factors (e.g. SFA reduction) which have already failed in numerous other better controlled trials.”
Which trials are you referring to? LA Veterans comes to mind – but it really doesn’t support your claim, now does it? 🙂
“Hence, if you look at ALL trials, what separates the more successful trials (consistent large reductions across most or all endpoints including total mortality) from the failed ones is not changes in saturated fat, but rather omega-3 specifically.”
Err, nope if you go for the big picture. See Ramsden et al: trials which involved MIXED n-3 & n-6 resulted in a decreased risk of non-fatal MI and CHD death. Once again: MIXED, not n-3 specific nor n-6 specific.
“It would be so much easier if you sat down with me in person.”
Who knows? But as that’s not going to happen, we’ll just have to made do with what we’ve got.
Mie, please clarify two things before I reply to your points:
Mie: “but just like Eric pointed out, a) did also include SUPPLEMENTATION trials (you do know the difference between “exchange” and “supplementation”, right?)”
Please distinguish those terms for me, because I don’t get how it is relevant to your claims.
Mie: “did not indicate the results in “X% of SFA –> PUFA) as e.g. Skeaff and Miller”
Where exactly in Skeaff and Miller do they do this in the trial analysis? Are you talking about a regression analysis?
I don’t think that higher consumption of seed oils is granted at all given all of its potential effects beyond short term coronary heart disease one (long term benefit is at least highly dubious). Just take a look at all the clues (papers) pointed out by David Gillespie from their posts linked in the third paragraph. Nothing against nuts though.
Seed oils are the newcomers. A prudent approach is to avoid them while waiting for the controversy to settle.
Z.M.
“Please distinguish those terms for me, because I don’t get how it is relevant to your claims.”
Supplementation = adding. Exhancge = not adding.
Clear enough for you?
“Where exactly in Skeaff and Miller do they do this in the trial analysis? Are you talking about a regression analysis?”
Err, Skeaff & Miller is a meta-analysis in which metaregression is kinda necessary, right?
Mie: “Supplementation = adding. Exhancge = not adding. ”
You would have to list for me the trials that are supplementation trials and those that are exchange trials or give specific examples, because all dietary trials included in Skeaff and Chowdhury involved a reduction in animal fat that was replaced by something else i.e. it involved a reduction + an addition, which is essentially an exchange.
Mie: “Err, Skeaff & Miller is a meta-analysis in which metaregression is kinda necessary, right?”
No, meta-regression is something else often done as a secondary analysis and is observational in nature, pull out your stats book 🙂 For example, Hooper et al. 2012 did a meta-regression in addition to the main analysis.
“You would have to list for me the trials that are supplementation trials and those that are exchange trials or give specific examples, because all dietary trials included in Skeaff and Chowdhury involved a reduction in animal fat that was replaced by something else i.e. it involved a reduction + an addition, which is essentially an exchange.”
Ah, my apologies, it seems I lost you for a moment there. Yes, Chowdbury et al. stated that they inspected “replacement of saturated fat with omega-6 polyunsaturated fatty acid” which, of course, is precisely the problem in these trials that distorts the results …
… the n-6 issue, that is. I’ll refer back to Ramsden et al. And yes, I remember you referring to Ramsden et al speculating on the reasons for the benefits of SFA-for-PUFA exhange possibly being n-3 -related. Now, this is more or less an unfounded attempt to underline their own relevant findings of
a) positive effects due to BOTH n-3 & n-6 replacement of SFA
and it also
b) ignores the likely explanation for n-6 exchange trials not being of any benefit (the amount of ALA being ridiculously high, up to 16% of tot. E; studies of poor quality in e.g. reporting –> yet, no statistically significant increased risk).
Now, do I recall correctly you mentioning something about having to stick to what the trials show instead of “speculating” on why they show what they show? 🙂
And about Skeaff and Miller, my bad. They carried out random effects meta-analysis. Which doesn’t change the issues I mentioned initially – and which you haven’t addressed.
Furthermore, could you now mention these “better controlled trials” indicating that SFA –> PUFA is useless?
I read your blog for the first time today and was thrilled to see this post on the change in recommendations from Up To Date. I blog on issues similar to your posts at http://www.theskepticalcardiologist.com and in particular I’ve focused on the bad advice to avoid full fat dairy and eat non fat dairy. With your permission I would like to reference your post on this with my own commentary. I’ll also put up links to your excellent writing and I’ll be following you closely. Keep up the good work!
Thanks Anthony
Of course, feel free to refer to my article on your blog with your own comments.
Appreciate your interest.
Looking forward to have a look at your blog.
A really late response to Erik and Mie. In Chowdhury’s analysis omega-6 RCTs (Oslo Diet Heart, Sydney Diet, Finnish Mental Hospital Study etc.) were wrongly labelled as “supplementation” studies. They were actually genuine *substitution* studies, ie. saturated fat was replaced by PUFA oils/margarines mainly. You can find this information in supplement material of the meta-analysis, table 11. However, these studies are confounded by trans fat content margarine those days, multiple dietary instructions and many more points.
I’ve detailed many of these studies at my SlideShare account.
In other words, substitution analysis was done regarding linoleic acid (omega-6) based morbidity RCTs but NOT based on prospective cohorts.
Fantastic Thread going here. It has made my day finding this website and Axel F. Sigurdsson MD – thanks so much for this amazing resource! Seems simple to me; better to eat something natural like full cream milk which science is now showing is actually beneficial, than something that has been highly processed to remove the fat content. I would also be weary of eliminating avocados from your diet (even if you are overweight) without further research – they are a natural source of many important nutrients.
If you want to lower LDL, without lowering HDL, get 15-20 minutes of sunshine a day. UVB rays (from sunshine or a UVB light) make vitamin D through the skin and LDL cho is the raw fuel for that. I know this for a fact and use this to manipulate my LDL. Lowered my LDL from 154 to 98 in a month with daily sunshine and stopping my vitamin D supplements.
HDL can be raised quickly by taking T of coconut oil a day. Note: work up to a Tab a day as if you are not used to fats you could get the runs. In 2 months I raised my HDL from 38 to 78 by taking coconut oil (highly saturated fat, but not animal fat) coconut oil is full of very good things too…antifungal, anticeptic, antiviral and has a shelf life of two years, opened! Kills bacteria and is known to kill the herpes virus. I know I sound like a nut… websearch Dr. Mary Newport …