“We no longer suggest avoiding saturated fats per se …”

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.

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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.

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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.

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CheckItAndSeeEddie (@theedtalks)Reijo Laatikainen (pronutritionist)Axel F SigurdssonDr. AnthonyP Recent comment authors

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offshoretinker
Guest

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… Read more »

Mie
Guest
Mie

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.

offshoretinker
Guest

Thanks for the passive aggressive lesson in semantics Mie – somewhat undermined by you understanding completely my meaning.

offshoretinker
Guest
FrankG
Guest
FrankG

“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”.

davebrown9
Guest

“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… Read more »

Mie
Guest
Mie

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… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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?

davebrown9
Guest

“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… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

That’s interesting Dave. Thanks.

Pasi Saario
Guest
Pasi Saario

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….

Mie
Guest
Mie

Saario, use English if you want to bitch about something.

Or better not: don’t bitch. Contribute.

Mie
Guest
Mie

“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… Read more »

Someone
Guest
Someone

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… Read more »

Danrex
Guest

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.

George Henderson
Guest

@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.

Grace
Guest
Grace

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!

RichardOrnishForLife
Guest
RichardOrnishForLife

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… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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… Read more »

FrankG
Guest
FrankG

“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

Dee
Guest
Dee

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… Read more »

Marg
Guest
Marg

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… Read more »

Yossi Mandel
Guest
Yossi Mandel

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.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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… Read more »

Grace
Guest
Grace

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… Read more »

FrankG
Guest
FrankG

“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”?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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.

“Sleeping with one’s shoes on is strongly correlated with waking up with a headache.
Therefore, sleeping with one’s shoes on causes headache.”

FrankG
Guest
FrankG

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.

RichardOrnishForLife
Guest
RichardOrnishForLife

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… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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.

Mie
Guest
Mie

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.

FrankG
Guest
FrankG

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.

davebrown9
Guest

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… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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… Read more »

Erik Arnesen
Guest

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… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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… Read more »

Erik Arnesen
Guest

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 In prospective observational studies, dietary LA intake is inversely associated with CHD risk… Read more »

davebrown9
Guest

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… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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”.

Mie
Guest
Mie

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?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Yes Mie. Misunderstanding is the right word.

Mie
Guest
Mie

Ok, glad to hear it. Perhaps you could be more careful with the wording next time. 🙂

Z.M.
Guest
Z.M.

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.

Erik Arnesen
Guest

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… Read more »

Z.M.
Guest
Z.M.

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.

Erik Arnesen
Guest

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.”

Mie
Guest
Mie

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… Read more »

Z.M.
Guest
Z.M.

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… Read more »

Mie
Guest
Mie

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… Read more »

Z.M.
Guest
Z.M.

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%… Read more »

Mie
Guest
Mie

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… Read more »

Mie
Guest
Mie

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… Read more »

Z.M.
Guest
Z.M.

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… Read more »

Z.M.
Guest
Z.M.

BTW this is my last reply, so take the last word if you desire 🙂

Dee
Guest
Dee

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!

grace
Guest
grace

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?!

Dee
Guest
Dee

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

Hans
Guest
Hans

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… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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 🙂

Hans
Guest
Hans

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… Read more »

Grace
Guest
Grace

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!

Dee
Guest
Dee

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.

Gary Yerby
Guest
Gary Yerby

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.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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.

Mark Hunter
Guest
Mark Hunter

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…… Read more »

Hans
Guest
Hans

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… Read more »

Ari
Guest
Ari

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

Z.M.
Guest
Z.M.

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… Read more »

VEPA A MURARI
Guest
VEPA A MURARI

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,… Read more »

RichardOrnishForLife
Guest
RichardOrnishForLife

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,… Read more »

davebrown9
Guest

“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… Read more »

Z.M.
Guest
Z.M.

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”… Read more »

Mie
Guest
Mie

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… Read more »

Z.M.
Guest
Z.M.

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?

Andrés
Guest
Andrés

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.

Mie
Guest
Mie

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?

Z.M.
Guest
Z.M.

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… Read more »

Mie
Guest
Mie

“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… Read more »

Dr. AnthonyP
Guest

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!

Axel F Sigurdsson
Admin
Axel F Sigurdsson

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.

Reijo Laatikainen (pronutritionist)
Guest

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… Read more »

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