Friday, February 8, 2013

Study: double mortality after replacing animal fats with vegetable fats

.
Also a mystery of some "missing data" etc. I am reposting this quote from Barry Groves' blog:

Quote:

...
The new research, published online in the British Medical Journal, was carried out by experts from the US Government’s National Institutes of Health in Maryland. They recovered missing data from a study in the 1960s involving 458 men aged 30-59 who had suffered a heart attack or angina. Using modern statistical methods to compare death rates, they found there was no evidence of the benefit of replacing saturated fats with omega-6 linoleic acid, found in vegetable fats. In fact, they said replacing the animal fats with polyunsaturated fatty acids (PUFAs) from vegetable fats increased risk of death in those patients with cardiovascular disease. Those who increased their intake of the “healthy” fats over three years were almost twice as likely to die. The omega-6 linoleic acid group in the study had a higher risk of death from all causes (62 per cent), as well as from cardiovascular disease (70 per cent) and coronary heart disease (74 per cent), compared to others. Linoleic acid is present in high amounts in some commonly used vegetable oils such as corn, sunflower, safflower and soya bean.
...

The study was published in BMJ on the 5-Februsary 2013: "Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis" (pdf)

More quotes (from the study, the highlights and the capitalized comments in [] brackets are mine):

Advice to substitute vegetable oils rich in polyunsaturated fatty acids (PUFAs) for animal fats rich in saturated fatty acids (SFAs) has been a cornerstone of worldwide dietary guidelines for the past half century.1 When this advice originated in the 1960s, PUFAs were regarded as a uniform molecular category with one relevant biological mechanism—the reduction in blood cholesterol.1 2 Omega 6 (n-6) linoleic acid (LA) was the best known dietary PUFA at the time.

...

Diet intervention
The intervention group received instructions to increase their PUFA intake to about 15% of food energy, and to reduce their intake of SFA and dietary cholesterol to less than 10% of food energy and 300 mg per day, respectively.10 To achieve these targets, intervention participants were provided with liquid safflower oil and safflower oil polyunsaturated margarine (“Miracle” brand, Marrickville Margarine). Liquid safflower oil was substituted for animal fats, common margarines and shortenings in cooking oils, salad dressings, baked goods, and other products, and was also taken as a supplement. Safflower oil polyunsaturated margarine was used in place of butter and common margarines.

Control
The control group received no specific dietary instruction. However, some participants began substituting polyunsaturated margarine for butter after their coronary event.33 Because the research team made no effort to alter the PUFA or SFA content of control diets, such dietary changes were allowed to continue.
...
In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.[IF THEY HAD BEEN PUBLISHED RATHER THAN GONE MISSING, AT THE TIME, FOURTY YEARS AGO!]
...
Increased all cause mortality in the safflower oil group was reported in 1978,10 although deaths due to cardiovascular disease and coronary heart disease were not reported by group.[BECAUSE THE DATA WENT MISSING!] Clinical outcomes for cardiovascular disease and coronary heart disease have been considered to be more relevant than all cause mortality when evaluating the evidence base25 and formulating dietary guidelines.26 Therefore, previous meta-analyses of PUFA intervention trials and risk of cardiovascular disease25 27 28 have been incomplete because they were not able to include these missing data from the SDHS. [SDHS=SYDNEY DIET HEART STUDY. CONCIDENTALLY, THE MISSING HEART MORTALITY DATA HAPPENED TO CONTRADICT, BY A LARGE FACTOR, THE EXPECTED OUTCOME! HAD THE HEART MORTALITY DATA NOT GONE "MISSING" FOURTY YEARS AGO, THE ENTIRE VEGETABLE OIL INDUSTRY WOULD PROBABLY NOT EXIST BY NOW!]



Interestingly, since the control group was found also shifting towards substituting all animal fats with vegetable oils and spreads, the degree of dietary change between the study group and the control group was most likely smaller than the nominal goal for PUFA intake increase to 15%. Yet, such a small difference of probably much less than 15% in PUFA (in absolute calories) have created a huge increase in cardiovascular disease, by about 70%. It indicates that the relative risk of cardiovascular disease rises proportionally to the absolute PUFA caloric intake, with a proportionality factor of about 5 or higher! (If the linear interpolation model holds true). Furthermore, an increase due to PUFA was even higher than an increase in cardiovascular mortality due to smoking (see Table 6)!

This high multiple factor seems to be confirm by the data from Table 5 indicating that for every 5% PUFA increase (in absolute energy%) the All cause mortality, the Cardiovascular disease mortality and the Coronary heart disease mortality increased by 31%, 35% and 26% respectively (relative risk factor).  This implies a proportionality factor of about 5-7.

 That is, for every 1% added Poly-Unsaturated Fatty Acids ( PUFA) in absolute calories % of the total, cardiovascular mortality INCREASED  by 5 to 7%. This is big news!

There is an even bigger news: Saturated fat is good for us! Table 5 exonerates the much maligned saturated fats from being implicated in heart disease (Dr. Ornish, please listen). For every 5% added saturated fat (in % of absolute total calories) the risk of mortality defined in the same categories as above DECREASED  by 30%, 28% and 28% respectively!  With the proportionality factor being also about 6, that is for every +1% of absolute saturated fat intake, mortality decreased by 6%!

This study has also neatly killed the second "bird" - the infamous cholesterol-heart disease hypothesis, quote:


As expected, increasing n-6 LA from safflower oil in the SDHS significantly reduced total cholesterol; however, these reductions were not associated with mortality outcomes (results not shown). Moreover, the increased risk of death in the intervention group presented fairly rapidly and persisted throughout the trial. These observations, combined with recent progress in the field of fatty acid metabolism, point to a mechanism of cardiovascular disease pathogenesis independent of our traditional understanding of cholesterol lowering.

It is interesting to observe the exact moment, around year 3.5 into the study on the graph Fig.2c below. I am speculating here, but a dramatic fall of mortality rates in both the intervention and in the control group coincidental with a sudden increase in quitting the study, may indicate a point when the participants and doctors realized that something is wrong and begun reverting to their previous diet. Butter, anyone?

Fig.2 (bottom) from the study.  

Notice how the number of deaths dropped to zero after year 3.5, and a dramatically higher rate of study-quitting by the patients. About 30 people used to leave the intervention group per year (out of which 5-16 were due to death) until year 3.5. Subsequently 49 and 36 patients quit but none died! There is probably more to be told that wasn't discussed in the paper, but the numbers reveal enough...



16 comments:

George Henderson said...

I've just blogged about this here:

http://hopefulgeranium.blogspot.co.nz/2013/02/the-results-show-that-omega-6-linoleic.html

Taking a somewhat different angle based on the ideas and criticisms in doctors' responses to the BMJ.
What will it take to satisfy some people? How can results be clearer?

Stan (Heretic) said...

Gutierrez criticism isn't very good, since the transfats issue was addressed satisfactory by the authors and total cholesterol reduction in intervention indicates that transfats could not have been the major part.

Yes indeed, what does it take to convince a Western tenured "scientist"? How did Galileo manage to convince his bishops to look through his telescope? He didn't, he just published his work and the bishop was @#$% regardless. Openess is the best defence!

George Henderson said...

I thought the authors did address the transfats, and the cholesterol says the influence was minimal, but it's still a then-unknown that would be quantified today.
There seems to have been a leak between the groups - at first some controls snuck in Miracle, while the Miracle group increasingly reverted to butter.

I am curious as to how the Standard Australian Diet (1966-1973) compares with the low-fat Mediterranean diet in the Lyon study (the Guyenet discussion I link to).
We can easily compare both because much the same prudent diet was contrasted in both. Well I can't, because I am something of a math illiterate, but they look pretty similar.
We have about 1.7 OR from SDHS and (the inverse) a 76% reduction in deaths from LDHT (more details here: http://wholehealthsource.blogspot.co.nz/2009/06/lyon-diet-heart-study.html ). How comparable are those? Is the SAD of 66-73 a valid alternative to the low-fat Med diet?

George Henderson said...

I've just been reading your post on mitochondrial destruction http://stan-heretic.blogspot.co.nz/2011/10/is-t2-diabetes-result-of-mitochondrial.html
ketone bodies stimulate mitochondrial replication, this is the mechanism when ketogenic diets are used to repair neurons.
http://www.sciencedirect.com/science/article/pii/S0165017308001045
Aubrey de Grey has some good semi-speculative papers on the fate of mitochondria.
http://www.sens.org/files/pdf/MiFRA-06.pdf

George Henderson said...

Aha, a 70% reduction is probably a greater difference than a 70% increase! Told you my math was bad.

Stan (Heretic) said...

Thanks for the link on mitochondria. Re: Lyon Study - it is an interesting question, weather the Omega-3 to Omega-6 ratio is the deciding factor or is it overconsumption of omega-6, linoleic acid in particular, that is the main problem? Hard to tell without more research. Also, it is not entirely certain if it is indeed the polyunsaturated omega-6 fats that is the main factor, or something else that is in the commercially manufactured vegetable oils. Partial oxidation? Transfats? Bottled vegetable oils are quite high in transfats (a few %), for example Canola oil (fresh) is supposed to contain about 4% omega-3, but it is unstable and converts all that omega-3 fat rather quickly into transfats, while in storage, catalized by the added anti-oxidants. There was an article about that by Dr. Mary Enig (see www.westonaprice.org).

I have seen some studies on nuts (nuts contain polyunsat fats mostly omega-6) added to patient's diet and they all seem to report a beneficial outcome. However, they are not long term studies.

Stan

Stan (Heretic) said...

[continuation of the Lyon Study thread from your message]
The fact that increased saturated fat consumption has had as much positive benefit as subtraction of the vegetable oil, may indicate that it is the excess of the omega-6 alone that is causing the problem, quite independently on the omega-3. One can also argue that this study may be suggesting that an addition of saturated fat could be almost as beneficial as adding omega-3.

The positive effect of adding omega-3 in the Lyon Study was almost twice as strong as the negative effect of adding omega-6, although it is hard to compare if the exact quantities of the supplements are not know (perhaps they are documented?). One thing about the French diet - it was and still is very high in animal fats therefore the Lyon Study simply added Omega-3 to an already high saturated fat diet, and the French heart disease risk is already one of the lowest in the Western world. On the other hand Australian diet in the Sydney Study may have been originally more "regressive" (American-like) and lower in animal fat than the French. Perhaps it was the removal of the saturated fat that has done most of the damage?

There are many possibilities/interpretations.

George Henderson said...

Yes, the removal of SFA stands out and it's interesting how commentators avoid mentioning it, some fool dietician from the UK theorized it was a lack of MUFA, which "protects against LA". Well, SFA does that too, and we know that SFA was restricted in the study, we don't know that about MUFA. And why the hell should we be eating something that we need to be "protected against"?

Drugs for side effects of drugs?
"I don't know why she swallowed the fly!"

George Henderson said...

Guyenet states that Lyon participants continued to eat cheeses on their low-fat diet.

Sydney diet of 1966 would have been rich in animal fat, but maybe some vege shortenings were used in baking.

Tony Mach said...

"… or something else that is in the commercially manufactured vegetable oils …"

Good question.

First of all, one nitpick, I think the problem is overconsumption of seed oils – commercially manufactured or not.

Then, while I think that BOTH the ratio and the absolute amount of n-6 is an problem (if not *THE* problem), there is one more thing in seed oil of which I don't have numbers: oil-solvent xenohormones.

(And here a short reminder to look into Bill Lands work, which focuses AFAIK on the n-3/n-6 metabolism, and how PUFAs get metabolized in prostaglandines, with n-3 and n-6 ending up in *different* series of prostaglandines – one potential pathogenic pathway)

Michael Barker said...

Hi Stan

Here's something for you.

I was on Pubmed looking up some other info and noticed that this paper apparently is now one of the most sought after papers on it.

Hopefully this paper is going to make worm turn.

Aaron said...

What do you think about this study? I know it is on worms, but it shows that polyunsaturated fats might not be as bad as you think.

Cellular renewal process may underlie benefits of omega fatty acids

"Study of tiny roundworms provides clue to observed human health benefits"

http://www.eurekalert.org/pub_releases/2013-02/mgh-crp021313.php

Stan (Heretic) said...

Aaron,

Re: the omega-6 and worms study

Activation of autophagy (beneficial) may be mediated by more than omega-6 arachidonic acid, its role may be coincidental, and the other issue is the dosage.

In fact it makes me suspect that the beneficial effects of low level ionizing radiation (see hormesis) and that a certain not too low level of stress (for example cold environment under ketogenic diet) may be perhaps related to this effect. Interesting topic.
Stan

Sam said...

Thanks for your blog. You've convinced me that omega-6's are bad. Wheat/corn carbs are bad. I'm still not convinced that saturated fats don't clog your arteries. I hope you understand this criticism is not of you personally. People get so upset these days over any kind of differences of opinion. Especially diet. I just want to get the facts straight and hopefully add something to your knowledge base. I read a blog page the other day that said that Inuit from before European times were found frozen and autopsied. They had atherosclerosis. Now maybe it was fire smoke or other bad diet that accounted for this but they did follow a diet heavy in saturated fats. Unfortunately I lost the page. I tried to find the study and maybe I did but I'm not sure.

Atherosclerosis-in-Pre-Westernized-Inuit.pdf

http://www.meandmydiabetes.com/wp-content/uploads/2010/03/Atherosclerosis-in-Pre-Westernized-Inuit.pdf

The next report I found is confusing. Some reports high Atherosclerosis some low.

Low incidence of cardiovascular disease among the Inuit*/what is the
evidence?

http://www.researchgate.net/publication/10943329_Low_incidence_of_cardiovascular_disease_among_the_Inuit--what_is_the_evidence/file/79e41509268714c56f.pdf

Here's what I think(at the moment, diet is complicated). Lots of fat included saturated fat helps the body function but maybe it clogs the arteries (not sure). I also believe that people can do well on a low fat- high carb diet if they watch what kind of carbs they eat. But who wants to eat like that? Is that even living? So I'm wondering what you think of Pauling therapy?

PAULING THERAPY Synopsis-short

http://www.internetwks.com/pauling/short.html

Chapter 7 The Pauling Therapy - extended

http://practicingmedicinewithoutalicense.com/protocol/excerpt_chp7.pdf

I tried this for over a month with doses slowly going up. I don't think I reached the maximum dose. I was also using liposomal vitamin C made like this:

http://www.quantumbalancing.com/liposomalC.htm

I had my blood tested before and my cholesterol was slightly high, (I don't have the numbers in front of me). After using the Pauling therapy for several weeks the results were my cholesterol went higher. Arrggh! Maybe it was washing out the cholesteral and that was the higher level measured? I then stopped for a few months and it went back down. I did feel better though with the Pauling therapy. Seemed that hiking up hills was easier. I was less winded. I'm going to try Pauling therapy again. The general idea being more saturated fats to feel better and clear out the mitochondria. Pauling therapy to clean out the resulting sludge from the saturated fats.

Stan (Heretic) said...

Sam, I am also puzzled by the Alskan and Andean mummies with athersosclerosis. This is somewhat contradicting the report of these peoples' good health prior to the adoption of European food. One issue is the small number of the corpses studied. Another possibility is that the atherosclerosis can be triggered by many factors other than the high carb or high wheat diet. Some of the3m are known such as hypothyrpidism/lack of iodine, deficiency of microeement such as magnesium and copper, and bacterial infections (chlamydia is one such documented in the literature, riketsia is another). Traces of arterial plaque are common, even among people who never or very rarely suffer from heart disease, for example Masai. Not every plaque is equal and not every form of plaque is deadly.

No I am not a diet fundamentalist - I am not upset if you bring contrary evidence or questions, I welcome it! My interest is purely scientific. I just like you, would like to know what is happening and why. Best regards,
Stan (Heretic)

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