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Friday, 8 February 2013

Doctors Respond to the Sydney Diet Heart Study


(music - Christmas in the Country, The Puddle)

“The results show that the omega-6 linoleic acid group had a higher risk of death from all causes, as well as from cardiovascular disease and coronary heart disease, compared with the control group.


We should be most skeptical of the research that best confirms our own beliefs. It may not contain an inaccurate result – in the case of the Sidney Diet Heart Study, the result is consistent with the totality of the evidence that is appearing from other sources – but it may not be as convincing to others as it appears to us. We should always be alert to the desirability of designing experiments to produce results that, one way or the other, will convince any reasonable person. In diet studies this may well be unattainable, and usually the “expert evidence” of clinical studies has to be considered in the context of circumstantial and eyewitness evidence from other sources, but it is the scientific ideal.



On the BMJ website where the study appears, doctors can send in their responses, and some of these responses give cogent reasons why a reasonable person, especially one not engaged with the Paleo discussion of seed oils over the past few years, might remain unconvinced by the latest revelations.

Perhaps the best response comes from Professor Jean Gutierrez, assistant professor of exercise science at Washington University. She points out that one of the products used in the trial probably contained high levels of trans fats:

Participants in the intervention group consumed “Miracle” Margarine, a product based on safflower oil. Hydrogenation of safflower oil itself creates a grainy product low in linoleic acid, so high-linoleic safflower oil margarine products were created by blending liquid safflower oil with another hydrogenated oil stock (3). Miracle Margarine used in the original study was either low in linoleic acid (due to hydrogenation of the safflower oil itself) or the oil was blended with another commercially hydrogenated fat to create a plastic margarine product. An investigation by Bernfeld, Homburger, & Kelley, published in 1962, indicated that the fatty acid composition of most margarines of the time were about 50-60% 18:1 monounsaturated fats (including oleic and trans isomers) and about 20-30% 18:2 linoleic acid, even in those products having high-PUFA claims on the label (4). None of the 22 margarines studied had a majority of fatty acids coming from PUFA. Another report from the same time period indicates that commercially produced hydrogenated fats, like those added to safflower oil to make margarine, were generally composed of about 25-40% trans fats (5). Fatty acid composition of margarines in the 1960s investigation were not comparable to liquid vegetable oil, despite package claims. The only reference supporting the healthful content of Miracle Margarine is a very general press release from the company who made the product (6). It is probable that Miracle Margarine had significant trans fatty acid content.

This is an obvious confounder, hard to dispute on science grounds. Morally it might not make much difference; if advice to reduce saturated fat and increase PUFA consumption lead to the use of such dodgy products such as Miracle Margarine, as it did, then it still stands condemned historically. Have there been studies where oil but not margarine was the intervention? Was the Rose Corn Oil Study really just a study of corn oil? Comments section please.

In the section "other dietary considerations" it appears that the "prudent diet" intervention group avoided the ordinary margarines allowed in the diet of the controls. We will probably never know which group ate most trans fats. The fact that the intervention group had low cholesterol and trans fats are supposed to elevate LDL cholesterol does seem to indicate that any harm trans fats may have done was not due to "lipid hypothesis" mechanisms.

Having established her scientific objectivity by drawing attention to the study’s biggest flaw, Professor Gutierrez strikes a home run with her last paragraph:

In addition to increasing PUFA intake, participants in the intervention group reported reduced dietary saturated fat, cholesterol, and calorie intake from baseline. A negative energy balance was verified with a slight mean drop in BMI. As expected, circulating total cholesterol and triglycerides were reduced in the intervention group, but mortality outcomes were not improved consequent to these circulating lipid and anthropometric changes, which is unexpected and interesting. The more important question arising from this study may be why a dietary intervention that improved all of these commonly used surrogate end points did not reduce all-cause mortality?

Why indeed, the world wonders.

Surgeon Basil D Fadipe from Dominica has an explanation for the result:


In a nutshell, the study shows LA is a 'substrate' for oxidative stress convertible to toxic derivatives, mechanistically adverse to the cardiovascular-coronary integrity; An otherwise good dietary item, LA's bad company (smoke/alcohol) wrecks its good potential.

This view has some merit – LA plus alcohol is definitely destructive to the liver via these mechanisms, and there are clearly links between high alcohol consumption and the negative effect of LA in the study (though it doesn't seem that abstinence removes the risk), but it does seem like special pleading. People will be exposed to oxidative stress in various ways, not all easily predicted or avoided. Why consume a dietary item that magnifies this insult in quantities greater than those required for essential functioning?

UK GP William K. Neville sums up the Paleo view;

Linoleic acid is an omega 6 fatty acid. It causes weight gain and inflammation. Omega 3 fats have the opposite effect. The ideal ratio of omega 6 to omega 3 in the diet is about 2:1 [9]. Modern diets have a ratio of 20:1 due to the false belief that linoleic acid is good for us. In pre-historic times weight gain from eating omega 6 fats in nuts and seeds, which were plentiful in the autumn, was an advantage to prepare humans for winter [10]. Meat from grass fed animals has a good amount of omega 3. But 99% of farmed animals are fattened on grain products such as brewery waste prior to slaughter which lowers their omega 3 levels to zero and the meat contains only omega 6. Similarly, farmed fish has reduced omega 3 levels due to being fed on grains.
Heart disease was rare before the introduction of industrial seed oils at the start of the 20th century [11]. Four meta-analyses recently prove saturated fat to be harmless [12]. The lesson of this article is that it is time we stopped demonising the really healthy fats such as butter, lard, beef dripping, coconut oil and palm oil [13, 14].

He makes more of the case against dairy than is perhaps justified by the evidence to date when he says:

The most important oxidising agent of LDL particles is the peptide BCM-7 produced by the digestion of A1 milk. The level of A1 milk consumption in countries is directly proportional to the rate of heart disease. Milk in the UK is mostly A1. Milk in Africa is mostly A2. France is in between. A few supermarkets have recently begun to sell A2 milk which has the potential to prevent many diseases such as type 1 diabetes and heart disease [6, 7, 8].

All I can say is that A2 milk tastes better, but is just as allergenic for my purposes. Milk is a complex food and there is no one factor that applies to everyone, but the BCM7 case outlined in “The Devil in the Milk” deserves study. I expect there are many other things that correlate with heart disease just as well as A1 milk does. Consider though, that when you eat meat, you eat from one or maybe two animals (unless it’s processed sausage meat). When you drink milk, the milk from large numbers of animals has been combined, each with its distinctive immunological factors. Our milk-drinking ancestors, if we had them, probably drank from one or two cows at a time. My granddad used to say that one secret of health was not to mix one’s drinks.
American Physician Megan I. Maurer makes a valid point that will also appeal to Paleo dieters:

I would like to point out that the source of the omega-6 fatty acids in this case was from safflower oil and safflower oil margarines which, despite being high in omega-6 fatty acids are still very calorically dense and in my opinion are not representative of what you might see had they used a whole food course of omega-6 fatty acids, such as sunflower kernels or walnuts. It has been consistently shown that a whole-food plant-based diet offers great cardiovascular protection. I think a study showing increased intake of omega-6 fatty acids in their whole form vs. saturated fats would have been more telling than just replacing it with oil.

Of course a diet of walnuts (an omega-3 nut, in fact) and sunflower seeds will introduce other confounders. But a worthwhile experiment would be to replace fatty meats with nuts and seeds, and butter and cooking fats with spreads and oils. The difference between intrinsic and extrinsic fats may be as important a confounder as the difference between intrinsic and extrinsic sugars.




The question is, more studies are needed, but are they ethically justified? It’s easy to test a dietary change when the evidence one has seen and the theories that seem to make most sense suggest it’ll be beneficial. Is it right to continue to experiment in this way as the evidence of harm accrues?
You might suspect it was the trans fats in the margarine that caused those extra deaths, but would you be prepared to re-run the study without them to find out?
However, the fact is that the experiment has overtaken our society and most of us have been enrolled in it, despite the actual results from the Sidney Diet Heart Study proper having been “lost” since 1973.
If PUFAS do have some potential for good instead of evil in certain cases, can we avoid discarding the baby with the bathwater? In 2009 Stephan Guyenet analysed a 1994 study that compared the so-called “prudent diet” used in Sydney with a diet that supplied limited omega-6 in the context of adequate omega-3; the LyonDiet Heart Trial. He writes:

Here's where it gets interesting. The intervention group ate three times as much omega-3 alpha-linolenic acid as the control group, and 32% less omega-6 linoleic acid. The ratio was 20 : 1 linoleic acid : alpha-linoleic acid in the control group, and 4.4 : 1 in the intervention group. This was due to the combination of a low-fat diet and the canola oil goop they were provided free of charge. 

But it gets even better. The intervention group reduced their omega-6 linoleic acid intake to 3.6% of calories, below the critical threshold of 4%. As I described in my recent post on eicosanoid signaling, reducing linoleic acid to below 4% of calories inhibits inflammation, while increasing it more after it has already exceeded 4% has very little effect if omega-3 is kept low*. This is a very important point: the intervention group didn't just increase omega-3. They decreased omega-6 to below 4% of calories. That's what sets the Lyon Diet-Heart trial apart from all the other failed diet trials. 

After five years on their respective diets, 3.4% of the control (prudent diet) group and 1.3% of the intervention ("Mediterranean") group had died, a 70% reduction in deaths. Cardiovascular deaths were reduced by 76%. Stroke, angina, pulmonary embolism and heart failure were also much lower in the intervention group. A stunning victory for this Mediterranean-inspired diet, and a crushing defeat for the prudent diet! 

There's a little gem buried in this study that I believe is the other reason it didn't get accepted to the New England Journal of Medicine: there was no difference in total cholesterol or LDL values between the control and experimental groups. The American scientific consensus was so cholesterol-centric that it couldn't accept the possibility that an intervention had reduced heart attack mortality without reducing LDL. The paper was accepted to the British journal The Lancet, another well-respected medical journal. 
[implications of the study here]

So in both the Sydney study and the Lyon trial, total cholesterol and LDL cholesterol had nothing to do with whether participants lived, or died of heart disease. Of course the Lyons “Mediterranean” diet only outperformed the “prudent” diet; the controls in the Sidney Diet Heart Study already seem to have done that by eating as people normally did in Sidney between 1966 and 1973.

The last word goes to Professor Dhastagir S. Sherrif of Benghazi University, Lybia:


Polyunsaturated fatty acids (PUFA) are essential fatty acids to be supplied in the diet. These are important for membrane function, producing eicosanoids; the endocannabinoids, the lipoxins and resolvins form lipid rafts for cellular signaling, act on DNA, activating or inhibiting transcription factors such as NF-κB - playing a vital role in physiological functions of the body. Yet there needs to be a balance between its intake and the form of PUFA taken in the diet.
Being polyunsaturated, they generate free radicals, cause lipid peroxidation and damage mitochondrial function. It is suggested that the intake of PUFA must be accompanied by adequate amounts of intake of anti-oxidants such as vitamin E. Human body and its metabolism cannot be viewed as parts but as whole body metabolism. Whole body metabolism needs to be viewed with the interplay of internal and external factors that regulate and maintain homeostasis. Extracellular factors including the dietary constituents need to be balanced with the internal physiological milieu unique to every individual. We need to remember the Daedalus effect: for every remedy there is an adverse side effect. How we balance them is the duty of true science that will help promote health.

(photos by Hayley Theyers (c) 2013)

36 comments:

Jeff Consiglio said...

I think the difference between fats from free-oils vs. whole foods such as nuts is perhaps huge.

I'm not a "plant based diet" advocate by any stretch...follow a LC diet actually...but can't help but notice 7th Day Adventists seem to do ok eating lots of NUTS.

Nuts have all kinds of plant compounds which may override any negative from the omega 6 they contain.

Most studies are based on nutritional reductionism, rather than whole foods.

I once emailed Dr. Walter Willet of Harvard fame, asking him why he thinks nuts are healthy, considering their high omega-6 content. He emailed back saying those who think nuts are unhealthy due to omega-6 are nuts, because lots of evidence showing them to be healthy.

In fact, in this video Willett actually goes as far as to say omega 6 is NOT inflammatory.

http://www.youtube.com/watch?v=fsSe1dKzbxI

George Henderson said...

I agree that omega-6 from nuts and similar plant whole foods may perform in different ways.
What seems unlikely to me is that someone with issues arising from excess omega-6 from oil (and chicken, see Paul Jaminet's recent post on how much omega-6 this brings to the average diet) will be able to reverse them by switching to omega-6 nuts.
A washout of omega-6 and a focus on omega-3 from seafood in the context of increased saturated/monunsaturated fat - as per Cooling Inflammation or the Perfect Health Diet - seems indicated (it worked for me). Once this has been achieved nuts should be OK.
I came across an interesting fact in John Lanchester's foodie novel "The Debt to Pleasure" (recommended reading for foodies and English lit buffs); in traditional English quisine ground almonds are a substitute for flour or potato, used for thickening soups and stews. Useful for low carbers.
On VLC diets there is evidence that omega-6 doesn't matter so much, as COX2 is inhibited (but what happens when one stops?).
Another gleaning from "The Debt to Pleasure"; James Joyce's description of cheese as "the corpse of milk".

Stan (Heretic) said...

Hi,

Re (Basil D Fadipe): An otherwise good dietary item, LA's bad company (smoke/alcohol) wrecks its good potential.

This is probably not the case since the study showed that the cardio mortality effect from smoking are smaller (about 50%) than the effect of PUFA increase from 6 to 15% (about 70%)

Stan (Heretic)

George Henderson said...

Hi Stan, what do you make of the alcohol stats?
The current paper links to several articles giving details from the original study published during its lifetime, but only the titles are in PubMed. I think these would be fascinating to dig up, I wish I still lived next to Otago Med School library which would have them in print. They seem to contain clinical observations and speculation from the doctors overseeing the study, and possibly supply details not mentioned today.


What do you think about the comparison between the SAD (Standard Australian Diet) as control in Sidney, and the Mediteranean diet in Lyon? Both beat the prudent diet - do you think they differed by much?
They seem pretty similar to my most rudimentary math brain.
Admittedly the duration of the 2 studies is different.

I'm considering pulling up some facts about what people ordinarily ate in Sydney 1966-1973 as it seems like a pretty healthy diet. I might promote it as an alternative to the Med diet.

George Henderson said...

Nah, actually a 70% reduction is NOT comparable to a 70% increase, I get that now. We might have to tweak the 1966 SAuD by removing the refined carbs and margarines to make it as good as the Mediterranean diet then.

George Henderson said...

The ratio between the advantages of the winning diets in the two studies is 2.6 to 1.6, with the Lyon Med diet leading. However, the Sidney subjects were at greater risk and actual % deaths was much lower in both arms of the Lyon trial compared to the SHDS.

Eliza said...

re: the comment by Jean Gutierrez:

She described the trans-fat potential as a "serious flaw"; however, I believe it is highly unlikely that Ramsden et al would not have done their homework on this topic, knowing that for many (justifiably or not) trans-fats are a deal-breaker.

Let's say for a moment, that Gutierrez is correct -- it was a margarine with nearly 40% transfats, and this was the greatest change (more so than the intervention group taking safflower supplements, etc).

She claims (from her comment at BMJ) "Another report from the same time period indicates that commercially produced hydrogenated fats, like those added to safflower oil to make margarine, were generally composed of 25-40%".

However, she neglects to mention that the report she's citing was actually published in 1959 – which can hardly be considered as retrospective of this same time period, as the Sydney trial did not begin until 1966 and ended in 1973.

Therefore, the publication by Carpenter and Slover in 1973 "Lipid composition of selected margarines" is a more appropriate timeframe, which is why Ramsden et. al cite it, stating: "Although the precise composition of this margarine was not specified, it was selected for the study because of its ability to lower blood cholesterol and its high PUFA to SFA ratio,22 two characteristics of margarines that contain comparatively low amounts of trans fatty acids.63 Because dietary trans fatty acids are predominantly 18-carbon MUFA isomers,64 the recorded changes in MUFAs probably included small amounts of trans-fatty acids in both groups."

Even if Gutierrez's first point is correct (unlikely, given the above info), it makes point #2 even more dubious because: If the intervention group was indeed consuming a large amount of trans-fats, it still leaves a burning question: why was their cholesterol lowered so successfully?

George Henderson said...

I agree. The controls were free to eat margarines and, probably more important, consume baked goods made with vegetable shortenings. these may have been transfat-heavy Crisco but may also have been Chefade™ (Goodman Fielder, 70% beef tallow, 30% oleo oil - oleo oil is an all-oleate triglyceride extracted from beef fat), popular in my childhood.

It looks as if the controls ate more and probably ate more fats in general, if so they were more exposed to whatever transfats were in their diets.

But only a portion of safflower in the intervention came from Miracle; some was used as cooking and salad oil and some was available as supplements.

The figure of 15% trans fats in Miracle is being bandied about on the internet, on what basis I don't know.

That trans fats were unquantified adds some uncertainty but as you say the fact of cholesterol being lowered goes against everything we expect of trans fats, so either trans fats were insignificant, or the experiment also disproves that facet of the lipid hypothesis.

One ill-effect of trans fats could be due to inhibition of the beta-oxidation of linoleic acid. PUFAs are oxidised by being converted to SFAs via a trans-configuration, using enzymes that may be competitively inhibited by trans fats. Or not, it just looks to me like a plausible interaction.

A confirmed interaction is similar: trans fat inhibits the metabolic conversion of linoleic acid to arachidonic acid and to other n-6 PUFAs.
http://www.scielo.cl/scielo.php?pid=S0716-97601999000400007&script=sci_arttext

George Henderson said...

Amusing selection from Experts on the Australian science Media Centre blog:
http://www.smc.org.au/2013/02/round-up-dietary-fats-and-heart-disease-bmj-experts-respond/

Many have ties to PUFA industry or previous wrong diet advice.
not one addresses the several aspects of the study and meta-analysis that contradict the lipid hypothesis.

George Henderson said...

If there is little or no connection between saturated fat and CVD death (not that CVD is the only way to die prematurely), and even less between animal fat and CVD, which I think is one of the few things we can take as proven, then why is advice to lower SFA still part of dietary recommendations?
Regardless of what one thinks about PUFA, this component of such advice is the sign that someone is either not thinking, or not free to speak.

George G said...

Thanks for pointing out this study, its results are very interesting.

Not related to this post, but noticed a new paper on Pubmed "Association of lipid droplet and hepatitis C virus proteins: Insights for virus replication."
http://www.ncbi.nlm.nih.gov/pubmed/23402989?dopt=Abstract
Unfortunately I can't access the text yet, but could be interesting, though it may be just a review of older research.

George Henderson said...

Thanks George G.
as Finn would say, I'm all about HCV and lipid droplets.
This is the facet of the HCV lifestyle that makes it possible to speed up or slow down replication and infection by adjusting lipids through diet, which is the original point of this blog.
The DGAT1 needed to supply these triglycerides is upregulated by HCV and dietary carbohydrate/insulin, and downregulated by carbohydrate restriction or fasting.

Here's the full text of that paper: http://www.jlr.org/content/early/2013/02/12/jlr.E036772.full.pdf+html

the new stuff here is about drug targets to inhibit intracellular HCV-lipid association.

George Henderson said...

In other words the whole carbohydrate-insulin hypothesis of obesity, propounded most recently by Gary Taubes, which is subject to considerable controversy in that context, seems to be a simple truism when it comes to the liver, especially under the influence of HCV, which sensitizes it to the various advertised ill-effects of glucose, insulin, fructose for its own purposes, to increase availability of these lipid droplets. Animal omega 3 and 6 fatty acids - DHA, EPA, AA - promote the breakdown of the droplets and slow viral replication.
Excess PUFAs will increase the peroxidative and inflammatory damage to the liver, and also increase HCV access to ininfected cells via increased LDL receptors, and probably allow easier ingress through more permeable membranes.
Combining a low-carb prescription with the basic paleo commandments (avoid seed oils, added sugars, and most grains and legumes, and don't be afraid of animal fat), while paying a bit of attention to antioxidants and probiotics (because of the immune tolerance vs inflammation aspect I haven't written about yet)... that's about where I'm at now. Seems to work.

Brendan Hannigan said...

To me, the idea that saturated fat and cholesterol cause heart disease is just so patently ridiculous that it's difficult to take this sort of research all that seriously.

Why is the idea that vegetable oils are "heart-healthy" even taken seriously enough to warrant investigation? It's a ridiculous notion, on the face of it. Why isn't that totally obvious to highly trained biologists after years of expensive education?

Frankly, it baffles me that there are so many apparently intelligent people out there still earnestly considering whether PUFA or SaFA are more likely to be causative factors in heart disease, or any other condition. I was under the impression that the study of evolution was one of the foundational disciplines of biology, and the argument that LA is healthy or even benign in all but the tiniest quantities is rather laughable in that context.

The "refined oil versus whole food" argument is mostly irrelevant. More than anything else, I think that these are cognitive mechanisms that people use to justify their continued belief in a scientific fairy tale.

George Henderson said...

Agreed.
i think the whole fallacy stems initially from the Western intellectual's sense of cultural inadequacy and guilt; that Eastern cultures are somehow purer and wiser. And one of the features of Eastern religious culture identified early on by early afficionados like Schopenhauer - because the things that are unusual in a culture attract attention first - was vegetarianism and non-violence. The reality of Buddhist and Hindu societies, like all human societies, was far from vegetarian or non-violent, but the ideal caught on.
We come to a point in history - the 60's - 70's counterculture - where the idea takes hold more widely, through music and other popular media, that vegetarianism (and other aspects of eastern religious thought) are the answer; simultaneously, the habits of one's parents generation are anathematized; including church-going, smoking, drinking, meat eating.
People who have soaked up this mindset in their formative years are unknowingly influenced by it; it becomes an obvious, unquestioned "fact" and animal fat is the casualty.
Science is distorted to reflect the current prejudice, and this suits industry. You have a perfect storm of error, because of the simultaneous invention of the cholesterol test, which seemed to support the new belief, and which has lent it a spurious validity.

We see the same thing at work today when veganism, despite its risks, is accepted as normal by government dieticians, as somehow being worth nurturing as the expression of a noble and virtuous impulse; whereas low-carb meat-based diets are not to be encouraged, not really because of any scientific evidence against them, but because they are seen as self-indulgent.
There are deep psychological forces at work deciding the values different foods are given, and science can have trouble taking root in such swampy ground.

Of course most people cannot stay vegetarian for very good reasons, so we have this slide back, but not all the way, only to the "vegan meat" chicken, to lean meats, low fat dairy and so on.
It's as if by avoiding what one thinks is "saturated" fat one can avoid the sinful part of meat.
The animal may be just as dead, but at least you're enjoying it less and feeling less satiated.

Chip Spitter said...

Our beloved nutrition experts in Australia have just updated their advice on eating healthy. It seems not much has changed in 10 years and they suggest we get between 4-10% of our energy intake from linoleic acid.

All those experts can't be wrong. Surely.

http://tinyurl.com/ahtryfo

http://tinyurl.com/a6g54nr

Nice blog, George.

George Henderson said...

The sure sign of the anserine advisor is the edict to eat "more" or "less" of something.
Sir, you do not know how much salt, red meat, fish, or fibre I ate yesterday. Do not attempt to guess when telling me what to eat today.
At least 4-10% is a real figure; taking the lower figure of 4% won't cause much harm.

"Replace high fat foods which contain predominantly saturated fats such as
butter, cream, cooking margarine, coconut and palm oil with foods which
contain predominantly polyunsaturated and monounsaturated fats such as oils,
spreads, nut butters/pastes and avocado."

No. You'd have to ignore the evidence that the highest consumption of dairy fats is associated with lower BMI and HALF the rate of type 2 diabetes.

Everything in the Food Guide pie chart is presented to look like a food product, even the meat and vege; of course half the foods are products, despite lip service paid to "wholefoods".

Oh look - consumption of fats and oils - a tiny part of boys' diet - actually went down between 1985 and 1995.

They are shuffling towards a less lipophobic position for future guidelines, in case the tide changes:

Fat: The 2003 edition of the dietary guidelines and many international public health organisations, including
the World Health Organization (WHO), 98 emphasised the major role of fat consumption in the development of overweight and obesity and of reducing fat intake as part of management. More recently, WHO has shifted its emphasis, stating that there is convincing evidence that energy balance is critical to maintaining healthy weight and ensuring optimal nutrient intakes, regardless of macronutrient distribution.
184
Although no specific macronutrient may be responsible for the development of obesity, the proportion of macronutrients in the diet does influence energy and nutrient intake, which may impinge on weight management and health outcomes.

Amazingly, the "limit saturated fat" advice (3.1) is only supported by one claim, supported by C grade evidence, about fish oil and dementia. Otherwise the lipid hypothesis is mentioned, and only with regard to markers, not outcomes:

Established evidence:
Saturated fat is the strongest dietary determinant of plasma LDL concentration.
Replacing saturated fat with polyunsaturated and monounsaturated fats is associated with improved blood lipids related to
cardiovascular disease.

And that's it. You can feel the props falling away as you read it.

Brendan Hannigan said...

George, your description of the psychological forces at work beneath these scientific fallacies was perfect.

I think the same applies to all of us, though, to some extent or another. In general, human beings make exceptionally poor scientists, because of the hidden emotional and psychological interference that inevitably dictates our unconscious assumptions. When the investigations of an entire scientific culture are guided by the same erroneous biases, the whole system starts to break down, and errors of really tragic proportions are committed.

"Science" is a beautiful abstract ideal, but in reality science is practiced by fallible, gullible, misguided, emotionally damaged human beings, with multiple conflicts of interest (career, family, past conditioning, emotional comfort). We are all in danger of succumbing to these fallacies. All we can do is try to be aware of them and work to diligently maintain our rationality and objectivity when they arise.

That being said, however, it's really amazing to me how little most nutritional scientists and government officials are actually thinking these days. That advice that you quoted relies entirely on the trivial fact that saturated fat raises LDL concentrations more than PUFA, with no consideration of the actual likely causes of heart disease (especially oxidized PUFA in the LDL membrane). Is that really the best they could do???

That last section you quoted is governed entirely by the psychological bias that you have identified, which, stripped to its essence, is basically this: "Saturated fat is bad for you because it's bad for you. And we know it's bad for you because, well, it's bad for you."

I'm sorry for beating a dead horse, but I'm just really amazed that such a high level of stupidity is now spreading around the world. Isn't there anyone involved in producing these recommendations that can still use their brain and recognize the absurdity of what they are recommending?

George Henderson said...

Scientists should take the Oath of Maimonides daily. It says in part;
"Grant me the strength, time and opportunity always to correct what I have acquired, always to extend its domain; for knowledge is immense and the spirit of man can extend indefinitely to enrich itself daily with new requirements. Today he can discover his errors of yesterday and tomorrow he can obtain a new light on what he thinks himself sure of today."
http://en.wikipedia.org/wiki/Oath_of_Maimonides

The problem of cholesterol is this: some interventions that lower LDL, such as eating more fish, probably do save lives. Others, such as high intakes of linoleate, do the opposite.
Similarly, saturated fat elevates LDL (maybe), eating lots of sugar and refined starch elevates LDL. Only one of those will kill you.

The error is to focus only on the "good" version of low LDL and the "bad" version of high LDL as indicating that low LDL is better.

The LDL is irrelevant; I'm pretty sure that fatty fish would be beneficial, saturated fats benign, sugar pernicious, linoleate toxic even in cases where they have no effect on LDL whatsoever.

George G said...

Thanks for that link to the article.
You really know how to find the article texts.
I just noticed another new abstract on "Elevated lipogenesis and diminished cholesterol synthesis in patients with hepatitis C viral infection compared to healthy humans."
http://www.ncbi.nlm.nih.gov/pubmed/23417775?dopt=Abstract
Seems very interesting new research and actually mentions the possibility of the need for PUFA supplementation in HCV patients.
I can't find the full text though.

George Henderson said...

I looked at the cholesterol lowering in a couple of earlier posts: HCV upregulates HMG-CoA reductase, but inhibits cholesterol completion; it uses the geraylgeranyl for extra geranylgeranylation of some protein (cool word eh?).
http://hopefulgeranium.blogspot.co.nz/2012/08/recent-blood-tests-hcv-genotype-3-and.html

Hence the idea that dietary cholesterol might become essential under such conditions, that some lives could be saved by adding cholesterol to the diet, that some symptoms of chronic hepatitis C are linked to this deficit.

If you add animal PUFAs to HCV cell cultures (which are always hepatoma cells BTW, it can't be cultured in healthy cells) they inhibit replication; this is probably due to activation of PPAR-alpha, the fat-burning transcription factor (and one of the least ambiguous control elements in metabolism; all it does is divert fats from triglycerides and storage into mitochondria via peroxysomes) thus matching what carb restriction, fasting, and naringenin do.

can't find that paper but there are others.

George Henderson said...

this Suppversity post mentions the mechanism by which DHA activates PPAR-alpha. EPA and AA have similar, weaker effects.
http://suppversity.blogspot.de/2011/12/some-things-fishy-oxidized-fish-oil.html

George G said...

Thanks George.
Would you recommend fish PUFA for HCV ?
I have increased my fish intake to 4 serves a week.
I have decided to swap tuna for canned Atlantic mackerel, because of the much higher fat content (13.8g/100g).
Tuna has very little fat.
Also canned sardines (13.5g/100g) and canned pink salmon (7.4g/100g)
and frozen NZ Hoki (3g/100g).
I am not so keen on fish oil tablets and farmed fish,
when wild caught fish is available.

George Henderson said...

Make sure the mackerel isn't canned in "vegetable oil" or "natural oil" as this is usually soy oil. The tomato sauce packed brands don't usually have added oil. Mackerel can have more mercury than the other fish, but as long as it's not your only fish that won't be a problem. I mostly use sardines, a little mackerel, and red salmon if I can afford it as this is a source of astaxanthin. I supplement krill oil sometimes, as a good anti-inflammatory for the joints.

George G said...

Yes I would avoid fish canned in oil.
I have also heard that this allows the good fish oil to escape from the fillet. And I would drain the liquid off the fillets.
Also Atlantic mackerel has a low level of mercury, compared to other mackerels and fish.
http://en.wikipedia.org/wiki/Mackerel_(food)

George Henderson said...

this is interesting, though I know a few people who'd dispute the fructose summary.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/#R76

Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?

If you also factor in high linoleic acid - which increases the cholesterol synthesis demand on the liver - you have a scenario that amplifies the effect they hypothesise. And would also be contributory to NASH and gallstones, conditions where cholesterol is produced in excess of bile salts and crystalises.

George G said...

On the topic of Fructose and HCV, this is an interesting new paper
"Dietary Fructose Intake and Severity of Liver Disease in Hepatitis C Virus-infected Patients"
http://www.ncbi.nlm.nih.gov/pubmed/23426443?dopt=Abstract

CONCLUSIONS: There were no significant associations between dietary fructose intake and hepatic fibrosis risk, as assessed by FibroSURE, in HCV-infected males. Additional research is needed to clarify the potential role of fructose intake and HCV-related hepatic inflammation.

George Henderson said...

I think that 0mega 6 would be a bigger driver of fibrosis than fructose. I don't actually know of animal experiments where fructose causes fibrosis, but oils do.
The lowest fructose intake was 30g, this is 60g sugar or 12 spoonsful.

If you had a wider range of intakes and looked at other markers like viral load or ALT you should see a difference, but it would be swamped by variations in PUFA intakes.

I don't know how reliable food questionaires that were filled out perhaps years earlier would be. Sugar intake is a very hard thing to judge if you're not counting it.

I'll try to find the fulltext and see if it does tell us anything.

George Henderson said...

Evidence for PUFA as driver of fatty liver in HCV:
http://www.medscape.com/viewarticle/585010

We found that a high intake of PUFA was associated with a higher degree of steatosis, and that a higher intake of lipids and carbohydrates was associated with fibrosis. Similar associations were found in animals with alcohol-induced liver damage and/or experimental NASH,[43-46] and in patients with NAFLD[47, 48]. It is noteworthy that obesity[49] and diabetes[50] have been found to be risk factors for hepatocellular carcinoma in case-controlled studies. Taken together, the foregoing data suggest a synergistic mechanism whereby alcohol, diet and HCV alter the metabolism of lipids and carbohydrates, which in turn, results in liver damage.

George Henderson said...

That link isn't free, try this one:
http://www.medscape.com/viewarticle/585010_4

then move to other pages.

George G said...

Thanks George, both links worked for me.
As you say it concludes :
"a higher intake of lipids and carbohydrates was associated with fibrosis" and recommends possible dietary changes.
But I think that fibrosis may be causing a higher intake of lipids and carbs, not the other way around.
Because liver malfunction causes some food malabsorption, so people have to eat more, just to achieve the same energy absorption.

George Henderson said...

The lipids tended to be high-PUFA anyway, and were consumed with carbohydrate. We see in lots of other research that carbohydrate promotes storage of fat and impedes fat-burning.
You are right that the mitochondrial dysfunction of HCV tends to promote overeating, especially of sugars, but also of fats as this is the combination that benefits the virus.

George Henderson said...

Here's the story of the missing data from the Sydney study:

http://www.cbc.ca/news/health/story/2013/02/11/f-crowe-omega-6.html

George Henderson said...

Although, if people with Hep C weren't absorbing the extra carbohydrate and/or lipids, it wouldn't be having the same metabolic consequences.
Unless we factor in gut bacteria and leaky gut:
The undigested carbohydrate could be driving dysbiosis and the PUFA and other lipids increasing transmigration of lipopolysaccharides (LPS) to the liver where they stimulate inflammation.

George Henderson said...

@George G.,
I also take your point that the worse someone's liver, the more likely that some of the food they eat will go straight through them. They may need to eat more for this reason or because fatigue promotes hunger, and it may not indicate causality at all.
In which case we're on safer ground with the proportional variations within the diet between PUFA/MUFA/SFA, which are independent of quantity.

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