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Tuesday, 29 April 2014

Saturated fat IS good for you, but how much polyunsaturated fat do you need?

Working on the "Real Food" AUT dietary guidelines submission it became clear that neither the epidemiology of the lipid hypothesis nor the RCT experiments testing it were designed to separate the supposed artery-clogging effect of saturated fat from the purported heart-healthy effect of polyunsaturated fat.
What we had was a series of comparisons of higher SFA and lower PUFA vs. lower SFA and higher PUFA. There were no investigations of either higher SFA in a diet with optimal PUFA, or of deficient PUFA in a diet also low in SFA.
The former of these, higher SFA in a diet with optimal PUFA, is what the low-carbohydrate, high-fat (LCHF) diet supplies. The latter is a danger on a low-fat diet, so "let them eat margarine".
1946 Dietary Guidelines - not bad at all.

Richard Lehman described the mindset in a recent BMJ blog
If I despair of meta-analyses, what can I say about dietary surveys? Actually, they’re quite fascinating, though they rarely bear any definable relation to human health. Diet and religion are often closely aligned. The authors of this paper have got religion bad: “Diet is one of the fundamental risk factors for health, disease, and disability in the world. Indeed, given that trends in metabolic risk factors such as blood pressure, cholesterol, glucose, and body mass index are being largely driven by nutrition, suboptimal diet is the single leading modifiable cause of poor health in the world, exceeding the burdens due to tobacco and excess alcohol consumption combined.” They then go on to look at fat. Why, I know not. But it is quite interesting to see which countries eat what types of fat. Where people eat more saturated fat, they often eat more unsaturated fat. For all I know this may help to explain why nearly everyone everywhere is enjoying their food more and living longer.
In the paper Richard Lehman is discussing, we find the alarming statement that the Centre for Disease Control (which really should be worrying more about emergent viruses and antibiotic-resistant bacteria and less about fat) thinks that getting 13% of our energy from linoleic acid (omega 6 PUFA) will be "optimal". If that's optimal, what do they consider an excess? This crazy figure is certain to be based on the amount of linoleic acid required to reduce serum LDL to a particular "healthy" target across a Western population, with no thought given to metabolic health, and bearing no relation to any intake humans might have been exposed to for any period in their evolutionary history.

As Peter D. said in a recent comments thread, "
You have a basic assumption that blood lipids cause CVD. You will make many wrong choices based on this hypothesis." Now, I don't know what causes CVD. It could be blood lipids - there are intelligent people who think that small, dense LDL particles typical of refined-carbohydrate diets rip up the arterial walls like stilettos on a ballroom floor. But I do know that the assumption that blood lipids cause CVD has led to many wrong choices. Wrong choices in the supermarket. Wrong choices in the design of experiments. Wrong choices in the interpretation of epidemiological data. Imagine what useful drugs statins might be if they were not over-prescribed on the basis of LDL counts, with results like this.

Many analyses of the "lipid hypothesis" epidemiology and RCTs failed to distinguish between omega 6 and omega 3 PUFA, or between vegetable PUFA (linoleic acid and alpha linolenic acid) and long chain polyunsaturated fats found in animal foods like EPA, DPA, DHA and arachadonic acid. This is understandable because, when Ancel Keys cooked up the lipid hypothesis, no-one knew that omega 3 fatty acids existed, let alone that they were essential nutrients. I'm not even sure if anyone realised that omega 6 was essential back then.
We are stuck with an article of faith from the Dark Ages. A diet high in saturated fats that happens to be deficient in polyunsaturated fats - say with fats supplied exclusively from tallow and hydrogenated shortening, with over-cooked boiled meat or deep-fried fish, milk, boiled greens, sugar, and highly refined grains - which was the mid-20th century diet for many in the Westernised world - can be deficient in PUFA. Smoking and drinking and the general lack of antioxidants in the diet, as well as the effect of insulin from the refined carbohydrate, will tend to squander what PUFA there is. Not surprising if this population has more CVD. What will be surprising is, if the saturated fat has anything to do with it. That diet will also be high in monounsaturated fat (beef olein is the MUFA from tallow, used in old-school chip shop fryers), but somehow MUFA gets a pass. It's all very unsatisfactory.

Is there any research that can help us sort out the difference between a lack of PUFA and an excess of SFA? Well, maybe. We can at least see the difference between an excess of PUFA, and a lack of SFA.
This study by Amin A. Nanji and Samuel French is an ecological study comparable to Ancel Key's "7 Countries" study, except that it includes 17 countries.
Mortality from cirrhosis in many countries deviates markedly from that expected for a given per capita alcohol intake. We investigated the possibility that dietary factors might explain the deviation expected and actual mortality rates in different countries. Deviations from expected cirrhosis mortality was calculated as a percentage for 17 different countries, all of whom had carrier rates for hepatitis B virus of less than 2%. The percentage of deviation was correlated with dietary intake of saturated fat, polyunsaturated fat, cholesterol, and also with mortality from ischemic heart disease. The percentage of deviation correlated inversely with dietary cholesterol (
r= -0.86, p 0.001) and saturated fat (r= -0.80, p 0.001) and positively with polyunsaturated fats (r= -0.55 p 0.05). This suggests that both saturated fat and cholesterol protect against alcoholic cirrhosis while polyunsaturated fats promote cirrhosis. The correlation between percentage of deviation and ischemic heart disease (r= -0.78, p 0.002) suggests that those factors that promote ischemic heart disease protect against alcoholic cirrhosis.

If the factors that promote IHD protect against alcoholic liver disease (ALD), what are they? 
We can perhaps discard the red herring of cholesterol, which is a marker for animal fat, and which indicates consumption of foods (such as eggs) which are also rich in the essential hepatoprotective nutrient choline. Cholesterol does protect against ALD tested separately, but coconut MCTs (no cholesterol, no PUFA) gives the same protection as tallow (cholesterol, 1% PUFA) when the two are compared.
There has been a large body of animal experimentation designed to elucidate the link between alcoholic liver disease and dietary fats, with occasional testing of acetaminophen (paracetamol) toxicity in the same model. These papers have been analysed expertly by Victoria Prince on her blog and I will not duplicate her efforts.
It can quite clearly be seen in Victoria Prince's third liver-and-lipids post below that there are mechanisms whereby saturated fats can have health benefits, distinct from the restriction of PUFA, because saturated fats from coconut and cocoa protect the liver in different ways.
Thus it seems that dietary MCTs work in a way that maintains the expression of gut tight junction proteins, preventing endotoxin from making it into the circulation, while long chain saturated fats work in a way that increases endotoxin-binding proteins in the liver.  Both prevent endotoxin-induced damage in the liver, but in very different and distinct ways." This is not just relevant to alcoholics and people who consume paracetamol; the fact that long-chain SFAs make the liver less sensitive to LPS is relevant to the studies showing serum markers of dairy fat intake are associated with diabetes protection, because liver inflammation is a precursor to diabetes. And the fact that MCT, made from fats you can only get in significant amounts from coconut or dairy fat, maintains the integrity of the gut, is relevant to the epidemiological studies showing that children who eat margarine and drink low-fat milk have a higher rate of allergies and asthma compared to children who eat butter and drink full-fat milk.
Saturated fats are good for you. Get over it.

The high fat model of alcoholic liver disease was developed because rats fed normal chow plus alcohol would not develop ALD. The researchers concluded that polyunsaturated fats are "essential for the development of alcoholic liver disease", and that saturated fats are protective.

Diets enriched with saturated fatty acids protect against alcohol-induced liver injury, whereas diets containing polyunsaturated fatty acids promote liver injury (Nanji and French, 1989Nanji et al., 19891994a). Saturated fatty acids have also been reported to reverse established alcoholic liver injury (Nanji et al., 19951996,1997b).

Now, the fats that promote liver injury are vegetable oils, typically in these tests corn oil and soy oil*. Thanks to the campaign against saturated fats, these are the kind of oils that the fast food eaten by drunken New Zealanders is prepared with today. This seems to be a failure in public health planning.

"You have a basic assumption that blood lipids cause CVD. You will make many wrong choices based on this hypothesis."
(*interestingly fish oil, which has a stronger association with CVD prevention than omega 6, also has a greater promoting effect on alcoholic liver disease, albeit in quantities many times greater than anyone would ever include in their diet. And deficiencies of PUFA, particularly AA, EPA, and DHA, also play a part in ALD, so Samuel French suggsts that alcoholics be advised to replenish these fats by eating "Mediterranean diet" type foods whenever they're in recovery).

The rat model of alcoholic liver disease demonstrates that in this case the effects of high PUFA, while they can be confused with those of low SFA, are not the same. It also demonstrates that the SFA/MUFA ratio of the non-PUFA fat makes little difference (olive oil is almost as protective as beef tallow against acetaminophen liver damage; it seems an oversight that olive oil has not been included in the alcohol experiments, considering how widely it is consumed).
The link between SFA and CVD disappears when SFA is considered separately ("monotonically"), rather than as a marker for PUFA deficiency. The protective association between omega 3 PUFA (the PUFA less likely to be optimal) and CVD remains about the same when these nutrients are considered monotonically, as in the 2013 Singapore Chinese Health study by Koh et al. People who ate more DHA, EPA, and ALA had significantly lower rates of CVD mortality - and they also ate more saturated fat, monounsaturated fat, and omega 6 PUFA, all increasing stepwise with omega 3 across the quartiles as CVD mortality decreased.
"Where people eat more saturated fat, they often eat more unsaturated fat. For all I know this may help to explain why nearly everyone everywhere is enjoying their food more and living longer." 
The inverse association between omega 3 and CVD (0.83 OR) is seen with total omega 6 intakes of, on average, 9.9g per day, or 4-5% of energy - almost exactly the same as healthy New Zealanders ate in this paper, and much less than the crazy CDC projection of 13%. 
All things being equal, the people who eat the most fat, assuming they are not eating solely hydrogenated industrial fats or exclusively low-PUFA fats such as tallow, but are instead getting some fats from wholefoods, including fish, are surely eating enough PUFA to have an optimal intake for CVD prevention, regardless of any effect on blood lipids.

Polyunsaturated fats are essential nutrients, but also highly reactive and bioactive molecules. This means that the association between intake and mortality will follow a fairly steep U-curve, with a "sweet spot" in the middle. Saturated fats are inessential nutrients with low reactivity. The association curve between intake and mortality is likely so flat my dog could skate it.

(not my actual dog)

PUFA, MUFA and SFA occur together in whole foods and in traditional fats and oils. They are not easily separated, even in the laboratory. You can buy pure sugar for a few dollars in the supermarket, it's easily separated from the foods it occurs in, usually to be ladled back into some other food in excessive quantities. You can probably buy purified long-chain saturated fats like palmitic acid from Sigma Aldrich if you have the money and inclination, and MCT is a processed form of medium-chain saturated fat that is sometimes supplemented by ketogenic dieters; I've never seen it, but I've heard it's expensive.
Most people eating a LCHF diet, even those who think "saturated fat is good for you", are not going to go that far. Few are even going to use butter or coconut oil as their only fats, and anyone eating a variety of wholefoods that have been made palatable but not cooked to death is likely to have an optimal PUFA intake, whatever that is.


Wednesday, 23 April 2014

AUT's Submission on Proposed "Changes" to New Zealand's Dietary Guidelines

For the last wee while I've been helping Prof Grant Schofield and his team write a response to the New Zealand dietary guidelines (low fat, high grain, no SFA).
The paper is the PDF linked to in this post.

The first time I've had my name on a scientific submission, and a fine one it is too, with the collected wisdom of a bunch of scientists from various disciplines, all working together, to a deadline (we had only a few days warning about the new guidelines, and received no background material on the scientific evidence used in their making). I'm proud of what we achieved, see what you think, and spread this document around.

George Henderson
"Everyone should eat what I eat, 'specially cats!"