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Sunday, 14 September 2014

The World's Longest-Running Refined Seed Oil Experiment

This table is from Dr Malcolm Kendrick's latest blog post, which is about the possibility of a retrospective "publication bias" deleting findings that don't support the lipid hypothesis on certain websites. The data, from the European Heart Study 2008, has been tabulated by Dr Kendrick to show the correlation between saturated fat consumption and CHD mortality between countries.


What's striking is the big gap between the countries of the former Soviet Union and the Western European states (and, for some reason, Israel). France, with the lowest CHD mortality, has the world's highest per capita butter consumption, Switzerland is similar, and olive oil countries don't come out too badly either. The UK, with its chicken twizzlers, mars bars, and fish fingers, and Israel, with its combination of soy oil plus high tech medical care, don't come out quite so well.

The massive rate of CHD in former Soviet states is attributable to many things - industrial and agricultural pollution, smoking and alcohol, untreated chronic infections, overwork, malnutrition, higher birthrate, lower incomes (the US CHD rate in 2008 was 126 per 100,000 - this is both sexes, age adjusted, so not exactly comparable to Dr Kendrick's table; see here for more age-adjusted data and discussion). To look at the correlations between these things and CHD is enough to question the existence of any diet-heart link whatsoever. What significance does a RR of 1.17 have in a world where RRs of 11.13 exist?

If, however, we must look at these statistics in diet-heart terms, one thing stands out to this student of history. Russia is the world's oldest producer, and consumer of vegetable seed oils. The sunflower was brought to Europe by the Spanish around 1510, and were established in the Netherlands (then part of the Spanish Empire) soon after. Peter the Great then brought the sunflower to Russia after his visit to the Netherlands in 1698. In 1716 a patent was granted in Great Britain for a method of extracting oil from sunflower seeds, and during the 1840s the Tsarist government of Russia began the manufacture of sunflower oil on an industrial scale.
Because the Lent restrictions of the Russian Orthodox Church forbade the consumption of fat, this seemed like a good idea at the time (once again the ascetic impulse will be the driver for a dietary change later to be justified and entrenched by theories about health).
The Great Soviet Encyclopaedia of 1979 naturally downplays the Tsarist achievement.

There were about 10,000 small vegetable oil and fat production shops and about 400 licensed, poorly equipped oil and fat plants in tsarist Russia. The vegetable oil output in 1913 was 538,000 tons; in addition, the equivalent of 192,000 tons of soap was produced (figured at a 40-percent fatty-acid content).

Under Soviet power, the vegetable oil and fat industry has become one of the major sectors of the food-processing industry, relying on advanced technology and a stable raw materials base. There are enterprises of the vegetable oil and fat industry in all of the Union republics. The largest are combines in Krasnodar, Moscow, Tashkent, Dushanbe, Irkutsk, Saratov, Kirovabad, Sverdlovsk, Gomel’, and Kazan, which account for 45 percent of the USSR’s total output of vegetable oil, about 65 percent of its margarine, and more than 75 percent of its soap and detergents.

In 1972 the vegetable oil and fat industry accounted for 5.4 percent of the gross output of the food-processing industry of the USSR, 2.5 percent of the work force, and 2.7 percent of the fixed industrial production assets.

The USSR is the world’s second largest producer of vegetable oils, soap, and margarine (after the USA). It accounts for more than 14 percent of the world’s vegetable oil. The output of vegetable oil in the USSR is growing steadily; production in 1972 was 3.6 times that of 1940 (see Table 1).

Owing to the increase in agricultural production, state purchases of oil-yielding crops in 1972 were twice the 1940 figure. The oil content of sunflower seeds, which account for 50 percent of all seeds processed by industry, has risen significantly. The material and technical basis for the vegetable oil and fat industry has grown. Production capacities for processing oil-yielding seeds have been increased primarily by modernizing existing extraction plants and building new ones. Introduction of the extraction method of processing oil-yielding seeds has made it possible to increase labor productivity, mechanize and automate production processes, and sharply increase the oil output from raw materials (see Table 2).

The proportion of oil-yielding raw materials processed by progressive extraction methods increased from 9.9 percent in 1940 to 81 percent in 1972.

Production in the margarine and soap industries is fully mechanized.

In the other socialist countries the vegetable oil and fat industry is based primarily on local raw materials. The volume of production has generally satisfied the needs of these countries. In 1972 the vegetable oil output in Rumania was 360,000 tons; in Poland, 213,000 tons; in Yugoslavia, 165,000 tons; in Bulgaria, 145,000 tons; in the German Democratic Republic, 131,-000 tons; in Czechoslovakia, 88,000 tons; and in Hungary, 80,000 tons.

The production of vegetable oil in certain capitalist countries was as follows: 830,000 tons in Italy (1972), 801,000 tons in the Federal Republic of Germany (1971), and 520,000 tons in France (1971). In the USA vegetable oil production in 1972 came to 4.6 million tons; the output of margarine was 2.6 million tons, and that of soap and synthetic detergents was 3.5 million tons.

And so on - the communist love of boring statistics was useful after all.
But wait - there's more. If the Tsars boosted the seed oil industry, the Bolsheviks, for political reasons, destroyed whatever dairy industry there was in Russia during their genocidal campaign against the "kulaks", which they defined as any farmer rich enough to own a cow, plus anyone they didn't like or who opposed their seizures of food, summary executions, and so on.
To destroy the dairy farmers they needed a substitute - so Soviet Russia, beginning in the 1920s, became the first large scale producer of soy products.
The USSR was the first nation in Europe and the second nation in the Western world (after the USA) to become a major producer of soybeans. Soybean production, which reached significant levels in the mid-1920s, rose to a remarkable peak of 283,000 tonnes in 1931, but had fallen back to a low of 54,000 tonnes in 1935, after which it increased steadily. At the time of this peak, starting in 1931, the USSR built a large Soybean Research Institute in Moscow, attracted some of the top soybean and soyfoods researchers from western Europe (Rouest, Berczeller), and did extensive soyfoods research, focusing on soymilk and tofu, durin
g the early 1930s.

So by any utopian diet-heart, lipid hypothesis theory of history, those former Soviet states should have had CDH beat years ago.
By the test of reality, on the other hand, you would be better off living in France on butter, cheese, cream and, hey, if you like it why not, olive oil. 

Thursday, 4 September 2014

Who put the Fox in charge of the Henhouse? Dirty Politics contaminates the food supply.

Those of my readers from outside New Zealand might be interested in this local story. Especially you Australians.

It starts here:
Katherine Rich, a former National party MP, now the chief executive of the New Zealand Food and Grocery Council, an industry lobby groupis on the advisory board responsible for the health star rating system. For some reason the N.Z. Government takes the position that we can only counter diet-related ill health by paying the food industry to do something about it on their own terms.

This kind of assumes some basic honesty and interest in science on their part. Instead, we get this:

Embedded image permalink

Katherine Rich, in her role as pretend responsible person working with government (and presumably collecting pay for that), can't attack the anti-sugar lobby as virulently as she'd like, so hires blogger Cameron Slater (wide following, no morals) to do it for her.

Meanwhile, she's on the board overseeing the Health Star food labeling system, which is more industry reps (Unilever, Nestles, etc.) than scientists. As wikipedia says:

Emails leaked to political writer Nicky Hager claim that Rich, in her role as Chief Executive of the Food and Grocery Council, has while on the board of the Health Promotion Agency (a Crown entity) fed prominent blogger, Cameron Slater, with posts that denigrate individuals in academia and the media who report on news or support health initiatives inimical to the interests of the food, alcohol, tobacco and soft drink industries. The posts have been published as if by Slater himself on his blog Whale Oil Beef Hooked as recently as February 2014.
Here is Whale Oil's "soft drink" archive, if you want to see what your tax dollars have been paying for.  These are the people our government thinks it can work with.
Actually, Slater is someone the National Government already works with; the bigger fish of the Whale Oil saga are the Prime Minister (or his office, no-one's sure how much he even knows what's going on), and the Justice Minister, Slater's closest friend in power, who has already fallen on her sword. The Katherine Rich Health Star business is a minor part of the scandal to most people.
Here's what she paid Slater to say about the soda tax:


The question is rather clumsy. Imagine the result if they had asked “Do you think it is a good idea to tax ALL Kiwis with a sugar tax, increasing food and drink prices across the board, when it is only fat bastards who should be taxed?”. 

These are the people our government puts in charge of your health when you shop.
Blogger the Jackal has the wider story and a link to
the emails here.
Direct download here:

Slater is in the tradition of the scurrilous and venal Restoration pamphleteer, selling spicy stories about the enemies of his patrons. He's kind of admirable in his whole-hearted and public commitment to turpitude. And sometimes the Slater/Graham/Rich hydra comes up with lines like:

So long as the health nazis promote the food pyramid that is heavy on carbohydrates and low on proteins then we will continue to get fatter, especially if we don't exercise to burn those calorie loadings. Taxing sugars and fats won’t work.   

Nice try, but it still doesn't buy my trust.

P.S. Katherine Rich is also on the Health Promotion Agency board. This is more balanced than the Health Star food labeling board, on the HPA board Rich is the only industry rep. And AUT's own Grant Schofield is on the HPA board. Should make for interesting meetings. 

Sunday, 31 August 2014

Plasma phospholipid linoleic acid is a marker of health.

A nicely controversial new paper from the American Heart Association, in which linoleic acid in plasma phospholipids is the only PUFA with negative correlation with total mortality. The more LA n-6 in the membranes of your red and white blood cells, together with your lipoproteins, the longer you live. So should we switch back from butter to margarine? 
(tl;dr; if you really care eat some nuts, nuts are the only LA source convincingly associated with reduced mortality, although nuts also being associated with exercise, wealth, not smoking and other markers of virtue, it's hard to be sure, but this latest research does help the nut case).
Here's the abstract

Circulating Omega-6 Polyunsaturated Fatty Acids and Total and Cause-Specific Mortality: The Cardiovascular Health Study

Background—While omega-6 polyunsaturated fatty acids(n-6 PUFA) have been recommended to reduce CHD, controversy remains about benefits vs. harms, including concerns over theorized pro-inflammatory effects of n-6 PUFA. We investigated associations of circulating n-6 PUFA including linoleic acid(LA, the major dietary PUFA), γ-linolenic acid(GLA), dihomo-γ-linolenic acid(DGLA), and arachidonic acid(AA),with total and cause-specific mortality in the Cardiovascular Health Study, a community-based US cohort.
Methods and Results—Among 2,792 participants(age≥65y) free of CVD at baseline, plasma phospholipid n-6 PUFAwere measured at baseline using standardized methods. All-cause and cause-specific mortality, and total incident CHD and stroke, were assessed and adjudicated centrally. Associations of PUFA with risk were assessed by Cox regression. During 34,291 person-years of follow-up (1992-2010), 1,994 deaths occurred (678 cardiovascular deaths), with 427 fatal and 418 nonfatal CHD, and 154 fatal and 399 nonfatal strokes. In multivariable models, higher LA was associated with lower total mortality, with extreme-quintile HR=0.87 (P-trend=0.005). Lower death was largely attributable to CVD causes, especially nonarrhythmic CHD mortality (HR=0.51, 95%CI=0.32-0.82, P-trend=0.001). Circulating GLA, DGLA, and AA were not significantly associated with total or cause-specific mortality; e.g., for AA and CHD death, the extreme-quintile HR was 0.97 (95%CI=0.70-1.34, P-trend=0.87). Evaluated semi-parametrically, LA showed graded inverse associations with total mortality (P=0.005). There was little evidence that associations of n-6 PUFA with total mortality varied by age, sex, race, or plasma n-3 PUFA. Evaluating both n-6 and n-3 PUFA, lowest risk was evident with highest levels of both.
Conclusions—High circulating LA, but not other n-6 PUFA, was inversely associated with total and CHD mortality in older adults.

You'll notice the name of Dariush Mozzafarian as senior author (he's from the U.S. but the research was done in Sydney, Australia, so it's unlikely he supervised it in person). Mozaffarian is open-minded about saturated fat and low-carb diets and has played a major role in rehabilitating dairy fat, which ought to lay to rest conspiracy theories about the study (publication bias might be another question). The result makes sense to me.
Remember that these are plasma phospholipids, that is, they exist in the oxidising environment of human blood. We make use of this dual state system of redox balance; antioxidant enzymes and glutathione keep the intracellular balance in favour of reduction, and the non-enzymatic reactions inevitable in the anarchic extracellular environment, and the relative lack of extracellular antioxidant enzymes, reverse that, so that insulin and amylin molecules and immunoglubulins adopt their active, oxidised structures only after exiting cells, and ascorbic acid is oxidised to dehydroascorbic acid before being taken up and regenerated - reduced - inside cells.
Everyone knows what happens if this balance is lost either way; reductive stress limits the cell's ability to perform metabolic functions, oxidative stress degrades cellular structures and closes them down.
Cardiolipin - the 4 radicals are predominantly C18:2, linoleate.
Linoelic acid is a major determinant of cellular health, because it's incorporated into a phospholipid called cardiolipin, which sits in mitochondrial membranes; the linoleate is essential precisely because it's the most easily oxidisable PUFA in living systems. When cardiolipin oxidises faster than glutathione and its enzymes can repair it, it's time to close that mitochondrion and start another - in this way, inefficient mitochondria that spew free radicals aren't kept alive forever. This isn't the only function of cardiolipin, but canary in the metabolic coalmine is a pretty useful job.
Cardiolipin radicals

Therefore it seems to me that the presence of higher levels of LA in plasma phospholipids, in an oxidising environment, is not a mere indication of its dietary ingestion, but rather a marker of the antioxidant status of the blood and of the lipoproteins, which carry carotenoids, coQ10, retinol, tocopherol and other lipid antioxidants to and from cells. This explains why nut consumption is inversely associated with mortality, but overall LA consumption is not (if it was, the authors of this study would have mentioned it - senior author Hu is the nut guy).
It would be pretty hard to have a less than adequate LA intake on a high-fat paleo diet, as I discussed here.

Another process destructive of plasma phospholipid LA is inflammation; the conversion of arachidonic acid to prostaglandins and eicosanoids. Because AA itself is essential and conserved in the cell membrane, there is a flux through AA, with a constant replacement from LA. And guess what? Plasma phospholipid PUFAs, including LA, are preserved on very low carb diets - one of the anti-inflammatory benefits.

In other words, the paper under discussion seems to support the good, old-fashioned, free radical theory of disease and ageing, as well as the inflammatory theory of CHD. It doesn't support the intake of high levels of high LA seed oils, because what is going to happen to that LA? Almost all of it is going to be oxidised in the liver, with 22% of the acetyl-CoA produced going to make cholesterol.
You heard me - linoleic acid has the opposite effect from statins, increasing hepatic cholesterol synthesis. It also increases hepatic LDL receptors and pulls cholesterol in from the blood stream. Sometimes too much cholesterol, because all this free cholesterol oxidises easily, and when it does, cardiolipin also oxidises and mitochondria die (all this is referenced in my NASH series, see the Labels sidebar). Statins, if you overlook the side effects, are probably anti-inflammatory; I don't think there's much chance that seed-oils are.

Tuesday, 26 August 2014

Amylin - the "root cause" of diabetes?

When this story broke, I had to look up amylin in my biochemistry (Mathews, Van Holde, Aherne 2000) and physiology (Best and Taylor, 1984) texbooks. Neither has amylin indexed. Nor do I remember any insightful blogs about amylin from the usual suspects recently. Flyin' blind here. Thank God for wikipedia.

This news story linking amylin build up to diabetes, based on new research conducted jointly in Auckland, New Zealand and Manchester England, makes the case reasonably clearly:

What does it mean?

Diabetes is defined as the loss  of beta-cells, so that insulin production ceases - the insulin dependent stage. Interestingly, amylin allegedly plays the same role in type 1 and 2 diabetes, and the aggregates of amylin are amyloid formations similar to those seen in alzheimers. Before you start thinking of type 3 diabetes, though, the amyloids in Alzheimers aren't made of amylin. Amyloid just means "starch-like". What they have in common is beta-sheet protein structures (nothing to do with beta-cells) misfolding in a contagious, prion-like process.

What is amylin?

Amylin, AKA Islet Amyloid Polypeptide (IAPP) is a protein produced by beta-cells in tandem with insulin. Insulin promotes glucose uptake and metabolism in cells, amylin slows glucose - and other food - uptake from the gut, by delaying gastric emptying, and decreases appetite; it also seems to be responsible from the switch from muscle glycogenogenesis to adipose lipogenesis, so probably has a role in obesity. According to wiki the ratio is 100:1 in favour of amylin (unless I've read it wrong and it's the other way round). Is the ratio always constant? Does amylin have any independence from insulin? In any case, amylin plus glucose represents a two-pronged approach to preventing systemic over-exposure to glucose; insulin pulls glucose out of, amylin slows access into, the blood.
Some people think amylin should be included with injectible insulin for type 1 diabetics.

Amylin overproduction results in incompleted (proamylin, or proIAPP) molecules being retained in cells; these serve to promote crystalization of further amylin beta-sheets in the cell, the amyloid clumps then initiate apoptosis, killing of the beta-cells with eventual loss of insulin - and amylin - production.

This looks like the end-stage of hyperinsulinaemia; this over-production of amylin (and insulin) is being driven by excess glucose intake, the amylin incompletion and insulin resistance may also indicate an overall micronutrient deficiency, and the out-of-phase insulin response to begin with indicates a) salivary amylase polymorphism, b) presence of excess omega 6 -> PGE2, c) absence of factors inhibiting PGE2, e.g. omega 3, CLA (the most likely reason for the diabetes-protective effect of dairy fat, or, if you don't eat dairy, ruminant fats).
Note that PGE2, an omega 6 series prostaglandin, inhibits glucose uptake, and to a somewhat lesser extent fructose, in sheep, but increases it in rats - probably the better model for human response. If this is the case, PGE2 is increasing glucose uptake as it decreases first phase insulin response, which is already diminished in individuals with fewer salivary amylase gene copies. The compensatory rise in second phase insulin response - exacerbated by 12-HETE, an omega 6 series eicosanoid - results in a larger area under the curve for both glucose and insulin; i.e., in hyperglycaemia and hyperinsulinaemia.

It is interesting that this hyperinsulinaemia-related problem with amylin is also causative in type 1 diabetes. It means that lower carb diets can be recommended to those at risk of this disease.
The T1D connection is really interesting. .I have a friend who is T1 diabetic; he said when he was 12 he got a craving to eat dry Milo (Nestles chocolate flavoured drink sweetened with maltose, i.e. glucose), ate a big tin of it in one day, crashed into a coma and woke up in hospital on insulin. That seems to show pronounced hyperinsulinaemia immediately preceding beta-cell burn out. Perhaps a combination of sudden hyperinsulinaemia from an inflammatory, infective, or autoimmune cause together with a low tolerance for amylin production.

Both insulin and amylin contain disulfide bridges (Cys-S-S-Cys) and this is interesting as the bridges are only meant to form outside the cell (the peptide is expressed as a string from the reducing environment of the cell, where the cysteine residues exist as 2x Cys-S-H, into the more oxidising serum enviroment, where the sulfur bonds snap together as the cysteine residues are oxidised to Cys-S-S-Cys plus H2O). If insulin output is very high, this puts a heavy demand on the reducing systems of the cell; glutathione, glutathione reductase, thioredoxin reductase and so on. Hydrogen sulfide - H2S - is also protective in the beta-cell for some reason. These are mostly selenocysteine enzymes, and selenocysteine is also required for a protein folding enzyme. (note though, supplying 200mcg Se as selenomethionine in America, not overall a selenium deficient country, has been associated with double the rate of diabetes in one study that was not directed at glycemic endpoints).  

Selenoprotein S is involved in retrotranslocation of misfolded proteins from the endoplasmic reticulum to the cytosol. This protein may also be involved in inflammatory and immune responses

Here is the Wiki page on amylin. It's interesting, has the background to the latest research, and I wonder why we never hear about this hormone in diet-health discussions? I guess that from now on we will be hearing more of it.

The take home - keep insulin production under control by counting carbs and avoiding vegetable seed oils, and amylin should tag right along, ensuring beta-cell function lasts a lifetime.

Sunday, 17 August 2014

The Difficulty of Attributing Ends to Means - Selenium and Heart Disease

One of the arguments used by New Zealand's Public Health experts still opposed to LCHF and Paleo diets - opposed, that is to the idea of the more saturated animal fats being safe, either overall, or in a mainly wholefood, low carb context - is that low-fat dietary guidelines, and the decreased intake of butter, with increased use of margarine and seed oils, ought to be given some of the credit for a decreased rate of heart disease in the past 30 years.
They'll acknowledge that smoking cessation (to be fair, they had a bit to do with this too) accounts for some of the decrease.
But is that accounting for every factor likely to be significant? Most people who had heart attacks In New Zealand prior to 1984 went through the Great Depression, World War 2, and the 1951 Waterfront Strike. They had parents who lived through the 1919 influenza outbreak. Their lives were different in many ways from those of the generation dying early or living longer today.

One of those differences is environmental - the toxicity of industrial, urban, and rural environments has changed, mostly for the better; testing and legislation is mainly a product of 1970's environmental activism. And particulate vehicle emissions, to give the best-researched example, do seem to be causative of atherosclerosis. The last few decades have seen tighter and tighter restrictions on vehicle exhaust emissions on our roads and on the burning of fossil fuels and wood in private fireplaces in our cities.

Another change is genetic - in 1984, Wang was not the most common surname in Auckland. New Zealand has always had a small population, with a tendency for Kiwis to seek their fortunes offshore, and this loss has been offset and the population increased steadily through immigration, with the migrants' countries of origin altering over time.

Another change is in the micronutrient content of the diet. In early days, the poor were at more risk of deficiency diseases than they are today. Vitamins and minerals are added to junk food to give the advertisers something to boast about, and even to improve shelf life; the use of ascorbic acid as an antioxidant (E300-304) is no doubt a safeguard against scurvy in the least-well fed populations.

This change also applies to wholefoods - since the 80's, NZ's importation of foods - esp grains, legumes and fruit has increased, which means a wider spread of micronutrition. There is a wider variety of foods, and of ingredients; market d
eregulation since the 1980's means the New Zealand food environment has altered significantly.

See, for example Medsafe on selenium
The intake of selenium by New Zealanders has increased since the earlier Total Diet Surveys in 1982 and 1987/88. To prevent animal diseases, farm animals are drenched with selenium-enriched products and the meal fed to poultry has selenium added. Generally bread made in the South Island is lower in selenium than bread made in the North. Since deregulation of the grain industry much North Island bread has a significant proportion of imported, largely Australian wheat which is selenium-rich. But South Island bread is made predominantly with wheat grown locally in low-selenium soils. Current practices need to continue for the selenium intake of New Zealanders to remain around recommended levels.Meats, eggs, dairy products and bread are the main sources of selenium in New Zealand diets.6 Kidney, liver and seafood, and for the vegetarian, imported legumes are rich in selenium.

The relevance of this is that Finland - a seriously deficient country like NZ was 30 years ago - mandated selenium in fertilizer in the 1980s to reduce CVD incidence, raising serum Se levels within a short time.
Result? (or, correlation?)

Between 1982 and 1997, coronary heart disease mortality rates [in Finland] declined by 63%, with 373 fewer deaths in 1997 than expected from baseline mortality rates in 1982. Improved treatments explained approximately 23% of the mortality reduction, and risk factors explained some 53–72% of the reduction.

This, of course, has been attributed to lipids and SFA too - selenium has been completely forgotten, it seems - but this was a huge, and brave, public health effort in Finland, comparable to iodised salt being introduced to iodine-deficient societies in the 1920s. And matched by what NZ has done, albeit by chance more than by design. Finland was one of Ancel Key's strongest statistical supports - and the methodologically questionable Finnish Mental Hospital Study is still a mainstay of lipid hypothesis epidemiology. We are not talking selenium supplementation above requirements, which doesn't prevent CVD, but correcting selenium deficiency. (If you ask me, the micronutrient theory of diet-health correlations is sadly neglected at present. What slows the oxidation of lipoproteins? Not so much any antioxidant tested separately at megadose intakes - just the whole antioxidant defense system working smoothly on a little bit of everything it needs. Selenium, zinc, etc., etc., etc.).
2014 is not just 1984 with less saturated fat.

There is more detail about the Finnish selenium program here.

I bought this 45RPM record at a thrift shop the other day. Blue Band, by Bobongo Stars - the full version (it covers both sides) is pretty cool, with a great old-school synthesizer solo. The story of the song, and of Marsavco margarine is told here; it's a palm oil product (so not much need for hydrogenation), and today it's fortified with vitamins including nicotinamide; probably a good thing in the corn-eating regions of Africa. The song is credited to Marsavco-Zaire.

Tuesday, 29 July 2014

A Guest Post on Prof. Grant Schofield's Blog

This is just a short post to direct readers to my guest post here:

Which contains all my thoughts about dietary fat recommendations and the lipid hypothesis, without too many distracting details.

I also want to supply a link to a most enjoyable book, Bertha M. Wood's "Foods of the Foreign-born in Relation to Health" from 1922.
I think this is the first record of "dietary transitions", adverse changes to the traditional diets of migrants in a new land. It was written at the height of U.S. xenophobia (in the immediate aftermath of the Great War and the Bolshevik revolution) and can also be seen as a response to prejudice. Though the Hungarian child's diet below might not have helped much.

In 1922, diabetics were treated by restricting starch, especially from grains and legumes; this was replaced with non-starchy vegetables. Fat was not generally restricted (though this is said to be necessary in some cases, perhaps because sugar doesn't seem to have been reduced).

I learnt about Bertha M. Wood's book from The Old Foodie blog.

Sunday, 22 June 2014

Epidemiology can be Interesting

      Hat tip to Nigel Kinburn for pulling up two studies from Siri-Tarino et al.’s 2010 saturated fat meta-analysis that did show correlations with heart disease. These were also the studies with the widest range of intakes. So what can they tell us?
      The first is by Jim Mann and colleagues from 1993, and straight up I am surprised that this has been included in any meta-analysis, because it uses a self-selected vegetarian cohort, with friends and family standing in for the rest of the population.
      “The study differs from
previous prospective studies of diet and IHD in that the volunteers were individuals whose self-selected diet resembled, in nutrient content, current dietary recommendations rather than the relatively high saturated fat diet typical of most affluent societies. The findings may not only help to explain which attributes of a vegetarian diet protect against IHD but also which foods and nutrients are important in the aetiology of IHD in populations who modify their diets along the lines of present guidelines.”
      It’s odd that such high-bias methodology isn’t excluded from meta-analysis, and makes me wonder what else is included.
      What does Mann et al. tell us?
“Results—IHD mortality was less than half that expected from the experience reported for all of England and Wales. An increase in mortality for IHD was observed with increasing intakes of total and saturated animal fat and dietary cholesterol—death rate ratios in the third tertile compared with the first tertile: 3.29, 95% confidence interval (CI) 1.50 to 7.21; 2.77, 95% CI 1.25 to 6.13; 3.53, 95% CI 1.57 to 7.96, respectively. No protective effects were observed for dietary fibre, fish or alcohol. Within the study, death rate ratios were increased among those in the upper half of the normal BMI range (22.5 to under 25) and those who were overweight (BMI over 25) compared with those with BMI 20 to under 22.5.
(Relative risk figures have been converted from 100 to 1.0)

      IHD was significantly associated with higher consumption of eggs, cholesterol, animal fat, and saturated fat.
      But, here’s the surprising finding; none of those dietary factors was associated with any increase in total mortality, significant or non-significant. People who avoided dying of IHD by following the healthy eating guidelines were dying at the same rate – the same ages - as their less health-conscious friends and family. This wasn’t pinned down to any particular cause of death.

      The fact that BMI under 20 was associated with as much increased risk of overall mortality as BMI over 25 (“total mortality was significantly higher in those with an initial BMI under 20, and a similar though not statistically significant trend is apparent for IHD mortality.”) wasn’t mentioned in the abstract, and is underplayed in the text (if it can be explained by undiagnosed pre-existing disease, so can the correlation with higher BMI). A bit like this dodgy AHF BMI calculator. Set this to BMI 7 (maximum height, minimum weight) and you still look healthy; muscular or curvy depending on gender. Results in real life may vary.

      The main dietary finding pertaining to all-cause mortality in Mann et al.;
“all cause mortality for all subjects was significantly lower in the middle and highest intakes of green vegetables (0.62, 95% CI 0.46–0.83; and 0.74, 95% CI 0.56–0.99) and among those consuming the highest intake of nuts (0.76, 95% CI 0.60–0.97) compared with the lowest intakes of these foods.”

     The second paper is by Bonniface et al., and unfortunately doesn’t supply all-cause mortality data.
      “Not consuming alcohol, smoking, not exercising and being socially disadvantaged were related to high saturated fat intake and CHD death. Cox survival analyses adjusting for these factors found that a level of saturated fat 100 g per week higher corresponded to a relative risk for CHD death for men of 1.00 (0.86-1.18) and 1.40 (1.09-1.79) for women. This difference between the effects of saturated fat in men and women was statistically significant (P=0.019).”

     Mean intakes of SFA in Bonniface et al. - Men: 47.0 g/d Women: 34.4 g/d. A respectable ~20%E (similar to the consumption by Indians eating food prepared with ghee in Raheja et al. 1995).
“The cut-off points for the quintiles of saturated fat in grams per week were 220, 276, 337 and 427 for men and 159, 202, 252 and 319 for women. There was a clear trend to higher CHD death rates associated with higher total and saturated fats and Keys' fat difference in women.”

      Keys' fat difference? This is the ratio between SFA and PUFA.
      “The result for the Keys statistic indicates that a higher level of saturated fat can be compensated by a lower level of polyunsaturated fat, in the ratio 2:1.”
      PUFA by itself showed no correlations, but the Keys difference did. In fact, the correlation between Keys' difference and CHD in table 3 is pretty striking.

     Both populations were in Britain. Perhaps the take-home is, that in Britain, at least at a certain point in time, you could choose how you wanted to die to some extent by choosing your diet around heart guidelines. Or by watching your Keys' ratio if you were female (women today, with vegetable oil diets, would not have ideal Keys' ratios by these tables). But living longer than those around you by restricting saturated fat is not a prediction supported by this epidemiology, or by any meta-analysis, as was discussed by Simon Thornley, Grant Schofield and I in our letter to the NZMJ.

     Diet epidemiology is interesting stuff. It’s incredibly hard to do well, and the things we can take away from it are sometimes unexpected. The papers that go into meta-analyses, even for something like SFA, are wildly heterogeneous in design and in quality. Jim Mann et al.’s 1993 paper told me just about everything I wanted to know that it was possible to tell from the data collected. Bonniface et al. were more obscure; critical data points for the Keys' difference were not included. What use are quintiles without means or cut-offs?
      I was surprised, as I said, that the Mann et al. paper, good though it is, is being included in meta-analysis, because of the self-selection bias (so, self-selection in Paleo or LCHF diet studies shouldn't be a barrier to being taken seriously either). That it was included speaks to the impartiality of meta-studies like Siri-Tarino et al. 2010 that exculpate saturated fat. Meta-studies give the overall truth that is relevant for public health planning, but miss the finer details of what is happening in specific communities at specific times. For example:
      In Mann et al., nuts are protective. This is a common finding, e.g. in Hu et al. 1998. In Bonniface et al. PUFA is not associated with harm, but the Keys' difference is. In Britain at the time of this study, among the mainly middle and upper classes, perhaps vegetable oils were not in common use. Perhaps nuts were a major source of linoleic acid, enough to attenuate its relationship with disease. And in Bonniface et al., with its more working class catchment (and this being Britain, class distinctions do matter), perhaps the ideal Keys' difference of 2:1 is what you get closer to eating nuts and fish with meat and dairy fat, and the adverse lower and higher ratios are what you get either not eating nuts and fish, or using vegetable oils and spreads instead of animal fats.
(the mean PUFA intake of 63.1g/week for women is ~4%E).
     Because it may turn out that when diet-heart epidemiologists one day separate PUFA in nuts and fish from PUFA in oils they will get very different values, as these AMD researchers did.

     Take home: For someone who has the disease of CHD, especially someone following a moderate fat, higher carbohydrate diet like most of the population (the dietary pattern at the heart of all epidemiology) it makes sense to follow these clues, as well as recognising the modern risk factors of sugar and refined flour; eat some nuts, fish, don’t eat red meat every day, eat only a few eggs per week, eat some full-fat dairy, and so on.
      On the other hand, for the average person to eat a pleasurable diet that has been designed around avoiding CHD risk factors from animal foods risks inviting in a host of other diseases that they may be susceptible to in ways they were never susceptible to CHD. Advice to the general population should be limited to recommending those protective factors for CHD that a) supply micronutrients, and b) are also protective factors in a wider sense (nuts, fish, fruit and vegetables, and full fat dairy), instead of messing with Keys' difference based on theories about blood lipids, as opposed to consistent findings based on real food inputs and hard endpoints.