Bernard Shaw goes to Samoa

I’ve been lucky enough to have worked as an extra on the latest fantasy series, and this means I have finally had the time and the freedom from digital poisoning to read some of the books I have wanted to finish.

Like Thomas Mann’s Doctor Faustus. A Thomas Mann book is long and its characters and ideas only really come into focus in the second half. But when they do, wow. Hitler – what were the Germans thinking? Mann describes not the rise of the Nazis but the fall of reason and cults of irrationality that preceded it. And which could precede any form of extreme collectivism anywhere. What he describes isn’t the Popper analysis everyone bandied about cack-handed back when we thought that any reinvigorated conservative critique of progressive radicalism was an impending fascist coup. It’s something more general, something latent in our own instinct to find the self-serving pattern of submission and permission to suit any uncertain times, and also latent in the instinct of intellectuals to make all times seem so uncertain that shit like that can be made to happen in them.
I also read four plays by Ibsen, all good and Ghosts and Hedda Gabbler being perfect marvels, the best plays I can remember having read. Seeing these plays as a bourgeoise in a Victorian theatre must have felt like finding a bomb under your seat.
I was also able to start part 2 (having already read parts 1 and 3) of Michael Holroyd’s biography of Bernard Shaw, covering the years 1898-1918. Shaw, a playwright (and disciple of Ibsen), is an unsympathetic character, with his vegetarianism, chastity, self-regard and urge to pontificate on everything, but he’s also the man who was a tireless cheerleader, inventor, and, behind the scenes, a diligent planner for much of what we call progress in the Western world. Everyone being paid the same amount, men and women being treated by society as if they were physiologically and psychologically identical – these were Shaw’s ideas, expressed frequently enough during an age when they only seemed outlandish and attention-seeking to become familiar, if still attention-seeking, concepts in our own times. And so much more (renewable energy, pacifism, animal rights, the list is quite possibly endless) – Shaw was the original SJW, with the important exception that he could and did laugh at himself, and was prepared to do the grinding political work needed to make civics work well – better schools, better drains, that sort of thing. And not a typical SJW either in that he courted and tolerated opposition in order to better spread his views. Thus he debated G.K. Chesterton, in debates chaired by Hilaire Belloc in a friendly but no-holds barred fashion, for many years. 

And most importantly for our purposes, Shaw was an antivaxxer who debated the most famous vaccinationist of his days, Sir Almroth Wright, regularly for decades. Wright, in fact, sought out Shaw first for publicity purposes.
Shaw’s opposition to vaccination was in part emotional (as an anti-vivisectionist), in part mystical (as a believer in a Life Force which trumped Darwinian evolution), in part envious of the prestige belonging to the freemasonry of Medicine over that of Art.
But he also sensed the role of bunkum in medicine, the unproven theories presented as fact, the faked experiments presented as proof, the corrupting influence of money, and the hollowness of appeal to authority (when the British government wanted to promote Wright’s serum they gave him a knighthood, then used his “Sir” as a selling point).    

“Shaw’s sense of vulnerability to the power of this medical elite, replacing his fear of death, gives his satire its edge…Behind these years of correspondence and controversy with Wright, and the play [The Doctor’s Dilemma] that resulted from their association, there lay a wish to take authority from the orthodoxly educated and give it to outsiders… the medical freemasonry was a closed circle of privileged people whose mesmeric power over other human beings angered Shaw.”

Most relevantly to the present day, he saw vaccination as a shameful cover-up for poverty. No need to fix the drains, supply decent housing, or feed the poor properly if you can stop a pandemic breeding in the slums, or at least the fear of one, or at least reduce the chances of it reaching the bourgeoisie, with a cheap jab. And this point – which perhaps acknowledges that vaccination can be effective, but highlights the social cost of its success – remains valid today.

Modern medical opinion, as reported by Holroyd, seems to be, that Sir Almroth Wright’s tuberculosis serum was worthless. There is even a theory that a similar vaccine technology gave the Spanish flu what it needed to get going. I don’t have the reading or expertise to comment on that. But I do know that Wright’s certainty that women were psychologically unfit to vote was misplaced (because, as Shaw noted, and as we can clearly see today, men are not any less prone to pseudoscientific reasoning) and that his repeated opinion that “the effect of hygiene is aesthetic” was positively dangerous, even if it always gave Shaw the opening to argue the case for Art.  

Which brings us to today. Diet is an arm of hygiene just as surely as hand-washing and the avoidance of crowded indoor spaces, both effective in reducing the spread of COVID19 and other infectious diseases. We can see from China and other places that an adequate selenium level of the diet alone quite possibly reduces the case fatality rate (CFR) for COVID-19 by a factor of 4. We can see that higher vitamin D levels (a sign of good diet quality overall, and not only sunlight exposure or vitamin D intake, because vitamin C, iron and magnesium are among the factors contributing to the serum vitamin D level) are associated with a greatly reduced CFR. And that higher levels of unsaturated fat in fat stores (as in the US population) increase the risk of lung damage and death when infected with SARS-CoV-2. Unsaturated fat is the main component of margarines and the cheap oils used to cook the food of the poor; white bread helps to keep it from being burned for fuel; meanwhile the wealthy eat butter and steak, and are not so prone to the storage of excess fat, despite needing to do less work.
Most of these risk factors, as I’ve said before, are actually the unintended consequences of earlier scientific error regarding the risk of skin cancer (which unsaturated oils also promote) and heart disease (which is mainly driven by the excessive insulin response to the modern diet).

A recent example of how the pro-vax narrative ignores the effects of poverty, and hygiene including diet, appeared in the blog of David Farrier. I’ve mentioned Farrier before in this blog because he’s quite a good bellwether of right-thinking opinion, and because he’s worth reading for his own sake. He’s the creator of an entertaining film, Tickled, about the human capacity for deception, and has a pretty good take on conspiracy theory and its psychology. But it depends whose conspiracy theory, because beneath all his quirkiness Farrier is a bog-standard PMC worrywart and always defers to the interests of his class, acting, on the blog at least, as a gatekeeper who's never met an expert he didn't agree with, or at least submit to meekly.

In this article on fake news written by Farrier’s friend Byron Coley, which is otherwise an intelligent and insightful guide to the current conspiracy theory and misinformation landscape inside NZ, we get an example of misinformation by omission, regarding the measles epidemic in Samoa, in a section on some Covid grifters who ran for parliament on the New Conservative platform.

" In April on Talano Sa’o, Tildsley spent an episode interviewing a man she described as “an unsung hero in Samoa” Edwin Tamasese.

“During the measles pandemic — which was devastating to our people, killed around seventy of our babies — he was right in the middle of it, and he was part of sharing vitamin D, vitamin A, vitamin C, and he did what he needed to do.”

Tamasese, who has no medical training, spread the false claim during the measles outbreak that authorities were “seeding” the country with measles through the emergency mass immunisation program deployed to stem the epidemic."  

So far, so bad. But the story of the Samoan measles outbreak is being manipulated here. The outbreak happened after Samoa’s regular measles vaccination program was stopped, and it was stopped after two babies died from a botched vaccination. It was the deaths of these two babies, and not the activities of anti-vax grifters, that lead to the deaths of 70 children. The Samoan health service, for reasons that are still not clear, could not run a safe vaccination program. Understandably parents chose not to take further risks, until the cost of not having vaccinated their children became obvious. Samoa has a population of 202,506, and 83 people died in the measles epidemic, among 5,700 confirmed cases. New Zealand has a population of 5 million, the same epidemic was described as the worst since 1938, with 2,194 confirmed cases, and two unborn fetuses in the second trimester died as a result of the outbreak. New Zealand many have higher vaccination rates than Samoa, at least among children, but it also has a thriving population of privileged unvaccinated kids.

This is a huge difference in impact. It is the kind of inequality of outcomes that is usually attributed to systemic racism, colonization etc. But when we see a difference so extreme that it really can be interpreted as evidence of those things by anyone with eyes to see, everyone is strangely silent.
Because systemic racism and neo-colonial exploitation could be real features of life in Samoa, if New Zealand’s experience is anything to go by. What else do we call the replacement of traditional foods with imported rubbish, under a system that promotes Western dietary values? New Zealand has a large Samoan population, and New Zealand’s dietary guidelines are dismissive of all the traditional Pacific energy foods in favour of grains. The use of coconut is confused with coconut oil and discouraged in patronising statements like “The Heart Foundation considers that when indigenous people consume coconut flesh and milk along with fish and vegetables, and they are also physically active, the coconut consumption is unlikely to put them at risk of cardiovascular disease. They are in a very different situation from people who consume coconut oil along with a typical western diet.”
Which if true (and the claim is still untested, as Shaw would have recognized, but likely to be untrue) would be true of any food supplying energy. Is it also saying that coconut is unhealthy for a sedentary population? That’s also unlikely to be true.
Traditional diets, and decent diets aligned with them, have long been disrupted in the Islands by Western-trained medical freemasons and commercial traders of imported goods, often working hand-in-hand. If you want to call it structural racism I won’t stop you. But weird how silent the usual suspects are.

Would the grifter’s supplements have saved lives? A silver bullet nutritional approach to systemic deprivation is rarely highly effective, but according to the Cochrane Collaboration, the ultimate in evidence-based medicine “Vitamin A reduces the risk of death from measles by 87% for children younger than 2 years”.
Yet the Samoan authorities were telling parents to ignore the grifters. Did they throw the babies out with the bathwater, or were they also supplying the vitamins to the unvaccinated, preferably before they got measles?

I don’t know the answers. But I do read the papers, watch the TV news, and look at stories on the internet. If I don’t know then it’s likely that very few people know. They only know what they’re told, and the narrative is owned by people who won’t tell you these important things. It’s still owned by Sir Almroth Wright. There’s an alternative narrative, of course, but you certainly can’t trust the people who own that.

Which leaves it up to the people who claim to be investigative – including your David Farriers and Byron Coleys – to find out the truth for us, even if this does rattle their class interests. Summary:  I'm always hopeful that my blog posts may attract people not familiar with my preoccupations and body-of-knowledge, such as it is. So to avoid confusion, here is a summing up:
Vaccines, which have been improved since Sir Almroth Wright's day, are a huge contributor to population health. You shouldn't have needed me to tell you that. However:  There was no Covid vax for a year and most people will still have no Covid vax this time next year. Over 3 million people have died. The drugs are not that effective at preventing this.  Look at environmental factors. The strong associations that exist - selenium, vitamin D and unsaturated/saturated fatty acid ratios - should have been exhaustively tested by now. But instead fuck all has happened. Why? Who is in charge of deciding what to test and how, and why have they not heard of Austin Bradford Hill?

There was no measles vax in Samoa due to a vaccine disaster. Such accidents are always possible, and antivaxers, paradoxically, will always be with us. Why were nutritional interventions - including those with known value - neglected and, indeed, scorned?
And were the other effective hygiene interventions - lockdown, masks, hand sanitizer, social distancing, quarantine - used to control spread, and if so, at what stage of the epidemic? They certainly weren't being used in the NZ outbreak.


The pertussis vax in DPT is also ineffective at preventing outbreaks and needs more frequent boosters than most people can manage. Again, lockdown, masks, hand sanitizer, social distancing, quarantine could be used to control spread, for which to work diagnostic criteria need to be more pragmatic and affordable, and environmental factors should be researched.

It's also relevant that the DPT vaccine is too dangerous to use in sub-Saharan Africa (due to local infectious disease risks that would not be at all relevant in the Pacific). Think of something else there. Why does the development of a vaccine prevent research into alternatives? They will often still be needed.

Is cannabis protective against an adverse effect of the modern diet? Cannabinoid signaling in the omega 3/6 hypothesis of obesity and mood disorders.

(this post originally appeared for subscribers on my Patreon blog in Dec 2020, and is now unlocked. If you want to support my blogging habit and see these posts before they happen, subscribe here!
The rest of you, enjoy.)

It’s pretty well accepted that cannabis is an appetite stimulant in the normal dose range. In fact, it’s pretty much been the unofficial standard-of-care drug for the treatment of appetite loss during illness or chemotherapy for a long time.
So we’d expect people smoking cannabis to have higher rates of obesity and type 2 diabetes, because of the munchies.
Yet it’s been a consistent epidemiological finding that the opposite is true – and the explanation that’s been proposed may give us an insight into why cannabis has become the modern panacea, a drug that has been proposed to treat almost everything and why its legalisation, especially for medical use, is being welcomed by such a large chunk of the population.

How consistent is the association between cannabis use and obesity? In a meta-analysis of BMI data:
“Nine studies were included that reported BMI of users and nonusers and met selection criteria, and an additional two studies were identified that reported lower BMI in Cannabis users, but did not provide numerical data. Of these studies, all reported lower values of BMI in Cannabis users, and only one of these did not reach statistical significance. A second study did not report statistical analysis of the BMI data. Of those studies reporting significant negative correlations, two reported that longer duration of Cannabis use was associated with reduced BMI.”(Clark 2018)

That’s a convincing association as far as it goes, but is there a mechanism that explains it?

In another paper, we read that “Suppressing hyperactive endocannabinoid tone is a critical target for reducing obesity.”(Alvheim 2012) The endocannabinoids, 2-arachidonoylglycerol (2-AG) and anandamide (AEA), promote both appetite and the growth and expansion of fat cells.(Naughton 2013, Banni 2010, Madsen 2012) This is a useful adaptation to store energy after a meal (or in the autumn, when linoleic acid, like sugar, is most easily found in nature) - but if it becomes a constant state can lead to obesity; with higher food (and especially carbohydrate) intake insulin levels also rise, ensuring more synthesis and storage of fat. When this fat exceeds the capacity of the body to store it, type 2 diabetes is one possible outcome, and at this stage it is very difficult to get the appetite to normalise; at which point removing carbohydrate from the diet seems to be the most effective way to reduce food intake without hunger.(van Zuuren 2018)

A drug that antagonises 2-AG and AEA, Rimbonabant, looked promising in animal studies but turned out to cause depression in humans.

Cannabis, of course, has similar effects to 2-AG and AEA, but the body’s response differs in an important way; we respond to the stimulation of endocannabinoid tone from THC and CBD by downregulating it, and this inhibition lasts longer than the effect of the drug does. In a sense, smoking pot inoculates us against excessive endocannabinoid signalling. This counter effect means that our cells burn more energy, rather than store it, and our appetite decreases, for quite a while after a session, even if we did have the munchies at some point.(Clark 2018) In a recent epidemiological study even historical cannabis use was associated with lower BMI and better insulin sensitivity. The rebound effect seems to last. Users probably don’t want to be saturated in cannabis all the time, but be using it intermittently to benefit.

But where does this excess endocannabinoid tone come from in the first place? 2-AG and AEA are made in the body from arachidonic acid, an omega-6 (ω-6 or n-6) fatty acid only found in animal foods – but the amount of AA in these foods is very low. Most AA in the body is synthesised from linoleic acid, the main polyunsaturated fatty acid in cheap vegetable oils (corn oil and soy oil, for example, are around 60% LA).
 

https://www.hindawi.com/journals/ije/2013/361895/fig1/

(Pathways for anandamide synthesis, from Naughton et al 2013)

So, what counters the obesogenic effect of anandamide and 2-AG naturally? The action of omega-6 endocannabinoids is opposed by omega 3 (ω-3, n-3) endocannabinoids, docosahexanoyl ethanolamide (DHEA) and eicosapentaenoyl ethanolamide (EPEA), which have a weaker binding affinity to CB1 and CB2 receptors.(Naughton 2013, Watkins 2014) The omega-3 cannabinoids are synthesized from DHA and EPA, the fatty acids in oily fish (pastured lamb or mutton is also a pretty good source). EPA and DHA can also be synthesized from alpha-linolenic acid (ALA), the omega-3 fatty acid found in flaxseed, canola oil and hemp oil (and present in small amounts in most green veges). However, it looks as if too high an intake of ALA also suppresses blood levels of EPA and DHA.(Gibson 2018)
(There is also an omega-9 cannabinoid, made from the main monounsaturated fat oleic acid, which counters the effects of the omega-6 series, decreasing appetite and increasing fat-burning, but this does not seem to depend on dietary intake. Oleic acid is produced in the body as well as an item of diet; it is synthesised after meals from carbohydrate and other fats, so its cannabinoid probably acts as a fullness signal).


It’s been known for a while that a higher intake of LA drives synthesis of AA and inhibits the conversion of ALA to EPA and DHA.(Gibson 2018) This is probably why fish oil became popular as a supplement, but fish oil has had relatively disappointing results in human trials. The only fish oil product approved as a drug (for cardiovascular disease) is VASCEPA, a synthetic variant of EPA which is reliably able to raise the EPA level in the bloodstream.

However, research out of Australia and France shows that saturated fat, especially dairy fat, increases the level of EPA or DHA in the bloodstream, in people fed omega 3 fatty acids from fish oil or canola oil respectively, compared with people instructed to use vegetable oils as per common governmental health advice.(Dias 2016, Dabadie 2005)  The Australians achieved a doubling of the EPA level when the other fat in the diet was more saturated. Yet the LDL (so-called “bad cholesterol”) level also increased.(Dias 2016)

Why would this be? EPA and DHA trigger the burning of fat in the liver – this is a good thing, lowering triglycerides, but it means these omega-3 fatty acids are destroyed in the process so less will reach the bloodstream in the lipoprotein (“cholesterol”) particles. Some saturated fats, especially the longer medium-chain fatty acids in dairy and coconut, also trigger fat burning and lower triglycerides – and this tends to spare some of the EPA and DHA present, so that other cells in your body can use it.(Drouin 2018)  But removing triglycerides from lipoproteins in the liver means they come out with less fat, and therefore more cholesterol. This raises your LDL-cholesterol, yet these cholesterol-rich LDL particles are less likely to harm your blood vessels than cholesterol-depleted ones.(Hirayami 2012)

It’s noticeable that the true relationship between dietary saturated fat and omega-3 is thus the opposite of that described in influential early books about omega-3 fatty acids, such as Horrobin’s “The Madness of Adam and Eve” and Allport’s “The Queen of Fats”, which painted them as enemies, based on a priori assumptions.

Our diets used to be very low in omega 6 LA. This changed for two reasons – first we were told to replace animal fat with polyunsaturated vegetable oil for cooking because this would lower cholesterol and so reduce the risk of heart disease. But human experiments have never supported this idea. In particular, a meta-analysis of those trials replacing saturated fat with oils and foods high in LA (rather than omega 3 fats) found that the risk of heart disease and death was non-significantly increased in those trials that were properly controlled.(Hamley 2017)
The second reason is that more of our animal-based food today comes from animals fattened on grains. The fat of chickens and pigs fed on corn and soy waste can be very high in LA and higher in AA compared with the fat of the same animals in the past, and even ruminant fat gets higher in LA and AA, and lower in EPA and DHA, when sheep and cattle are fattened on grains.

Guyenet and Carlson analysed all the different studies done over the years measuring the fatty acid percentages of fat stores in samples from people in the USA and found “that adipose tissue LA has increased by 136% over the last half century and that this increase is highly correlated with an increase in dietary LA intake over the same period of time”.(Guyenet 2015)

Adipose LA in Sweden, for example, is significantly lower than in the USA – Scandinavians still eat plenty of meat and dairy fat, and when they do use plant oils prefer canola, which has 1/3 the LA content of soy or corn oil, or olive oil with 1/6 as much; they are also more likely to eat oily fish than Americans. The official recommended limit of saturated intake in some Scandinavian countries is significantly higher than the 10% of energy limit recommended in the USA, UK or NZ. The Swedes enjoy lower rates of obesity, type 2 diabetes, and heart disease than we do with a saturated fat limit which they seem to ignore.

As Clark et al stated in their hypothesis paper,

“…populations with diets characterized by a high omega-6/omega-3 ratio will see significantly larger health improvements from Cannabis use than those eating diets with more moderate ratios of omega-6/omega-3 FAs. This may explain some of the inconsistencies in the data on the metabolic impact of Cannabis use; for example, Cannabis use by Swedish populations may not have the same health impacts as Cannabis use by Americans due to the different dietary backgrounds and obesity rates of these populations.
Cannabis use in the United States appears to provide significant public health benefits due to partial or complete reversal of the metabolic dysregulation caused by the strongly elevated omega-6/omega-3 ratio of the American diet.”


(Note: If “cannabis use… appears to provide significant public health benefits” in a preventive sense, then the distinction between medicinal and recreational uses of the drug becomes a little blurred, as some medications, such as aspirin or statins, can be legally be prescribed to perfectly healthy people for their purported preventive effects, despite there not being strong evidence for such effects outweighing harms.)


Are governments blind to the possible harms of a high omega-6 intake? The New Zealand MOH is still recommending that high-omega 6 seed oils replace animal fats and coconut oil. Why?

Some public health experts still want us to have low cholesterol levels, despite a lack of evidence that the cholesterol effect of food (as opposed to genes or drugs) has any effect on disease risk.
Some also point to epidemiology in which higher linoleic acid intakes appear to be associated with benefit.
Unfortunately, this isn’t as reliable as it might be – the only foods that supply zero LA are sugar, alcohol, and highly refined flour. The less of these foods you consume, the better – and the higher your LA intake will be. None of these studies separates out the LA consumed from seed oils, as opposed to chicken or nuts and seeds, foods which might reasonably be expected to keep you healthy for other reasons than the type of fat they contain – there is no epidemiology of seed oils. How do you even measure cooking oil accurately in a questionnaire? Those takeaway chips you ate last week – do you remember what they were fried in?

But despite only weak evidence for benefit, plenty of negative evidence, and growing evidence of harm, the push continues. In 1987 the government of Mauritius introduced a raft of health measures, most of which were sensible (smoking, exercise, blood pressure control) but also ordered that soy oil replace palm oil in the cheap “ration” oil used for cooking by most people. 5 years later public health experts applauded a decrease in saturated fat intake, a large increase in polyunsaturated fat, and lower cholesterol levels.(Uusitalo 1996) But what was the outcome 10, 20 years later? Cardiovascular mortality increased a bit, BMI increased– and the prevalence of type 2 diabetes increased from 12.8% in 1987, to 15.2% in 1992, and 17.9% in 1998.(Morrell 2019, Söderberg 2005) Mauritius is now fighting the same type 2 diabetes epidemic seen in most other countries after seed oils were introduced. Yet the government of Fiji imposed a tax on palm oil in 2015 to try to get the same outcome, citing the Mauritius experiment as if it had been successful – because no-one involved had published anything suggesting that it wasn’t.(Coriakula 2018)
But while governments and establishment public health experts may appear to be blind to this problem, behind the scenes efforts to lower the amount of omega-6 in the food supply have been going on for decades. These initiatives include the development of canola and more recently the breeding of “high-oleic” oil seeds that are much lower in omega-6. For example, recently Pic’s peanut butter and peanut oil switched to using a high-oleic peanut, and these products now contain a far lower dose of linoleic acid than most other brands.
At present high-oleic oils and nut butters cost a bit more. The linoleic acid in the food supply, found in cheap oils, margarines and mayonnaise, and deep fried food, especially chicken (the cheapest meat), is tilted towards the diets of the poor, and alongside the similarly cheap refined carbohydrates is doing them no favours, whatever diet epidemiology, which is generally done in more privileged populations, might say.

Is this theory relevant to the psychotropic uses of cannabis in modern society?
I haven’t researched this question deeply, but here are some pointers -

The omega-3/6 balance also influences inflammation and pain perception; a high omega-3 and low omega-6 diet in people with chronic headache reduced pain. The control group restricting omega-6 alone, with no extra omega 3, had a lesser reduction in pain and saw some raising of EPA in the blood, but did not experience the drop in AA that was seen in the omega-3 arm.(Ramsden 2013, Taha 2014) Of course, pain relief is an important use of cannabis.

Omega-3 fatty acids supress some effects of PTSD in animals, and Hibbeln and Gow, writing in the journal of Military Medicine, proposed that improving the omega-3/6 ratio in military rations would reduce depression, suicide, and impulsive aggression among US troops.(Hibbeln 2014) In a case-control study, low DHA status was more strongly associated with suicide in US troops than having witnessed the death or wounding of colleagues in combat (OR 1.62 vs 1.54).(Lewis 2011)

There’s an interesting study on the effect of cannabis use during CBT therapy for PTSD and substance use disorders – “results revealed a crossover lagged effect, whereby higher cannabis use was associated with greater PTSD symptom severity early in treatment, but lower weekly PTSD symptom severity later in treatment. Cross-lagged models revealed that as cannabis use increased, subsequent primary substance use decreased and vice versa”.(Ruglass 2017)

A high-dose EPA supplement in children with ADHD aged 6-18 significantly improved measures of attention and vigilance in those subjects with low EPA at baseline.(Chang) A trial of Sativex in adults with ADHD found “nominally significant” improvement in some measures tested, not contradicting the anecdotal reports from this population of cannabis users.(Cooper)

Acetaminophen (paracetamol) is a painkiller that enhances cannabinoid signalling through CB1 receptors in the pain centre of the brain.(Klinger-Gratz 2018) Paracetamol also reduces the pain of social rejection, empathy for the pain of others, and the experience of existential angst after exposure to material that provokes what psychologists call a “meaning threat”, defined as “whenever one is assaulted by thoughts and experiences that are at odds with one’s expectations and values” - represented in the experiment by the films of David Lynch played to people who hadn’t seen them before!(Mischkowski 2016, Slavich 2019, Randles 2013)

And now we’re getting into deep psychological and sociological territory indeed. Has the remodelling of diets (and reformulation of infant formulas) since the 1970s altered our social functioning? Should it join the long queue of factors proposed to account for our current malaise? Or has David Lynch just made too many films?

More research is needed.
But one thing does seem clear – for good or bad, cannabis probably is an appropriate medication for our times, and the widespread modern awareness of its efficacy may have complex roots in the recent history of our society.

References

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Banni, S. and Di Marzo, V. (2010), Effect of dietary fat on endocannabinoids and related mediators: Consequences on energy homeostasis, inflammation and mood. Mol. Nutr. Food Res., 54: 82-92. doi:10.1002/mnfr.200900516

Chang, J.P., Su, K., Mondelli, V. et al. High-dose eicosapentaenoic acid (EPA) improves attention and vigilance in children and adolescents with attention deficit hyperactivity disorder (ADHD) and low endogenous EPA levels. Transl Psychiatry 9, 303 (2019) doi:10.1038/s41398-019-0633-0

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Hirayama S, Miida T. Small dense LDL: an emerging risk factor for cardiovascular disease. Clin Chim Acta 2012; 414: 215–224.

Klinger-Gratz PP, Ralvenius WT, Neumann E, et al. Acetaminophen Relieves Inflammatory Pain through CB1 Cannabinoid Receptors in the Rostral Ventromedial Medulla. J Neurosci. 2018;38(2):322–334. doi:10.1523/JNEUROSCI.1945-17.2017

Lewis MD, Hibbeln JR, Johnson JE, Lin YH, Hyun DY, Loewke JD. Suicide deaths of active-duty US military and omega-3 fatty-acid status: a case-control comparison. J Clin Psychiatry. 2011;72(12):1585–1590. doi:10.4088/JCP.11m06879

Madsen L, Kristiansen K. Of mice and men: Factors abrogating the antiobesity effect of omega-3 fatty acids. Adipocyte. 2012;1(3):173–176. doi:10.4161/adip.20689

Mischkowski D, Crocker J, Way BM. From painkiller to empathy killer: acetaminophen (paracetamol) reduces empathy for pain. Soc Cogn Affect Neurosci. 2016;11(9):1345–1353. doi:10.1093/scan/nsw057

Morrell, S., Taylor, R., Nand, D. et al. Changes in proportional mortality from diabetes and circulatory disease in Mauritius and Fiji: possible effects of coding and certification. BMC Public Health 19, 481 (2019) doi:10.1186/s12889-019-6748-7


Naughton SS, Mathai ML, Hryciw DH, McAinch AJ. Fatty Acid modulation of the endocannabinoid system and the effect on food intake and metabolism. Int J Endocrinol. 2013; 2013:361895. doi:10.1155/2013/361895

Ramsden CE, Faurot KR, Zamora D, et al. Targeted alteration of dietary n-3 and n-6 fatty acids for the treatment of chronic headaches: a randomized trial. Pain. 2013;154(11):2441–2451. doi:10.1016/j.pain.2013.07.028

Randles D, Heine SJ, Santos N. The common pain of surrealism and death: acetaminophen reduces compensatory affirmation following meaning threats. Psychol Sci. 2013 Jun;24(6):966-73. doi: 10.1177/0956797612464786. Epub 2013 Apr 11.

Ruglass LM, Shevorykin A, Radoncic V, et al. Impact of Cannabis Use on Treatment Outcomes among Adults Receiving Cognitive-Behavioral Treatment for PTSD and Substance Use Disorders. J Clin Med. 2017;6(2):14. Published 2017 Feb 7. doi:10.3390/jcm6020014


Simopoulos AP. Dietary omega-3 fatty acid deficiency and high fructose intake in the development of metabolic syndrome, brain metabolic abnormalities, and non-alcoholic fatty liver disease. Nutrients. 2013;5(8):2901–2923. Published 2013 Jul 26. doi:10.3390/nu5082901


Slavich GM, Shields GS, Deal BD et al. Alleviating Social Pain: A Double-Blind, Randomized, Placebo-Controlled Trial of Forgiveness and Acetaminophen. Ann Behav Med. 2019 Dec; 53(12): 1045–1054.

Söderberg S, Zimmet P, Tuomilehto J, de Courten M, Dowse GK, Chitson P, Gareeboo H, Alberti KG, Shaw JE. Increasing prevalence of Type 2 diabetes mellitus in all ethnic groups in Mauritius. Diabet Med. 2005 Jan;22(1):61-8.

Taha AY, Cheon Y, Faurot KF, et al. Dietary omega-6 fatty acid lowering increases bioavailability of omega-3 polyunsaturated fatty acids in human plasma lipid pools. Prostaglandins Leukot Essent Fatty Acids. 2014;90(5):151–157. doi:10.1016/j.plefa.2014.02.003

Uusitalo U, Feskens EJM, Tuomilehto J, Dowse G, Haw U, Fareed D, et al. Fall in total cholesterol concentration over five years in association with changes in fatty acid composition of cooking oil in Mauritius: cross sectional survey. BMJ 1996;313:1044­6.

van Zuuren EJ, Fedorowicz Z, Kuijpers T, Pijl H, Effects of low-carbohydrate- compared with low-fat-diet interventions on metabolic control in people with type 2 diabetes: a systematic review including GRADE assessments, The American Journal of Clinical Nutrition, Volume 108, Issue 2, August 2018, Pages 300–331

Watkins BA, Kim J. The endocannabinoid system: directing eating behavior and macronutrient metabolism. Front Psychol. 2015;5:1506. Published 2015 Jan 6. doi:10.3389/fpsyg.2014.01506

.

The most important post - a new Nutrition and Mental Health article and book

The Better Brain: How nutrition will help you overcome anxiety, depression, ADHD and stress is a new book (not to be mistaken with the David Perlmutter book of similar name) by Bonnie Kaplan and Julia Rucklidge.

I was invited to review this very important book - by the authors of multiple RCTs and cross-over studies, who are announcing new findings in nutrition and mental health scientific research in book form for the first time, for NZ mainstream media channel Newsroom, where I've managed to place a few nutrition articles in the past.
Basically, the more hits this gets the more likely it becomes that I'll be asked back, and that I'll thus be able to keep placing ideas about LCHF, keto, ancestral diets, and the failings of the food industry and dietary guidelines in the MSM.

Please click here:

https://www.newsroom.co.nz/book-of-the-week-the-wrong-diet-makes-you-insane

My earlier posts in Newsroom can be accessed from the link.

Thank you

Zombies of the Risk Society

How the Risk Society model of “progress” explains the COVID-19 paralysis, how Zombies were enlisted in the cause, and what hope there is left of not becoming Zombies ourselves. (Note: this article was originally posted on Pearl Harbor day 2020, as a subscriber-only post on my Patreon account - to stay up-to-date with my research (except matters of urgent public interest, such as selenium and Covid-19 theories, which will always be free) in these low-employment times, please subscribe!)

“Whereas the utopia of equality contains a wealth of substantial and positive goals of social change, the utopia of the risk society remains peculiarly negative and defensive. Basically, one is no longer concerned with attaining something ‘good’, but rather with preventing the worst.

The dream of the old society is that everyone wants and ought to have a share of the pie. The utopia of the risk society is that everyone should be spared from poisoning.”
Ulrich Beck, Risk Society, 1986

In the summer of late 1968, two years after I arrived in New Zealand with my family as an 8-year old, what would become known as the Hong Kong Flu arrived. We were all sick and could barely move to feed ourselves. I remember to this day the feeling of one’s sinuses and bronchial passages being encased in and fossilized by concretions of phlegm day after day. Getting back to normal, if I ever did, took forever. The Hong Kong Flu killed a million people world-wide; 100,000 of these were in the USA. When mortuary room ran out, bodies were stacked in the subways in Berlin. Given that there are many more people alive today than in the 60’s who can be killed by such an infection, the Hong Kong Flu seems a decent approximation of the virulence of COVID-19.
Yet, Woodstock, and Altamont, went ahead in 1969, at the height of the epidemic in the USA. I’ve never seen the flu mentioned in any hippie memorial. The Vietnam War went on – if the flu is mentioned in histories of the Tet offensive, it doesn’t seem to have influenced strategy or logistics.
This wasn’t a result of ignorance. In the 1966 Star Trek episode The Naked Time (series 1, episode 4), Lt (jg) Joe Tormolen is infected by an alien virus while inspecting facilities on the planet Psi 2000. We first see Lt (jg) Joe wearing a biohazard suit (with an oddly feminine-patterned facemask – the props crew, probably, having used offcuts of material bought to scantily clad the green-skinned dancing girls on some other planet) then see him put his hand under the mask to scratch his face. Even though this will not be the route of infection, the scene is included to signal that Lt (jg) Joe is the crew member who is going to catch something.

If people weren’t any more stupid in the past than they are today – always a safe bet – then how do we explain the difference in the world’s reaction to today’s pandemic?

In my day job, I have helped a Professor of Public Health stay up-to-date with the evidence, and most of this evidence is conceptualised in terms of risk. Risk influences policy – will taxing sugar, or fat, improve population health? Hugely complicated rearrangements of hopelessly confounded data are lobbied at politicians who want to be seen to be doing something that will add a few extra days to the average lifespan, which, by the miracle of statistics, can then easily be sold in far more grandiose terms. The data sets are riddled with class bias – does eating red meat reduce your risk of cancer? I cannot tell you that, because in Western societies red meat signifies labour, labourers are more likely to be exposed to workplace carcinogens than academics and clerical workers, and no-one measures carcinogen exposure in diet epidemiology.

The differences in risk that appear are usually small, and the certainty is low, so why do we care so much? A few years ago I came across a blog post by documentary maker Adam Curtis which explains this important change in the function of society through the “risk society” predictions of Ulrich Beck, quoted above. Curtis says:

That was written in 1986 - and it is remarkably prescient. Because that short paragraph pretty much describes the present day mood in our society. A world where individuals are constantly calibrating risks in their lives, while politicians are expected to anticipate and avoid all future risks and dangers.

And everyone gives up on the idea of creating equality, which allows inequality to increase massively.

Beck’s book is extraordinary - because he came from the liberal left. Yet he is basically saying that in the face of these new potential risks we will have to move away from the political idea of progress and social reform - and instead hunker down in the brace position and try and anticipate all dangers that might be coming at us out of the darkness.

In 1968 a lot of people, from Ho Chi Min to LBJ to the crowd at Woodstock, had progress and social reform on their minds. Lockdown after MLK’s murder? Good luck with that. Suspend flights to and from Vietnam? Not going to happen for other reasons. The world’s machinery was simply being applied to different ends, and few thought it could or should be diverted to stop a pandemic.

At some point faith that the world could be radically changed, and that wars could be convincingly won, faded away. And science, perverted by the political and economic demands placed on it by the Cold War and the opportunities of consumerist capitalism, became a source of extra risk – leaky nuclear reactors, persistent pollutants, dodgy drugs, instead of the engine and arbiter of progress.

Curtis again:
“I think the truth probably is that it was the baby boomers losing their youth - and finding themselves unable to face the fact of their own mortality - they started to project their fears onto the rest of society. But somehow people like Beck transformed this into a grand pessimistic ideology.”

Beck’s original risk society theorem was about limiting man-made risk, but a pandemic, once you can do something about it, easily becomes such a risk; for example, jet aircraft are man-made vectors for transmitting pathogens rapidly around the world. Just as Godzilla represented the risk of nuclear power to a generation of Japanese, the Centres for Disease Control decided, about a decade ago, to use Zombies in their pandemic education programs.
You heard me right – Zombies. Imaginary monsters of undead human lineage derived from Afro-Caribbean folk tradition, and introduced to modern audiences by some relatively progressive film-makers who side-stepped any possible racist implications to create a more generalized myth of “the Other”. The Zombie film is basically an exercise in imagining genocide at a remove. You wake up one day and your neighbours are mindlessly intent on killing you and there’s nothing you can do about it – a common enough experience in mid 20th-century Europe. In the usual Zombie film, the tables will be turned, as they were in Europe. There will then be a genocide of Zombies, but it’s ethical because Zombies, though in human form and formerly known to us as our fellow humans, have become convincingly subhuman. It may be cathartic, but it’s not reassuring.

(Table from Walter Dehority, Infectious Disease Outbreaks, Pandemics, and Hollywood—Hope and Fear Across a Century of Cinema., JAMA 2020)

But the Zombie idea appealed to educators globally, as a way of getting kids interested in scientific concepts like exponential spread. And just as a way of pleasing kids and keeping them entertained – “look up from your video game, because this lesson’s like a video game!” – which is what education is turning into (anything too rigorous rapidly becomes financially and socially “risky”). I remember the kids coming home from school and talking about their Zombie lessons and wondering WTAF?

As discussed in an NZ Medical Journal article in 2018, the evidence that teaching kids about Zombies improves their preparedness as young adults is lacking. But it certainly allows them to see pandemics in dehumanizing terms, because no-one cares what happens to Zombies.
And so New Zealand went, overnight, from being a society where any expression of concern about immigration numbers for any reason was automatically flagged as “racist” and shouted down, to being the most “Build the Wall!” society on earth, a Hermit Kingdom jealously guarding its borders, with those members of society most progressive in normal times tending to be most vocal in defence of the new isolationism and any other restrictive measure needed to eliminate risk.
Not, I should add, that NZ’s approach has been overtly repressive – unlike Australia we haven’t implemented large fines, and have avoided violent arrests, for breaches of Covid decorum. Police are more likely to tell you that your behaviour is very disappointing and they expected better from you - and no-one wants to hear that.
As Prime Minister Jacinda Ardern says, “Be Kind”. You can take this as a reference to Albert Camus’ The Plague or Ellen DeGeneres’ The Ellen Show, or both, depending on your background, but it’s been useful advice to fall back on. Like most of the government’s messaging so far, it’s on point, easy to conceptualise, and leaves little room for confusion.

Nor has the NZ government’s reaction been entirely regressive. The slow claw-back of workers’ rights by a Labour party which famously surrendered to neo-liberalism in the 1980s has if anything strengthened under Covid; wages and benefits have been increased as more workers have lost their jobs and small businesses have failed. The idea that everyone is in the same boat here – a kind of Covid-class consciousness - is generally accepted.
NZ is a small country, we all know each other, and back in the early 90’s now-finance minister and deputy Prime Minister Grant Robertson, then head of the Otago Student’s Union, asked my band to play at his 21st. As bandleader I shared a common mission with Grant as host, that of keeping the party going and the inevitable Nazi skinhead gatecrasher contingent peaceful, which when you think about it is not unlike the mission of any successful left-leaning government in a democracy.

Talking about gatecrashers, QAnon and the associated plandemic theorists have indeed made inroads here. A few thousand people attended an illegal “Freedom” march in Auckland during the brief second lockdown of that city. And the right-thinking rest of NZ society – the Lockdown Liberals, to use Anton Jäger’s phrase, are being taught to see the spread of QAnon – a lab-grown virus if ever there was one - as another kind of Zombie pandemic.

(Since I wrote the first draft of this essay, NZ investigative journalist David Farrier, who is well-informed on QAnon, has begun sharing comics by Dan Vernon portraying conspiracy theorists as Zombies. One of these portrays cancelled, delusional chef Pete Evans* as a Zombie and describes the MAGA hat as a “neo-Nazi” symbol. More realistically, and more in keeping with the neo-Nazi cartoon shared by Evans that the comic was an outraged response to, the MAGA hat will go down in history as the symbol of a grifter-capitalist grab at political power - “say what you like about the tenets of National Socialism, Dude, at least it's an ethos.”)

Lockdown liberals also look askance on another group in NZ known as Plan B,  academics who warn that we can’t stay hermits forever, that lockdowns have both predictable and unforeseen consequences, and that we should be openly debating the alternatives whether we choose to embrace them or not.
The argument against these Covid-relativists is that it is heartless to consider the economy when lives are at stake - as if poverty no longer kills, as if life-extending medical treatments are cheap.
It's a trolly problem where the view on both lines is obscured by distance, and the categorical imperative is to preserve the lives that seem closest in time – those that would be lost to Covid – by diverting the runaway trolly off towards the lives unseen.


We’ll open the country when “we” have a vaccine, even though that will inevitably result in the infections we’ve been postponing, albeit hopefully at a lower rate. In the meantime, we seem to have done nothing in New Zealand to identify and quantify, let alone treat, the risk factors that are most likely to influence the virulence of COVID-19; from here these look like vitamin D deficiency, selenium deficiency (endemic in New Zealand), diabetes and obesity, and the polyunsaturated fat content of one’s fat stores – most of which are unintended consequences of earlier Risk Society initiatives - all of which are metabolically interlinked in their interaction with the virus, and all of which can easily be modified in whatever time we have - if the Risk Society so decides.

Ironically, we’d know a lot more about the factors influencing SARS CoV-2 virulence if we used more often the methods of the father of risk epidemiology, Austin Bradford Hill. In the 1960’s, Hill conceptualised the scientific argument against cigarettes in a way that could be seen as conclusive. Hill’s criteria are neglected today (or sometimes rewritten in order to weaken them as a form of special pleading) because, taken as a whole, they tend to screen out the small, confounded, possibly imaginary, and practically meaningless risks that are so popular for generating media articles and influencer pay-days today, like the story that inspired Curtis’s Vegetables of Truth.

We can become more like Bradford Hill, and less like Ulrich Beck, if and when we decide to stop being Zombies and start living.


* It’s a theme for another day, what caused Pete Evans, who did help expose one Big Lie and was pilloried for it by the corrupt Aussie dietetics establishment and the predatory press, to start seeing Big Lies everywhere and malign “elites” behind everything till his mind turned to mush.

Letter – Selenium supplementation may improve COVID-19 survival in sickle cell disease.

Further to Ulfberg and Stehlik’s letter of Sept 29^th, further evidence supports the role of selenium in COVID-19 virulence.[1]

In their pre-print analysis by machine learning of Medicare patients Dun et al. found that the leading comorbidity associated with COVID-19 mortality, adjusted for age and race, was sickle cell disease (aOR, 1.73; 95% CI, 1.21-2.47), followed by chronic kidney disease (aOR, 1.32; 95% CI, 1.29-1.36).[2]

Both SCD and kidney disease can lower selenium levels by decreasing tubular selenium resorption, and are associated with deficient selenium status.[3,4]

Selenium status or intake has been correlated with COVID-19 outcomes, including mortality and recovery rates, in four patient groups in China, Germany, South Korea, and southern India.[5,6,7,8] SARS-CoV-2, like other RNA viruses, sequesters selenium causing selenium levels to drop during infection.[6,9] SARS-CoV-2 may infect cells in bone marrow, suppressing red blood cell formation.[10] Selenium status is inversely associated with haemolysis in SCD, and selenium may both inhibit haemolysis and enhance erythropoiesis in SCD.[3,11]

Selenium is required for the actions of both vitamin D and dexamethasone.[12,13] Selenite infusion is safe, including in critically ill and dialysis patients, and selenium supplementation has had favourable effects in other RNA virus infections.[14,15,16]

It should be noted that vitamin C and magnesium are also commonly deficient nutrients and are required for the activation of vitamin D3 by hydroxylation.[17,18,19] Deficiency of ascorbate has been associated with COVID-19 and COVID-19 outcomes in hospital populations.[20]

Selenium, supplemented if necessary with its cofactors in vitamin D metabolism, is proposed to be an important protective factor in the general population, but has the potential to reduce mortality from SARS CoV-2 infection in the sickle cell disease population to an even greater extent.


[1] Ulfberg, J., & Stehlik, R. (2020). Finland’s handling of selenium is a model in these times of coronavirus infections. British Journal of Nutrition, 1-2. doi:10.1017/S0007114520003827

 
[2] Dun C, Walsh CM, Bae S et al. A Machine Learning Study of 534,023 Medicare Beneficiaries with COVID-19: Implications for Personalized Risk Prediction. medRxiv 2020.10.27.20220970; doi: https://doi.org/10.1101/2020.10.27.20220970

[3] Delesderrier E, Cople-Rodrigues CS, Omena J, et al. Selenium Status and Hemolysis in Sickle Cell Disease Patients. Nutrients. 2019;11(9):2211. Published 2019 Sep 13. doi:10.3390/nu11092211

[4] Iglesias P, Selgas R, Romero S, Díez JJ. Selenium and kidney disease. J Nephrol. 2013 Mar-Apr;26(2):266-72. doi: 10.5301/jn.5000213. Epub 2012 Sep 18. PMID: 23023721.

[5] Zhang J, Taylor EW, Bennett K, Saad R, Rayman MP. Association between regional selenium status and reported outcome of COVID-19 cases in China, The American Journal of Clinical Nutrition, Volume 111, Issue 6, June 2020, Pages 1297–1299, https://doi.org/10.1093/ajcn/nqaa095

[6] Moghaddam A, Heller RA, Sun Q et al. L. Selenium Deficiency Is Associated with Mortality Risk from COVID-19. Nutrients 2020, 12, 2098.

[7] Im, JH et al. Nutritional status of patients with coronavirus disease 2019 (COVID-19) Int J Infectious Diseases, August 11, 2020

[8] Majeed, M et al. An Exploratory Study of Selenium Status in Normal Subjects and COVID-19 Patients in South Indian population: Case for Adequate Selenium Status: Selenium Status in COVID-19 Patients. Nutrition. Available online 11 November 2020, 11105

[9] Wang, Y et al. SARS-CoV-2 suppresses mRNA expression of selenoproteins associated with ferroptosis, ER stress and DNA synthesis. Preprint, 2020/07/31. 10.1101/2020.07.31.230243

[10] Reva, I., et al. Erythrocytes as a Target of SARS CoV-2 in Pathogenesis of Covid-19. Archiv EuroMedica. 2020. doi.org/10.35630/2199-885X/2020/10/3.1

[11] Jagadeeswaran R, Lenny H, Zhang H et al. The Impact of Selenium Deficiency on a Sickle Cell Disease Mouse Model. Blood 2018; 132 (Supplement 1): 3645. doi: https://doi.org/10.1182/blood-2018-99-111833

[12] Schütze N, Fritsche J, Ebert-Dümig R, et al. The selenoprotein thioredoxin reductase is expressed in peripheral blood monocytes and THP1 human myeloid leukemia cells--regulation by 1,25-dihydroxyvitamin D3 and selenite. Biofactors. 1999;10(4):329-338. doi:10.1002/biof.5520100403

[13] Rock C, Moos PJ. Selenoprotein P regulation by the glucocorticoid receptor. Biometals. 2009;22(6):995-1009. doi:10.1007/s10534-009-9251-2

[14] Zhao Y, Yang M, Mao Z, et al. The clinical outcomes of selenium supplementation on critically ill patients: A meta-analysis of randomized controlled trials. Medicine (Baltimore). 2019;98(20):e15473. doi:10.1097/MD.0000000000015473

[15] Manzanares W, Lemieux M, Elke G, Langlois PL, Bloos F, Heyland DK. High-dose intravenous selenium does not improve clinical outcomes in the critically ill: a systematic review and meta-analysis. Crit Care. 2016;20(1):356. Published 2016 Oct 28. doi:10.1186/s13054-016-1529-5

[16] Steinbrenner H, Al-Quraishy S, Dkhil MA, Wunderlich F, Sies H. Dietary selenium in adjuvant therapy of viral and bacterial infections. Adv Nutr. 2015;6(1):73-82. Published 2015 Jan 15. doi:10.3945/an.114.007575

[17] Cantatore FP, Loperfido MC, Magli DM, Mancini L, Carrozzo M. The importance of vitamin C for hydroxylation of vitamin D3 to 1,25(OH)2D3 in man. Clin Rheumatol. 1991 Jun;10(2):162-7. doi: 10.1007/BF02207657. PMID: 1655350.

[18] Dai Q, Zhu X, Manson JE, et al. Magnesium status and supplementation influence vitamin D status and metabolism: results from a randomized trial. Am J Clin Nutr. 2018;108(6):1249-1258. doi:10.1093/ajcn/nqy274

[19] Cooper ID, Crofts CAP, DiNicolantonio JJ, et al. Relationships between hyperinsulinaemia, magnesium, vitamin D, thrombosis and COVID-19: rationale for clinical management. Open Heart. 2020;7(2):e001356. doi:10.1136/openhrt-2020-001356

[20] Carr, A.C.; Rowe, S. The Emerging Role of Vitamin C in the Prevention and Treatment of COVID-19. Nutrients 2020, 12, 3286.

[3] Delesderrier E et al. Selenium Status and Hemolysis in Sickle Cell Disease Patients. Nutrients. 2019;11(9):2211. Published 2019 Sep 13. doi:10.3390/nu11092211

[4] Iglesias P et al. Selenium and kidney disease. J Nephrol. 2013 Mar-Apr;26(2):266-72. doi: 10.5301/jn.5000213. Epub 2012 Sep 18. PMID: 23023721.

 [5] Zhang J et al. Association between regional selenium status and reported outcome of COVID-19 cases in China, The American Journal of Clinical Nutrition, Volume 111, Issue 6, June 2020, Pages 1297–1299, https://doi.org/10.1093/ajcn/nqaa095

[6] Moghaddam A et al. L. Selenium Deficiency Is Associated with Mortality Risk from COVID-19. Nutrients 2020, 12, 2098.

[7] Im, JH et al. Nutritional status of patients with coronavirus disease 2019 (COVID-19) Int J Infectious Diseases, August 11, 2020

[8] Majeed, M et al. An Exploratory Study of Selenium Status in Normal Subjects and COVID-19 Patients in South Indian population: Case for Adequate Selenium Status: Selenium Status in COVID-19 Patients. Nutrition. Available online 11 November 2020, 111053

 

[9] Wang, Y et al. SARS-CoV-2 suppresses mRNA expression of selenoproteins associated with ferroptosis, ER stress and DNA synthesis. Preprint, 2020/07/31. 10.1101/2020.07.31.230243

 

[10] Reva, I., et al. Erythrocytes as a Target of SARS CoV-2 in Pathogenesis of Covid-19. Archiv EuroMedica. 2020. doi.org/10.35630/2199-885X/2020/10/3.1

 

[11] Jagadeeswaran R et al. The Impact of Selenium Deficiency on a Sickle Cell Disease Mouse Model. Blood 2018; 132 (Supplement 1): 3645. doi: https://doi.org/10.1182/blood-2018-99-111833

Mauritius - When the effects of saturated fat replacement failed to conform to the modelling, no-one cared.

There may be no country in the world in which a suggested limit on saturated fat has not been followed by a relatively rapid increase in the incidence of diabetes and obesity.

Of course this is a matter of observation not experiment, but so is most of the evidence that various dietary guidelines organizations have relied on over the years.

 

A particularly egregious case seems to have occurred in Mauritius, after the Mauritian Government changed the fat content of ration oil, a cheap cooking oil used by most of the population, by decree. In 1987 it had been 75-100% (median 87.5%) palm oil, with (by then) some soybean oil – overnight this was changed to 100% soybean oil. This change was based on predictions from the research of Ancel Keys into heart disease, in particular the 7 Countries study and the intervention in East Finland.

This took PUFA intakes (almost all linoleic acid) to 8.6%E for men and 8.8%E for women, and lowered SFA intakes to 7%E and 7.5%E respectively. These were, as reported, not high fat diets, and it may be relevant that Mauritius is a sugar-producing nation.[1,2]

 5 years later, in 1992, researchers, including experts from Finland and the WHO, measured the changes in fat intake and cholesterol in the Mauritian population, focusing on Hindu Indians.

 

"In the 5-year survey of lipids and other biomarkers, mean population serum total cholesterol concentration fell appreciably from 5.55 mmol/l to 4.7 mmol/l (P<0.001). The prevalence of overweight or obesity increased, and the rates of glucose intolerance changed little."[1]

 

However, in a letter to the BMJ, N Chandrasekharan, a consultant chemical pathologist and Kalyana Sundram, senior research officer of the Palm Oil Research Institute of Malaysia disputed these findings -

 "On the purported fall in serum cholesterol concentration from 5.7 mmol/l in 1987 to 4.6 mmol/l in 1992, it is not evident whether the samples were from the same subjects.

The data for 1992 on the per caput fat intake of 56.2 g per day based on a 24 hour dietary recall is a far cry from the 73.7 g reported by the Food and Agriculture Organisation. The figures for edible oil intake seem erroneous. In 1987 palm oil accounted for only 27.5% of the edible oils consumed and its saturated fatty acids contributed 1.89% of the total energy intake and this fell to 0.33% in 1992."[3]

 

However, we have previously found FAO fat consumption estimates to be unreliable, overestimating NZ butter consumption in recent years by a factor of 4. And Chandrasekharan and Sundram’s letter contains this statement:

 "Although we are also concerned about the need to reduce the prevalence of non­communicable diseases in Mauritius, we disagree on the kind of simplistic thinking and draconian measures advocated."[3]

 

In other words, whatever the effect on fat intakes or cholesterol, the change was a radical one. It put more linoleic acid into the Mauritian food supply, and as in other places, the change in mandated fats would have been accompanied by voluntary changes along the same lines. We may doubt whether cholesterol levels changed, but not that people began to consume more soybean oil.

 So what happened? The 1987 intervention included several good ideas – exercise more, smoke less, drink less – as well as less certain ones – eat less salt, eat less saturated fat and more soybean oil.

 However, it seems unlikely that CVD went down – circulatory mortality as a percentage of mortality increased after 1987. [4]

 "Over 1981–2004 the proportion of circulatory disease mortality rose from 44% to 49% in males, and from 46% to 57% in females."

 

Mauritius is now #2 in the world for diabetes mortality. However, a coding change in 2004 meant that much of what had been recorded as circulatory disease mortality was shifted to diabetes mortality. What we do know is that diabetes prevalence increased, as has incidence of pre-diabetes.

 "The prevalence of Type 2 diabetes increased significantly during the period studied, from 12.8% in 1987, to 15.2% in 1992, and 17.9% in 1998."[5]

 

Note that this contradicts the 1992 claim – by some of the same authors – that “the rates of glucose intolerance changed little” between 1987 and 1992, a discordance not mentioned in the 2002 paper.[1]

 "The age-standardized prevalence of diabetes in 2009 was 22.3% (95% CI 20.0–24.6) among men and 20.2% (18.3–22.3) among women, representing an increase since 1987 of 64 and 62% among men and women, respectively".[6]

 

The Mauritius fat change paper has been cited just 17 times in 25 years, and not one of the citing papers includes any follow up on the consequences of the change there. For example, an AHA paper mentions the Mauritius change in glowing terms without following up whether benefit or harm ensued, beyond the claimed 5-year drop in cholesterol.[7] Palm oil reduction was modelled for India in 2013, and a doubled palm oil tax has been implemented in Fiji since, all in papers citing the 1987-1992 Mauritius cholesterol drop.[8, 9]
But none follows that citation up with any hard outcomes.

 Conversely, none of the papers on health in Mauritius since 1992, charting worsening trends, and in which the Finns still feature as authors, mentions the oil change of 1987. However, the earlier paper had contained a warning:[2]

 "Whether the replacement of palm oil by soya bean oil, rich in n-6 polyunsaturated fatty acids, is the optimal dietary change may be questioned... the consumption of fats high in polyunsaturated fatty acids may lead to increased concentrations of free radicals and oxidised low-density lipoprotein, which may promote the progression of atherosclerosis. Therefore, notwithstanding the apparent success of the intervention in Mauritius, an oil high in monounsaturated fatty acids, such as olive oil or rapeseed oil, might be preferable if such an oil substitution were currently being planned."

 

It appears now that both saturated fat in the diet, and a low intake of omega 6 linoleic acid,  are beneficial in terms of the incorporation of the omega 3 fatty acids EPA and DHA into circulating lipids and cells.[10, 11, 12, 13] EPA in particular is anti-inflammatory, and is an approved drug for the prevention of CVD.[14]

 "These observations indicate that the efficacy of n-3 fatty acids in reducing arachidonic acid level is dependent on the linoleic acid to saturated fatty acid ratio of the diet consumed."[11]

 "The results suggest that dietary substitution of SFA with n-6PUFA, despite maintaining low levels of circulating cholesterol, hinders n-3PUFA incorporation into plasma and tissue lipids."[13]

 

The conversion of linoleic acid to arachidonic acid, and the peroxidation of arachidonic acid to aldehydes which interfere with insulin signaling, as well as its conversion to cannabinoids which increase adipocyte growth, in a context of decreased omega 3 availability from high LA and low SFA diet, are pathways that may explain the eventual adverse outcomes in Mauritius, especially in a population with high sugar availability.[15,16]

 "Our recent finding that sucrose and other high glycemic index carbohydrates abrogate the antiobesity effect of n-3 PUFAs might, at least in part, provide an explanation to the apparent discrepancy between human and rodent intervention studies, and the lack of effect in some human trials. In addition to the amount and type of carbohydrates, the levels of n-6 PUFAs, linoleic acid in particular, in the background diet might influence the antiobesogenic effect of n-3 PUFAs."[15]

 

It seems that, in the matter of diet, public health experts cannot be relied on to investigate the possibility that they have made a mistake. They control the narrative so that a (questionable) historical change in cholesterol within a 5-year period is considered evidence that a lifetime intervention is valuable, yet a nation-wide worsening of hard endpoints after that intervention can be ignored. Certainly the diabetes disaster in Mauritius can have had many causes, but the possibility that the soya bean oil intervention was one of them has not even registered in the medical literature over a 30 year period, let alone been tested.

 H/T Louise Stephen @LouiseStephen9 author of  'Eating Ourselves Sick' for bringing this intervention to my attention.

Postscript: it will be obvious to students of evidence-based medicine that the quality of evidence used to create this argument has left much to be desired. With the exception of the date and intent of the intervention and the diabetes incidence data, nothing here tells us quite what we want to know. For example, circulatory disease as a percentage of mortality is a suggestive but imperfect measure, even before the coding change. So there will be those who read this article and feel justified in dismissing the need for it.
But I ask them to look at things another way - the data in this page is, to the best of my knowledge, the sum total of the published, peer-reviewed evidence on the subject. The Mauritius intervention - a legal disruption of the saturated fat supply to replace it with unsaturated fat within an entire community, in a way designed to target its most vulnerable members - has been the masturbation fantasy of a certain type of public health epidemiologist for as long as I can remember. There is a constant supply of peer-reviewed publications modelling the long-term effect of such an intervention on the putatively preventable causes of mortality, and there have been none directly investigating the impact on those causes in this case - where the long-planned intervention actually happened.
The reasons for this neglect are a matter for conjecture; we may hear future tales of suppressed data and publication bias as we did with the Sydney Heart Study and Minnesota Coronary Experiment studies (both of which also involved changes of fat products given to a population, rather than the less certain changes of mere advice given in most other diet-heart studies)[17] but the conclusion ought surely to be that the modelling should stop until the facts have been checked. 

References

[1]  Dowse GK, Gareebo H, Alberti KGMM, Zimmet P, Tuomilehto J, Purran A, et al. Changes in population cholesterol concentrations and other cardiovascular risk factor levels after five years of the non­communicable disease intervention programme in Mauritius. BMJ 1995;311:1225­9.

 

[2]  Uusitalo U, Feskens EJM, Tuomilehto J, Dowse G, Haw U, Fareed D, et al. Fall in total cholesterol concentration over five years in association with changes in fatty acid composition of cooking oil in Mauritius: cross sectional survey. BMJ 1996;313:1044­6.

 

[3]  Chandrasekharan N, Sundram K. Fall in cholesterol after changes in composition of cooking oil in Mauritius. BMJ. 1997;314(7079):516. doi:10.1136/bmj.314.7079.516

 

[4]  Morrell, S., Taylor, R., Nand, D. et al. Changes in proportional mortality from diabetes and circulatory disease in Mauritius and Fiji: possible effects of coding and certification. BMC Public Health 19, 481 (2019) doi:10.1186/s12889-019-6748-7

 

[5]  Söderberg S, Zimmet P, Tuomilehto J, de Courten M, Dowse GK, Chitson P, Gareeboo H, Alberti KG, Shaw JE. Increasing prevalence of Type 2 diabetes mellitus in all ethnic groups in Mauritius. Diabet Med. 2005 Jan;22(1):61-8.

 

[6]  Magliano DJ, Söderberg S, Zimmet PZ, et al. Explaining the increase of diabetes prevalence and plasma glucose in Mauritius. Diabetes Care. 2012;35(1):87–91. doi:10.2337/dc11-0886

 

[7]  Mozaffarian D, Afshin A, Benowitz NL, et al. Population approaches to improve diet, physical activity, and smoking habits: a scientific statement from the American Heart Association. Circulation. 2012;126(12):1514–1563. doi:10.1161/CIR.0b013e318260a20b

 

[8]  Basu S, Babiarz KS, Ebrahim S, Vellakkal S, Stuckler D, Goldhaber-Fiebert JD. Palm oil taxes and cardiovascular disease mortality in India: economic-epidemiologic model. BMJ. 2013;347:f6048. Published 2013 Oct 22. doi:10.1136/bmj.f6048

 

[9]  Coriakula J, Moodie M, Waqa G, Latu C, Snowdon W, Bell C. The development and implementation of a new import duty on palm oil to reduce non-communicable disease in Fiji. Global Health. 2018;14(1):91. Published 2018 Aug 29. doi:10.1186/s12992-018-0407-0

 

[10]  Gibson, Robert A. Musings about the role dietary fats after 40 years of fatty acid research. Prostaglandins, Leukotrienes and Essential Fatty Acids, Volume 131, 1 – 5

 

[11] Garg ML, Thomson ABR, and Clandinin M T. Interactions of saturated, n-6 and n-3 polyunsaturated fatty acids to modulate arachidonic acid metabolism.

The Journal of Lipid Research, February 1990 , 31, 271-277.

 

[12] Dabadie H, Motta C, Peuchant E, LeRuyet P, Mendy F. Variations in daily intakes of myristic and alpha-linolenic acids in sn-2 position modify lipid profile and red blood cell membrane fluidity. Br J Nutr. 2006 Aug;96(2):283-9.

 

[13] Dias Cintia B, Wood LG, and Garg Manohar L. Effects of dietary saturated and n-6 polyunsaturated fatty acids on the incorporation of long-chain n-3 polyunsaturated fatty acids into blood lipids. European Journal of Clinical Nutrition. 2016; 70: 812-818

 

[14] Budoff M, Brent Muhlestein J, Le VT, May HT, Roy S, Nelson JR. Effect of Vascepa (icosapent ethyl) on progression of coronary atherosclerosis in patients with elevated triglycerides (200-499 mg/dL) on statin therapy: Rationale and design of the EVAPORATE study. Clin Cardiol. 2018;41(1):13–19. doi:10.1002/clc.22856

 

[15] Madsen L, Kristiansen K. Of mice and men: Factors abrogating the antiobesity effect of omega-3 fatty acids. Adipocyte. 2012;1(3):173–176. doi:10.4161/adip.20689

 

[16] Clark TM, Jones JM, Hall AG, Tabner SA, Kmiec RL. Theoretical Explanation for Reduced Body Mass Index and Obesity Rates in Cannabis Users. Cannabis Cannabinoid Res. 2018;3(1):259-271. Published 2018 Dec 21. doi:10.1089/can.2018.0045


[17] Ramsden Christopher E, Zamora Daisy, Majchrzak-Hong Sharon, Faurot Keturah R, Broste Steven K, Frantz Robert P et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73) BMJ 2016; 353 :i1246
https://www.bmj.com/content/353/bmj.i1246