Search This Blog

Tuesday, 13 April 2021

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.

Thursday, 4 March 2021

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

Further to Ulfberg and Stehlik’s letter of Sept 29th, 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:

[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,

[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.

[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:

[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,

[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.


[11] Jagadeeswaran R et al. The Impact of Selenium Deficiency on a Sickle Cell Disease Mouse Model. Blood 2018; 132 (Supplement 1): 3645. doi:

Monday, 16 November 2020

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. 


[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

Sunday, 27 September 2020

Selenium reduces COVID-19 risk - a back-of-the-envelope Bradford Hill analysis.

Bradford Hill introduced a checklist for assessing the strength of epidemiological evidence for causality, which is useful in the current pandemic when nutritional factors have been insufficiently tested by experiment in favour of drugs with, so far, relatively weak effects.[1]
Remember, a long time has passed and a lot of people have died while Evidence-Based Medicine was facing the wrong way.
And asking the wrong question. "What new treatment will save more lives in the ICU?" is an important question, but one with few answers and no great ones - "What can stop people who catch SARS-CoV-2 coming to the ICU?" is a better one in a pandemic, and one that might also lead to better treatment protocols.

Selenium reduces COVID-19 mortality: A Bradford Hill analysis

1) Strength of association. Very Strong.

1) On inspection of the Hubei data, it is notable that the cure rate in Enshi city, at 36.4%, was much higher than that of other Hubei cities, where the overall cure rate was 13.1% (Supplemental Table 1); indeed, the Enshi cure rate was significantly different from that in the rest of Hubei (P < 0.0001). Enshi is renowned for its high selenium intake and status [mean ± SD: hair selenium: 3.13 ± 1.91 mg/kg for females and 2.21 ± 1.14 mg/kg for males]—compare typical levels in Hubei of 0.55 mg/kg (10)—so much so that selenium toxicity was observed there in the 1960s. Selenium intake in Enshi was reported as 550 µg/d in 2013.
Similar inspection of data from provinces outside Hubei shows that Heilongjiang Province in northeast China, a notoriously low-selenium region in which Keshan is located, had a much higher death rate, at 2.4%, than that of other provinces (0.5%; P < 0.0001). The selenium intake was recorded as only 16 µg/d in a 2018 publication, while hair selenium in the Songnen Plain of Heilongjiang was measured as only 0.26 mg/kg (Supplemental Table 2).

Finally, we found a significant association between cure rate and background selenium status in cities outside Hubei (R2 = 0.72, F test P < 0.0001; Figure 1, Supplemental Table 2).[2]

Correlation between COVID-19 cure rate in 17 cities outside Hubei, China, on 18 February, 2020 and city population selenium status (hair selenium concentration) analyzed using weighted linear regression (mean ± SD = 35.5 ± 11.1, R2 = 0.72, F test P < 0.0001). Each data point represents the cure rate, calculated as the number of cured patients divided by the number of confirmed cases, expressed as a percentage. The size of the marker is proportional to the number of cases.

2) Serum samples (n = 166) from COVID-19 patients (n = 33) were collected consecutively and analyzed for total Se by X-ray fluorescence and selenoprotein P (SELENOP) by a validated ELISA. Both biomarkers showed the expected strong correlation (r = 0.7758, p < 0.001), pointing to an insufficient Se availability for optimal selenoprotein expression. In comparison with reference data from a European cross-sectional analysis (EPIC, n = 1915), the patients showed a pronounced deficit in total serum Se (mean ± SD, 50.8 ± 15.7 vs. 84.4 ± 23.4 µg/L) and SELENOP (3.0 ± 1.4 vs. 4.3 ± 1.0 mg/L) concentrations. A Se status below the 2.5th percentile of the reference population, i.e., [Se] < 45.7 µg/L and [SELENOP] < 2.56 mg/L, was present in 43.4% and 39.2% of COVID samples, respectively.
The Se status was significantly higher in samples from surviving COVID patients as compared with non-survivors (Se; 53.3 ± 16.2 vs. 40.8 ± 8.1 µg/L, SELENOP; 3.3 ± 1.3 vs. 2.1 ± 0.9 mg/L), recovering with time in survivors while remaining low or even declining in non-survivors.[3]

Vitamins B1, B6, B12, D (25-hydroxyvitamin D), folate, selenium, and zinc levels were measured in 50 hospitalized patients with COVID-19. A total of 76% of the patients were vitamin D deficient and 42% were selenium deficient. No significant increase in the incidence of deficiency was found for vitamins B1, B6, and B12. folate, and zinc in patients with COVID-19. The COVID-19 group showed significantly lower vitamin D values than the healthy control group (150 people, age/sex matching). Severe vitamin D deficiency (based on 10 ng/dL) was found in 24% of the patients in the COVID-19 group and 7.3% of the control group. Among 12 patients with respiratory distress, 11 (91.7%) were deficient in at least one nutrient. However, patients without respiratory distress showed deficiency in 30/38 people (78.9%, P-value 0.425). These results suggest that a deficiency of vitamin D or selenium may decrease the immune defenses against COVID-19 and cause progression to severe disease; however, more precise and large-scale studies are needed.[18]

100% of the patients in this study with severe outcomes, including death, were selenium deficient; 75% were vitamin D deficient; none were zinc deficient.

2) Consistency - Very Strong

All epidemiological data about selenium and COVID-19 is consistent in direction and effect size. However, tests that could be done comparing COVID-19 risk in high and low selenium regions of Brazil, Scandinavia (selenium is supplemented in the food supply of Finland), and the USA would establish consistency further.

[edit 16/11/202o] - New study from South India is consistent with those from Germany, China, and South Korea:

We analysed the blood serum levels in apparently healthy (N=30) individuals and those with confirmed COVID -19 infection (N=30) in the southern part of India. Patients showed a significantly lower selenium level of 69.2 ±8.7 ng/ml than controls 79.1 ± 10.9 ng/ml, the difference was statistically significant (P=0.0003). Interestingly the controls showed a borderline level of selenium, suggesting that the level of this micronutrient is not optimum in the population studied.[19]

[edit 14/12/2020] letter from Finland in BJN compares death rate with Sweden's.

[edit 15/12/2020 deficiency of both zinc and selenium predicts COVID-19 severity in EPIC data]
"This combined deficit was observed in 0.15% of samples in the EPIC cohort of healthy subjects, in 19.7% of the samples collected from the surviving COVID-19 patients and in 50.0% of samples from the non-survivors."[22]

3) Specificity - Strong

Selenium has much weaker or less consistent associations with other diseases, except those caused by other RNA viruses, e.g. when risk of hepatocellular cancer in viral hepatitis patients is compared with risk of osteoporosis.[4, 5]

4) Temporality - Strong

Prospective ecological comparisons are temporal by design.[2] In the German study, the temporal association between low serum selenium levels and COVID-19 symptom severity was closely tracked.[3]

Nutrients 12 02098 g003 550

5) Dose-response gradient - Very Strong

A strong, consistent dose-response is seen, even at levels where the risk of selenium toxicity exists, and despite the fact that toxic levels of soil selenium are often a legacy of industrial pollution in China.[2]

6) Plausibility - Very High

Reading references 2 and 3, as well as this review of the evidence written before reference 2 was published, should be persuasive.[6] See also ref 17 for antiviral effects. This one goes up to 11.

7) Coherence - Very High

Selenium is well-studied and nothing in its story seems to contradict the idea that higher intakes will protect against COVID-19 mortality and reduce the severity of disease.
Dexamethasone, a drug which can reduce COVID-19 mortality in the ICU, enhances 1α,25-dihydroxyvitamin D3 effects by increasing vitamin D receptor transcription.[7] 
Selenium sufficiency is essential for the function of vitamin D in peripheral blood monocytes.[8] Vitamin D status also correlates with COVID-19 survival.[9]

[Edit: 20/11/20] Two conditions which are associated with selenium depletion through effects on tubular mineral resorption, sickle cell disease (aOR, 1.73; 95% CI, 1.21-2.47), and chronic kidney disease (aOR, 1.32; 95% CI, 1.29-1.36), are the comorbidities most strongly associated with COVID-19 mortality in a large US MEDICARE patient analysis.[20] Selenium status in sickle cell disease is inversely associated with markers of hemolysis, a feature of severe COVID-19 pathology.[21]

8) Experiment - Weak (Insufficient)

This is an area of neglect, but overlaps with the next section as there are several trials of selenium supplementation in other viral diseases, and animal experiments in analogous conditions, and many mechanistic experiments that are non-specific. However the interaction between SARS-CoV-2 and selenoproteins has been confirmed by experiment.[10]

9) Analogy - Strong

Selenium intake is protective, and selenium supplementation has been useful, in other viral illnesses.
However, the protective effect of high selenium intakes before infection in epidemiology appears stronger than the protective effect of selenium as a late intervention in disease.[6, 11]

10) Risk - Weak in short-term, Well-Established in long term.

We can add the most relevant of extra questions to any given set of criteria - "strength of the alternative hypothesis" would be a good one for any lipid hypothesis.
Bradford Hill stated that some interventions are easier to justify than others.

On fair evidence we might take action on what appears to be an occupational hazard, e.g. we might change from a probably carcinogenic oil to a non-carcinogenic oil in a limited environment and without too much injustice if we are wrong. But we should need very strong evidence before we made people burn a fuel in their homes that they do not like or stop smoking the cigarettes and eating the fats and sugar that they do like. In asking for very strong evidence I would, however, repeat emphatically that this does not imply crossing every ‘t’, and swords with every critic, before we act.

With nutrient intakes there is often an identifiable risk, with a J-shaped curve. With selenium the risk is selenosis, which is a condition that requires chronic high exposure (I have given myself mild selenosis with around 900mcg selenium a day and it was not a terrible condition to experience and was reversible). There could be other risks. Luckily we have an experiment that tells us where the limit is.
In a low selenium country, like New Zealand or Denmark, you don't want to take more than 200mcg of extra selenium long term.[12] Pity the low dose arms here weren't retained in the intervention.


During 6871 person-years of follow-up, 158 deaths occurred. In an intention-to-treat analysis
the hazard ratio (95% confidence interval) for all-cause mortality comparing 300 µg selenium/d to placebo was 1.62 (0.66, 3.96) after 5 years of treatment and 1.59 (1.02, 2.46) over the entire follow-up period. The 100 and 200 µg/d doses showed non-significant decreases in mortality during the intervention period that disappeared after treatment cessation. Although we lacked power for endpoints other than all-cause mortality, the effects on cancer and cardiovascular mortality appeared similar.

Howsoever that may be, taking extra selenium above 200mcg per day may yet be advised if one becomes ill with COVID-19,  but an inorganic salt of selenium like sodium selenite (which is anyhow probably safer than the selenomethionine form long-term, as I'll discuss below) is preferable, according to the selenovirus expert, Ethan Will Taylor. 
(this video link does not show in the mobile version of this post but can be reached through the web view option at the bottom)

[Edit: 1/09/20] There is also very good evidence that intravenous high dose selenite is safe in the ICU setting.

Totally 19 RCTs involving 3341 critically ill patients were carried out in which 1694 participates were in the selenium supplementation group, and 1647 in the control. The aggregated results suggested that compared with the control, intravenous selenium supplement as a single therapy could decrease the total mortality (RR = 0.86, 95% CI: 0.78–0.95, P = .002, TSA-adjusted 95% CI = 0.77–0.96, RIS = 4108, n = 3297) and may shorten the length of stay in hospital (MD −2.30, 95% CI −4.03 to −0.57, P = .009), but had no significant treatment effect on 28-days mortality (RR = 0.96, 95% CI: 0.85–1.09, P = .54) and could not shorten the length of ICU stay (MD −0.15, 95% CI −1.68 to 1.38, P = .84) in critically ill patients.[13]

This, and an earlier analysis which found less benefit, did not single out viral illnesses as a subgroup - this is only evidence for safety - but the earlier analysis did find a) slightly lower mortality in trials without an initial bolus dose, b) no increased risk in patients with renal disease.[14]

I will hypothesize briefly on selenium increasing mortality at 300 mcg/day in the Danish intervention study, a dose far too low to cause selenosis.
(The conventional signs of selenosis result from selenocysteine replacing cysteine in proteins, and the relative weakness of the Se-Se bond compared with the S-S bond.)
[Edit - hypothesis improved, 23/09/20]
The question of selenium causing insulin resistance and increasing mortality in high-dose supplements, not mirrored as far as I can see in natural high-dose populations, may have a simple explanation - supplements allow us to consume micronutrients without protein.
If you have no cysteine or methionine coming in when you take Se (either because you're not eating protein, or perhaps it can happen naturally if the Se level is high in a low-protein food and diet) then the selenocysteine formed will be incorporated into all proteins, not just the ones that require it. Including the insulin receptors, which will suffer a relative loss of function.
(similarly, though for different reasons, pyridoxine toxicity can be triggered by supplementing on a low-protein diet)

If we think that insulin resistance causes CVD, then the increased risk from (mostly) natural high Se levels is not great, see fig 5 here [15], but the intervention studies have more alarming results, and I think the competition of selenium- vs sulphur-amino acids in protein fed vs unfed states can explain this. There is next to no evidence of Se toxicity from Brazil nuts, which are high in both Se and protein.

It makes sense to me that selenomethionine, very useful as it will increase selenoprotein levels quickly if you don't have much time, should be replaced with sodium selenite for long-term coverage.

Brazil nuts are a variable quantity, a sample of nuts sold in NZ in 2008 had an average of 19 mcg per nut and increased selenoprotein levels more than selenomethionine.[16]

Plasma selenium increased by 64.2%, 61.0%, and 7.6%; plasma GPx by 8.3%, 3.4%, and -1.2%; and whole blood GPx by 13.2%, 5.3%, and 1.9% in the Brazil nut, selenomethionine, and placebo groups, respectively. Change over time at 12 wk in plasma selenium (P < 0.0001 for both groups) and plasma GPx activity in the Brazil nut (P < 0.001) and selenomethionine (P = 0.014) groups differed significantly from the placebo group but not from each other. The change in whole blood GPx activity was greater in the Brazil nut group than in the placebo (P = 0.002) and selenomethionine (P = 0.032) groups.

[Edit 02/09/20] - thanks to Mike Angell for this link; while all selenium sources are probably protective against death and ongoing harm from COVID-19, only selenite is likely to have an additional antiviral effect, and has low toxicity.[17]

A rational protocol for using selenium in prevention and treatment of COVID-19, fully consistent with the evidence discussed here, is described at the end of this paper:

All scientific work is incomplete - whether it be observational or experimental. All scientific work is liable to be upset or modified by advancing knowledge. That does not confer upon us a freedom to ignore the knowledge we already have, or to postpone the action that it appears to demand at a given time.

Austin Bradford Hill, 1965.


[1] Hill AB. The environment and disease: association or causation? Proc R Soc Med. 1965;58(5):295-300.

[2] Jinsong Zhang, Ethan Will Taylor, Kate Bennett, Ramy Saad, Margaret P Rayman, 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,

[3] Moghaddam, A.; Heller, R.A.; Sun, Q.; Seelig, J.; Cherkezov, A.; Seibert, L.; Hackler, J.; Seemann, P.; Diegmann, J.; Pilz, M.; Bachmann, M.; Minich, W.B.; Schomburg, L. Selenium Deficiency Is Associated with Mortality Risk from COVID-19. Nutrients 2020, 12, 2098.

[4] Yu MW, Horng IS, Hsu KH, Chiang YC, Liaw YF, Chen CJ. Plasma selenium levels and risk of hepatocellular carcinoma among men with chronic hepatitis virus infection. Am J Epidemiol. 1999;150(4):367-374. doi:10.1093/oxfordjournals.aje.a010016

[5] Wang, Y., Xie, D., Li, J. et al. Association between dietary selenium intake and the prevalence of osteoporosis: a cross-sectional study. BMC Musculoskelet Disord 20, 585 (2019).

[6] Bermano, G., Méplan, C., Mercer, D., & Hesketh, J. (2020). Selenium and viral infection: Are there lessons for COVID-19? British Journal of Nutrition, 1-37. doi:10.1017/S0007114520003128

[7] Hidalgo AA, Deeb KK, Pike JW, Johnson CS, Trump DL. Dexamethasone enhances 1alpha,25-dihydroxyvitamin D3 effects by increasing vitamin D receptor transcription. J Biol Chem. 2011;286(42):36228-36237. doi:10.1074/jbc.M111.244061

[8] 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

[9] Martín Giménez, V.M., Inserra, F., Ferder, L. et al. Vitamin D deficiency in African Americans is associated with a high risk of severe disease and mortality by SARS-CoV-2. J Hum Hypertens (2020).

[10] 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

[11] 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

[12] Rayman MP, Winther KH, Pastor-Barriuso R, et al. Effect of long-term selenium supplementation on mortality: Results from a multiple-dose, randomised controlled trial. Free Radic Biol Med. 2018;127:46-54. doi:10.1016/j.freeradbiomed.2018.02.015

[13] 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

[14] 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

[15] Angelica Kuria, Hongdou Tian, Mei Li, Yinhe Wang, Jan Olav Aaseth, Jiajie Zang & Yang Cao (2020) Selenium status in the body and cardiovascular disease: a systematic review and meta-analysis, Critical Reviews in Food Science and Nutrition, DOI: 10.1080/10408398.2020.1803200

[16] Thomson CD, Chisholm A, McLachlan SK, Campbell JM. Brazil nuts: an effective way to improve selenium status. Am J Clin Nutr. 2008;87(2):379-384. doi:10.1093/ajcn/87.2.379

[17] Kieliszek M, Lipinski B. Selenium supplementation in the prevention of coronavirus infections (COVID-19) [published online ahead of print, 2020 May 24]. Med Hypotheses. 2020;143:109878. doi:10.1016/j.mehy.2020.109878

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

[19] 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

Chen Dun, Christi M. Walsh, Sunjae Bae, Amesh Adalja, Eric Toner, Timothy A. Lash, Farah Hashim, Joseph Paturzo, Dorry L. Segev, Martin A. Makary. A Machine Learning Study of 534,023 Medicare Beneficiaries with COVID-19: Implications for Personalized Risk Prediction.
medRxiv 2020.10.27.20220970; doi:

[21] 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

Thursday, 2 July 2020

A Reading List, and I Shill for a New Cookbook

It's been a time for reading lists; in lockdown I enjoyed discovering the books of T.H. White (The Goshawk and The Age of Scandal) and Evan S. Connell (Mrs Bridges) and reading Hillary Mantel's memoir (Giving Up the Ghost).
Sam Kriss also has a great reading list in Damage magazine, which features some of the best political writing I've read in ages - kind of a Leftist Spectator, if you get my drift, i.e. an honest journal, in a time when honesty is a rare and dangerous thing.

This is a reading list I compiled for PreKure a while back, of books most worth reading if you're interested in the nutrition-and-health ideas this blog has covered over the years.

The Perfect Health Diet, Paul and Shou-Ching Jaminet, 2012

This was one of the first “Paleo” books I read and, in my opinion, still one of the best. There are all sorts of sensible ideas, lots of references, and it’s not exclusively low carb. Some of their theoretical objections to keto diets haven’t come to much, and can be taken with a grain of salt, but there’s so much of value here to compensate. As far as population health goes, this is a clever and coherent interpretation of the evidence.

The Daughter of Time, Josephine Tey, 1951

This amusing 1950’s British detective story is a “research thriller”. The action, such as it is, takes place in a hospital bed as an injured detective sends his friends to libraries in search of the evidence in the case of a well-known historical mystery. Tey’s genius, and the lasting appeal of this book (Christopher Hitchens called it one of the most important ever written) is to show us how the most cherished received beliefs can be based – if we look closely – on lies and hearsay, the suppression of evidence, and self-serving propaganda. (*cough* saturated fat *cough*) And when Tey’s detective comes around to her alternative hypothesis, he oversells it – we suspect the author’s bias by now, and already know the evidence is too corrupt to accept; so its very flaws help to make this book perfect. If you want to inoculate young adults against fake news without getting mired in any modern controversies, convince them to read The Daughter of Time.

Foods of the Foreign Born in Relation to Health, Bertha M. Wood, 1922

Wood was a US dietitian and wrote this book at a time when the US was receiving migrants and refugees from all over Europe, as well as Mexico and the Middle East; some had brought political terrorism with them, xenophobia was if anything more extreme than it is today, and in this climate Wood wanted to familiarise nursing and dietetic students with the variety of immigrant diets so that they could help these populations in what we would today call a culturally appropriate manner. Thanks to her research we can learn about the real Mediterranean diets of 100 years ago, and that Hungarians gave children whiskey instead of milk on their cereal. A feature of this book is that Wood tells us how to adapt each population’s diet for diabetics by removing the starchy carbs. Foods of the Foreign Born is available free online at

. Mathews, van Holde, Ahern. 3rd edition. 2000.

This is a second-hand biochemistry textbook. I recommend older editions like this, which you can sometimes find in op shops, because they give less space to the biochemistry of the genome, which isn’t useful information if you’re interested in nutrition, and thus have more nuts-and-bolts detail than whatever they’re selling today. It also says on page 841 that “Adult onset diabetes can often be controlled by dietary restriction of carbohydrate”. Only experts in biochemistry were allowed to tell us something that simple and true in 2000 - the rest of the world back then only cared about saturated fat and felt that the Mediterranean Diet was quite daring.

This book is, amongst other things, your essential guide to what functions vitamins and minerals really perform in the body. Disclaimer – I understand few of the many mathematical formulas in this book that are an essential part of a real biochemistry education, but enjoyed this book nonetheless, making especial use of the index.

The Meat Fix: How a Lifetime of Healthy Living Nearly Killed Me! John Nicholson, 2012

This is a light, funny read by a UK sports journalist who wrecked his gut and metabolic health by trying to be a good vegetarian. I recommend it as a consumer’s eye view of the path many are on today, and also an insight into what popular low-carb science looks like to an ordinary convert – a bit pseudoscientific from our perspective, but still thoroughly effective.

And, of course, The Big Fat Surprise (Nina Teicholz) and Why We Get Fat (Gary Taubes) – these are the books that best explain how we got to where we are today.

Now, I've never run advertising on this blog. I did try at one stage, when I ran out of money, but Google weren't interested. Their loss, my escape.

However, given a chance to sell out in a good cause, in a time when paid work ain't what it used to be, I've leapt at it.

Ally Houston from PaleoCanteen has written "Low Carb on a Budget" with chef John Meechan and this is the book I've long meant to write but never had time for.
Lower income people are most likely to suffer from the conditions for which low carb is the specific cure, from metabolic syndrome to obesity to type 2 diabetes to depression, anxiety and chronic pain.
Yet low-carb cookbooks are often written by foodies and include a wide variety of expensive, hard to find, and - not to put too fine a point on it - unnecessary - ingredients. Even without these, there is still some extra cost over white bread, sugar, margarine and processed meat, but nothing you won't soon make back from your dentist, doctor, pharmacy and snack bills.
Low Carb on a Budget gets high praise from those most worth listening to in the UK diet-and-public health debate; if you don't know the names of some of those praising it, check out their work.
Another great selling point is that I'll get a pound, whatever that is, for every copy sold through the link above, and the  Public Health Collaboration, a very effective lobby group in the UK, will get 50p.

Wednesday, 27 May 2020

My Letter to Cochrane on the Hooper 2020 saturated fat meta

I submitted this on the Cochrane form at

Others will have points to add about study quality and other factors, I have stuck to what I know (not wanting to waste my life battling an opponent who can obviously be reanimated an unlimited number of times).

The introduction to this meta-analysis includes an error uncorrected from the 2015 version.

Oliver 1953 measured total cholesterol, not LDL cholesterol. Further, it is relevant that every subject in Oliver 1953 had been eating the same hospital diet for at least 5 weeks before the cholesterol samples were taken, which does not support a diet-heart interpretation of the results.[1] (The presence of FH in the sample, and/or survivorship bias, are probably more reasonable interpretations)

[1] The Plasma Lipids in Coronary Artery Disease. Oliver MF, Boyd GS. Br Heart J. 1953 Oct;15(4):387-92. 

The section headed "Agreements and disagreements with other studies or reviews" has not addressed any written after 2014, meaning that this section has not been updated. There are several analyses of the diet heart trials since 2015 that should have been addressed (indeed, that should have been read before the current Cochrane review was designed). Some are listed below.[2,3.4]

[2] Hamley, S. The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials. Nutr J 16, 30 (2017).

[3] Thornley S, Schofield G, Zinn C, Henderson G. How reliable is the statistical evidence for limiting saturated fat intake? A fresh look at the influential Hooper meta-analysis. Intern Med J. 2019;49(11):1418‐1424. doi:10.1111/imj.14325

[4] Jeffery L Heileson, Dietary saturated fat and heart disease: a narrative review, Nutrition Reviews, Volume 78, Issue 6, June 2020, Pages 474–485,

The discussion of Siri-Tarino 2010 in "Agreements and disagreements with other studies or reviews" claims that adjustment for lipids has confounded its null result, however Siri-Tarino at al had already addressed this by isolating studies not adjusted for lipids with no difference in their null result. This is quite understandable as adjusting for lipids also means adjusting for TG and HDL, cardiometabolic risk markers which can be beneficially infuenced by saturated fat and worsened by carbohydrate.
Studies which do not adjust for lipids can be favourable to saturated fat, for example the Malmo DCS, a high-quality observational study using a 7-day food diary and more rigorous exclusion criteria than is usual, or the 2019 dose-response meta-analysis of observational studies by Zhe et al.[5,6]

[5] Leosdottir M, Nilsson PM, Nilsson JA, Månsson H, Berglund G. Dietary fat intake and early mortality patterns--data from The Malmö Diet and Cancer Study. J Intern Med. 2005;258(2):153‐165. doi:10.1111/j.1365-2796.2005.01520.x

[6] Zhu, Y., Bo, Y. & Liu, Y. Dietary total fat, fatty acids intake, and risk of cardiovascular disease: a dose-response meta-analysis of cohort studies. Lipids Health Dis 18, 91 (2019).

The claim that greater lowering of LDL in trials being associated with greater reduction of events supports the diet-heart hypothesis may be unsound. Persons in good metabolic health are at significantly lower risk of CVD events despite other risk factors.[7] Persons who are obese, have diabetes, or the metabolic syndrome do not usually experience drops in LDL cholesterol when fat in the diet is changed; the subjects in the feeding studies cited, who did experience such drops, were healthy volunteers.[8,9,10]

[7] Jeppesen J, Hein HO, Suadicani P, Gyntelberg F. Low triglycerides-high high-density lipoprotein cholesterol and risk of ischemic heart disease. Arch Intern Med. 2001;161(3):361‐366. doi:10.1001/archinte.161.3.361

[8] Flock MR, Green MH, Kris-Etherton PM; Effects of Adiposity on Plasma Lipid Response to Reductions in Dietary Saturated Fatty Acids and Cholesterol, Advances in Nutrition. 2011;2,(3):261–274,

[9] Benatar JR, Sidhu K, Stewart RAH. Effects of High and Low Fat Dairy Food on Cardio-Metabolic Risk Factors: A Meta-Analysis of Randomized Studies. Tu Y-K, ed. PLoS ONE. 2013;8(10):e76480. doi:10.1371/journal.pone.0076480.

[10] Lefevre M, Champagne CM, Tulley RT,et al. Individual variability in cardiovascular disease risk factor responses to low-fat and low-saturated-fat diets in men: body mass index, adiposity, and insulin resistance predict changes in LDL cholesterol. Am J Clin Nutr. 2001;82(5):957–963,

It is also relevant that from 2004 the Swedish population began to reject diet-heart advice, to such an extent that butter sales rose and margarine sales dropped; cholesterol levels also rose.[11] Yet as recently as 2018 mortality from, and incidence of, AMI was continuing to decline in Sweden. In fact incidence of AMI had stayed stable from 1987 to 2005, after which it began to drop from 42,263 PA to 25,789 PA in 2018.[12]

[11] Johansson I, Nilsson LM, Stegmayr B, Boman K, Hallmans G, Winkvist A. Associations among 25-year trends in diet, cholesterol and BMI from 140,000 observations in men and women in Northern Sweden. Nutr J. 2012;11:40.

[12] Data accessed from Swedish Social Registry website 28/05/20