Selenium reduces COVID-19 risk - a back-of-the-envelope Bradford Hill analysis [originally posted 28/09/20, last updated 13/06/22]

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.

a) 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]

b) 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]

c) 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.

d) In regression models, serum Se levels were inversely associated with lung damage independently of other markers of disease severity, anthropometric, biochemical, and hemostatic parameters.[23]

e) The association between soil Se level and the incidence of COVID-19 was observed in different cities of Hubei Province. The incidence of COVID-19 was more than 10 times lower in Se-enriched cities (Enshi, Shiyan, and Xiangyang) than in Se-deficient cities (Suizhou and Xiaogan).[25]

See also refs 19 and 22, discussed below.

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 13/06/2022] - New study from the USA shows a two-fold higher mortality rate in low-selenium regions.[30]
Discussed in more detail on my Patreon blog - the only way I make any part of a living from this work, so help a brother out!

[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]

Statistically significant and often very strong associations between selenium intake, selenium status, and various COVID-19 outcomes have been reported from China, South Korea, Germany, South India, Russia and Europe. No null association has yet been reported.

Rigorous re-analysis of updated Chinese pandemic data published recently confirms the original observations, this time using the case-fatality rate:

A total of 147 cities each reporting over 20 cases were included in the current analysis. In these cities, 91% (14,045) of total cases and 85.8% (103) of total mortality from COVID-19 in China had been reported.
Totally, 14,045 COVID-19 cases were reported from 147 cities during 8 December 2019–13 December 2020 were included. Based on selenium content in crops, the case fatality rates (CFRs) gradually increased from 1.17% in non-selenium-deficient areas, to 1.28% in moderate-selenium-deficient areas, and further to 3.16% in severe-selenium-deficient areas (P = 0.002). Based on selenium content in topsoil, the CFRs gradually increased from 0.76% in non-selenium-deficient areas, to 1.70% in moderate-selenium-deficient areas, and further to 1.85% in severe-selenium-deficient areas (P < 0.001). The zero-inflated negative binomial regression model showed a significantly higher fatality risk in cities with severe-selenium-deficient selenium content in crops than non-selenium-deficient cities, with incidence rate ratio (IRR) of 3.88 (95% CIs: 1.21–12.52), which was further confirmed by regression fitting the association between CFR of COVID-19 and selenium content in topsoil, with the IRR of 2.38 (95% CIs: 1.14–4.98) for moderate-selenium-deficient cities and 3.06 (1.49–6.27) for severe-selenium-deficient cities.[24]

UPDATE 23/11/2021

A recent review of in-hospital selenium data shows consistent associations between lower Se and adverse outcomes in 9/10 comparisons where the population selenium level is below the optimal range of 130-150 mcg/dL. The outlier is an n=9 study (the smallest) in which length of hospital stay is the outcome and supplementation during the stay may be a confounder. In the one study where Se went over the optimal range a higher Se was found in more severe cases.[26]

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]



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 Strong

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. The effects of selenium and selenite align to support the associational results across multiple mechanisms.


7) Coherence - Very Strong

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 (Neglected)

This is an area of sufficient neglect to make you despair about medical humanity, if you know that there have been thousands of trials of potentially useless drugs for COVID-19 already. However this criteria 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. The interaction between SARS-CoV-2 and selenoproteins has been confirmed by experiment.[10]

UPDATE 23/11/15

This team in Wuerzburg Germany have ben steadily researching selenium in COVID-19 patients in ICU and have got to the stage of testing an intervention.

There's no control arm but we have proof of safety for 1mg sodium selenite and proof of concept in that people in whom the intervention raised SelenoP did better.

We don't yet know that this effect isn't an artifact of disease severity, but such careful work brings the needed RCT closer.

"According to intensive care unit (ICU) standard operating procedures, patients received 1.0 mg of intravenous Se daily on top of artificial nutrition, which contained various amounts of Se and Zn. Micronutrients, inflammatory cytokines, lymphocyte subsets and clinical data were extracted from the patient data management system on admission and after 10 to 14 days of treatment. Forty-six patients were screened for eligibility and 22 patients were included in the study. Twenty-one patients (95%) suffered from severe ARDS and 14 patients (64%) survived to ICU discharge. On admission, the majority of patients had low Se status biomarkers and Zn levels, along with elevated inflammatory parameters. Se supplementation significantly elevated Se (p = 0.027) and selenoprotein P levels (SELENOP; p = 0.016) to normal range. Accordingly, glutathione peroxidase 3 (GPx3) activity increased over time (p = 0.021). Se biomarkers, most notably SELENOP, were inversely correlated with CRP (rs = −0.495), PCT (rs = −0.413), IL-6 (rs = −0.429), IL-1β (rs = −0.440) and IL-10 (rs = −0.461). Positive associations were found for CD8+ T cells (rs = 0.636), NK cells (rs = 0.772), total IgG (rs = 0.493) and PaO2/FiO2 ratios (rs = 0.504). In addition, survivors tended to have higher Se levels after 10 to 14 days compared to non-survivors (p = 0.075). Sufficient Se and Zn levels may potentially be of clinical significance for an adequate immune response in critically ill patients with severe COVID-19 ARDS.[27]

In comparison to patients with a fatal outcome (n = 8), survivors (n = 14) significantly responded to supplementation with an increase in Se (p = 0.008), SELENOP (p = 0.004), GPx3 (p = 0.039) and Zn levels (p = 0.020) over the course of the ICU stay (Figure 5). Decedents had a median ICU course of 17.5 days (12–22), whereas patients with a favorable outcome were treated for significantly longer (40 days, 20–44; p = 0.025)."

There are also two tests of mixtures including selenium for COVID-19 with favourable results, the first is a survey of a clinic's patients already taking selenium, zinc, and vitamin D for  Hasimoto's thyroiditis.[28]

After adjusting for age, gender, BMI, smoking status, we found an association between the absence of supplements and the risk of hospitalization, and invasive mechanical ventilation. Patients with Hashimoto’s thyroiditis who had COVID-19 infection and who had previously taken supplements such as selenium, zinc, and vitamin D had milder clinical outcomes, or no symptoms compared to those who did not receive supplements who had a moderate or severe outcome (P <0.05)

The next is an RCT from the South Indian doctors cited earlier, of a mixed supplement supplying 40 mcg selenium (a very modest dose in this context, but not insignificant), n=100.[29]


ImmuActiveTM 500 mg capsule containing curcuminoids (100 mg), andrographolides (50 mg), resveratrol (50 mg), zinc (10 mg), selenium (40 mcg), and piperine (3 mg) or placebo was administered orally to subjects once daily after breakfast.

Results. The ordinal scale at the end of the study was significantly lower in COVID-19 patients supplemented with ImmuActive (0.57) than placebo (1.0), with a  value of 0.0043. The ordinal scale decreased by one unit within 2.35 days in ImmuActive-supplemented patients, while it took 3.36 days in placebo-supplemented patients. Days of hospitalization and time required to turn RT-PCR negative were comparatively lower in the ImmuActive arm than the placebo arm. Change in modified Jackson’s Symptom Severity Score and COVID-19 QOL were significant from screening to the end of the study in both ImmuActive and placebo arms. There were no adverse events observed during the study period.

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]



Those are the nine canonical Bradford Hill criteria. The discussion about selenium suggests that an ad hoc 10th criteria will also be useful:

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.[1]

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:
https://www.frontiersin.org/articles/10.3389/fnut.2020.00164/full

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.

References:

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

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1898525/pdf/procrsmed00196-0010.pdf

[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, https://doi.org/10.1093/ajcn/nqaa095

[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). https://doi.org/10.1186/s12891-019-2958-5

[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
https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/selenium-and-viral-infection-are-there-lessons-for-covid19/BE3AC78D5C92725BE83C4E474ECBB548

[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). https://doi.org/10.1038/s41371-020-00398-z

[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

https://www.researchgate.net/publication/343365020_SARS-CoV-2_suppresses_mRNA_expression_of_selenoproteins_associated_with_ferroptosis_ER_stress_and_DNA_synthesis

[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  https://www.tandfonline.com/doi/full/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
https://academic.oup.com/ajcn/article/87/2/379/4633360

[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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7246001/

[18] Im, JH et al. Nutritional status of patients with coronavirus disease 2019 (COVID-19) Int J Infectious Diseases, August 11, 2020
https://www.ijidonline.com/article/S1201-9712(20)30647-0/fulltext

[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
https://www.sciencedirect.com/science/article/pii/S0899900720303361

[20] 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: https://doi.org/10.1101/2020.10.27.20220970

[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

[22] Raban Arved Heller, Qian Sun, Julian Hackler, Julian Seelig, Linda Seibert, Asan Cherkezov, Waldemar B. Minich, Petra Seemann, Joachim Diegmann, Maximilian Pilz, Manuel Bachmann, Alireza Ranjbar, Arash Moghaddam, Lutz Schomburg,

Prediction of survival odds in COVID-19 by zinc, age and selenoprotein P as composite biomarker, Redox Biology, Volume 38, 2021, 101764,

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574778/

[23] Skalny AV, Timashev PS, Aschner M, et al. Serum Zinc, Copper, and Other Biometals Are Associated with COVID-19 Severity Markers. Metabolites. 2021;11(4):244. Published 2021 Apr 15. doi:10.3390/metabo11040244
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8071197/

[24] Zhang, HY., Zhang, AR., Lu, QB. et al. Association between fatality rate of COVID-19 and selenium deficiency in China. BMC Infect Dis 21, 452 (2021). https://doi.org/10.1186/s12879-021-06167-8

[25] Liu Q, Zhao X, Ma J, et al. Selenium (Se) plays a key role in the biological effects of some viruses: Implications for COVID-19. Environ Res. 2021;196:110984. doi:10.1016/j.envres.2021.110984
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[26] Fakhrolmobasheri, M., Mazaheri-Tehrani, S., Kieliszek, M. et al. COVID-19 and Selenium Deficiency: a Systematic Review. Biol Trace Elem Res (2021). https://doi.org/10.1007/s12011-021-02997-4
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[27] Notz, Q.; Herrmann, J.; Schlesinger, T.; Helmer, P.; Sudowe, S.; Sun, Q.; Hackler, J.; Roeder, D.; Lotz, C.; Meybohm, P.; Kranke, P.; Schomburg, L.; Stoppe, C. Clinical Significance of Micronutrient Supplementation in Critically Ill COVID-19 Patients with Severe ARDS. Nutrients 2021, 13, 2113.
https://doi.org/10.3390/nu13062113

[28]  Zelija Velija Asimi, Almira Hadzovic-Dzuvo, & Djinan Al Tawil. Selenium, zinc, and vitamin D supplementation affect the clinical course of COVID-19 infection in Hashimoto’s thyroiditis. Presented ePosters 14: COVID-19 Endocrine Abstracts (2021) 73 PEP14.2 | DOI: 10.1530/endoabs.73.PEP14.2

https://www.endocrine-abstracts.org/ea/0073/ea0073pep14.2

[29] Muhammed Majeed, Kalyanam Nagabhushanam, Kalpesh Shah, Lakshmi Mundkur, "A Randomized, Double-Blind, Placebo-Controlled Study to Assess the Efficacy and Safety of a Nutritional Supplement (ImmuActiveTM) for COVID-19 Patients", Evidence-Based Complementary and Alternative Medicine, vol. 2021, Article ID 8447545, 9 pages, 2021. https://doi.org/10.1155/2021/8447545

[30] JinsongZhanga, EthanWill Taylorb, KateBennett, Margaret P. Rayman. Does atmospheric dimethyldiselenide play a role in reducing COVID-19 mortality? 

Gondwana Research, Available online 6 June 2022 https://doi.org/10.1016/j.gr.2022.05.017

Yes, but, what will you do when the Covid comes?

This post was originally published on Patreon. You don't have encourage the speculations of the likes of me, but if you want to try, please subscribe!   Every day on NZ twitter people are debating what they would do were they the Government about vaccine roll-outs, MIQ, lockdowns, DJ's, and any other thing they can think of that they have absolutely no influence over.

Maybe, like me, you're double-chipped, using the app, wearing the mask, and annoying AF. Maybe you're even boostered up the wazoo. Well done. But y'know what? You're probably going to catch covid. Even if you don't, someone you care about is going to, even if you no longer care about the unvaccinated except as targets of your spite.

And yet, what no-one is talking about, or better yet arguing about in order to straighten out, is what they're doing now to reduce their risk of taking up hospital space when that happens, and what they're going to do to make themselves feel better once they get sick.

The good news is that the symptoms of Omicron are basically flu symptoms - scratchy throat, muscle ache, fatigue, night sweats, no loss of smell of taste. These, apart from the cough, were basically the second shot vax effects for many people. And even for those hospitalised, the average stay is 4 days vs 8 days with Delta. But why go to hospital at all if you can help it? Some people - morons, mostly - posit a false dichotomy between government policy and personal responsibility. But in every area, these are on completely different planes and complement each other. You taking responsibility for your health eases the pressure on a government trying to help those unfortunates who can't or won't.

So without further ado, as they say in places where there is an oversupply of further ado, here are the things I do.

Firstly, I exercise regularly and keep the sugar, seed oil, and refined starch real low; another way of saying this is that I eat whole food (of the cheapest sort, e.g. eggs, mince, the fruit and vege in season), play frisbee or swim every day, and walk the dog. I get as much sun as I can handle, and will take vitamin D in winter, or after a while during the prolonged cloudy weather typical of much of NZ.

Secondly, I eat a little sauerkraut or yoghurt with my meals, or take a cheap probiotic.

Thirdly, I take some supplements - Clinicians Selenium drops (Sodium Selenite), around 150 mcgs (three drops) a day, and x4 if I think I'm coming down with an RNA virus. This works out at around $17 a year. The cheapest Zinc tabs from chemist warehouse, one a day, but mostly when exposure is likely.  The cheapest chelated magnesium in the supermarket, 150 mg, most days (but I was taking this already).

If I get sick or obviously exposed, I'll increase the selenium drops to 300mcg 2x daily and take Sanderson's ViraMax, a mixture of elderberry (great, works for flu), echinacea, (great, works for cold), olive leaf extract (olive leaf extract has never worked for me, ever), and andrographis (works very well for all viral respiratory infections, but has a rare side-effect risk of liver damage, probably in people with compromised antioxidant defenses). When I had the RSV last year this combo eliminated symptoms so quickly I wondered if I'd just imagined coughing, sneezing and snotting all over the place on the first day.

Maybe you have different ideas? Please discuss them here or in a public forum. More:
https://www.newsroom.co.nz/readingroom/book-of-the-week-will-salad-cure-covid

My review of selenium, probiotics and vitamin D for COVID-19, meat for mental health, and LCHF for diabetes reversal in MSM

Greetings readers!

Every so often I am asked to review new or best-selling books related to diet for Newsroom and am encouraged by the Reading Room editor Steve Braunias, a very fine writer indeed, not to hold back.

Here's my "review" of two books on vegetables, which is mostly on the role of selenium, probiotics, and vitamin D in the Covid pandemic, as well as the value of meat in the preservation of mental health, and the promise of LCHF, keto and fasting diets for type 2 diabetes remission.

The more clicks and readers it gets, the more chance I'll have of presenting these types of ideas in mainstream media forums in future.

https://www.newsroom.co.nz/readingroom/book-of-the-week-will-salad-cure-covid

Virta Health vs Seidelmann - of ketones and COVID-19

You would have seen this paper; senior author is Sara Seidelmann of the infamous "low carb kills" paper, the reviewers were one vegan propagandist David Jenkins (a friend of the family, so to speak) and an Iranian prof with a decent publications list in the plant-based area - neither with any infectious diseases expertise.

There were 568 COVID-19 cases and 2316 controls. Among the 568 cases, 138 individuals had moderate-to-severe COVID-19 severity whereas 430 individuals had very mild to mild COVID-19 severity. After adjusting for important confounders, participants who reported following ‘plant-based diets’ and ‘plant-based diets or pescatarian diets’ had 73% (OR 0.27, 95% CI 0.10 to 0.81) and 59% (OR 0.41, 95% CI 0.17 to 0.99) lower odds of moderate-to-severe COVID-19 severity, respectively, compared with participants who did not follow these diets. Compared with participants who reported following ‘plant-based diets’, those who reported following ‘low carbohydrate, high protein diets’ had greater odds of moderate-to-severe COVID-19 (OR 3.86, 95% CI 1.13 to 13.24). No association was observed between self-reported diets and COVID-19 infection or duration.

you'll find good criticisms in the rapid responses attached, and my PubPeer comment here.

 The methods state 
Lastly, we combined ‘low carbohydrate’ diets and ‘high protein’ diets into another category (‘low carbohydrate, high protein diet’, n=483) to evaluate whether these dietary patterns are associated with COVID-19 severity.

Why? No reason is given for combining these 2 categories. 

There was a keto option, so why didn't they add keto + low carb?

Methods state
Before analyses, we selected dietary patterns with sufficient ‘yes’ responses (‘yes’ response of at least 100 individuals). To increase precision, we analysed three dietary patterns after combining dietary patterns that are similar in terms of dietary intake.

Perhaps keto had less that 100 responses? But there was no registered protocol, those decisions were post-hoc - even if keto had fewer than 100 responses, adding it would have still increased numerical power, which was presumably the point of combining categories as they did. And there's nowhere it says how many responses, and we also have no way of knowing how similar low carb and high protein really were (everything was pretty similar really, these were for most respondents just the virtue-signaling labels they gave to their eating habits).

Anyway, there was no association once people with a negative or no PCR test were excluded.
That's not in the abstract.

But, you know, people are using the keto and LCHF diets to treat diabetes and reduce COVID19 mortality associated with type 2 diabetes, MetSyn, or obesity, so this is a nasty thing to say if it's not true. It's a bit like trying to get people to stop taking vaccines based on your bias and some shit you didn't understand.

Fortunately Vitra Health have ridden to the rescue with a survey of their own T2D population on a ketogenic diet. We know these people are actually following the diet, or adhering closely to it.

The abstract (presented at an ADA conference) is 
COVID-19 Severity in a Geographically Diverse, U.S.-based, Ambulatory Population with Type 2 Diabetes on a Medically Supervised Ketogenic Diet

Data were obtained from medical records and from surveys sent to T2D patients who self-reported COVID-19 diagnosis; 47.8% (294/614) responses and one known COVID-related death yielded a sample of 295 (50% male, 54±9 years, across 41 US states). We observed low reported rates of hospitalization (10.9%), ventilation (2.0%), and death (0.3%) relative to national reports.
Let's compare with the Seidelmann paper - 1) we know the diet is real. 2) COVID-19 is self-reported (some will have tests some not, as in Seidelmann) but - we do have people being hospitalised, unlike Seidelmann, and we even have one death, so Virta are able to capture events that people weren't able to report directly, because their model includes liaison with primary providers likely to report deaths to them. 3) the event rates are low for a population with type 2 diabetes, as shown by the comparison with this population. The populations, though much the same age, aren't identical, but the biggest difference seems to long term inclusion in the Virta Health population (note the "baseline" HbA1c data in Virta - before treatment with the ketogenic diet - is similar to the overall HbAic data in the comparator vs standard practice, but many of the Virta Health population have put their T2D in remission. At this stage, we have to say that the EFFECTS of the keto program are protective - weightloss and euglycaemia, etc. We don't have evidence that keto per se is protective apart from those factors. But that may well be hidden in the data, once the whole set is fully written up. But once again, it looks like Harvard is a bad actor, an ill informant in the nutrition-and-health space, interfering with effective treatments to preserve its own ill-gotten (by a process of bloviation if not graft) dietary hegemony.

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.

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.