Response to a BMJ article which did not make it past there Disqus-based moderation system

This is an outrigger page from a particular part of the main page cv19/#uk-bame  .  Below is the response I wrote to this article:

Inequality in our ethnic minorities: we must act before the next pandemic
Dipesh P Gopal and Sonia Adesara BMJ Opinion 2020-06-02

Robin Whittle .   2020-06-07

To the main COVID-19 page of this site:
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An important and easily-modifiable risk factor for COVID-19 severity and death is low vitamin D levels.  Vitamin D deficiency is widespread in Ireland and the UK, and the BAME community is at even higher risk. 

Please see the research from the Philippines ( and Indonesia ( Both show that these risks are much higher for people whose 25OHD levels are less than 30ng/ml (75nmol/L) compared to those with higher levels.

Kawasaki disease has been recognised for 50 years and most doctors and researchers regard its etiology as being due to a viral or bacterial trigger combined with other factors which remain elusive, but which are generally believed to be genetic. Yet they note its prevalence, in Paris, among dark-skinned children (, its correlation with winter and early spring ( , and the involvement of an exaggerated inflammatory response.  Of the 15 articles I found concerning COVID-19 and Kawasaki disease 9 mentioned inflammation. None of these articles mentioned vitamin D, despite vitamin D deficiency being a very well known cause of weak and dysregulated, overly-aggressive, pro-inflammatory immune responses (

2016 research from Italy:

Severe vitamin D deficiency in patients with Kawasaki disease: a potential role in the risk to develop heart vascular abnormalities?
Stefano Stagi et al. Clinical Rheumatology volume 35, pages 1865–1872 (2016)

shows that children with Kawasaki disease had very low 25OHD levels: 9.2ng/ml compared to 23.3ng/ml for age-matched healthy controls.  Those children who developed coronary artery abnormalities averaged 4.9ng/ml. These averages are 20% to 11% of the 46ng/ml average of African herders and hunter gatherers: .

It is easy to understand vitamin D deficiency, combined with genetic and probably other nutritional factors, causing such weakened and dysregulated immune response that COVID-19 triggers Kawasaki disease in children and severe lung inflammation, followed by a hypercoagulative state in adults: and

While there may be some parallel causation (unseen factors driving both disease severity and vitamin D deficiency) and perhaps some reverse causation (if it could be shown that inflammatory diseases significantly lower 25OHD levels) these considerations are minor compared to the surely largely causative relationship between low vitamin D levels and weakened and excessively inflammatory immune responses.

It is more difficult to understand why most doctors and researchers remain unaware this 2016 Italian research.  Likewise, few seem to be aware of the Philippino and Indonesian research.

There has long been a need to raise everyone's 25OHD to at least 30ng/ml - aiming for 40 to 60ng/ml - to ensure strong and well-regulated immune responses and so to protect against a plethora of chronic illnesses, including MS, neurodegeneration, diabetes etc.  With COVID-19 threatening to infect most people in the months to come, there is an urgent need for robust vitamin D supplementation to prevent the current pattern of harm and death.  This is unlikely to occur until most doctors recognise the need for this.

Yet, in a widely reported article Susan Lanham-New and twenty colleagues support the UK standards for vitamin D3 supplementation (400IU/day for adults) and its aim for most of the population to have more than 10ng/ml 25OHD. This is 1/3 of the level reported by Philippino and Indonesian researchers as an apparent threshold of relative safety.

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