Dr. Weeks’ Comment: Let’s simplify all this talk about COVID-19: What kills people with COV-19 – an acute respiratory distress syndrome (ARDS) – is hyper inflammation. “patients with severe COVID-19 might have a cytokine storm syndrome“. It is the hyper inflammation which kills: “hyperinflammatory syndrome characterised by a fulminant and fatal hypercytokinaemia with multiorgan failure”. The recommendation as regards screening people at risk involves checking for inflammation: “All patients with severe COVID-19 should be screened for hyperinflammation using laboratory trends (eg, increasing ferritin, decreasing platelet counts, or erythrocyte sedimentation rate)”

So putting aside all the hysteria, we see clearly that COVID-19 is dangerous primarily because of excessive inflammation so one we see that, let’s ask “What is the most logical treatment protocol? An expensive, entirely experimental, dangerous guess at a vaccination? No. Think! To optimize your survival, you simply need to reduce inflammation in order to prevent developing problems with COVID-19. Reducing inflammation with also reduce the danger once you learn that you are testing positive for COVID-19. The mortality rate is less that 4% – huge yes! (the yearly influenza is 1%), but you just learned that currently – of all the people who get serious symptoms of COVID-19, a huge % 96 to be exact out of 10o people survive and recover.

Now you also understand that the difference between life and death once infected is simply your ability to lower your experience of inflammation. What is sensible now is, of course, to minimize your chances of being exposed to COVID-19 … (social distancing!)… but more importantly, to eat the anti-inflammatory diet and specifically to eat powerful organic, anti-inflammatory seeds which are 1) nutrient dense in order to give your physician within all the tools it needs to survive and thrive (Did you know that seeds concentrate nutrients 20-30x more than the fruit or vegetable it grew in?), 2) Synergistic anti-inflammatory seeds (black cumin, raspberry. grape), 3) get the cellular debris and metabolic junk out with Detoxifying seeds with alkalinizing greens: milk thistle seed , cranberry seed and black cumin seed) .

Also: stop handicapping your body by eating inflammatory foods like dairy, sugar, alcohol, whey and instead, why not help your body help you? You need to drink plenty of good quality water (no fluoride and chloride) and supplement with the essential elements of a corrective approach to COVID. We recommend high quality zinc, vitamin A palmitate, methylselenocysteine and the other 7 essential remedies.

Remember to KISS…. keep it simple silly! Here is what the article below tells is in plain English “mortality might be due to virally driven hyperinflammation.” Eat the seeds!

COVID-19: consider cytokine storm syndromes and immunosuppression

• Puja Mehta et al
• SOURCE The Lancet… https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30628-0/fulltext?rss=yes

As of March 12, 2020, coronavirus disease 2019 (COVID-19) has been confirmed in 125 048 people worldwide, carrying a mortality of approximately 3·7%,¹ compared with a mortality rate of less than 1% from influenza. There is an urgent need for effective treatment. Current focus has been on the development of novel therapeutics, including antivirals and vaccines. Accumulating evidence suggests that a subgroup of patients with severe COVID-19 might have a cytokine storm syndrome. We recommend identification and treatment of hyperinflammation using existing, approved therapies with proven safety profiles to address the immediate need to reduce the rising mortality.Current management of COVID-19 is supportive, and respiratory failure from acute respiratory distress syndrome (ARDS) is the leading cause of mortality.² Secondary haemophagocytic lymphohistiocytosis (sHLH) is an under-recognised, hyperinflammatory syndrome characterised by a fulminant and fatal hypercytokinaemia with multiorgan failure. In adults, sHLH is most commonly triggered by viral infections³ and occurs in 3·7–4·3% of sepsis cases.⁴ Cardinal features of sHLH include unremitting fever, cytopenias, and hyperferritinaemia; pulmonary involvement (including ARDS) occurs in approximately 50% of patients.⁵ A cytokine profile resembling sHLH is associated with COVID-19 disease severity, characterised by increased interleukin (IL)-2, IL-7, granulocyte-colony stimulating factor, interferon-γ inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α, and tumour necrosis factor-α.⁶ Predictors of fatality from a recent retrospective, multicentre study of 150 confirmed COVID-19 cases in Wuhan, China, included elevated ferritin (mean 1297·6 ng/ml in non-survivors vs 614·0 ng/ml in survivors; p<0·001) and IL-6 (p<0·0001),² suggesting that mortality might be due to virally driven hyperinflammation.

As during previous pandemics (severe acute respiratory syndrome and Middle East respiratory syndrome), corticosteroids are not routinely recommended and might exacerbate COVID-19-associated lung injury.⁷ However, in hyperinflammation, immunosuppression is likely to be beneficial. Re-analysis of data from a phase 3 randomised controlled trial of IL-1 blockade (anakinra) in sepsis, showed significant survival benefit in patients with hyperinflammation, without increased adverse events.⁸ A multicentre, randomised controlled trial of tocilizumab (IL-6 receptor blockade, licensed for cytokine release syndrome), has been approved in patients with COVID-19 pneumonia and elevated IL-6 in China (ChiCTR2000029765).⁹ Janus kinase (JAK) inhibition could affect both inflammation and cellular viral entry in COVID-19.¹⁰All patients with severe COVID-19 should be screened for hyperinflammation using laboratory trends (eg, increasing ferritin, decreasing platelet counts, or erythrocyte sedimentation rate) and the HScore¹¹ (table) to identify the subgroup of patients for whom immunosuppression could improve mortality. Therapeutic options include steroids, intravenous immunoglobulin, selective cytokine blockade (eg, anakinra or tocilizumab) and JAK inhibition.