A Covid pill by autumn is highly unlikely, yet the safest, cheapest treatment for COVID-19 is being ignored.
Shortly after UK Prime Minister Boris Johnson declared that we will have ‘a tablet you can take at home that will reduce the chance of the COVID-19 infection turning into more severe disease’ by autumn, Pfizer announced the start of trials on a new experimental drug it hopes to have available by the end of the year.
Pfizer’s spokesperson Dr Neeta Ogden told CBS News, said: ‘I think that with this drug we really have to look at it as a game changer. We haven’t seen medication even discussed on the horizon that one can take early on or prophylactically if you’ve been exposed, kind of like what we have for the flu.’
New drugs, however, have to go through many stages to establish safety, the effective dose, then, finally a placebo-controlled trial. Given that this has to be with infected people it’s a tall order to get all that done properly, without short-cuts, this year, and get the drug licensed. Therefore, an autumn release date seems unlikely.
What’s the difference between anti-viral drugs, like the one touted by Pfizer, and vaccines? How do anti-viral drugs actually work?
Unlike vaccines, which aim to induce ‘acquired or learnt’ immunity thereby priming the immune system to produce antibodies which attack the virus, anti-viral agents aim to be more general in interfering with a virus’s ability to take hold.
The first anti-viral was AZT for HIV infection. AZT blocks an enzyme called reverse transcriptase used by infected cells to make new viruses. It’s part of a class of anti-retroviral drugs used against AIDS.
When swine flu struck in 2009, the UK government spent £500 million on Tamiflu, a drug that inhibits another enzyme, neuraminidase, which viruses use to break out of cells in order to infect others. Neuraminidase inhibitor drugs tend to end in ‘mivir’ such as oseltamivir (Tamiflu) or zanamivir (Relenza).
The British Medical Journal (BMJ) fought for four years to get full disclosure of the drug company’s trial data to enable independent analysis. Once undertaken, this independent analysis showed that they were much less effective than originally claimed, with significant side-effects. According to a BMJ report Tamiflu ‘causes nausea and vomiting and increases the risk of headaches and renal and psychiatric syndromes’ with many children reporting nightmares.
An independent meta-analysis of all trials showed that oseltamivir reduced duration of infection by 13%, from 6.7 days to 5.8 days but made no difference to hospitalisations. Even worse results were reported for zanamivir reducing infection duration by 10%. There’s a mad scramble right now to see if any of these existing drugs can be repurposed for COVID-19.
But there are already safe, effective alternatives. For example, vitamin C.
The first trial on COVID-19 infected people, published in the Journal of the American Medical Association (JAMA) in February, gave 8 grams of Vitamin C a day to PCR positive outpatients (i.e those testing positive for COVID-19) and showed an 18% reduction in duration from 6.7 days, with standard treatment, to 5.5 days for those taking vitamin C. This was reported as ‘not significant’ but it actually represented a highly significant 70% improved recovery rate, not disclosed in the JAMA paper but teased out on independent analysis by professor of public health at the University of Helsinki, Dr Harri Hemila.
For those with longer infection the vitamin C reduced duration by 30%, from 9 days to 6 days. According to Hemila, based on previous trials ‘doses of 6–8 g/day may shorten viral upper respiratory infections by some 20%.’ One trial giving 8 grams, reported that almost half (46%) became symptom free within 24 hours. The more you give and the sooner you give it upon infection, the better the results.
Unlike the drug contenders, vitamin C has many mechanisms of action, both supporting healthy immunity as well as suppressing viruses. Vitamin C increases the production and improves the function of all critical immune cells and protects them from virally induced ‘oxidative’ damage. It also boosts interferon, which interferes with viral replication and is anti-bacterial. Many critical Covid patients develop secondary bacterial pneumonia and sepsis – both of which can be reduced by vitamin C.
Back in 1990, twice Nobel prize winner Linus Pauling and colleagues infected human T-cells with HIV then exposed them to vitamin C. The virus was effectively inactivated – reverse transcriptase was reduced by more than 99% and outsurpassed the drug AZT in a further study on human T-cells.
Studies exposing type-A flu viruses, which includes bird and swine flu, to a nutrient mixture high in vitamin C show profound inhibition of the virus and inhibition of neuraminidase and outperformed oseltamivir (Tamiflu) when tested on Asian bird flu (A/H5N1).
The UK Government’s Therapeutics Taskforce set up ‘to search for the most promising new medicines to be made safely and rapidly available’ has a study planned for critical treatment using intravenous vitamin C, but none for early intervention. This is a shame because vitamin C is unpatentable, hence pharma companies, reliant on profits from man-made patentable drugs, have no incentive to research vitamin C. Given that vitamin C, if taken at onset of symptoms, cuts duration better than any anti-viral drug to date, is safe, inexpensive and rapidly available, one has to ask: ‘Why not vitamin C?’.