H1N1 Influenza
The H1N1 virus (a sub type of the Influenza A virus) that appears to have become a very serious human contagion and pathogen in recent months, has some history to it that may prove to be very useful. So before beginning the discussion of how to prevent and treat it, it is important to look back at the 1918 pandemic that appears to have been caused by a virus that is quite similar to the one causing the current outbreak.
In 1918 more than 20 million people died as a direct result of this infection--and that is based on fairly primitive tools for gathering such statistics. Others estimate that it is likely that more than 50 million died if we applied today's statistical criteria. The Global Initiative on Sharing All Influenza Data (GISAID) is a very up to date resource regarding the scientific specifics of this current outbreak. Their website will be totally locked down for weeks owing to the explosion of scientists seeking to gain registration privileges (it is an enrolled info site and requires some academic credentials for enrollment). Nonetheless, we expect the information regarding the genetic uniquenesses of this novel hybrid of swine, avian, and human H1N1 subtypes to be unveiled and dispatched within the next several weeks or possibly months.
Some of the early genetic characterization of the virus responsible for the new H1N1 outbreak tells us that this bug just does not have the teeth that it otherwise might and will not likely kill a lot of people. A rogue protein in certain influenza virus types – the PB -1F2 protein – seems to confer a lethal capacity for the virus to kill immune cells theoretically releasing massive amounts of the inflammatory proteins they contain thereby causing the so-called “cytokine storm”. This is the phenomenon that kills the healthiest humans. If it does mutate such that it has the PB-1F2 protein, we then have the H1N1 virus of 1918.
Since the 1976 flu epidemic was an H1N1 variety without the PB-1F2 protein, it was not a killer. But many people got it and might still have some cross immunity to it’s more lethal PB-1F2 cousin. This would have a favorable effect. But most of the current “young and the strong” were not alive then. The folks with some cross immunity are likely 45 or older now.
The fact that the current virus has emerged “out of season” in a sense is a testimony to its slightly more aggressive and infectious nature. The worst case scenario will be the apparent lull over the hot summer months with a mutation to the PB-1F2 rogue by the time the flu season gets underway in October 2009.
Without getting too bogged down in these specifics, it is imperative to apply what information we do have toward practical applications for treatment and prevention. This virus does not seem to damage the respiratory epithelium or tissue lining the airways as much as it hits the immune cells lining or embedded in the respiratory mucosa. It either “reprograms” or agitates them to release massive amounts of inflammatory cytokines (small miniature proteins or peptides that are the "messenger molecules" of one's immune system) or in its more lethal form, it makes them commit apoptosis or cellular suicide. In other words, one's immune cells can become a liability. This can be too much for the tissues of the airways and lungs to handle. The horrendous outpouring of inflammatory by products (imagine your thumb hit hard by a hammer, then imagine this happening to your lungs) overwhelms our capacity to maintain effective airways, and severe difficulty with oxygenation occurs. The next stage of this immunologic tragedy is the now-vulnerable respiratory tissue developing secondary bacterial infection with common pathogens such as strept or staph. Compound this with the potential for the rapid emergence of resistant strains of these bacteria in the population due to much greater antibiotic use, and one has the makings of a real "situation".
Those with the strongest and most vigilant immune systems (young males between 18-45) may be the most susceptible to getting the sickest if infected. I would even go further and suggest that individuals who have already demonstrated an overly vigilant immune system (type I diabetics or others with autoimmune diseases not treated with immunosuppressives) might be at particular risk in the absence of some of the measures I will describe below.
Preventing this disease may be impractical if not impossible. Quarantine and isolation will simply buy time until the virus is better understood, antiviral medications that seem effective can be dispensed to a broader set of communities, and perhaps some eventual vaccine developed and dispensed fairly and effectively. Remember, however, that the public health record with rapidly developed influenzae vaccines is not particularly good. The vaccine currently being dispensed (and required in certain situations) is neither proven effective nor safe at this point. There is a fear that it might lead to an inordinate number of Guillain-Barre cases (a polio-like illness sometimes requiring respiratory support which usually resolves in weeks or months).
Nonetheless, there is likely some value in avoiding efforts to acquire the bug. This bug should be considered extremely contagious through primarily airborne routes with very few viral particles necessary to begin human incubation (3-4 days) and eventual infection of the host. I would suggest simply smiling in church at your neighbor for the peace greeting this year, and if anyone sneezes without some reasonable attempt to use a handkerchief, they should be flogged.
Treatment is of two types: 1) prophylactic treatment applied in the case of possible exposure or incipient infection (already exposed but not yet sick) and 2) treatment for those already experiencing symptoms. Prophylactic treatment may be the most important to understand and prepare for given the risks and uncertainties of getting and treating full blown disease.
If exposed or even thought to be at risk for exposure, I would start with several primary nutritional tools that have reasonable scientific proof of being beneficial. I will list these by number for clarity:
1. Selenium -- make sure one is taking a good multivitamin with at least 200 mcg of selenium/d. Then add a second 200 mcg capsule daily. For those who weigh less than 150# (including children), the rule of thumb is a total daily intake of 2 mcg/pound of body weight/day. This will not cause toxicity! The thoroughbred polo horses who died from selenium toxicity this past year in Florida received hundreds of times that dose. Selenium is very important in promoting healthy antioxidant enzyme activity and also seems to be important insofar as hosts who are selenium deficient appear to promote much greater virulence of the virus once infected. There is some discussion that the mutation to the PB-1F2-containing virus will be more likely to take place in selenium deficient individuals.
2. Vitamin D -- this is the critical nutrient in my opinion and may determine the difference between a fatal and a mild infection with H1N1. It is important to understand that vitamin D is a cell signalling molecule that governs the release of inflammatory cytokines. Vitamin D deficient individuals will be at much greater risk for severe morbidity or mortality. The rule of thumb is ~ 25-30 international units of vitamin D3/pound of body weight orally per day unless major sun exposure without sunscreen (minimum of 1 hour in shorts and T shirt--adjust for season; this type of exposure in the Minnesota December sun does not cut it). If exposure is imminent or threatened, I suggest doubling this dose for ~ 10 days. If infection is known and manifest, I suggest 3 days of 250 units/pound/day (yes, 10x the usual), then back to the doubled dose until the infection is resolving, then back to baseline dosing. I suggest avoiding calcium supplements during these periods of higher vitamin D dosing. Individuals with comorbidities such as renal failure, the need for prescription vitamin D analogs, etc, should consult their physician or a knowledgeable naturopath before doing any of this.
3. Botanical antivirals -- there is a rich history of strong herbal antivirals and few if any known side effects when used temporarily for viral illnesses (outside of the occasional skin rash). I have a particular source we vend to patients in our practice, but any local naturopath can be an extremely useful source for the acquisition and utilization of botanical antivirals.
4. Homeopathy -- most homeopaths will tell you that this is highly individualized treatment and that there is no good "one size fits all" approach with this modality. Nonetheless, for those unfamiliar with what homeopathy actually is, please go to www.flusolution.net for a refresher course. The 3 remedies that were clearly associated with a dramatic reduction in mortality (20% vs 1%) during the 1918 pandemic in areas of the United States where conventional MD experiences were compared with local homeopathic or naturopathic practitioners are Gelsemium, Eupatorium, and Bryonia. Whether one believes in this art and science or not, anyone who really looks at those treated with these remedies for viruses like influenza will be impressed with the results. I suggest finding a local naturopathic doctor or homeopath for a session (your insurance will not cover it) and obtain some of these remedies for you and your family. It could be critically important if we do indeed get in to a major situation with this virus.
5. Antiinflammatory fatty acids -- the EPA/DHA of fish oil is important, yes, but there are other novel fatty acids that downregulate inflammatory mediation much more effectively. I prescribe a product called Immunoviva -- liquid or gelcaps -- made by Botanical Oils in Spooner, Wisconsin. It is simply superior in terms of reducing inflammatory mediation in the chronically ill. I would take 2-3 tsps/d or 3-6 gelcaps/d based on the risk or presence of illness. Another interesting application is to use high doses of limonene, a very unsaturated and antiinflammatory fatty acid derived from the rind of citrus fruits, particularly limes (from which it is named). It is marketed as Esophagard, a novel approach for those with reflux based on the principle that reflux has an inflammatory cause rooted in immune reactions to processed, agricultural (ie, grains and dairy) foods. I started giving this product to people with standard influenza this past year, and they were not as sick nor sick as long as usual. I would take 2-3 Esophagard daily if I caught the bug.
6. Tamiflu (oseltamivir) is a pro drug that is metabolized once taken into an inhibitor of the viral enzyme, neuraminidase, which is important for the virus to multiply. This drug can be taken by young and old alike and is used both prophylactically and for those who are ill. It will definitely blunt the illness depending on the virulence of the bug. There is no guarantee that taking this drug will prevent serious illness or death if not taken early enough nor will it prevent serious illness in everyone who is exposed. But it will likely help. It can be obtained through any primary care MD. I have already had patients who want to stockpile it a little, and it should be emphasized that production has some limitations. If a rapid pandemic took hold, supplies would likely be exhausted quickly. There have also been reports of drug resistance in several different influenza A strains.
In summary, the H1N1 Pandemic of 2009 might not happen. The bug might not have the teeth that it’s 1918 ancestor had. A vaccine might be quickly developed, but always remember that vaccines have hazards and being "vaccinated" is not the same as being "immunized". Public health measures are improved and more expedient. But we live in a more crowded world, nutrition can be very suboptimal re things like selenium, and it could mutate into a very deadly monster. There are a number of simple measures that together might confer much greater resilience to those most vulnerable – the young and the strong. Those with hypervigilant immune systems should be particularly wary and prepared.
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Minnesota Natural Medicine
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