Gabor Szendi:
The new coronavirus and the health crisis in the West

Many considered the emergence of the SARS-Cov2 virus and the consequences of the pandemic an out of the blue occurrence. Whereas according to virologists and health economists nothing surprising had happened. To put events into a wider perspective, in fact only another alarming turn of events had come true in the ever-increasing health crises of Western civilization.

 

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G Szendi: The new coronavirus and the health crisis in the West

Many considered the emergence of the SARS-Cov2 virus and the consequences of the pandemic an out of the blue occurrence. Whereas according to virologists and health economists nothing surprising had happened. To put events into a wider perspective, in fact only another alarming turn of events had come true in the ever-increasing health crises of Western civilization.

It is like the climate crisis. Things deteriorate slowly over a long period of time, enough for people to notice, then suddenly the quantitative deterioration manifests in loss of quality, and most people believe something new and unusual has happened.

The Titanic effect

From the point of view of evolution, the "original sin" was the development of agriculture and animal husbandry. That was the time that man formed a close relationship with animals. The dangerous pathogens of the modern era (Rabies, Spanish flu, TB, HIV, Ebola, Lyme, Zika, MERS-Cov, Sars-Cov, bird flu) were all transmitted from animals to people just like the current Sars-Cov2 virus strain, which is the cause of the Covid-19 infection. The name of this phenomenon is zoonosis. Countless infections occur due to newer pathogens, only these are either not recognized or they don't receive media attention. (1) Globalization guarantees the fast spreading. Already in historic times the plague and cholera were carried from Asia into the Western world by merchants and travelers. If we consider to the continuous presence of known and unknown pathogens, it is only a matter of time before they come into contact with people, and them which one will be able to spread from human to human. Though a lot of virologists may feel like Cassandra, the Trojan princess and priestess who was blessed by the gods with the ability of foresight, but also cursed, so that nobody would believe her words. Several virologists wrote books and articles on the subject saying that in terms of epidemics there can only be battles won, but the war never ends. Academic medicine presumptuously believed that dangerous pathogens had been eradicated with vaccination. The appearance of HIV then Ebola were considered as exceptional incidents, and not as predictable events coming true. The goal of politics always was and always will be to ensure that nothing disturbs the peaceful slumber of voters until the next election. In the constant intoxication of development there is no time to learn from the past. When something does happen, great efforts are made to solve the issue, but enthusiasm lasts only until the problem is neutralized. This way of thinking never prepares for the future and only wakes up when trouble arises. This is what I call the Titanic effect: a memorable story, where there were not enough lifeboats, the warnings of icebergs were in vain, and the ship raced forward in the hope of setting a new speed record. (2)

The new coronavirus was - retrospectively - detected last December in the sewage water, but more serious regulations were only introduced in March. Protective gear and medical equipment necessary for treatment were in short supply worldwide, although predictable new epidemics would require a steady supply of necessary resources. This caused panic in the entire developed world, the unpreparedness and the premature overreaction created an economic crisis. It is hard to judge what has caused bigger damage, the virus itself, or the measures taken against it.

Why are we always unprepared?

Focusing only on coronavirus, there were warning signs. In 2002 SARS-Cov was discovered in Asia. The acronym for the virus is derived from Severe Acute Respiratory Syndrome Coronavirus. The virus caused a total of 8,096 cases in 27 countries, and out of those infected, 774 died. The structure of the virus was determined and the mechanism was discovered - that it gets into cells through the ACE2 receptors, just like the current SARS-Cov2. But because there was success in containing the epidemic, which phased out, so did the motivation to develop suitable medication and vaccines. Then all hell broke loose when 10 years later MERS-Cov (Middle East Respiratory Syndrome Coronavirus) was discovered, which was spread by camels and was even more deadly: out of 2,494 infected, 858 died. At that point, vaccine development was started in various directions, but once again funding and enthusiasm dwindled. If there is no pandemic, why bother with vaccination? (3) How much more advanced the world would be right now, if we had developed a vaccine against SARS-Cov, which uses the same pathways to get into cells. Actually, there are seven known coronaviruses that are capable of infecting people. One of these is the HCoV-NL63, which uses the same ACE2 receptors to enter cells, has been around for centuries, and causes lower respiratory illnesses - mainly in children. So, there would have been enough time to develop a vaccine.

So what is the reason that epidemics continuously find mankind unprepared, when experience shows that old and new viruses cause epidemics again and again? Beyond the Cassandra syndrome there are two fundamental factors that play a decisive role in this: the financial interests of the pharmaceutical and vaccine industry, and the narrow-mindedness of governments.

After 1950 governments gradually lost control over pharmaceutical and vaccine development that turned into a line of business of the profit oriented pharmaceutical giants. The consequence of this is that only something profitable is worth developing. After a contained epidemic who will invest their capital into developing a vaccine that might come in handy one day? Of course governments could help by subsidizing research, what's more, they could even step in as the contractor. But the same question arises: out of the always tight budget for the many research subjects urgently needing support, why choose to finance something that might never be needed? In other words, generally short-term profits win over long-term interests. Although the restrictions introduced for SARS-Cov has caused $54 billion damage to the world economy, not one country or government wants to spend money on sparing damage to others. During the last 60 years the prevalence of new illnesses quadrupled every decade, and since 1980 the number of epidemics has tripled every year. (4) Which one should they take seriously?

A typical story is the development of the Ebola vaccine, that lasted 20 years (registration was announced in December 2019). Several research labs came up with significant results, but the vaccine industry rejected further developments that could have led to a registered vaccine. The reason: vaccine development is not very profitable. The yearly turnover of the pharmaceutical industry is more than a trillion dollars and only 3% of this comes from vaccines. (4) The development of that vaccine only sped up when the WHO and the leading powers realized in 2014 that Ebola had reached West-Africa and from there it would soon arrive to the First World. (5) Merck produced the first Ebola vaccine almost as a favor, based on calculations of making a financial loss on production. This approach can work once, but defense against epidemics cannot be built on behind the curtain deals.

The health crisis of Western medicine

In the entire developed world the management of the pandemic, to a different degree in each country, was hindered by severe lack of capacity. This could be explained by the sudden increase of needs, but with this the real reason of the worldwide health crisis was masked. The crisis has been ongoing for 50-60 years, and the pandemic only made it more obvious. Public health is the disadvantaged child of every government because it proves to be a bottomless pit, where no amount of money is enough to satisfy demands. However this is only an explanation of current budgeting.

The other reason for the crisis is much deeper: Western lifestyle during the 20th and 21st centuries made such illnesses widespread that were once considered a rarity in the 19th century, and are unknown amongst the tribal people same genetics as contemporary Western people. (6) Western diseases such as cardiovascular and autoimmune diseases, cancer, diabetes and allergies are hardly curable with the tool kit of academic medicine, they can only be treated. But treatment must last a lifetime, and the mass of people needing treatment is an ever increasing one, because of the increase in expected lifespan. In addition, illnesses are manifesting in ever younger generations. The latest developments in the pharmaceutical industry are not more effective, only more expensive, and because everyone wants the latest treatments this also means increasing expenses.

There are 3 reasons treatments do not lead to healing.

  • The fundamental problem is that Western diseases are lifestyle diseases. In other words, they can only be prevented - and in many cases cured - by lifestyle changes. Western diseases are maintained by the wrong lifestyle choices. Attempting to substitute a healthy lifestyle with treatment is ineffective because medical treatment cannot outweigh a sickness-promoting diet, micro-nutrient deficiencies, and the lack of physical activity.
  • You cannot change one single parameter in the body (eg: blood glucose, blood pressure, or inflammation levels) by medicating, without damaging the entire system. This is notably proven by an analysis which shows that the death rate caused by medical treatment exceeds death by cardiovascular diseases and cancer. (7; 8) In the USA the deaths of one million people a year have been decisively shown to be caused not by medical malpractice, but by the side effects and interactions between medications, unjustified treatments, hospital infections, over-diagnosis, and overtreatment as a result of screening.
  • Western medicine treats diseases based on wrong paradigms, so the lack of adequate treatment in itself continues or further worsens illnesses. (8) One of the well-known examples of this is the cholesterol hypothesis and the treatment based on it.
  • In short: no amount of money can resolve the problems. Most medical interventions are not healing but merely life extending.

When two pandemics meet

I did not present the futile struggle of medicine against Western diseases without a reason. Covid-19 is also a Western disease, although in an indirect sense.

If we look at susceptibility to the new coronavirus, and disease outcome, it is completely clear that there is a close relationship with obesity and related metabolic immunological disorders. According to a report from the CDC (Centers for Disease Control and Prevention) on the 26th August, out of the 161,000 deaths related to Covid-19, only in 6% of cases was Covid-19 identified as the sole reason of death. In all the remaining cases the deceased individuals had on average 2.6 chronic illnesses or pathological conditions. 92% of the deceased were older than 55, out of which 57% were over 75. (9) The reason for this is that chronic diseases are more common and accumulate in old age.

71% of the US population over 20 are overweight (BMI>25kg/m2) out of which 38% are obese (BMI>30kg/m2). (10) (The Hungarian data is hardly any better). 25% of US citizens over 65 are type 2 diabetics, but the percentage of pre-diabetics is even higher. (11) 34% of the adult population suffer from metabolic syndrome. (12) (The symptoms of metabolic syndrome are hypertonia, high insulin and blood glucose levels, unfavorable blood lipid composition, and abdominal fat gain). It is 1.5 times more likely that obese people will get infected by the new coronavirus, 2.1 times more likely that they will require hospital treatment, 1.8 times more likely they will end up in intensive care, while the severely obese are 2.3 times more likely to die of Covid-19. (13;14) People with diabetes carry a similar risk: among them severe cases of Covid-19 are 2.5 times more probable, they are 4.7 times more likely to develop pneumonia and acute respiratory distress syndrome, and their risk of mortality is 2.1 times higher. (15)

The situation could also be described as that an otherwise harmless pathogen entered the system, and this was able to tip over that fine balance provided by the medical treatments of Western diseases. Typically, people who suffer from chronic illnesses manifest symptoms in response to infection, healthy people who do not have any illnesses get through the infection without any or only mild symptoms. A similar phenomenon can be observed during the yearly flu epidemics. During the 2009-2010 epidemic the severely obese (BMI>40 kg/m2) were five times more likely to end up in hospital with the flu, the mortality was three times higher among obese people, and 7.6 times higher among the severely obese. (16) 90 % of influenza deaths happened in people over 65. (17) In essence, a similar scenario is being manifested, only the leading character is new.

If we entertained the idea that they are no obese people and Western diseases caused by obesity, then the new Coronavirus pandemic would hardly cause any disturbance.

Are mortality rates exaggerated?

Unfortunately according to the recommendations of the WHO, for every person who ever had a positive coronavirus test result then presumably (or actually) died of it - regardless of how much time passed between the diagnosis of infection and death - has to be recorded as a coronavirus death. (18) In an article by two British statisticians titled "Why no-one can ever recover from COVID-19 in England - a statistical anomaly" they criticized British medical records which included in the daily numbers of Coronavirus deaths all the people who were ever infected, and died from anything at a later date. (19) When the government adjusted the statistics and only counted those who died within 28 days of infection, the number of deceased immediately dropped by 5,377. Considering, that according to estimates 5-80% of people with positive test results are symptom free, we don't know how many who died from another cause are still included in the adjusted British statistics. (20)

Many dispute just how justifiable it is to classify someone as a victim of coronavirus when they ultimately died of a chronic disease. For a person who underwent an organ transplant, or is immune deficient for any other reason, a mild infection can be fatal, yet it is not correct to consider them a "common cold casualty". Because of the nature of chronic and old age diseases these deaths would unfortunately happen sooner or later, therefore the increased mortality of epidemic months can be considered as "premature" mortality, or the result of an overburdened medical system. It is also a known fact that half of Covid-19 deaths world-wide originate from old people's care homes. In the USA for instance, 41% of total Covid-19 mortality was in that 0.6% who live in old people's care homes. (21) On the basis of the accessible early data the situation is also similar in other developed countries. (22) It is very possible that - similar to the Hungarian situation - hospitals have become the primary focal sources in other countries too. In Hungary every third Covid-19 patient caught the infection in a hospital (23) which accounts for half of fatal cases. (24)

The publication of the raw data for mortality without proper analysis creates general panic. One would minimally expect not to intermingle the deaths of different risk groups and their causes.

Why does the Western lifestyle increase Coronavirus mortality?

It is not obesity itself that is dangerous, but the dysfunction of the body related to it. One of the highest risks of Covid-19 mortality is high inflammation, and high blood glucose levels.

The abundance of high glycemic index carbohydrates and omega 6 fatty acids, so typical of the Western diet, causes the level of IL-6 inflammation factor to rise, even without obesity, (25;26) and the consumption of these over time causes high insulin - and high blood glucose - levels that lead to obesity and insulin resistance.

Fat cells, especially abdominal, or in other words visceral fat, produces compounds and inflammation factors (IL-6, TNF-alfa, etc.) that cause insulin resistance and prompt the liver to upscale the production of another inflammation marker called CRP. Inflammation factors result in symptomless general inflammation. (14) Various factors further deteriorate the situation. For example, because of their excess weight, those who breathed faster had 33-fold higher levels of IL-6 than those of normal weight. (27) Obese diabetics have three times higher IL-6 levels. (28) High inflammation levels cause phlebosclerosis that causes high blood pressure. (29)

Covid-19 and inflammation

In complicated cases of Covid-19, patients' IL-6 levels are 3 times higher than in uncomplicated cases. High levels of IL-6 are one of the causes of respiratory failure, shock, and multi-organ dysfunction. Patients whose condition improved also had lower IL-6 levels, but for those whose condition worsened, IL-6 levels further increased. Patients who died had twice as high IL-6 levels compared to those who survived. (30)

A study which continuously measured the IL-6 levels of patients found that those who had more than 80 pg/ml were 22 times more likely to end up on a ventilator. The IL-6 levels demonstrated this with a 92% of accuracy. (31) Earlier studies had already proved that in pneumonia cases high IL-6 levels predict the death of a patient. (32)

Unfortunately, ventilators used as life-saving interventions have been found to double COVID-19 mortality compared to cases of influenza pneumonia. (33) Amongst other things the reason for this might be that lung damage caused by ventilation further increases the IL-6 levels. (34)

The role of IL-6 in determining disease outcome has been demonstrated in clinical trials in which IL-6-neutralizing drugs (tocilizumab, heparin) have shown significant success in the treatment of patients. (30;35)

Sugar and Covid-19

On average 14% of Covid-19 patients were diabetic, but the ratio in the over 60 group was 23%, while in the under 60 group 8.7%. Diabetics were 2.1 times more likely to develop severe or critical states from the infection, and were 3 times more likely to die in relation to the infection. (36) Naturally high blood glucose levels lead to worsening of symptoms even without a diabetes diagnosis. Patients who had higher than 7 mmol/l fasting blood glucose levels at the time of hospital admission, had a 4 times higher risk of complications, and people with 6.1-7 mmol/l had a 2.7 times higher risk compared to the ones below 6.1 mmol/l. (37) This increased risk is due to multiple reasons. There is a higher inflammation level in diabetes, the body's resistance against infections is weaker, and specifically in diabetes there are more ACE2 receptors - which are the gateways for the new Coronavirus to enter cells.

It is a characteristic of the Sars-Cov2 virus to shift the energy production of cells from mitochondrial function to oxygen-free fermentation (glycolysis). Because it produces 16 times less energy than normal energy-producing processes, cells working with fermentation have high sugar requirements. This is exactly what we see in the case of cancer cells as well, and it is for the same reason that high blood glucose levels also represent a danger from the point of view of cancer. Another aggravating factor is that immune cells in the lungs also gain their energy through fermentation, and high blood sugar levels stimulate them to increase the production and release of inflammatory factors, which again only leads to worsening of the disease. This is called a cytokine storm. (38)

What influences the risk of infection?

I do not discuss here the recommended and compulsory epidemiological control methods, as they are widely known.

Age

Age is a significant risk factor, but here it is important to distinguish between healthy old people, and those typically suffering from chronic diseases. As we age, the function of the adaptive immune system decreases as our innate immune system increases, leading to an inflammatory overreaction, the extreme example of which is the cytokine storm, which kills half of elderly COVID-19 patients. (39) This process is considered to be inherent in aging, although it is mainly typical of elderly chronic patients. Examination of centennials - or older - demonstrates that aging is not necessarily associated with high levels of inflammation and chronic diseases. (40) 'Centennials' typically eat a low-calorie diet. Research in other directions has also shown that the processes associated with aging can be significantly slowed by calorie restriction. (41)

Normalizing blood glucose levels and weight loss

Given that obesity and the resulting dysfunctions are one of the main risk factors, changing diet, weight loss and normalizing blood sugar levels would be one of the best tools to avoid infection and more severe symptoms. Weight loss also reduces inflammation, and losing 5 kg can result in a 4.5 / 3.5 mmHg decrease in blood pressure. (42) Studies have shown that type 2 diabetes is reversible through weight loss. (43) In acute cases, the creation of ketosis (when the body produces energy from fatty acids and ketone bodies) eliminates high blood sugar and inflammation, as macrophages that produce inflammatory factors can only get energy from sugar. (44) Irrespective of weight loss, blood glucose can be controlled with a number of drugs and dietary supplements that reduce blood glucose levels and insulin resistance. Metformin is a well-known drug for stabilizing blood sugar levels. In various studies, metformin reduced mortality by 20 to 80%. (45) Berberine, chromium, vanadium, magnesium, vitamins C and D, Ceylon cinnamon, garlic extract, Portulaca oleracea (common purslane), cumin, black cumin, etc. have been shown to be effective in lowering blood glucose.

Vitamin-D

The protective effects of vitamin D have been repeatedly confirmed by research. The direct protection provided by vitamin D can be attributed to the production of antimicrobial proteins in the trachea that kill invading bacteria and viruses. (46) In general, this has been confirmed in relation to infectious diseases of the upper respiratory system (47) and the anti-influenza effect has already been demonstrated in several studies. (46) Vitamin D also has an anti-inflammatory effect. (25) In addition it lowers blood sugar levels. (48). Adequate daily magnesium intake is also important, as without it vitamin D is not utilized. Magnesium also improves blood glucose control (49) and is an anti-inflammatory. (50)

The rapid spread and dangers of the epidemic may have been greatly influenced by the very low average vitamin D levels in developed countries, (51) and even in Africa. (52) This is especially true for older people, who have a reduced ability to synthesize vitamin D, and who typically avoid sunlight.

The protective effects of vitamin-D against Covid-19 has been demonstrated in several studies.

In one study, COVID-19 patients were divided into 4 groups based on their symptoms and condition: mild, moderate, severe, and critical. Severe patients already had difficulty breathing and critically ill patients had to be placed in an intensive care unit. The vitamin D levels of the four groups were as follows (in ng / ml): 31.2 ± 1.08; 27.4 ± 2.14; 21.2 ± 1.12; 17.1 ± 2.39. That is, the lower the vitamin D levels in patients, the more severe the condition. (53) Participants with higher vitamin D levels were 8 times more likely to come through the illness with mild symptoms, while those with the lowest vitamin D levels were 20 times more likely to develop a critical condition. Comparing the annual UV radiation of 100 countries with their morbidity and mortality rates, it has been clearly shown that both values are lower in southern countries than in northern countries. (54) In an Indonesian study, Covid-19 patients with insufficient vitamin D levels (21- 29 ng/ml), and patients with vitamin-D deficiencies (<20 ng/ml) were 12.5 times and 19.1 times, respectively, more likely to die compared to patients with normal vitamin-D levels (>30 ng/ml). (55)

According to the results of the first placebo-controlled study, only 2% of COVID-19 patients who were treated with vitamin D had to be admitted to intensive care, while in the group that wasn't treated with vitamin D the ratio was 50%. Mortality was 7% in the vitamin D-free group. (56)

Mitochondria

Previously, purely on a theoretical basis, I recommended to stimulate mitochondria with NAD+ and other dietary supplements supporting mitochondrial function, as a defense against Sars-Cov2. (57) Since then several studies have addressed this issue. On one hand, the new coronavirus has been shown to arrest mitochondrial function and switch cells to glucose fermentation, (38) on the other hand, it neutralizes the mitochondrial virus-detecting protein to suppress the cell's immune defense and enhance inflammation. The virus then multiplies in the mitochondria itself. One reason for the high level of inflammation is increased NLRP3 inflammasome activity due to mitochondrial aging (58), which can be inhibited by sirtuin-1 and 2 genes (SIRT 1 and 2). (59) However, the function of sirtuin genes can be stimulated by mitochondria. So for several reasons, anything that improves mitochondrial function reduces the effect of infection. (60) Further research confirmed that the new coronavirus inhibits the production of NAD +, a precursor of the ATP energy molecule that provides cellular energy. The authors also demonstrated that substances that increase NAD + levels (Nicotinamide Mononucleotide or Nicotinamide Riboside) inhibit viral replication. (61) Unfortunately, many people try to control the Sars-Cov2 virus by taking one single 'miracle solution'. Supplements that raise vitamin D or NAD + levels are of little value on their own if the body is suffering from micronutrient deficiencies.

Vitamin-C

Vitamin C in higher doses (6-10 grams / day) undoubtedly plays an important role in the prevention of various infections, and also shortens the duration of the disease even in the development of upper respiratory diseases. (62) However, only intravenous vitamin C offers significant benefits against Sars-Cov2 virus. (63)

Quercetin

Quercetin has emerged as an anti-Sars-Cov2 agent because, when taken in sufficient amounts, it inhibits the penetration of coronavirus into cells. (64) In addition, quercetin, like curcumin, resveratrol and berberine, stimulates the Sirt2 gene activity, which inhibits inflammation. Another benefit of quercetin is that it promotes the entry of zinc into cells, which enhances the cells' ability to defend themselves. (65) A number of other biochemical properties have been described which, in principle, make quercetin suitable for the prevention and treatment of COVID-19, but so far only clinical trials have been initiated to confirm the effect. The studies used 1,000 mg a day. The absorption and utilization of quercetin are variable, ranging from 0 to 50%, and as it is rapidly oxidized, it is recommended to be taken with vitamin C, because vitamin C regenerates quercetin. The combined use enhances the antiviral effect of both agents. (66)

Melatonin

The potential antiviral effect of melatonin has attracted attention for three reasons. On one hand, melatonin is produced throughout the body, not only in the pineal gland, and is a powerful antioxidant that is also involved in protecting mitochondria. On the other hand, over a lifetime, its production gradually decreases, i.e., its levels are already low in the age group most vulnerable to COVID-19. Thirdly, bats have much higher levels of melatonin, and although they carry and distribute Sars-Cov and Sars-Cov2, they are asymptomatic. During coronavirus infection, free radicals cause damage to lung tissue. One molecule of melatonin neutralizes 10 free radicals, while vitamin C only neutralizes one. Melatonin inhibits the inflammatory effect of the NLRP3 inflammasome. (67) Another important effect of melatonin is that the 'self-extracting' protein-degrading enzyme of Sars-Cov2 virus is inhibited by melatonin, i.e. by preventing the virus from activating. In addition, it inhibits the action of a special protein that keeps the ACE2 receptor on the cell surface, also reducing infection. (68) It is calculated that in more serious Covid-19 cases, 8 mg / kg body weight / day should be administered in 5 divided doses (69). As a precaution, it is worth taking a larger dose at night.

Zinc

One-third of the world suffers from zinc deficiency, but the only obvious consequence is an increased susceptibility to infection. The WHO estimates that zinc deficiency is responsible for 16% of lower respiratory tract infections. Zinc has been shown to have antiviral activity against a number of viruses known to date. Among other things, it inhibits the adhesion of the virus to the cell surface, inhibits the growth of the virus, and destabilizes the coating of the virus. It also has anti-inflammatory and immunostimulant effects. Studies have shown that zinc deficiency is common in groups of patients susceptible to COVID-19 (heart, lung, cancer, diabetes, autoimmune diseases, etc.) and the obese. Although clinical trials have not directly confirmed the anti-Sars-Cov2 effect, zinc is definitely worth taking, mostly with quercetin, as it also helps the zinc enter cells. (70)

Conclusions

Many conclusions can be drawn from the current pandemic. Understandably, the media and experts always focus on the present and look for better solutions in the given circumstances. A more forward-looking way of thinking should put the above issues into a broader context: The real problem is not Sars-Cov2 itself, but the vulnerability of Western civilization because of our current way of living. Sars-Cov2 just holds up a mirror to Western society, reflecting that we are on a wrong path.

 

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References

1 Quammen, D: Spillover: Animal Infections and the Next Human Pandemic W. W. Norton, 2012. ssrn.com/abstract=3585561

2 Henig, RM: Experts warned of a pandemic decades ago. Why weren't we ready? National Geographic 2020, július.

3 Diamond MS, Pierson TC. The Challenges of Vaccine Development against a New Virus during a Pandemic. Cell Host Microbe. 2020;27(5):699-703.

4 Walsh, B: The World Is Not Ready for the Next Pandemic. Time, 2017, május 4.

5 Branswell, H: 'Against all odds': The inside story of how scientists across three continents produced an Ebola vaccine. STAT, 2020, jan. 7

6 Lindeberg, S: Food and Western Disease. Health and Nutrition from an Evolutionary Perspective. Wiley-Blackwell, 2010

7 Null, G;Feldman, M; Rasio, D; Dean, C: Death by medicine. Praktikos books, 2011.

8 Szendi G: Medicine on the Wrong Path. Caught in the dogma trap. Jaffa, Budapest, 2018.

9 CDCa: https://www.cdc.gov/nchs/nvss/vsrr/covid_weekly/index.htm

10 CDCb: https://www.cdc.gov/nchs/fastats/obesity-overweight.htm

11 Saklayen MG. The Global Epidemic of the Metabolic Syndrome. Curr Hypertens Rep. 2018;20(2):12.

12 Shi TH, Wang B, Natarajan S. The Influence of Metabolic Syndrome in Predicting Mortality Risk Among US Adults: Importance of Metabolic Syndrome Even in Adults With Normal Weight. Prev Chronic Dis 2020;17:200020.

13 Popkin BM, Du S, Green WD, Beck MA, Algaith T, Herbst CH, Alsukait RF, Alluhidan M, Alazemi N, Shekar M. Individuals with obesity and COVID-19: A global perspective on the epidemiology and biological relationships. Obes Rev. 2020 Aug 26. doi: 10.1111/obr.13128.

14 Lockhart SM, O'Rahilly S. When Two Pandemics Meet: Why Is Obesity Associated with Increased COVID-19 Mortality? Med (N Y). 2020;10.1016/j.medj.2020.06.005.

15 Huang I, Lim MA, Pranata R.: Diabetes mellitus is associated with increased mortality and severity of disease in COVID-19 pneumonia - A systematic review, meta-analysis, and meta-regression. Diabetes Metab Syndr, 2020, 14(4):395-403.

16 Morgan OW, Bramley A, Fowlkes A, Freedman DS, Taylor TH, Gargiullo P, Belay B, Jain S, Cox C, Kamimoto L, Fiore A, Finelli L, Olsen SJ, Fry AM. Morbid obesity as a risk factor for hospitalization and death due to 2009 pandemic influenza A(H1N1) disease. PLoS One. 2010 Mar 15;5(3):e9694.

17 Thompson WW et al. Mortality associated with influenza and respiratory syncytial virus in the United States. JAMA, 2003, 289:179-186.

18 WHO: INTERNATIONAL GUIDELINES FOR CERTIFICATION AND CLASSIFICATION (CODING) OF COVID-19 AS CAUSE OF DEATH. WHO, 2020

19 Loke, YK; Heneghan, C: Why no one can ever recover from Covid-19 in England. The Spectator 17 July 2020,

20 Heneghan, C; Brassey, J; Jefferson, T: COVID-19: What proportion are asymptomatic? CEBM, April 6, 2020.

21 NYT: More Than 40% of U.S. Coronavirus Deaths Are Linked to Nursing Homes. New York times2020, aug. 13.

22 Wikipedia: Impact of the COVID-19 pandemic on long-term care facilities. Wikipedia, 2020.

23 Kaszás F: Coronavirus: Every Third Patient Got Infected in Hospital. Hungary Today, 2020a, 06.25.

24 Kaszás F: Coronavirus: Half of Deceased Contracted Infection in Hospitals. Hungary Today, 2020b.07.17.

25 Heber, D; Henning, S: Biomarkers of Inflammation and the Western Diet. in: Bharat B. Aggarwal David Heber (eds): Immunonutrition Interactions of Diet, Genetics, and Inflammation. CRC Press 2014. pp:53-65.

26 Goletzke J, Buyken AE, Joslowski G, Bolzenius K, Remer T, Carstensen M, Egert S, Nöthlings U, Rathmann W, Roden M, Herder C. Increased intake of carbohydrates from sources with a higher glycemic index and lower consumption of whole grains during puberty are prospectively associated with higher IL-6 concentrations in younger adulthood among healthy individuals. J Nutr. 2014 Oct;144(10):1586-93.

27 Roytblat L, Rachinsky M, Fisher A, Greemberg L, Shapira Y, Douvdevani A, Gelman S. Raised interleukin-6 levels in obese patients. Obes Res. 2000 Dec;8(9):673-5.

28 Mohamed-Ali V, Goodrick S, Rawesh A, Katz DR, Miles JM, Yudkin JS, et al. Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-alpha, in vivo. J Clin Endocrinol Metab. 1997;82:4196-200.

29 Bautista LE, Vera LM, Arenas IA, Gamarra G. Independent association between inflammatory markers (C-reactive protein, interleukin-6, and TNF-alpha) and essential hypertension. J Hum Hypertens. 2005;19(2):149-54.

30 Coomes, EA; Haghbayan, H: Interleukin-6 in COVID-19: A Systematic Review and Meta-Analysis. medRxiv ,2020, doi:10.1101/2020.03.30.20048058

31 Herold, Tobias ; Jurinovic, Vindi ; Arnreich, Chiara ; Hellmuth, Johannes C ; von Bergwelt-Baildon, Michael ; Klein, Matthias ; Weinberger, Tobias: Level of IL-6 predicts respiratory failure in hospitalized symptomatic COVID-19 patients. medRxiv, 2020, doi:10.1101/2020.04.01.20047381

32 Bacci MR, Leme RC, Zing NP, Murad N, Adami F, Hinnig PF, Feder D, Chagas AC, Fonseca FL. IL-6 and TNF-? serum levels are associated with early death in community-acquired pneumonia patients. Braz J Med Biol Res. 2015 May;48(5):427-32.

33 Auld SC, Caridi-Scheible M, Blum JM, Robichaux C, Kraft C, Jacob JT, Jabaley CS, Carpenter D, Kaplow R, Hernandez-Romieu AC, Adelman MW, Martin GS, Coopersmith CM, Murphy DJ; Emory COVID-19 Quality and Clinical Research Collaborative. ICU and Ventilator Mortality Among Critically Ill Adults With Coronavirus Disease 2019. Crit Care Med. 2020 Sep;48(9):e799-e804.

34 Gurkan OU, He C, Zielinski R, Rabb H, King LS, Dodd-o JM, D'Alessio FR, Aggarwal N, Pearse D, Becker PM. Interleukin-6 mediates pulmonary vascular permeability in a two-hit model of ventilator-associated lung injury. Exp Lung Res. 2011 Dec;37(10):575-84.

35 Buijsers B, Yanginlar C, Maciej-Hulme ML, de Mast Q, van der Vlag J. Beneficial non-anticoagulant mechanisms underlying heparin treatment of COVID-19 patients. EBioMedicine. 2020 Aug 24;59:102969. doi: 10.1016/j.ebiom.2020.102969.

36 Mantovani A, Byrne CD, Zheng MH, Targher G. Diabetes as a risk factor for greater COVID-19 severity and in-hospital death: A meta-analysis of observational studies. Nutr Metab Cardiovasc Dis. 2020 Jul 24;30(8):1236-1248.

37 Wang, S., Ma, P., Zhang, S. et al. Fasting blood glucose at admission is an independent predictor for 28-day mortality in patients with COVID-19 without previous diagnosis of diabetes: a multi-centre retrospective study. Diabetologia (2020). doi:10.1007/s00125-020-05209-1

38 Codo AC, Davanzo GG, Monteiro LB, et al. Elevated Glucose Levels Favor SARS-Cov2 Infection and Monocyte Response through a HIF-1?/Glycolysis-Dependent Axis [published correction appears in Cell Metab. 2020 Sep 1;32(3):498-499]. Cell Metab. 2020;32(3):437-446.e5.

39 Mueller AL, McNamara MS, Sinclair DA. Why does COVID-19 disproportionately affect older people?. Aging (Albany NY). 2020;12(10):9959-9981

40 Franceschi C, Ostan R, Santoro A. Nutrition and Inflammation: Are Centenarians Similar to Individuals on Calorie-Restricted Diets?. Annu Rev Nutr. 2018;38:329-356.

41 Blagosklonny MV. From causes of aging to death from COVID-19. Aging (Albany NY). 2020;12(11):10004-10021.

42 Neter JE, Stam BE, Kok FJ, Grobbee DE, Geleijnse JM. Influence of weight reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension. 2003;42(5):878-884.

43 Lean MEJ, Leslie WS, Barnes AC, et al. Durability of a primary care-led weight-management intervention for remission of type 2 diabetes: 2-year results of the DiRECT open-label, cluster-randomised trial. Lancet Diabetes Endocrinol. 2019;7(5):344-355.

44 Sukkar SG, Bassetti M. Induction of ketosis as a potential therapeutic option to limit hyperglycemia and prevent cytokine storm in COVID-19. Nutrition. 2020;110967.

45 Scheen AJ. Metformin and COVID-19: From cellular mechanisms to reduced mortality [published online ahead of print, 2020 Aug 1]. Diabetes Metab. 2020;S1262-3636(20)30098-7.

46 Gruber-Bzura BM. Vitamin D and Influenza-Prevention or Therapy?. Int J Mol Sci. 2018;19(8):2419.

47 Martineau AR, Jolliffe DA, Hooper RL, et al. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. 2017;356:i6583.

48 Hu Z, Chen J, Sun X, Wang L, Wang A. Efficacy of vitamin D supplementation on glycemic control in type 2 diabetes patients: A meta-analysis of interventional studies. Medicine (Baltimore). 2019;98(14):e14970.

49 Veronese N, Watutantrige-Fernando S, Luchini C, et al. Effect of magnesium supplementation on glucose metabolism in people with or at risk of diabetes: a systematic review and meta-analysis of double-blind randomized controlled trials [published correction appears in Eur J Clin Nutr. 2016 Dec;70(12 ):1463]. Eur J Clin Nutr. 2016;70(12):1354-1359.

50 Zhang X, Li Y, Del Gobbo LC, et al. Effects of Magnesium Supplementation on Blood Pressure: A Meta-Analysis of Randomized Double-Blind Placebo-Controlled Trials. Hypertension. 2016;68(2):324-333.

51 Cashman KD, Dowling KG, Škrabáková Z, et al. Vitamin D deficiency in Europe: pandemic?. Am J Clin Nutr. 2016;103(4):1033-1044.

52 Mogire RM, Mutua A, Kimita W, Kamau A, Bejon P, Pettifor JM, Adeyemo A, Williams TN, Atkinson SH. Prevalence of vitamin D deficiency in Africa: a systematic review and meta-analysis. Lancet Glob Health. 2020 Jan;8(1):e134-e142.

53 Alipio, Mark, Vitamin D Supplementation Could Possibly Improve Clinical Outcomes of Patients Infected with Coronavirus-2019 (COVID-2019) (April 9, 2020). .doi:10.2139/ssrn.3571484

54 Panarese A, Shahini E. Letter: Covid-19, and vitamin D. Aliment Pharmacol Ther. 2020;51:996-998

55 Raharusun, Prabowo and Priambada, Sadiah and Budiarti, Cahni and Agung, Erdie and Budi, Cipta, Patterns of COVID-19 Mortality and Vitamin D: An Indonesian Study. 2020, doi:10.2139/ssrn.3585561

56 Castillo, ME; Costa, LME; Barrios, JMV; Díaz, JFA; Miranda, JL; Bouillon, R; Gomez, JMQ: Effect of Calcifediol Treatment and best Available Therapy versus best Available Therapy on Intensive Care Unit Admission and Mortality Among Patients Hospitalized for COVID- 19: A Pilot Randomized Clinical study The Journal of Steroid Biochemistry and Molecular Biology Available online 29 August 2020, 105751 doi:10.1016/j.jsbmb.2020.105751

57 Szendi G: Bard against coreonavirus. Whereof doctors not always talk. 2020, 5: 20-22.

58 Yu JW, Lee MS. Mitochondria and the NLRP3 inflammasome: physiological and pathological relevance. Arch Pharm Res. 2016 Nov;39(11):1503-1518.

59 Kitada M, Ogura Y, Monno I, Koya D. Sirtuins and Type 2 Diabetes: Role in Inflammation, Oxidative Stress, and Mitochondrial Function. Front Endocrinol (Lausanne). 2019;10:187.

60 Singh: Am J Physiol Cell Physiol, 2020, 319(2):C258-C267.

61 Heer CD, Sanderson DJ, Alhammad YMO, et al. Coronavirus and PARP expression dysregulate the NAD Metabolome: a potentially actionable component of innate immunity. Preprint. bioRxiv. 2020;2020.04.17.047480.

62 Hemilä H. Vitamin C and Infections. Nutrients. 2017;9(4):339.

63 Cheng RZ, Kogan M, Davis D. Ascorbate as Prophylaxis and Therapy for COVID-19-Update From Shanghai and U.S. Medical Institutions. Glob Adv Health Med. 2020;9:2164956120934768.

64 Williamson G, Kerimi A. Testing of natural products in clinical trials targeting the SARS-Cov2 (Covid-19) viral spike protein-angiotensin converting enzyme-2 (ACE2) interaction. Biochem Pharmacol. 2020;178:114123.

65 Yanuck, SF; J PizzornoH MessierK N Fitzgerald: Evidence supporting a phased immuno-physiological approach to COVID-19 from prevention through recovery integrative medicine. 2020, 19(Suppl 1):8-35

66 Colunga Biancatelli RML, Berrill M, Catravas JD, Marik PE. Quercetin and Vitamin C: An Experimental, Synergistic Therapy for the Prevention and Treatment of SARS-Cov2 Related Disease (COVID-19). Front Immunol. 2020;11:1451.

67 Shneider A, Kudriavtsev A, Vakhrusheva A. Can melatonin reduce the severity of COVID-19 pandemic?. Int Rev Immunol. 2020;39(4):153-162.

68 Feitosa EL, Júnior FTDSS, Neto JADON, Matos LFL, Moura MHDS, Rosales TO, De Freitas GBL. COVID-19: Rational discovery of the therapeutic potential of Melatonin as a SARS-Cov2 main Protease Inhibitor. Int J Med Sci 2020; 17(14):2133-2146.

69 Tan, D.-X. and Hardeland, R. 2020. Estimated doses of melatonin for treating deadly virus infections: focus on COVID-19. Melatonin Research. 3, 3 (Jun. 2020), 276-296.

70 Wessels I, Rolles B, Rink L. The Potential Impact of Zinc Supplementation on COVID-19 Pathogenesis. Front Immunol. 2020;11:1712.