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Alzheimer’s disease continues to be a leading cause of death in the U.S., with 1 in 3 seniors dying with Alzheimer’s or dementia — more than the number killed by breast and prostate cancers combined.1
While a cure has remained elusive, the connection between brain health and gut microbiota has grown clearer, and research suggests that the bacteria in your intestines may influence brain functioning and can even promote neurodegeneration.2
A team of Swiss and Italian researchers has taken the correlation a step further, with research showing a connection between imbalanced gut microbiota and the development of amyloid plaques in the brain;3 Alzheimer’s is characterized by an accumulation of beta-amyloid plaques and neurofibrillary tangles in the brain.
Proteins Produced by Gut Bacteria May Trigger Alzheimer’s

The study involved a cohort of 89 people between 65 and 85 years of age. Some of them suffered from Alzheimer’s disease or other neurodegenerative diseases while others were healthy with no memory problems.
The researchers used PET imaging to measure amyloid deposition in their brains, then measured markers of inflammation and proteins produced by intestinal bacteria, such as lipopolysaccharides and short-chain fatty acids, in their blood.
Lipopolysaccharides (LPSs) are dead bacteria or, more specifically, the cell walls of dead bacteria. Your immune system treats them as living bacteria and mounts immune defenses against the perceived invaders. LPSs are pro-inflammatory and have been found in amyloid plaques in the brains of Alzheimer’s patients.4
The study revealed that high blood levels of LPSs and the short-chain fatty acids (SCFAs) acetate and valerate were associated with large amyloid deposits in the brain. Other SCFAs, namely butyrate, appeared to have a protective effect; high levels of butyrate were associated with less amyloid.
Butyrate — an SCFA produced when gut bacteria ferment fiber — activates the secretion of brain-derived neurotrophic factor (BDNF),5 reduced levels of which have been linked to Alzheimer’s disease.
“Our results are indisputable: Certain bacterial products of the intestinal microbiota are correlated with the quantity of amyloid plaques in the brain,” explains Moira Marizzoni, a study author with the Fatebenefratelli Center in Brescia, Italy.6
Probiotic ‘Cocktail’ May Act as an Early Preventative

The study represents a continuation of prior research by the team, which found that the gut microbiota in people with Alzheimer’s disease differs from those without the condition. In those with Alzheimer’s, microbial diversity is reduced, with certain bacteria being overrepresented and other microbes decreased.
“Furthermore,” said neurologist Giovanni Frisoni, study author and director of the University Hospitals of Geneva (HUG) Memory Center in Switzerland, “we have also discovered an association between an inflammatory phenomenon detected in the blood, certain intestinal bacteria and Alzheimer’s disease; hence the hypothesis that we wanted to test here: Could inflammation in the blood be a mediator between the microbiota and the brain?”7
With the connection growing stronger, the team is planning further research to reveal which specific bacteria or groups of bacteria may be responsible for the effect, which could ultimately lead to a preventive treatment “cocktail.” Frisoni said in a news release:8

“Indeed, we must first identify the strains of the cocktail. Then, a neuroprotective effect could only be effective at a very early stage of the disease, with a view to prevention rather than therapy.

However, early diagnosis is still one of the main challenges in the management of neurodegenerative diseases, as protocols must be developed to identify high-risk individuals and treat them well before the appearance of detectable symptoms.”

The Fasting Connection

One reason why fasting is so beneficial for neurodegenerative diseases such as Alzheimer’s is because it helps your body to cycle through autophagy and the rebuilding phase.
Autophagy is the process by which your body cleans out damaged organelles, encouraging proliferation of new, healthy cells, which relates to Alzheimer’s because the refolding process is one of several factors that need to work in order for your brain to function.
Importantly, fasting activates autophagy, which is your body’s way of taking out the trash, and will also trigger the regeneration of stem cells. In our 2017 interview, Dr. Steven Gundry explained that this also may have a direct connection with LPSs, and giving your gut a rest from these pro-inflammatory proteins via fasting may be healing:

“We have an amazing repair system that goes to work when you’re fasting. Not the least of which is [letting] your gut rest. It’s probably one of the smartest things that any of us can do — putting the wall of your gut at rest, not having to absorb nutrients, not having to deal with the constant inflow of lectins or toxins. But I think more importantly, it gives [your body] a chance to finally do some serious cleaning of your brain …

Alzheimer’s and Parkinson’s have a unifying cause, and that is the brain is defending itself against perceived threat, a lot of which are LPSs. If you put your gut at rest and don’t have LPSs coming into your system, and the longer you can maintain that, realistically, the better off you are.

As Jason Fung would say, intermittent fasting is great; doing a modified calorie-restricted diet is great, but it technically is so much easier to just stop eating … The second level of my modified food pyramid is ‘Don’t eat anything.'”

Probiotics Show Promise for Alzheimer’s
The effect of beneficial bacteria on brain health is well-established, including in people with Alzheimer’s disease. A 2016 study of 60 Alzheimer’s patients looked into the effect of probiotic supplements on cognitive function, with promising results.9 Those who drank milk containing probiotics experienced significant improvements in cognitive function.
While average Mini-Mental State Examination (MMSE) scores increased among the probiotics group and the control group, which drank plain milk, had a decrease in scores.
The probiotics group also had beneficial metabolic changes, including lowered triglycerides, very low-density lipoprotein and C-reactive protein, a measure of inflammation, as well as reduced markers for insulin resistance.
The researchers suggested the beneficial metabolic changes may be responsible for the cognitive improvements. Walter Lukiw, a professor at Louisiana State University who was not involved in the study, further explained to Medical News Today that your gut and brain are intricately connected:10

“This is in line with some of our recent studies which indicate that the GI [gastrointestinal] tract microbiome in Alzheimer’s is significantly altered in composition when compared to age-matched controls …

… and that both the GI tract and blood-brain barriers become significantly more leaky with aging, thus allowing GI tract microbial exudates (e.g. amyloids, lipopolysaccharides, endotoxins and small non-coding RNAs) to access central nervous system compartments.”

Probiotics May Inhibit Neurodegeneration
Probiotics are thought to influence the central nervous system and behavior via the microbiota-gut-brain-axis, and researchers have suggested they may have both preventive and therapeutic potential for Alzheimer’s disease (AD) by modulating the inflammatory process and counteracting oxidative stress, among other mechanisms.11 Writing in the open-access Impact Journal on Aging, researchers explained:12

“It has been found that dysfunction in behavior and cognition is associated with GM [gut microbiota] dysbiosis. Activation of gut inflammation has been regarded as a possible pathogenic cofactor in cognitive deterioration and dementia.

Moreover, the most distinctive alterations in the GM of AD patients are decreased abundance of anti-inflammatory bacterial species (e.g. Bifidobacterium brevestrain A1) and increased abundance of pro-inflammatory flora phyla (e.g. Firmicutes and Bacteroidetes).

And restoring GM homeostasis could slow down the progression of AD. Therefore, the GM has been proposed as a key player in the pathogenesis of AD and might be a new potential therapeutic target for the prevention and treatment of AD.”

They conducted a meta-analysis involving five studies and 297 subjects, which revealed a significant improvement in cognition and a significant reduction in malondialdehyde and high-sensitivity C-reactive protein — inflammatory and oxidative biomarkers — in probiotic groups compared to controls.13
Research is still uncovering which bacteria are most beneficial, but the Bifidobacterium breve strain A1 may be of particular use in Alzheimer’s treatment. Using Alzheimer’s disease model mice, researchers were able to confirm that daily oral administration of B. breve A1 reduced the cognitive dysfunction normally induced by amyloid beta.14
One of the mechanisms behind these protective effects was found to be suppression of amyloid-beta-induced changes in gene expression in the hippocampus. In short, the bacterium had an ameliorating effect on amyloid-beta toxicity.
Still other research suggests gut microbiota may contribute to Alzheimer’s risk via multiple avenues, including by influencing aging, diabetes, sleep and circadian rhythm.15
It’s also possible, researchers hypothesize, that decades of factors such as diet, stress, aging and genetics, combine to disrupt gut permeability and the integrity of the blood-brain barrier, allowing the entry of inflammatory agents and pathogens and inducing an inflammatory response that triggers a neuroinflammatory response in the brain.16
“There is mounting evidence that the gut microbiota interacts with AD pathogenesis by disrupting neuroinflammation and metabolic homeostasis,” they noted, adding that “the gut microbiota has gone from being the forgotten organ to a potential key player in the AD pathology.”17
Alzheimer’s Prevention Strategies
Optimizing your gut flora is a key strategy to preventing Alzheimer’s and a host of other chronic diseases. To do this, avoid processed foods, antibiotics and antibacterial products, fluoridated and chlorinated water, and be sure to eat traditionally fermented and cultured foods, along with taking a high-quality probiotic if needed.
Maintaining a healthy gut is one of the healthy lifestyle parameters outlined by Dr. Dale Bredesen, professor of molecular and medical pharmacology at the University of California, Los Angeles School of Medicine, and author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline.”18
Bredesen’s ReCODE protocol evaluates 150 factors, including biochemistry, genetics and historical imaging, known to contribute to Alzheimer’s disease. This identifies your disease subtype or combination of subtypes so an effective treatment protocol can be devised.
Time-restricted eating, or fasting, is another important strategy, as is reducing your intake of polyunsaturated fatty acids, also called PUFAs, found in vegetable oils, edible oils, seed oils, trans fat and plant oils. A high-fat, moderate-protein, low net-carb ketogenic diet is ideal for preventing degeneration that can lead to Alzheimer’s,19 and this will also help to nourish a healthy gut.
Overall, nourishing your brain health is best done with a comprehensively healthy lifestyle. By leveraging 36 healthy lifestyle parameters, Bredesen was able to reverse Alzheimer’s in 9 out of 10 patients.
This included the use of exercise, ketogenic diet, optimizing vitamin D and other hormones, increasing sleep, meditation, detoxification and eliminating gluten and processed food. For more details, you can download Bredesen’s full-text case paper online, which details the full program.20

Mid-March 2020 predictions said COVID-19 would kill 2.2 million Americans if allowed to run its course.1 By the end of March, Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, downgraded the projected death toll, saying we were probably looking at 100,000 to 240,000 Americans dying.2
April 8, 2020, a new model referred to as the Murray Model3 downgraded the threat further, predicting COVID-19 will kill 60,000 in the U.S. by August 20204 — a number that is still 20,000 lower than the Centers for Disease Control and Prevention’s death toll numbers attributed to the seasonal flu the winter of 2017/2018.5
Now, nine months into the pandemic, mortality statistics clearly show the truth: The COVID-19 pandemic is a pandemic in name only. In reality, there’s no excess mortality,6,7,8 and had it not been for the World Health Organization changing the definition of “pandemic,” COVID-19 would no longer be an issue.
I know some will balk at the concept of no excess mortality but the truth is the truth, and when you examine the existing numbers, that is what you find. If you integrate the U.S. Centers for Disease and Prevention’s comments that 94% of those who died had comorbidities, which could easily be the real cause of the reported “COVID-19 deaths,” it then becomes obvious that the numbers were highly inflated.
Definition of Pandemic Substantially Altered

The WHO’s original definition of a pandemic was:9,10

“… when a new influenza virus appears against which the human population has no immunity, resulting in several, simultaneous epidemics worldwide with enormous numbers of deaths and illness.”

The key portion of that definition is “enormous numbers of deaths and illness.” This definition was changed in the month leading up to the 2009 swine flu pandemic. The change was a simple but substantial one: They merely removed the severity and high mortality criteria, leaving the definition of a pandemic as “a worldwide epidemic of a disease.”11

This switch in definition allowed the WHO to declare swine flu a pandemic after a mere 144 people had died from the infection, worldwide, and it’s why COVID-19 is still promoted as a pandemic even though it has caused no excess mortality in nine months.12,13,14
We now have plenty of data showing the lethality of COVID-19 is on par with the seasonal flu.15,16,17,18,19 It may be different in terms of symptoms and complications, but the actual lethality is about the same. The absolute risk of death is equivalent to the risk of dying in a car accident.20,21
By removing the criteria of severe illness causing high morbidity, leaving geographically widespread infection as the only criteria for a pandemic, the WHO and technocratic leaders of the world were able to bamboozle the global population into giving up our lives and livelihoods.
As noted by Reiner Fuellmich, an attorney and founding member of the German Corona Extra-Parliamentary Inquiry Committee, the COVID-19 pandemic is “probably the greatest crime against humanity ever committed.”22,23,24,25
This certainly isn’t the first time doom and gloom predictions of mass casualties have completely collapsed. It’s also not the first time that fast-tracked pandemic vaccines have been issued, with devastating effect.
In that regard, we can learn a lot from the 1976 swine flu pandemic, detailed in the 1979 “60 Minutes” episode featured above. This was also the first time drug companies were indemnified against liability for any harm that might result from a fast-tracked vaccine. 
The Swine Flu Fraud of 1976

In February 1976, secretary of health F. David Matthews warned the American people there were indications that the virus responsible for the deadly 1918 flu pandemic had returned. In January that year, a 19-year-old Army private had died from flu-related pneumonia, despite being in good health, and by the end of the month, 155 soldiers at Fort Dix tested positive for swine flu antibodies.
Projections suggested the dreaded virus would kill 1 million Americans before the end of 1976.26 “The government propaganda machine cranked into action,” “60 Minutes” says, urging all Americans to get vaccinated against the swine flu.
Americans who got the swine flu vaccine were told it had been properly field tested. What they were not told was that the vaccine they received was not the actual vaccine that had undergone testing.
According to “60 Minutes,” 46 million Americans got the vaccine, and over the next few years, thousands of Americans filed vaccine damage claims with the federal government.27
This was well before the 1986 Vaccine Compensation Act, so vaccines were still liable for damages at that time. Congress did grant the swine flu vaccine special immunity, though, and wound up paying (actually U.S. taxpayers did) for the $3.5 billion in damages the vaccine caused. A 1981 report by the U.S. General Accounting Office to Sen. John Durkin reads, in part:28

“Before the swine flu program there were comparatively few vaccine-related claims made against the Government. Since 1963, Public Health Service records showed that only 27 non-swine flu claims were filed.
However, as of December 31, 1979, we found that 3,839 claims and 988 lawsuits had been filed against the Government alleging injury, death, or other damage resulting from the 45 million swine flu immunizations given under the program.
A Justice official told us that as of October 2, 1980, 3,965 claims and 1,384 lawsuits had been filed. Of the 3,965 claims filed, the Justice official said 316 claims had been settled for about $12.3 million …”

$3.5 Billion Dollars in Damages Paid for Vaccine Injuries

According to “60 Minutes,” the final claims amount for the nearly 4,000 claimants ended up totaling $3.5 billion. Two-thirds of the claimants suffered neurological damage and at least 300 of them died from vaccine side effects. In the end, the pandemic itself never materialized.29 An article by Real Clear Politics described the timeline of the pandemic that wasn’t, and the circumstances that led to the indemnification of vaccine makers:30

“All of the reported swine flu cases had been limited to the soldiers in Private Lewis’ camp. The virus wasn’t spreading. For some reason this information did not mollify the doctors, and on Feb. 14, 1976, the CDC issued a notice to all U.S. hospitals to be on the lookout for any cases of swine flu.

By March … not one case of swine flu had been reported outside of Fort Dix. For some reason this news did not placate the doctors either, and on March 13, 1976, the director of the CDC asked Congress for money to develop and test enough swine flu vaccine to immunize at least 80% of the population of the United States …
By July, [scientists] were pretty much agreed that a flu pandemic in 1976 would not lead to 1 million U.S. dead. The flu strain extracted from Private Lewis, they learned, was much less virulent that the 1918 strain …
The World Health Organization ordered hospitals to keep a global lookout for swine flu, but it did not request mass immunization … But the U.S. government was unstoppable. Congress began to pressure the drug companies to work faster toward development of a swine flu vaccine …
The drug companies suggested that they could work faster if they were given immunity from lawsuits in the event something went wrong with the vaccine. Congress refused. The issue of legal liability remained at an impasse until Aug. 2, 1976.
On that day, two members of the American Legion died of a strange respiratory disease they acquired at the Legion’s convention in Philadelphia. Congress collectively freaked.
Panicky news reports out of Philadelphia hinted that the deaths were the beginning of the Great Swine Flu Epidemic of 1976. On Aug. 3, Congress agreed to completely indemnify the drug companies against any and all lawsuits they might incur as a result of the distribution of swine flu vaccine.”

CDC Lied About Swine Flu Vaccine Safety

According to “60 Minutes,” Americans who got the swine flu vaccine were told it had been properly field tested. What they were not told was that the vaccine they received was not the actual vaccine that had undergone testing.
What’s more, according to Dr. Michael Hattwick, who directed the surveillance team for the 1976 swine flu vaccination program at the U.S. Centers for Disease Control and Prevention, there was evidence showing influenza vaccinations could, and had, caused neurological complications in the past.
He claims he warned his superiors of this possibility, as it pertained to the swine flu campaign. Yet the CDC denied the evidence and the American public was never informed of this risk. “60 Minutes” also reveals the CDC was proven to have lied in its marketing materials for the vaccine.
Judy Roberts was one of the victims of that 1976 vaccination campaign. She was paralyzed by the vaccine, and suffered permanent damage. Her husband, who also was vaccinated and suffered no ill effects, ends the “60 Minute” segment saying:

“I told Judy to take the shot … I’m mad with my government. They knew the facts but they didn’t release those facts, because if they had released them, people wouldn’t have taken it.
And they can come out tomorrow and tell me there’s going to be an epidemic, and they can drop off like flies next to me, and I will not take another shot that my government tells me to take.”

The Origin of the Anti-Vaccine Movement

The 1976 swine flu vaccine program has sometimes been cited as the origin of the anti-vaccine movement, and for good reason. Thousands were seriously injured and hundreds died after placing their trust in scientists and the government. Many of them, just like Roberts in the “60 Minutes” segment, vowed never to be that naïve again. As reported by Smithsonian Magazine in 2017:31

“In the spring of 1976, it looked like that year’s flu was the real thing. Spoiler alert: it wasn’t, and rushed response led to a medical debacle that hasn’t gone away.
‘Some of the American public’s hesitance to embrace vaccines — the flu vaccine in particular — can be attributed to the long-lasting effects of a failed 1976 campaign to mass-vaccinate the public against a strain of the swine flu virus,’ writes Rebecca Kreston for Discover.
‘This government-led campaign was widely viewed as a debacle and put an irreparable dent in future public health initiative, as well as negatively influenced the public’s perception of both the flu and the flu shot in this country.'”

Pandemic Threats Have Repeatedly Turned to Naught

Sadly, the embarrassment of the 1976 swine flu debacle did not put an end to faux pandemics. In the last 15 years alone we’ve had to defend against wave upon wave of pandemic pandemonium, none of which turned out to be the global killer that “experts” predicted.
The 2005 bird flu outbreak, for example, was predicted to kill anywhere from 2 million to 150 million people. In reality, the death toll topped out at just 98 people, globally, in 2005; 115 in 2006; and 86 in 2007.32 No one in the U.S. died from this infection, and the sheer brazenness of this fake pandemic prompted me to write my New York Times best seller book “The Great Bird Flu Hoax.”
In 2006, 2007 and again in 2008, hyped warnings over the bird flu were repeatedly exposed as little more than a cruel hoax, designed to instill fear and line the pocketbooks of industry and various vested individuals.
Then came the now infamous H1N1 swine flu of 2009.33 The CDC estimates that from April 12, 2009, to April 10, 2010, there were 60.8 million cases of H1N1 infection, 274,000 hospitalizations and 12,469 deaths in the United States. The infection fatality rate was a mere 0.02%. Then, as now, vaccines were fast-tracked. Lo and behold, within months, cases of disability and death from the H1N1 vaccine were reported in various parts of the world.
In 2010, the ASO3-adjuvanted swine flu vaccine Pandemrix (used in Europe but not in the U.S. during 2009-2010) was causally linked34 to childhood narcolepsy, which had abruptly skyrocketed in several countries during the vaccination campaign.35,36

In the aftermath, the Council of Europe Parliamentary Assembly (PACE) raised serious questions about the WHO’s handling of the pandemic and the role drug companies may have played in its drug and vaccine recommendations.
In June 2010, PACE concluded “the handling of the pandemic by the WHO, EU health agencies and national governments led to a ‘waste of large sums of public money, and unjustified scares and fears about the health risks faced by the European public.'”37
Specifically, PACE concluded there was “overwhelming evidence that the seriousness of the pandemic was vastly overrated by WHO,” and that the drug industry had influenced the organization’s decision-making.38
The sad reality is that the WHO is little more than a front group for Big Pharma and the technocratic elite that seek to “reset” the global economic and social structure. It would indeed be naïve to expect this private organization to do what’s right for public health while simultaneously taking direction from Bill Gates (its primary funder) and the drug industry.
While the 2009 swine flu pandemic was the most significant in terms of the fearmongering brought to bear, in the summer of 2012, dire predictions of mutating bird flu again filled the media, followed by urgent calls for yet another fast-tracked vaccine.

Two years later, in 2014, the Ebola virus turned into a global health emergency after epidemics in Liberia, Guinea and Sierra Leone had been largely ignored. Interestingly enough, a UN resolution called for no restrictions on international travel to Ebola-stricken countries — a decision that led to an infected passenger bringing the infection to the U.S.
Another two years after that, in 2016, Zika virus hit pandemic status,39 triggering travel alerts and restrictions in and out of affected regions. All of these pandemics defied experts’ predictions of mass casualties. None turned into a global killer, and COVID-19 is no different.40,41,42
Why We Must End Gain-of-Function Research

Time and again, serious safety breaches have been identified at laboratories working with the most lethal and dangerous pathogens in the world,43,44,45,46,47,48,49 and mounting evidence suggests SARS-CoV-2 may be a lab creation as well.

Scientists defend and promote gain-of-function research by insisting it allows us to prepare for pandemics.50 In reality, this kind of research does not appear to have improved governments’ pandemic responses in the least. If anything, it’s a curious coincidence that the very viruses undergoing gain-of-function research are the ones causing pandemics.

As just one example, an article51 by Mark Denison, editor of mBio, presents a hypothesis for the 1977-1978 H1N1 swine flu pandemic, often referred to as the Russian flu, as the first cases were reported in the USSR. According to Denison, the pandemic “was probably not a natural event, as the genetic sequence of the virus was nearly identical to the sequences of decades-old strains.”

The lab hypothesis has “gained popularity in discussions about the biosafety risks of gain-of-function influenza virus research, as an argument for why this research should not be performed,” he writes. Another possibility being kicked around is that the infection spread through a live-vaccine trial. A third option: a deliberate release as a bioweapon.
As noted in a 2009 New England Journal of Medicine review article, which provided a historical perspective on the emergence of H1N1 viruses:52

“Even though human influenza A (H1N1) virus had not circulated since 1957 and the swine influenza A (H1N1) virus that had been identified at Fort Dix did not extend outside the base, in November 1977, the H1N1 strain reemerged in the former Soviet Union, Hong Kong, and northeastern China.
This strain affected primarily young people in a relatively mild presentation. Careful study of the genetic origin of the virus showed that it was closely related to a 1950 strain but dissimilar to influenza A (H1N1) strains from both 1947 and 1957.
This finding suggested that the 1977 outbreak strain had been preserved since 1950. The reemergence was probably an accidental release from a laboratory source in the setting of waning population immunity to H1 and N1 antigens.”

Can history repeat itself? There are no guarantees that it can’t or won’t, which is why it’s so important we find out where SARS-CoV-2 really came from. As noted by the National Review,53 getting to the bottom of the origin of SARS-CoV-2 is crucial if we want to prevent a similar pandemic in the future:

“If it originated from a person eating bat or pangolin at a wet market, then we need to take steps to ensure that bat and pangolin consumption and trade stops …
Bat guano is used as fertilizer in many countries, and that guano can be full of viruses … If this is the source of the virus, we need to get people to stop going into caves and using the guano as fertilizer …
In a strange way, the ‘lab accident’ scenario is one of the most reassuring explanations. It means that if we want to ensure we never experience this again, we simply need to get every lab in the world working on contagious viruses to ensure 100% compliance with safety protocols, all the time.”

As temperatures drop, rates of respiratory infections — the common cold and influenza, primarily — increase exponentially. Many believe this has to do with the drop in temperature, but cold exposure actually ramps up your immune system, making you less prone to infection.
According to a 2002 study1,2 by the U.S. and Canadian armies, cold exposure can double the number of natural killer (NK) cells in your body, which are part of your first line of defense against pathogenic infiltration and other types of cell damage.
As detailed by retired nurse and academic teacher John Campbell in the video above, a scientific review3 published in 2006 concluded that epidemic seasonal influenza is most likely related to the prevalence of vitamin D deficiency during winter months. According to the authors:4

“In 1981, R. Edgar Hope-Simpson proposed that a ‘seasonal stimulus’ intimately associated with solar radiation explained the remarkable seasonality of epidemic influenza.
Solar radiation triggers robust seasonal vitamin D production in the skin; vitamin D deficiency is common in the winter, and activated vitamin D, 1,25(OH)2D, a steroid hormone, has profound effects on human immunity.
1,25(OH)2D acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the ‘oxidative burst’ potential of macrophages.
Perhaps most importantly, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in neutrophils, monocytes, natural killer cells, and in epithelial cells lining the respiratory tract where they play a major role in protecting the lung from infection.”

Source: Cannel et.al. 20065: Temperate latitudes show seasonal variation in viral infection rates that correspond to changes in solar irradiance. Tropical latitudes do not, because the solar variation is minimal.

Inverse Relationship Between Flu Deaths and UVB Exposure

While vitamin D has been linked to many health benefits, the relationship between vitamin D and infectious disease is particularly robust. For example, a 2010 study6 by Norwegian researchers found there’s an inverse relationship between UVB sun exposure — which is how your body synthesizes vitamin D naturally — and influenza deaths. According to the authors:7

“Non-pandemic influenzas mostly occur in the winter season in temperate regions. UVB calculations show that at high latitudes very little, if any, vitamin D is produced in the skin during the winter.
Even at 26°N (Okinawa) there is about four times more UVB during the summer than during the winter. In tropical regions there are two minor peaks in vitamin D photosynthesis, and practically no seasonality of influenza.
Pandemics may start with a wave in an arbitrary season, while secondary waves often occur the following winter. Thus, it appears that a low vitamin D status may play a significant role in most influenzas The data support the hypothesis that high fluences of UVB radiation (vitamin D level), as occur in the summer, act in a protective manner with respect to influenza.”

Vitamin D Protects Against Fatal Lung Disease

Other studies8,9,10 have confirmed the long-held belief that vitamin D protects against tuberculosis, a fatal lung disease that kills an estimated 1.8 million people around the world each year.11 This is largely related to vitamin D stimulating antimicrobial peptides (AMPs) like cathelicidin (LL37).
In the past, tuberculosis was treated by making sure patients got plenty of sun exposure. In fact Finsen was given the Nobel Prize in 1903 for this determination. Around the turn of the 20th century regular sun exposure was the most effective clinical strategy for the treatment of tuberculosis, but was eventually phased out with the development of antibiotics.
A 2011 study in Science Translational Medicine examined the mechanisms responsible for your immune system’s ability to ward against tuberculosis, concluding that T cells play a central role. They release a protein called interferon-g, which in turn activates the release of AMPs so your immune cells can mount an effective attack against the tuberculosis bacteria.
However, in order for this activation to occur, you have to have sufficient levels of vitamin D. In patients with low vitamin D levels, this immune response was not activated. Meanwhile, among those with adequate levels, there was an 85% reduction of colony-forming tuberculosis bacteria. As reported by UCLA:12

“The team noted that vitamin D may help both innate and adaptive immunity, two systems that work synergistically together to fight infections. Previous research by the team found that vitamin D played a key role in the production of a molecule called cathelicidin, which helps the innate immune system kill the tuberculosis bacteria.
Humans are born with innate immunity, which is the preprogrammed part of the immune system. The current research findings demonstrate that vitamin D is also critical for the action of T cells, key players in adaptive immunity, a highly specialized system that humans acquire over time as they encounter different pathogens.”

More Than 80% of COVID Patients Are Vitamin D Deficient

Currently, the respiratory infection of note is of course COVID-19, and vitamin D appears to have a lot to do with your risk of this infection as well. According to a Spanish study13,14,15 published online October 27, 2020, in The Journal of Clinical Endocrinology & Metabolism, 82.2% of COVID-19 patients tested were found to be deficient in vitamin D. As reported by the authors:16

“In COVID-19 patients, mean± SD 25OHD levels were 13.8±7.2 ng/ml, compared to 20.9 ±7.4 ng/ml in controls. 25OHD values were lower in men than in women. Vitamin D deficiency was found in 82.2% of COVID-19 cases and 47.2% of population-based controls.
25OHD inversely correlate to serum ferritin and D-dimer levels. Vitamin D deficient COVID-19 patients had a greater prevalence of hypertension and cardiovascular diseases, raised serum ferritin and troponin levels, as well as a longer length of hospital stay than those with serum 25 OHD levels ? 20 ng/ml.”

While this particular study failed to find a correlation between vitamin D levels and disease severity, other studies have shown patients with higher levels do tend to have milder disease. In fact, one such study17,18 found your risk of developing a severe case of, and dying from, COVID-19 virtually disappears once your vitamin D level gets above 30 ng/mL (75 nmol/L).
SARS-CoV-2 positivity is strongly and inversely associated with circulating 25(OH)D levels, a relationship that persists across latitudes, races/ethnicities, both sexes, and age ranges. ~ PLOS ONE September 17, 2020
Other research19 looking at vitamin D and COVID-19 mortality found those with a vitamin D level between 21 ng/mL (50 nmol/L) and 29 ng/mL (75 nmol/L) had a 12.55 times higher risk of death than those with a level above 30 ng/mL. Having a level below 20 ng/mL was associated with a 19.12 times higher risk of death.
Vitamin D Lowers Your Risk of a Positive COVID-19 Test

Vitamin D has also been linked to a lower risk of testing positive for COVID-19. This, the largest observational study20 to date, looked at data for 191,779 American patients who were tested for SARS-CoV-2 between March and June 2020 and had had their vitamin D tested sometime in the preceding 12 months.
Of those with a vitamin D level below 20 ng/ml (deficiency), 12.5% tested positive for SARS-CoV-2, compared to 8.1% of those who had a vitamin D level between 30 and 34 ng/ml (adequacy) and 5.9% of those who had an optimal vitamin D level of 55 ng/ml or higher. As noted by the authors:21

“SARS-CoV-2 positivity is strongly and inversely associated with circulating 25(OH)D levels, a relationship that persists across latitudes, races/ethnicities, both sexes, and age ranges.”

How Vitamin D Impacts COVID-19
In June 2020, I launched an information campaign about vitamin D that included the release of a downloadable scientific report. This report, as well as a two-minute COVID risk quiz is available on StopCovidCold.com.

October 31, 2020, my review paper22 “Evidence Regarding Vitamin D and Risk of COVID-19 and Its Severity,” co-written with William Grant, Ph.D., and Dr. Carol Wagner, both of whom are part of the GrassrootsHealth expert vitamin D panel, was also published in the peer-reviewed journal Nutrients. You can read the paper for free on the journal’s website.

As noted in that paper, dark skin color, increased age, pre-existing chronic conditions and vitamin D deficiency are all features of severe COVID disease, and of these, vitamin D deficiency is the only factor that is readily and easily modifiable.
You may be able to reverse chronic disease, but that typically takes time. Optimizing your vitamin D, on the other hand, can be achieved in just a few weeks, thereby significantly lowering your risk of severe COVID-19.
In our paper, we review several of the mechanisms by which vitamin D can reduce your risk of COVID-19 and other respiratory infections, including but not limited to the following:23

Reducing the survival and replication of viruses24
Reducing inflammatory cytokine production
Maintaining endothelial integrity — Endothelial dysfunction contributes to vascular inflammation and impaired blood clotting, two hallmarks of severe COVID-19
Increasing angiotensin-converting enzyme 2 (ACE2) concentrations, which prevents the virus from entering cells via the ACE2 receptor — ACE2 is downregulated by SARS-CoV-2 infection, and by increasing ACE2, you also avoid excessive accumulation of angiotensin II, a peptide hormone known to increase the severity of COVID-19

Vitamin D is also an important component of COVID-19 prevention and treatment for the fact that it:

Boosts your overall immune function by modulating your innate and adaptive immune responses
Reduces respiratory distress25
Improves overall lung function
Helps produce surfactants in your lungs that aid in fluid clearance26
Lowers your risk of comorbidities associated with poor COVID-19 prognosis, including obesity,27 Type 2 diabetes,28 high blood pressure29 and heart disease30

Data from 14 observational studies — summarized in Table 1 of our paper31 — suggest that vitamin D blood levels are inversely correlated with the incidence and/or severity of COVID-19, and the evidence currently available generally satisfies Hill’s criteria for causality in a biological system.32
COVID-19 Features Related to Vitamin D Status
Our paper33 also details several features of COVID-19 that suggest vitamin D deficiency is at play. For starters, SARS-CoV-2 emerged in the winter in the northern hemisphere, and as we moved into summer, positive tests, hospitalizations and death rates fell. So, generally, COVID-19 prevalence has been inversely correlated with solar UVB doses and vitamin D production, just like seasonal influenza.
Secondly, people with darker skin have higher COVID-19 case and death rates than Caucasians. Vitamin D is produced in your skin in response to sun exposure, but the darker your skin, the more sun exposure you need in order to maintain an optimal vitamin D level. As a result, vitamin D deficiency tends to be far higher among Blacks and dark-skinned Hispanics.

Thirdly, one of the lethal hallmarks of COVID-19 is the cytokine storm that can develop in severe cases, which manifests as hyperinflammation and tissue damage. Vitamin D is known to regulate inflammatory cytokine production, thereby lowering this risk. Lastly, vitamin D is an important regulator of your immune system, and dysregulation of the immune system is a hallmark of severe COVID-19.
England to Hand Out Free Vitamin D Supplements
According to a November 28, 2020, BBC News report,34 British health officials are now recommending people take supplemental vitamin D this winter to reduce their risk of respiratory infections, including COVID-19.
Similar recommendations have been issued to the government health officials in Scotland, Wales and Northern Ireland. Unfortunately, no such recommendations have been issued in the U.S., which is why sharing this information is so important.
Senior care homes in the U.K. will receive enough vitamin D supplements to cover all residents, and people on the “clinically extremely vulnerable” list35 will have the option to get four months’ worth of free vitamin D supplements delivered to their homes starting in January 2021.
Even though the dose she recommended is 100% to 180% lower than the ideal range of 6,000 to 8,000 units per day, nevertheless chief nutritionist at Public Health England, Dr. Alison Tedstone, told the BBC:36

“We advise that everyone, particularly the elderly, those who don’t get outside and those with dark skin, take a vitamin D supplement containing 10 micrograms (400IU) every day. This year, the advice is more important than ever with more people spending more time inside, which is why the government will be helping the clinically extremely vulnerable to get vitamin D.”

Co-Nutrients Reduce Your Vitamin D Requirement

If you cannot get sufficient amounts of sun exposure to maintain a vitamin D blood level of 40 ng/mL (100 nmol/L) to 60 ng/mL (150 nmol/L), a vitamin D3 supplement is highly recommended. Just remember that the most important factor here is your blood level, not the dose, so before you start, get tested so you know your baseline. This will help you determine your ideal dose, as it can vary widely from person to person.
Also remember that you can minimize your vitamin D requirement by making sure you’re also getting enough magnesium. Magnesium is required for the conversion of vitamin D into its active form,37,38,39,40 and research41 has confirmed higher magnesium intake helps reduce your risk of vitamin D deficiency by activating more of it.
A scientific review42,43 published in 2018 concluded that up to half of all Americans taking vitamin D supplements may not get significant benefit as the vitamin D simply gets stored in its inactive form, and the reason for this is because their magnesium levels are too low.
Research by GrassrootsHealth reveals taking supplemental magnesium can lower your vitamin D need by 146%. Vitamin K2 is another important cofactor, and taking both magnesium and vitamin K2 can lower your vitamin D requirement by as much as 244%.44

Take-Home Message

All in all, the evidence is unmistakable: Optimizing your vitamin D can go a long way toward minimizing your chances of contracting a respiratory infection, be it the common cold, seasonal influenza or COVID-19.

Mounting evidence also demonstrates that if you do end up contracting COVID-19, having adequate vitamin D will lower the odds of you requiring hospitalization45 and intensive care46,47,48,49 as it reduces the severity of the infection.50,51 As detailed earlier, vitamin D also lowers your risk of dying from COVID-19.52,53,54,55,56

I urge everyone to share this information so that we can minimize additional outbreaks. Again, if you live in the northern hemisphere, now is the time to check your vitamin D level and start taking action to raise it if you’re below 40 ng/mL (100 nmol/L). Experts recommend a vitamin D level between 40 and 60 ng/mL (100 to 150 nmol/L).

An easy and cost-effective way of measuring your vitamin D level is to order GrassrootsHealth’s vitamin D testing kit. Also, if you haven’t already visited www.stopcovidcold.com please do so now so you can take your free COVID risk test and grab a free PDF copy of my vitamin D report, which has far better graphics than what we were able to put into our Nutrients paper.
Once you know your current vitamin D level, use the GrassrootsHealth vitamin D calculator57 to determine how much vitamin D you might need to reach your target level, and remember that increasing your magnesium and vitamin K2 intake will optimize your vitamin D absorption and utilization.
Retest your vitamin D level in three to four months to make sure you’ve reached your target level. If you have, then you’re taking the correct dosage. If you’re still low (or have reached a level above 80 ng/mL), you’ll need to adjust your dosage accordingly and retest again in another three to four months.

Bay leaves are popularly used in pickling, marinating and flavoring stews, soups and stuffing. They come from the bay laurel tree native to Mediterranean countries. The leaves can be up to 3 inches long and are almond-shaped. You’ve likely seen cooking shows or read recipes that recommended adding a bay leaf to savory soups and stews, but removing it before eating. As Serious Eats describes the bay leaf:1

“It’s understandable why you may think they’re optional. Bay leaf, by its very nature, plays second fiddle to other, more prominent flavors. But just as a grind of black pepper, some sautéed anchovies, or a softened leek might not be instantly recognizable in a stew, they add a layer of subtle background music for the stars of your dish to play over.”

Although the initial flavor is reminiscent of Vicks VapoRub, originating from the chemical eugenol that’s the largest compound in the bay leaf, the flavor changes after simmering for an hour or two and adds a complex profile that many people enjoy in their soups and sauces.
Biting into a bay leaf is unpleasant, which is why they’re left whole in the cooking and fished out before serving. You can find fresh and dried bay leaves at most grocery stores. For the most part, dried bay leaves are generally imported from the Mediterranean region and fresh bay leaves are shipped from California.2 Although they’re both called bay leaves and used in nearly the same way, the plants are not directly related.
What Bay Leaf Is in Your Spice Rack?

The true bay leaf is also known as a bay laurel and is a broadleaf evergreen tree native to Western Asia, Northern Africa and southern Europe.3 The botanical name is Laurus nobilis and it can be grown as a houseplant.
However, you may have seen the leaves of other species commonly sold as bay leaves since the leaves are similar in morphology, aroma and sometimes flavor.4 These substitutes include:5

Cinnamomum tamala (Indian bay leaf)
Litsea glaucescens (Mexican bay leaf)
Pimenta racemosa (West Indian bay leaf)
Syzygium polyanthum (Indonesian bay leaf)
Umbellularia californica (Californian bay leaf)

While they look similar, the flavor and odor after cooking are not what you would expect from L. nobilis. As the writer at Serious Eats describes, throwing a fresh bay leaf into a bechamel sauce resulted in something that “tasted like I’d tipped a bottle of cold medicine into it.”6
In a recent study, researchers compared the Laurus nobilis, commonly sold in Nigerian markets, against the leaves of Syzygium guineense (S.guineense) and Syzygium eucalyptoides (S. eucalyptoides) in search of a possible replacement for the bay laurel.7
The researchers used a commercial sample of Laurus nobilis as the gold standard and compared essential oils obtained through hydrodistillation and analyzed by gas chromatography-mass spectrometry. The largest constituents in L. nobilis were eucalyptol, alpha pinene and camphene.
There were 75 compounds in L. nobilis, 16 of which matched S. guineense essential oil, with six matching compounds in S. eucalyptoides. Syzygium guineense has historically been used in folklore medicine by people in African countries. The researchers included it to analyze the antimicrobial and antioxidant properties in the essential oil.
Syzygium eucalyptoides is native to Western Australia, where the fruit is eaten to help prevent cancer, fight asthma and lower the risk of diabetes. The leaves, bark and fruit of the Syzygium polyanthum plant have a variety of traditional uses, including to treat high blood pressure, gastritis, diarrhea and skin diseases.
Bay Leaf Extract Lowers Fasting Blood Glucose Level

Past studies of Syzygium polyanthum demonstrated the ethanol extract of the essential oil had antioxidant activities and was safe for humans. In a study presented at the 6th International Conference on Public Health in Indonesia, researchers discussed their study in which they investigated the effects of the ethanol extract on fasting blood sugar in study participants with Type 2 diabetes.8
The pilot study used a randomized control trial design with a small sample size of eight individuals. Those receiving the intervention consumed 350 milligrams (mg) of the extract in capsule form once a day for 14 days. The control group took a placebo for the same time period.
Data were collected on the day before the intervention began and after the participants had taken the supplement for 14 days. Following the intervention, the fasting blood sugar in the group receiving the supplement was lower than in the control group.
The researchers believe the statistical nonsignificant difference was related to the small sample size in a pilot study and concluded the Syzygium polyanthum ethanol extract may be an effective means of lowering blood sugar in people with Type 2 diabetes.9
The results support an earlier animal study using a methanol extract of S. polyanthum testing for hypoglycemic activity. The researchers wrote that people with diabetes in Indonesia commonly included the leaf in traditional medicine to control blood sugar.10
The researchers evaluated the possible mechanisms through which the extract exerted the antihyperglycemic activity and found it inhibited the absorption of glucose from the intestines and increased the uptake in muscle tissue. A second animal study showed rats that received S. polyanthum extract had a 65.91% lower blood glucose than those in the control group.11
Bay Leaf and Soursop Help Lower Uric Acid Levels

In a study published in Scientific Reports, the researchers sought to investigate the potential bidirectional association between gout and Type 2 diabetes.12 They used data from the Singapore Chinese Health Study, and concluded that the results suggested having an incident of gout is related to the development of diabetes in normal weight individuals — yet those with diabetes had a lower risk of gout.
A second study also found people who developed gout had an increased risk of developing diabetes.13 Gout is caused by elevated levels of uric acid in the blood that’s the result of increased production or decreased excretion.14 According to the Partnership to Fight Chronic Disease, nearly 4 million people in the U.S. have gout, which is a form of inflammatory arthritis.15
In an evaluation by the same organization, the researcher found treatment for gout exceeded $11,000 per patient each year, which is much higher than previous estimates.16 Researchers from Perintis Institute of Health Science in Indonesia sought to compare the effect of Indonesian bay leaf drink against soursop juice to reduce uric acid levels and thus impact on gout development.17
Soursop fruit is also called graviola and is a creamy textured, strongly flavored fruit some compare to pineapple or strawberries.18 The researchers did a pretest and a post-test after intervention with 17 participants who drank the bay leaf drink and 17 who consumed soursop juice.
Although both groups had lower levels of uric acid at the end of the intervention, the researchers found those who consumed the soursop juice had a statistically greater reduction. However, bay leaves have been a traditional part of Ayurveda remedies in the treatment of gout, both in tea form and as an external application.19
Supplement Lowers Blood Pressure and Promotes Angiogenesis

Indonesian bay leaf (Syzygium polyanthum) also influences your vascular system. In one study from Indonesia published in 2020, the researchers evaluated the effect that bay leaf extract could have on vascular endothelial growth.20
They used an animal model in which acute coronary syndrome was surgically induced and the animals then treated with the bay leaf extract. On evaluation, the researchers found a significant expression of vascular endothelial growth factors in the treatment group as compared to the control group.
This led them to conclude bay leaf extract could have a potential effect on angiogenesis and act as an adjuvant treatment that may lead “to better prognosis for reperfusion on ischemic tissue.”21 This has the potential to improve recovery after cardiovascular events that trigger tissue ischemia and damage.
A second recent study published in the International Journal of Innovative Science and Research Technology evaluated the effect Indonesian bay leaf may have on the systolic and diastolic blood pressure of pregnant women with high blood pressure.22
The researchers engaged 39 pregnant women and split them into 19 in the intervention group and 20 in the control group. The women in the intervention group were given 14 days of 80 mg of Indonesian bay leaf nanoparticles with 10 mg of nifedipine, while the control group received just the nifedipine.
Nifedipine is a calcium channel blocker used to treat high blood pressure and control angina,23 and is prescribed in the treatment of high blood pressure in pregnancy.24 The data showed there was a greater decrease in systolic and diastolic blood pressure in the intervention group where the medication was augmented with bay leaf nanoparticles.
Multiple Health Effects Attributed to Laurus Nobilis

Many of these studies used Syzygium polyanthum extract, but other researchers have evaluated the health benefits of true bay leaf (Laurus nobilis) and found several successful pharmacological uses. Traditionally, the leaves have been used as antidiarrheal, anti-inflammatory or antidiabetic remedies. Animal studies have also found L. nobilis contributes to:25

Wound healing
Anticonvulsant activity
Analgesic capabilities

Antimutagenic processes
Immunostimulant capabilities
Antiviral uses

Anticholinergic action
Repellent qualities against the common mosquito
Antibacterial uses against Staphylococcus aureus, Bacillus subtilis, and Staphylococcus intermedius

It’s important to know that when you buy bay leaves with the scientific term Laurus nobilis, you want it to be the genuine article and not some knock-off from an ornamental plant. They must be from the laurel tree, so shop for quality. While some herbs, when dried, become powdery and tasteless, bay leaves can be dried with very little change in the aromatic components.26
Bay leaves are a classic ingredient in savory sauces, and delicious on seafood, meats and numerous vegetable dishes. One FYI: Due to the presence of a high concentration of eugenol, bay leaf oil (or bay oil) may be a skin and mucus membrane irritant. If you want your bay leaves to last, store them in the freezer, which is helpful if you want to buy them in bulk.