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The Effects of Vitamin D and COVID-Related Outcomes

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Reproduced from original article:

Analysis by Dr. Joseph Mercola    Fact Checked      July 08, 2021

vitamin d and covid-19


  • Researchers investigated the effects of Pulse D therapy — daily high-dose supplementation (60,000 IUs) of vitamin D — for eight to 10 days, in addition to standard therapy, for COVID-19 patients deficient in vitamin D
  • Vitamin D levels increased significantly in the vitamin D group — from 16 ng/ml to 89 ng/ml — while inflammatory markers significantly decreased, without any side effects
  • Vitamin D has multiple actions on the immune system, including enhancing the production of antimicrobial peptides by immune cells, reducing damaging proinflammatory cytokines and promoting the expression of anti-inflammatory cytokines
  • A growing number of studies shows that vitamin D administration significantly reduces ICU admission and death in cases of COVID-19
  • Vitamin D is inexpensive, widely available and safe; getting your blood tested — and optimizing your levels — is one of the simplest and most straightforward steps you can take to improve your health, including in relation to COVID-19

Do you know your vitamin D level? If not, getting your blood tested — and optimizing your levels — is one of the simplest and most straightforward steps you can take to improve your health, including in relation to COVID-19. Vitamin D, as an immunomodulator, is a perfect candidate for countering the immune dysregulation that’s common with COVID-19.1

As early as November 2020, it was known that there were striking differences in vitamin D status among people who had asymptomatic COVID-19 and those who became severely ill and required ICU admission. In one study, 32.96% of those with asymptomatic cases were vitamin D deficient, compared to 96.82% of those who were admitted to the ICU for a severe case.2

COVID-19 patients who were deficient in this inexpensive and widely available vitamin had a higher inflammatory response and a greater fatality rate. The Indian study authors recommended “mass administration of vitamin D supplements to populations at risk for COVID-19,”3 but this hasn’t happened, at least not in the U.S.

As of April 21, 2021, the date the U.S. National Institutes of Health (NIH) last updated their COVID-19 treatment guidelines/vitamin D page, they stated, “There are insufficient data to recommend either for or against the use of vitamin D for the prevention or treatment of COVID-19.”4 As you’ll see in the paragraphs that follow, however, the evidence for its use is beyond overwhelming.

Vitamin D Therapy Reduces COVID’s Inflammatory Storm

Vitamin D has multiple actions on the immune system, including enhancing the production of antimicrobial peptides by immune cells, reducing damaging proinflammatory cytokines and promoting the expression of anti-inflammatory cytokines.5 Cytokines are a group of proteins that your body uses to control inflammation.

If you have an infection, your body will release cytokines to help combat inflammation, but sometimes it releases more than it should. If the cytokine release spirals out of control, the resulting “cytokine storm” becomes dangerous and is closely tied to sepsis, which may be an important contributor to the death of COVID-19 patients.6

Many COVID-19 therapeutics are focused on viral elimination instead of modulating the hyperinflammation often seen in the disease. In fact, uncontrolled immune response has been suggested as a factor in disease severity, making immunomodulation “an attractive potential treatment strategy.”7

In one example, researchers investigated the effects of Pulse D therapy — daily high-dose supplementation (60,000 IUs) of vitamin D — for eight to 10 days, in addition to standard therapy, for COVID-19 patients deficient in vitamin D.8 Vitamin D levels increased significantly in the vitamin D group — from 16 ng/ml to 89 ng/ml — while inflammatory markers significantly decreased, without any side effects.

“Vit.D acts as a smart switch to decrease the Th1 response and pro inflammatory cytokines while enhancing the production of anti-inflammatory cytokines in cases of immune dysregulation. It is pertinent to note that SARS-CoV-2 virus activates Th1 response and suppresses Th2 response,” researchers wrote in the journal Scientific Reports.9

They concluded that Pulse D therapy could be safely added to COVID-19 treatment protocols for improved outcomes.

Vitamin D3 Reduces COVID-19 Deaths and ICU Admissions

Another group of researchers in Spain gave vitamin D3 (calcifediol) to patients admitted to the COVID-19 wards of Barcelona’s Hospital del Mar.10 About half the patients received vitamin D3 in the amount of 21,280 IU on day one plus 10,640 IU on Days 3, 7, 15 and 30. Those that received vitamin D fared significantly better, with only 4.5% requiring ICU admission compared to 21% in the no-vitamin D group.

Vitamin D treatment also significantly reduced mortality, with 4.7% of the vitamin D group dying at admission compared to 15.9% in the no-vitamin D group. “In patients hospitalized with COVID-19, calcifediol treatment significantly reduced ICU admission and mortality,” according to the researchers.11 In response to the findings, British MP David Davis tweeted:12

“This is a very important study on vitamin D and Covid-19. Its findings are incredibly clear. An 80% reduction in need for ICU and a 60% reduction in deaths, simply by giving a very cheap and very safe therapy – calcifediol, or activated vitamin D … The findings of this large and well conducted study should result in this therapy being administered to every COVID patient in every hospital in the temperate latitudes.”

At one point, the U.K.’s National Health Service was offering free vitamin D supplements to people at high risk from COVID-19,13 but they also state, like the U.S., “there is currently not enough evidence to support taking vitamin D to prevent or treat COVID-19.”14

While their guidance does urge Britons to take a vitamin D supplement between October and March “to keep your bones and muscles healthy,” it only recommends a dose of 400 IUs a day, which is easily 20 times lower than what most people require for general health and optimal immune function.

Dose matters when it comes to COVID-19 recovery. Researchers compared daily supplementation with either 5,000 IUs or 1,000 IUs oral vitamin D3 among patients with suboptimal vitamin D levels hospitalized for mild to moderate COVID-19.15 Those in the 5,000 IUs group had a significantly shorter time to recovery for cough and loss of the sense of taste compared to the 1,000 IUs group.

According to the researchers, “The use of 5000 IU vitamin D3 as an adjuvant therapy for COVID-19 patients with suboptimal vitamin D status, even for a short duration, is recommended.”16

If You’re Hospitalized With COVID-19, Ask for Vitamin D

The evidence continues to grow that treatment with vitamin D leads to significantly better outcomes for people hospitalized with COVID-19. In another example, hospitalized COVID-19 patients who received vitamin D3 had a mortality rate of 5%, compared to 20% for those who did not. The researchers explained:17

“… [T]he protective effect of calcifediol remained significant after adjustment for multiple confounder factors related to severity disease even after selecting those subjects who were older (≥65 years) and had worse oxygen saturation levels at admission (<96%).”

Similarly, 76 consecutive patients hospitalized with COVID-19 at Reina Sofia University Hospital in Córdoba,18 Spain, were randomized to receive either standard care or standard care plus vitamin D3 to rapidly increase vitamin D levels.

Of 50 treated with vitamin D, only one person was admitted to the ICU. Of 26 who were not treated with vitamin D, 13 (50%) required admission to the hospital. Researchers noted, “Calcifediol seems to be able to reduce severity of the disease.”19 Further:

“Of the patients treated with calcifediol, none died, and all were discharged, without complications. The 13 patients not treated with calcifediol, who were not admitted to the ICU, were discharged. Of the 13 patients admitted to the ICU, two died and the remaining 11 were discharged.”

In a previous review,20 the researchers explained that vitamin D has favorable effects during both the early viraemic phase of COVID-19 as well as the later hyperinflammatory phase,21 including for acute respiratory distress syndrome (ARDS), a lung condition that’s common in severe COVID-19 cases, which causes low blood oxygen and fluid buildup in the lungs.

“Based on many preclinical studies and observational data in humans, ARDS may be aggravated by vitamin D deficiency and tapered down by activation of the vitamin D receptor,” they said22 … “Based on a pilot study, oral calcifediol may be the most promising approach.”

Even regular “booster” doses of vitamin D, regardless of baseline vitamin D levels, appear to be effective in reducing the risk of mortality in people admitted to the hospital with COVID-19, particularly for the elderly.23,24 Those researchers noted, “This inexpensive and widely available treatment could have positive implications for the management of COVID-19 worldwide, particularly in developing nations.”25

Lower Vitamin D Levels May Increase Death Risk

Researchers in Indonesia, who looked at data from 780 COVID-19 patients, found those with a vitamin D level between 21 ng/mL (52.5 nmol/L) and 29 ng/mL (72.5 nmol/L) had a 12.55 times higher risk of death than those with a level above 30 ng/mL.26

Having a level below 20 ng/mL was associated with a 19.12 times higher risk of death. A “majority of the COVID-19 cases with insufficient and deficient Vitamin D status died,” they added,27 suggesting that research is needed to look into the role of vitamin D supplementation on COVID-19 outcomes.

One such study, a systematic review and meta-analysis published in the Journal of Endocrinological Investigation,28 included 13 studies involving 2,933 COVID-19 patients. Again, vitamin D was a clear winner, with use in COVID-19 patients significantly associated with reduced ICU admission and mortality, along with a reduced risk of adverse outcomes, particularly when given after COVID-19 diagnosis.

When it comes to data to support the use of vitamin D for COVID-19, 87 studies have been performed by 784 scientists. The results show:29

  • 53% improvement in 28 treatment trials
  • 56% improvement in 59 sufficiency studies
  • 63% improvement in 16 treatment mortality results

A number of clinical trials are also underway looking further into the use of vitamin D for COVID-19,30 including one by Harvard Medical School researchers looking into whether taking daily vitamin D reduces COVID-19 disease severity in those newly diagnosed as well as reduces risk of infection in household contacts.31

‘A Simple and Inexpensive Measure’

Some positive advances have already occurred that could make this potentially lifesaving strategy more widely used. The French National Academy of Medicine released a press release in May 2020, referring to the use of vitamin D as a “simple and inexpensive measure that is reimbursed by the French National Health Insurance” and detailing the importance of vitamin D for COVID-19.32

For COVID-19 patients over 60, they recommend vitamin D testing and if deficiency is found, a bolus dose of 50,000 to 100,000 IU. For anyone under the age of 60 who receives a positive COVID-19 test, they advise taking 800 IUs to 1,000 IUs of vitamin D per day. A vitamin D review paper published in the journal33 Nutrients in April 2020 recommends higher amounts, however, stating:

“To reduce the risk of infection, it is recommended that people at risk of influenza and/or COVID-19 consider taking 10,000 IU/d of vitamin D3 for a few weeks to rapidly raise 25(OH)D concentrations, followed by 5000 IU/d.

The goal should be to raise 25(OH)D concentrations above 40-60 ng/mL (100-150 nmol/L). For treatment of people who become infected with COVID-19, higher vitamin D3 doses might be useful.”

The best way to know how much vitamin D you need is to have your levels tested. Data from GrassrootsHealth’s D*Action studies suggest the optimal level for health and disease prevention is between 60 ng/mL and 80 ng/mL, while the cutoff for sufficiency appears to be around 40 ng/mL. In Europe, the measurements you’re looking for are 150 to 200 nmol/L and 100 nmol/L respectively.

Air Pollution Is Making Your Allergies Worse

Reproduced from original article:

Analysis by Dr. Joseph Mercola   Fact Checked    June 19, 2021

allergies worsened by air pollution


  • Air pollution attaches to pollen and can damage your lungs, which may help drive protein allergens deeper into your pulmonary system to trigger a significant allergic response
  • Rising levels of carbon dioxide gas have lengthened the growing season, contributing to more pollen in the air. However, the pollen has less protein, which may be contributing to the collapsing bee population
  • The number of people with food allergies is also rising, including adults who develop food allergies
  • Your allergic response is mediated by your gut microbiome. Another physiological biomarker tied to seasonal and food allergies is vitamin D; consider testing your level twice a year to identify your vitamin D requirements

With each passing year, more people are affected by seasonal allergies. In the quest to identify the mechanism behind the growing number of people experiencing allergies, scientists have identified several factors that play an important role. One of these is air pollution.1,2

According to the Asthma and Allergy Foundation of America,3 more than 50 million Americans have experienced a variety of types of allergies each year, and that number only continues to rise. The annual cost exceeds $18 billion for allergic rhinitis and $25 billion for food allergies.

The most common types of seasonal allergies are reactions to tree, grass and weed pollen. Allergic rhinitis, which is also called hay fever, affects 5.2 million children and 19.2 million adults. Although these numbers are staggering, scientists expect them to continue to rise as increasing levels of carbon dioxide (CO2) have affected plant growth and pollen production.

The most common symptoms of allergic rhinitis include sneezing, stuffy, runny nose, watery and itchy eyes and itching in your nose, throat or mouth. A sizable number of allergy sufferers experience noticeable brain fog as well. Food and seasonal allergies are your body’s reactions to particles it considers foreign.

The first time your body meets a protein allergen, plasma cells release immunoglobulin E (IgE).4 This attaches to the surface of mast cells, which are found in great numbers in your surface tissue such as skin and nasal mucus membranes. Mast cells release important chemical mediators, one of which is histamine.

The next time your body encounters this allergen, your mast cells become activated within minutes and release a powerful cocktail of histamines, leukotrienes and prostaglandins. This triggers the cascade of symptoms that you associate with allergies.

Rising Levels of CO2 Feed Flowering Plants

One of the major components of air pollution is carbon dioxide. According to the Center for Climate and Energy Solutions,5 carbon dioxide makes up 76% of all greenhouse gas emissions. Trees and other plants use carbon dioxide for photosynthesis. You might think rising levels of carbon dioxide may be good for plant life, but like most things, plants need a balance.

Gilles Oliver is an engineer from the National Aerobiological Surveillance Network, which tracks pollen throughout France. He spoke with a reporter from Vice France about the interaction between CO2 and plant life, saying,6 “But when the proportion of this CO2 in the air increases, plants grow faster and produce more pollen.”

An increase in pollen production raises your exposure to pollen, and thus produces more severe seasonal allergies. Changes in temperature and CO2 have also extended the frost-free season and thus lengthened pollen season.7 However, the pollen being produced by these plants may be contributing to the collapse of the bee population.

Scientists have found that increases in CO2 produce more pollen, but the pollen has lower protein levels.8 When bees harvest from flowers they first drink the nectar and then collect the pollen. Nectar is high in carbohydrates, while pollen offers long-term nutrition and provides the bees’ only natural source of protein.

When scientists compared flowers from Canada Goldenrod collected from 1842 to the present, they found the percentage of protein dropped by 33%.9 Over the same number of years, CO2 levels have risen by 30%. This increased the carbohydrates in the pollen making it essentially junk food for bees.10

The researchers confirmed the CO2 change in the environment played a role in dropping protein levels through testing published in the Proceedings of the Royal Society B.11

More than 100 past studies have demonstrated the change in atmospheric carbon dioxide reduces the nutritional value of plants, but this study was the first to examine the effects on bees. Mathilde Renard, an agricultural engineer at the Environmental Department of the Paris City Hall, also spoke with the Vice France reporter about the rising pollen counts in Paris.12

She attributes some of the urban pollen to the city’s planting efforts. One of the main strategies Paris is now using is to diversify the species to reduce the pollen concentration for each plant, in the hope of reducing citizens’ allergic response.

Other gardening choices that affect pollen count include preferentially planting male trees.13 Female trees shed more seeds and fruit, which need to be cleaned, but male trees tend to produce more allergic pollen. Some city planners have also chosen species based on their aesthetic value. For instance, birch trees are pretty, but birch tree pollen is one of the largest allergic triggers in the northern hemisphere.14

Pollution and Allergens Interact in Rising Allergies

Oliver attributes the increase in allergies in France to air pollution, saying,15 “It does two things. If you have allergies, it weakens your respiratory tract so you can get ill more easily. It also breaks up the pollen particles in the air, which allows them to penetrate deeper in our respiratory systems.”

The effect of air pollution on your body is insidious. The World Health Organization16 determined 92% of the global population is breathing polluted air. Most people associate air pollution with respiratory conditions since it has a significant impact on your pulmonary health.

However, while the damage to your lungs is significant, it’s important to remember air pollution affects more than your pulmonary system. For example, a study17 published in Environmental Health found a link between living close to busy roads and developing non-Alzheimer’s dementia and Parkinson’s disease.

According to the WHO, by 2016 air pollution was already responsible for respiratory diseases that killed 543,000 children aged 5 years and younger every year.18 Air pollution is also responsible for asthma in 14% of children around the globe. In April 2019, London launched an ultra-low emissions zone in central London in an attempt to reduce emissions by 45%.19

Researchers found that children living in these areas had a reduction in lung capacity by about 5% when pollution rose above legal levels.20 Dr. Ben Barrett commented on studies evaluating the effect air pollution has on pulmonary health in children, saying:21

“Air pollution has been found to restrict lung growth in children. Low lung function in childhood can persist into adulthood and is often associated with other health problems including chronic obstructive lung disease in later life.”

Air Pollution May Also Drive Pollen Deeper Into Your Lungs

As Oliver commented, air pollution increases the ability of pollen to penetrate your lungs. This can happen through several mechanisms.22 These include the facilitation of pollen release, stimulating the IgE-mediated response and enhancing the expression of allergens within pollen grains.

Grains of pollen do not only carry allergens, but can also elicit allergic responses in individuals who are sensitized. Pollen grains are too large to penetrate deep into the respiratory tract, so symptoms observed with patients who are allergic to pollen are more likely due to particles that are smaller than pollen grains. According to researchers:23

“Interestingly, air pollutants bind to these particles and exacerbate allergic disorders. Moreover, pollen grains release biologically active lipids, which activate immune cells in vitro.”

Researchers postulate that the interaction between air pollution and pollen grains outside the body may increase the amount of allergen released into the environment. This may happen through a variety of mechanisms that researchers have been studying in the lab and with human participants.24

They found that allergic reactions to grass pollen are greater in cities than in rural areas. Several types of air pollutants act “as adjuvants through binding to allergens and stimulating IgE synthesis, resulting in exacerbation of asthma symptoms.”25

A Clean Society May Increase Risk of Food Allergies

The number of people experiencing food allergies is also on the rise. One paper26 published by Yale University27 proposed the rising number may be the result of an exaggerated activation of the system that protects you against eating toxic foods. As many as 8% of children28 have a potentially deadly response to the major eight food allergens, often referred to as the “Big 8.”29

These include milk, eggs, wheat, soybeans, fish, crustacean shellfish, tree nuts and peanuts. Your body uses multiple sensory mechanisms to monitor what you eat, including chemosensory processes in the gut. The Yale University scientists argue that the body has a food quality control system in which an allergic response plays a significant role.

One prevailing theory for this rise in food allergies is living in a too-clean environment. This is also called the hygiene hypothesis, which some scientists have expanded to include processed foods, dishwashing detergent and other environmental chemicals.

In a paper30 written in Clinical and Experimental Immunology, the researchers argue these factors also play a role in disrupting your internal food quality control system.

There is a difference between a food sensitivity, intolerance and a food allergy.31 A true allergy is mediated by the immune system and triggered by a reaction to proteins found in your food or drink. Food intolerances are also called food sensitivities. These are usually an unpleasant gastrointestinal reaction, but the reaction is not mediated by your immune system.

Although most food allergies develop in childhood, it’s not unheard of for adults to develop a food allergy. Data32 gathered from October 2015 to September 2016 suggest 10.8% of adults are allergic to food. Scientists believe this contradicts the long-held belief that most allergies develop in childhood.

In a survey of 40,443 adults, 38.3% had food allergies that sent them to the emergency room and 48% had at least one triggered after the age of 18. Your gut microbiome is vital to the functioning of your immune system, which mediates an allergic response to food. You’ll find suggestions on how to optimize your gut microbiome in “How Your Gut Health Impacts Your Disease Risk.”

Vitamin D — Links to Seasonal and Food Allergies

One physiological biomarker tied to the risk of seasonal and food allergies is vitamin D. Researchers have found there is both experimental and clinical evidence that vitamin D is linked to allergic rhinitis.33

One double-blind placebo-controlled clinical trial34 evaluated the combined effect of vitamin D supplementation with an antihistamine medication. The study found that the people who received vitamin D and the medication had a significant decrease in their symptoms as compared to those who only received the medication.

The researchers measured vitamin D levels after eight weeks, finding those who received the supplement had a mean serum level of 24 nanograms per milliliter (ng/mL) and the level in the group who did not get vitamin D supplementation was 15 ng/mL.

It is important to note that the researchers did not use the supplement as a basis for concluding the vitamin D had a positive effect, but rather the serum level of vitamin D. The rising level of food allergies also corresponds to the increasing number of people with vitamin D deficiency. Vitamin D plays a significant role in the regulation of IgE, important in the development of food allergies.

The link between vitamin D deficiency, which has almost doubled in just over 10 years in the U.S.,35 and poor regulation of IgE responses, may be a significant factor. Both play a role in the development, severity and course of allergic diseases and may help explain, at least in part, why so many adults are developing food allergies.

Vitamin D deficiency has become so widespread it’s been called a pandemic by a Harvard Medical School researcher.36 The short list of health benefits attributed to vitamin D optimization include improving your immune system, strengthening muscles, bones and teeth and improving your cardiovascular health.

I recommend you get your vitamin D level tested twice each year — once when the level is likely to be at its lowest (midwinter) and once when it’s at its highest (midsummer). Grassroots Health offers vitamin D testing through its D*Action Study and has an online vitamin D calculator you can use to estimate your vitamin D requirements.

To read more about the interaction between vitamin D deficiency and allergies, how to optimize your vitamin D and the synergy between vitamin D3, magnesium, calcium and vitamin K2, see “Vitamin D Deficiency Can Lead to Increased Allergies.”

Quercetin: What It Is and Why You Need It

© May 25th 2021 GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC.
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Reproduced from original article:
Posted on: Wednesday, May 19th 2021 at 4:15 pm
Written By: GreenMedInfo Research Group
This article is copyrighted by GreenMedInfo LLC, 2021

Find out more about quercetin and how this potent antioxidant flavonoid offers significant therapeutic benefits against a wide range of conditions, from diabetes to DNA damage

Flavonoids are one of nature’s many therapeutic gifts. Widely found in fruits and vegetables, these phenolic substances have antioxidant properties that protect cells from free radical damage.[i] One of the most well-known and studied flavonoids is quercetin, a flavonol mostly found in onions, berries, citrus fruits, broccoli and grapes.

A potent antioxidant, quercetin boasts of anti-inflammatory, anti-hypertensive, antiobesity and anti-atherosclerotic actions. Since free radicals figure into the development of diseases, quercetin holds promise for benefitting conditions such as high blood pressure, vascular disorders and metabolic syndrome.[ii] Here is compelling evidence of the health benefits of quercetin.

Potential Anti-Diabetes Aid

The development of Type 2 diabetes has been linked to oxidant stress caused by an unhealthy diet.[iii] Toona sinensis leaves, which are rich in quercetin, may reduce the risk of diabetes by reducing oxidative stress in the liver.

A topical compound containing substances such as quercetin, ascorbyl palmitate and vitamin D3 was formulated to reduce the oxidative stress contributing to peripheral diabetic neuropathy.[iv] A preliminary study in 2005 showed that the compound may safely relieve the symptoms of diabetic neuropathy and enhance quality of life.

Quercetin displayed protective effects in the kidneys and liver of obese animal models with Type 2 diabetes.[v] Together with quinic acid, quercetin also helped ameliorate hyperglycemia, hyperlipidemia and insulin resistance in diabetic rats.[vi]

Protection From DNA Damage

A 2011 study investigated the potential protective effects of quercetin against DNA damage and oxidative stress induced by methylmercury in animal subjects.[vii] For over 45 days, animal models were orally treated with methylmercury and the flavonoid with doses reflecting human exposure. The team then measured DNA damage in liver cells called hepatocytes and peripheral leukocytes (white blood cells).

The results revealed that methylmercury reduced the concentration of glutathione in the body by 17% and caused DNA damage to liver and blood cells. With quercetin, no such effects manifested. “In summary, our results indicate that consumption of quercetin-rich foods may protect mercury-exposed humans against the adverse health effects of the metal,” the researchers wrote.[viii]

What makes this benefit particularly crucial is that the prevention of DNA damage is involved in preventing cancer via dietary compounds. An aqueous horseradish extract and its main flavonoids kaempferol and quercetin, for instance, demonstrated potential for DNA damage protection likely by acting as antimutagens.[ix]

Chemopreventive Properties

Epidemiological studies vouch for the protective effects of phytochemicals against cancer risk. As a ubiquitous flavonoid, quercetin is an ideal candidate to fight cancer due to its antioxidant and antiproliferative actions.[x]

It is known to modulate a plethora of molecules for multitargeted cancer prevention and therapy. Here are examples of quercetin’s chemopreventive abilities:

  • Incorporated in liposomes along with resveratrol, quercetin may be valuable in treating inflammation or oxidative stress associated with precancerous or cancerous skin lesions.[xi]
  • Quercetin exhibited a preventive effect on liver cancer in animal models.[xii] Hepatocellular carcinoma, the most common form of liver cancer, is on the rise in many countries, with an estimated 905,677 new cases globally in 2020.[xiii]
  • Quercetin inhibited tumor growth and enhanced the sensitivity to thermotherapy, indicating a potential treatment option for hepatocellular carcinoma.[xiv]
  • The combination of quercetin and ionizing radiation might be a promising therapy for colon cancer treatment through targeting colon cancer stem-like cells and inhibiting the Notch-1 signaling.[xv]
  • Quercetin suppressed the metastatic ability of lung cancer, with potential therapeutic applications for metastatic non-small cell lung cancer in particular.[xvi]

Prevention and Treatment of Various Infections

Quercetin may protect against the antibiotic-resistant Streptococcus pneumoniae infection mainly through inhibiting pneumolysin, a pore-forming cytotoxin and a major determinant of virulence.[xvii] Separate findings previously highlighted quercetin’s therapeutic potential in treating sepsis as well.[xviii]

The flavonoid derivative quercetin-3β-O-D-glucoside (Q3G) also showed promising antiviral activity against two distinct species of Ebola, outbreaks of which occur frequently in African countries.[xix]

Hyaluronic acid, chondroitin sulfate, curcumin and quercetin taken together were also effective in preventing recurrent urinary tract infections in postmenopausal women.[xx]

Read more about scientific proof of the therapeutic value and significance of quercetin across numerous health issues and conditions in the nearly 600 abstracts with quercetin research found on the database.



[i] David A et al “Overviews of Biological Importance of Quercetin: A Bioactive Flavonoid” Pharmacogn Rev. 2016 Jul-Dec; 10(20): 84-89.

[ii] David A et al “Overviews of Biological Importance of Quercetin: A Bioactive Flavonoid” Pharmacogn Rev. 2016 Jul-Dec; 10(20): 84-89.

[iii] Zhang Y et al “Quercetin Isolated from Toona sinensis Leaves Attenuates Hyperglycemia and Protects Hepatocytes in High-Carbohydrate/High-Fat Diet and Alloxan Induced Experimental Diabetic Mice” J Diabetes Res. 2016 ;2016:8492780. Epub 2016 Nov 15.

[iv] Valensi P et al “A multicenter, double-blind, safety study of QR-333 for the treatment of symptomatic diabetic peripheral neuropathy. A preliminary report” J Diabetes Complications. 2005 Sep-Oct;19(5):247-53.

[v] Lai L et al “Protective effects of quercetin and crocin in the kidneys and liver of obese Sprague-Dawley rats with Type 2 diabetes: Effects of quercetin and crocin on T2DM rats” Hum Exp Toxicol. 2020 Oct 6:960327120954521.

[vi] Arya A et al “Synergistic effect of quercetin and quinic acid by alleviating structural degeneration in the liver, kidney and pancreas tissues of STZ-induced diabetic rats: a mechanistic study” Food Chem Toxicol. 2014 Sep ;71:183-96. Epub 2014 Jun 19.

[vii] Barcelos G et al “Protective properties of quercetin against DNA damage and oxidative stress induced by methylmercury in rats” Arch Toxicol. 2011 Feb 1. Epub 2011 Feb 1.

[viii] Barcelos G et al “Protective properties of quercetin against DNA damage and oxidative stress induced by methylmercury in rats” Arch Toxicol. 2011 Feb 1. Epub 2011 Feb 1.

[ix] Molecules. 2014 ;19(3):3160-72. Epub 2014 Mar 14. PMID: 24637991

[x] Priyadarsini R et al “The flavonoid quercetin modulates the hallmark capabilities of hamster buccal pouch tumors” Nutr Cancer. 2011 Feb 2:1. Epub 2011 Feb 2.

[xi] Caddeo C et al “Effect of quercetin and resveratrol co-incorporated in liposomes against inflammatory/oxidative response associated with skin cancer” Int J Pharm. 2016 Nov 20 ;513(1-2):153-163. Epub 2016 Aug 5.

[xii] Seufi A et al “Preventive effect of the flavonoid, quercetin, on hepatic cancer in rats via oxidant/antioxidant activity: molecular and histological evidences” J Exp Clin Cancer Res. 2009 ;28:80. Epub 2009 Jun 11.

[xiii] Medscape January 31, 2021

[xiv] Dai W et al “Quercetin induces apoptosis and enhances 5-FU therapeutic efficacy in hepatocellular carcinoma” Tumour Biol. 2015 Dec 1. Epub 2015 Dec 1.

[xv] Li Y et al “Quercetin pretreatment enhances the radiosensitivity of colon cancer cells by targeting Notch-1 pathway” Biochem Biophys Res Commun. 2020 Jan 18. Epub 2020 Jan 18.

[xvi] Chang J et al “Quercetin suppresses the metastatic ability of lung cancer through inhibiting Snail-dependent Akt activation and Snail-independent ADAM9 expression pathways” Biochim Biophys Acta. 2017 10 ;1864(10):1746-1758. Epub 2017 Jun 23.

[xvii] Lv Q et al “Quercetin, a pneumolysin inhibitor, protects mice against Streptococcus pneumoniae infection” Microb Pathog. 2020 Mar ;140:103934. Epub 2019 Dec 17.

[xviii] Cui W et al “Quercetin Exerted Protective Effects in a Rat Model of Sepsis via Inhibition of Reactive Oxygen Species (ROS) and Downregulation of High Mobility Group Box 1 (HMGB1) Protein Expression” Med Sci Monit. 2019 Aug 4 ;25:5795-5800. Epub 2019 Aug 4.

[xix] Qiu X et al “Prophylactic efficacy of Quercetin-3-β-O-D-glucoside against Ebola virus infection” Antimicrob Agents Chemother. 2016 Jun 13. Epub 2016 Jun 13.

[xx] Torella M et al “Efficacy of an orally administered combination of hyaluronic acid, chondroitin sulfate, curcumin and quercetin for the prevention of recurrent urinary tract infections in postmenopausal women” Eur J Obstet Gynecol Reprod Biol. 2016 Dec ;207:125-128. Epub 2016 Nov 1.

GMI Research Group

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.

Vitamin D Supplementation Reduces COVID-19 Deaths by 64%

Reproduced from original article:

Analysis by Dr. Joseph Mercola      Fact Checked      February 22, 2021

vitamin d3 for coronavirus


  • A Spanish study found giving supplemental vitamin D3 (calcifediol) to hospitalized patients with PCR-confirmed COVID-19 — in addition to standard care — reduced ICU admissions by 82% and mortality by 64%
  • People who already had higher vitamin D at baseline were 60% less likely to die
  • Many are now calling for official vitamin D recommendations to be issued by their governments
  • Other recent research found vitamin D is a contributing factor to COVID-19 outbreaks and infection severity. Surges in daily positive tests during the fall of 2020 in 18 European countries linearly correlate with latitude, and, hence, sun exposure and vitamin D levels
  • One of the reasons vitamin D is so important against COVID-19 has to do with its influence on T cell responses. Vitamin D receptor signals regulate T cell responses and therefore play an important role in your body’s defense against viral and bacterial infections

Vitamin D plays an important role in most diseases, including infectious disease, which is why from the very beginning of the COVID-19 pandemic, I suspected that optimizing vitamin D levels among the general population would significantly lower COVID-19 incidence and death.

Since then, mounting evidence reveals this is indeed the case, as researchers have repeatedly demonstrated that higher vitamin D levels reduce rates of positive tests, hospitalizations and mortality related to this infection.

Vitamin D3 Reduces ICU Admissions and Mortality

Most recently, a Spanish study1,2 (which has yet to undergo peer-review) found giving supplemental vitamin D3 (calcifediol) to hospitalized patients with PCR-confirmed COVID-19 reduced ICU admissions by 82% and mortality by 64%.3 People who already had higher vitamin D at baseline were 60% less likely to die.

The study included 930 patients, 551 of whom received vitamin D3 — 532 micrograms on the first day of admission followed by 266 mcg on days 3, 7, 15 and 30. The remaining 379 patients served as controls.

All were given standard of care, which included hydroxychloroquine and an antibiotic (or two antibiotics in cases where bacterial infections were diagnosed), plus a steroid in cases involving pulmonary inflammation and/or cytokine storm.4 As reported by the authors:5

“ICU assistance was required by 110 (11.8%) participants. Out of 551 patients treated with calcifediol at admission, 30 (5.4%) required ICU, compared to 80 out of 379 controls (21.1%).

Logistic regression of calcifediol treatment on ICU admission, adjusted by age, gender, linearized 25(OH)D levels at baseline, and comorbidities showed that treated patients had a reduced risk to require ICU (RR 0.18).

Baseline 25(OH)D levels inversely correlated with the risk of ICU admission (RR 0.53). Overall mortality was 10%. In the Intention-to-treat analysis, 36 (6.5%) out of 551 patients treated with calcifediol at admission died compared to 57 patients (15%) out of 379 controls.

Adjusted results showed a reduced mortality for more of 60%. Higher baseline 25(OH)D levels were significantly associated with decreased mortality (RR 0.40).

Age and obesity were also predictors of mortality. Interpretation: In patients hospitalized with COVID-19, calcifediol treatment at the time of hospitalization significantly reduced ICU admission and mortality.”

Renewed Calls for Vitamin D Recommendations

In response to the Spanish findings, British MP David Davis tweeted that “The findings of this large and well conducted study should result in this therapy being administered to every COVID patient in every hospital in the temperate latitudes,” adding that:6

“Since the study demonstrates that the clear relationship between vitamin D and COVID mortality is causal, the U.K. government should increase the dose and availability of free vitamin D to all the vulnerable groups. These approaches will save many thousands of lives. They are overdue and should be started immediately.”

Many others are also calling for official vitamin D recommendations to be issued by their governments. Among them, Emer Higgins,7 a member of the Irish political party Fine Gael, who called on the Irish health minister, Stephen Donnelly, to include vitamin D supplementation in its “Living with COVID-19” strategy, slated for launch at the end of February 2021.

Higgins leaned on evidence from the Irish Covit-D Consortium,8 which shows vitamin D helps optimize your immune response. “There is negligible risk in this strategy and potentially a massive gain,” she said. According to the Covit-D Consortium, the nutrient can lower the risk of death from COVID-19 in the elderly by as much as 700%.9

Click here to learn more

Low Vitamin D Linked to COVID-19 Outbreaks and Severity

Another recent study10 published in the journal Scientific Reports confirmed vitamin D is a contributing factor to COVID-19 outbreaks and infection severity. According to the authors, the surges in daily positive test results during the fall of 2020 in 18 European countries linearly correlate with latitude, and hence sun exposure and vitamin D levels. They point out that:

“The country surge date corresponds to the time when its sun UV daily dose drops below ≈ 34% of that of 0° latitude. Introducing reported seasonal blood 25-hydroxyvitamin D (25(OH)D) concentration variation into the reported link between acute respiratory tract infection risk and 25(OH)D concentration quantitatively explains the surge dynamics …

The date of the surge is an intrapopulation observation and has the benefit of being triggered only by a parameter globally affecting the population, i.e. decreases in the sun UV daily dose.

The results indicate that a low 25(OH)D concentration is a contributing factor to COVID-19 severity, which, combined with previous studies, provides a convincing set of evidence.”

While it’s well-recognized that most elderly individuals are deficient in vitamin D, the problem is widespread in all age categories, including children.

As noted in a February 2021 study11 comparing vitamin D levels in breast milk collected in 1989 and 2016/2017, vitamin D concentrations are consistently higher during the summer, but overall, vitamin D levels have declined since 1989. As a result, pregnant and lactating mothers and their infants may require vitamin D supplementation for optimal health.

Vitamin D Is Crucial for Optimal T Cell Responses

One of the reasons why vitamin D is so important against COVID-19 has to do with its influence on T cell responses. Animal research12 published in 2014 explained how vitamin D receptor signals regulate T cell responses and therefore play an important role in your body’s defense against viral and bacterial infections.

As noted in that study, when vitamin D signaling is impaired, it significantly impacts the quantity, quality, breadth and location of CD8 T cell immunity, resulting in more severe viral and bacterial infections.

Strong antibody response correlates with more severe clinical disease while T-cell response is correlated with less severe disease.

What’s more, according to a December 11, 2020, paper13 in the journal Vaccine: X, high-quality T cell response actually appears to be far more important than antibodies when it comes to providing protective immunity against SARS-CoV-2 specifically:14

The first SARS-CoV-2 vaccine(s) will likely be licensed based on neutralizing antibodies in Phase 2 trials, but there are significant concerns about using antibody response in coronavirus infections as a sole metric of protective immunity.

Antibody response is often a poor marker of prior coronavirus infection, particularly in mild infections, and is shorter-lived than virus-reactive T-cells …

Strong antibody response correlates with more severe clinical disease while T-cell response is correlated with less severe disease; and antibody-dependent enhancement of pathology and clinical severity has been described.

Indeed, it is unclear whether antibody production is protective or pathogenic in coronavirus infections. Early data with SARS-CoV-2 support these findings. Data from coronavirus infections in animals and humans emphasize the generation of a high-quality T cell response in protective immunity.”

The authors go on to state that epitopes associated with SARS-CoV2 have been identified on CD4 and CD8 T-cells in the blood from patients who have successfully recovered from COVID-19, and that these epitopes “are much less dominated by spike protein than in previous coronavirus infections.”15

As a refresher, aside from SARS-CoV-2, there are six other coronaviruses known to cause respiratory disease in humans:16

  • Types 229E, NL63, OC43 and KHU1 are quite common and cause mild to moderate respiratory infections such as the common cold.
  • SARS-CoV (Severe Acute Respiratory Syndrome coronavirus), associated with severe respiratory illness.17,18
  • MERS-CoV (Middle East Respiratory Syndrome coronavirus) which, like SARS, causes more severe respiratory infections than the four common coronaviruses.19

Understanding the Role of Epitopes

What do they mean by “epitopes associated with SARS-CoV2 have been identified on CD4 and CD8 T-cells”? Epitopes20 are sites on the virus that allow antibodies or cell receptors in your immune system to recognize it. This is why epitopes are also referred to as “antigenic determinants,” as they are the part that is recognized by an antibody, B-cell receptor or T-cell receptor.

Most antigens — substances that bind specifically to an antibody or a T-cell receptor — have several different epitopes, which allow it to be recognized by several different antibodies. Importantly, some epitopes can cause autoimmunological pathogenic priming if you’ve been previously infected with SARS-CoV-2 or exposed via a COVID-19 vaccine.21

In other words, if you’ve had the infection once, and get reinfected (either by SARS-CoV-2 or a sufficiently similar coronavirus), the second bout has the potential to be more severe than the first. Similarly, if you get vaccinated and are then infected with SARS-CoV-2, your infection may be more severe than had you not been vaccinated.

For this reason, “these epitopes should be excluded from vaccines under development to minimize autoimmunity due to risk of pathogenic priming,” a recent paper22 in the Journal of Translational Autoimmunity warns.

One of the reasons why mRNA gene therapy “vaccines” are causing so many problems may in fact be because they have failed to “screen out unsafe epitopes to reduce autoimmunity due to homology between parts of the viral protein and the human proteome,” according to that Journal of Translational Autoimmunity paper.23

Natural SARS-CoV-2 Infection Induces Broad Epitope Coverage

The authors of the Vaccine: X paper point out that while most COVID-19 gene therapy “vaccines” focus on the SARS-CoV-2 spike protein as a natural antigen, “natural infection by SARS-CoV-2 induces broad epitope coverage, cross-reactive with other betacoronviruses.”

Indeed, this has been demonstrated in a number of studies, including a Singaporean study24,25,26 that found common colds caused by the betacoronaviruses OC43 and HKU1 might make you more resistant to SARS-CoV-2 infection, and that the resulting immunity might last as long as 17 years.

In other words, if you’ve beat a common cold caused by a OC43 or HKU1 betacoronavirus in the past, you may have a 50/50 chance of having defensive T-cells that can recognize and help defend against SARS-CoV-2. What the Vaccine: X authors are basically warning about is that the so-called vaccines are unlikely to provide the same level of immunity as natural infection does, and may even cause pathogenic priming.

Vitamin D Speeds Viral Clearance

Other research,27 published in November 2020 in the Postgraduate Medical Journal, shows oral vitamin D supplementation also helps speed up SARS-CoV-2 viral clearance. This study included only asymptomatic or mildly symptomatic SARS-CoV-2-positive individuals who also had vitamin D deficiency (a vitamin D blood level below 20 ng/mL).

Participants were randomly assigned to receive either 60,000 IUs of oral cholecalciferol (nano-liquid droplets) or a placebo for seven days. The target blood level was 50 ng/mL. Anyone who had not achieved a blood level of 50 ng/mL after the first seven days continued to receive the supplement until they reached the target level.

Periodically, all participants were tested for SARS-CoV-2 as well as fibrinogen, D-dimer, procalcitonin and CRP, all of which are inflammatory markers. The primary outcome measure of the study was the proportion of patients testing negative for COVID-19 before Day 21 of the study, as well as changes in inflammatory markers. As reported by the authors:28

“Forty SARS-CoV-2 RNA positive individuals were randomized to intervention (n=16) or control (n=24) group. Baseline serum 25(OH)D was 8.6 and 9.54 ng/mL, in the intervention and control group, respectively.

10 out of 16 patients could achieve 25(OH)D>50 ng/ml by day-7 and another two by day-14 … 10 (62.5%) participants in the intervention group and 5 (20.8%) participants in the control arm became SARS-CoV-2 RNA negative. Fibrinogen levels significantly decreased with cholecalciferol supplementation unlike other inflammatory biomarkers.

[A] greater proportion of vitamin D-deficient individuals with SARS-CoV-2 infection turned SARS-CoV-2 RNA negative with a significant decrease in fibrinogen on high-dose cholecalciferol supplementation.”

More Evidence Vitamin D Impacts COVID-19

If you haven’t already gone to the free website I created to educate the world about vitamin D, please do now. It’s You can download the free condensed version of the paper I had published last year that is easier to read and full of graphics to illustrate the information.

October 31, 2020, my own vitamin D review,29 co-written with William Grant, Ph.D., and Dr. Carol Wagner, both of whom are part of the GrassrootsHealth expert vitamin D panel, was 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:30

  • Reducing the survival and replication of viruses31
  • 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 distress32
  • Improves overall lung function
  • Helps produce surfactants in your lungs that aid in fluid clearance33
  • Lowers your risk of comorbidities associated with poor COVID-19 prognosis, including obesity,34 Type 2 diabetes,35 high blood pressure36 and heart disease37

Data from 14 observational studies — summarized in Table 1 of our paper38 — 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.39 Our paper40 also details several features of COVID-19 that suggest vitamin D deficiency is at play in this illness.

How to Optimize Your Vitamin D

While most people would probably benefit from a vitamin D3 supplement, it’s important to get your vitamin D level tested before you start supplementing. The reason for this is because you cannot rely on blanket dosing recommendations. The crucial factor here is your blood level, not the dose, as the dose you need is dependent on several individual factors, including your baseline blood level.

Data from GrassrootsHealth’s D*Action studies suggest the optimal level for health and disease prevention is between 60 ng/mL and 80 ng/mL, while the cutoff for sufficiency appears to be around 40 ng/mL. In Europe, the measurements you’re looking for are 150 to 200 nmol/L and 100 nmol/L respectively.

I’ve published a comprehensive vitamin D report in which I detail vitamin D’s mechanisms of action and how to ensure optimal levels. I recommend downloading and sharing that report with everyone you know. A quick summary of the key steps is as follows:

1.First, measure your vitamin D level — One of the easiest and most cost-effective ways of measuring your vitamin D level is to participate in the GrassrootsHealth’s personalized nutrition project, which includes a vitamin D testing kit.

Once you know what your blood level is, you can assess the dose needed to maintain or improve your level. If you cannot get enough vitamin D from the sun (you can use the DMinder app41 to see how much vitamin D your body can make depending on your location and other individual factors), then you’ll need an oral supplement.

2.Assess your individualized vitamin D dosage — To do that, you can either use the chart below, or use GrassrootsHealth’s Vitamin D*calculator. To convert ng/mL into the European measurement (nmol/L), simply multiply the ng/mL measurement by 2.5. To calculate how much vitamin D you may be getting from regular sun exposure in addition to your supplemental intake, use the DMinder app.42

Vitamin D-Serum Level

3.Retest in three to six months — Lastly, you’ll need to remeasure your vitamin D level in three to six months, to evaluate how your sun exposure and/or supplement dose is working for you.

Take Your Vitamin D With Magnesium and K2

As detailed in “Magnesium and K2 Optimize Your Vitamin D Supplementation,” it’s strongly recommended to take magnesium and K2 concomitant with oral vitamin D. Data from nearly 3,000 individuals reveal you need 244% more oral vitamin D if you’re not also taking magnesium and vitamin K2.43

What this means in practical terms is that if you take all three supplements in combination, you need far less oral vitamin D in order to achieve a healthy vitamin D level.

Vitamin D Dose-Response

– Sources and References

Warning: This unexpected physical problem could mean you’re lacking vitamin C in your diet

Reproduced from original article:

by:  | February 15, 2021

vitamin-c-deficiency(NaturalHealth365) If your gums bleed, you could be in the early stages of gingivitis, an inflammatory condition caused by a build-up of bacteria and plaque inside the mouth.  But a study just published in Nutrition Reviews suggests that poor dental habits and oral bacteria might not be the only explanation for bleeding gums.

Incredibly, a vitamin deficiency — vitamin C deficiency, to be exact — could be to blame.

New research suggests low levels of vitamin C in the blood may be at the root of this common oral health problem

The authors of the breaking study, titled “Bleeding tendency and ascorbic acid requirements: systematic review and meta-analysis of clinical trials,” assessed 15 clinical trials from six countries, representing 1,140 people.  The researchers also collected and analyzed data of over 8,200 Americans from the Centers for Disease Control and Prevention’s Health and Nutrition Examination Survey.

Based on their analysis, the researchers concluded that people who experienced bleeding of their gums and even bleeding in the eye (retinal hemorrhage), were more likely to have low levels of vitamin C (ascorbic acid) in their blood.  Furthermore, increasing vitamin C intake seemed to help reduce the bleeding problems!

The link between gum health and vitamin C isn’t a brand new discovery.  Swollen, bleeding, and discolored gums is one of the most well-recognized signs of scurvy, a potentially fatal disease caused by very low levels of vitamin C.  But this new data suggests that “setting human [vitamin C] requirements based on scurvy prevention leads to [vitamin C] plasma levels that may be too low to prevent an increased gingival bleeding tendency,” according to the study authors.

In other words, just because we can get enough vitamin C to avoid scurvy doesn’t necessarily mean we’re getting enough vitamin C for optimal health.

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How much of this vitamin do you need? Here’s a quick primer (and sample shopping list)

If you experience bleeding gums (or if you ever notice that your sputum or toothpaste has a pinkish tint to it), it could be time to visit the dentist or doctor for a check-up.  Bleeding gums are also a good reminder to improve your oral hygiene habits (e.g., twice-daily brushing and flossing, avoiding sugary foods and beverages, etc.).

But you should also take a look at your diet and ensure you’re eating plenty of vitamin C rich foods.  If low vitamin C levels are leading to bleeding gums, then no amount of flossing and brushing will fully resolve the underlying cause of your gum issues.

According to Mayo Clinic, the recommended daily amount for a typical adult is between 65 and 90 milligrams (or up to 120 mg for lactating women), while the upper limit is 2,000 mg per day.  Other than using a supplement, you can easily hit your recommended amount by adding more of these foods to your diet:

  • Sweet red pepper (half a cup has 95 mg)
  • Strawberries (half a cup has 49 mg)
  • Grapefruit (half of one has 39 mg)
  • Kiwifruit (1 has 64 mg)
  • Brussels sprouts (half a cup has 48 mg)

By the way, in case you needed another reason to quit smoking: the National Institutes of Health say research consistently shows that smokers have lower plasma levels of vitamin C because of smoking-induced oxidative stress.  For this reason, smokers should consume about 35 mg more than nonsmokers (or better yet, quit smoking altogether).

Sources for this article include:

NAD+ Helps Restore Age-Related Muscle Deterioration

Reproduced from original article:

Analysis by Dr. Joseph Mercola      Fact Checked      February 15, 2021

nicotinamide adenine dinucleotide benefits


  • Several studies have proposed that mitochondrial dysfunction in your motor neurons drive the development of sarcopenia (age-related muscle loss)
  • Scientists recently discovered that Alzheimer’s-like protein aggregates (amyloid beta) underlie the muscle deterioration commonly seen in aging, and that nicotinamide adenine dinucleotide (NAD+) is essential for combating this condition
  • When the NAD+ salvage pathways in muscle are impaired, mitochondrial dysfunction and decreased muscle mass ensue
  • NAD+ boosting molecules such as nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), nicotinamide (a form of vitamin B3 or niacin) and nicotinic acid (niacin) have been shown to protect against age-related muscle disease
  • NMN appears to be the best, as it activates the NAD+ salvage pathway and is a direct precursor to NAD+. Lifestyle strategies such as exercise, sauna bathing, fasting, recalibrating your circadian rhythm and avoiding excessive EMFs and alcohol will also address low NAD+

The tendency is to lose muscle as you age, a condition known as sarcopenia. If you don’t do anything to stop it you can expect to lose about 15% of your muscle mass between your 30s and your 80s.1 An estimated 10% to 25% of seniors under the age of 70 have sarcopenia and as many as half those over the age of 80 are impaired with it.2

Enforced bedrest, due to hospitalization, for example, can also have a dramatic impact on your muscle mass, even if you’re younger. According to a 2015 review3 in Extreme Physiology & Medicine, you can lose 5.2% of your muscle mass in the first two weeks of bedrest. By Day 23, you can have lost up to 10% of your quadriceps muscle mass.

Not only are strong muscles a requirement for mobility, balance and the ability to live independently, but having reserve muscle mass will also increase your chances of survival4 when sick or hospitalized. Since muscle is lost far more easily and quicker than it’s built, finding ways to continuously promote and maintain your muscle mass is of utmost importance.

The Crucial Role of NAD+

As reported by Science Daily,5 scientists recently discovered that Alzheimer’s-like protein aggregates underlie the muscle deterioration commonly seen in aging, and that nicotinamide adenine dinucleotide (NAD+) is essential for combating this condition.

Their study,6 published in the journal Cell Reports, showed that protein aggregates (amyloid) could be blocked by boosting the levels of NAD+, a biomolecule that is also essential for maintaining mitochondrial function.

Higher levels of NAD+ were found to turn on the defense systems of the mitochondria and restore muscle function. Aggregated proteins have long been thought to be a contributor to brain aging, and this study proves aggregated proteins also contribute to muscle aging.

“The most prominent component of these protein aggregates is beta-amyloid, just like in the amyloid plaques in the brains of patients with Alzheimer’s disease,” said Johan Auwerx at EPFL’s School of Life Sciences. “These abnormal proteotoxic aggregates could serve as novel biomarkers for the aging process, beyond the brain and muscle.”

The study points out that NAD+ homeostasis is required to maintain proteostasis, i.e., the regulation of protein creation, folding, trafficking and degradation. It turns out that boosting NAD+ in later life will reduce amyloidosis (the buildup of amyloid) and mitochondrial dysfunction.

The importance of NAD+ for healthy muscle function is also reviewed in “Sarcopenia and Muscle Aging: A Brief Overview,”7 published in the journal Endocrinology and Metabolism. The paper highlights:

“… recent findings that describe key pathophysiological phenotypes of this condition, including alterations in muscle fiber types, mitochondrial function, nicotinamide adenine dinucleotide (NAD+) metabolism, myokines, and gut microbiota, in aged muscle compared to young muscle or healthy aged muscle.”

As indicated by the Cell Report study, this Endocrinology and Metabolism paper highlights the connection between sarcopenia and mitochondrial dysfunction in both skeletal muscle and motor neurons.

People with sarcopenia have been found to have both reduced mitochondrial oxidative capacity and inhibited NAD+ biosynthesis, and several studies have proposed that mitochondrial dysfunction in your neurons actually drive the development of sarcopenia.8

Click here to learn more

What Is NAD+?

NAD+ is a substrate for a number of important enzymes, including poly(ADP-ribose) polymerase (PARP) and sirtuin 1 (SIRT1), which is known as a classic longevity protein. NAD+ is also essential in metabolic processes such as creating ATP in your mitochondria. It accepts and donates electrons and is used in oxidation-reduction reactions in the mitochondrial electron transport chain.

Interestingly, what scientists have observed is that NAD+ levels decline in most tissues over time, and is associated with aging in general and is therefore thought to play an important role in many age-related diseases.

According to the Endocrinology and Metabolism paper,9 researchers have shown that when the NAD+ salvage pathways in muscle are impaired, mitochondrial dysfunction and decreased muscle mass ensues.

NAD+ boosting molecules such as nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), nicotinamide (a form of vitamin B3 or niacin) and nicotinic acid (niacin) have all been shown to protect against age-related muscle disease.

How to Boost NAD+

Of those four, NMN is my personal favorite as it activates the NAD+ salvage pathway. As explained by Siim Land in a recent interview, featured in “Simple Strategies That Will Improve Your Immunity,” which also reviews the importance of NAD+ in COVID-19:

“A lot of the NAD that your body produces is recycled through the salvage pathway. Very little (less than 1%) of it is going to come from food, especially tryptophan or niacin. The easiest way to prevent losing your NAD as you get older or as you get immunocompromised is to promote the salvage pathway.”

I’ve previously recommended the use of NR over NMN but have since changed my stance. NR used to be considered superior because no NMN transporter — required to get it into cells — had been detected. We now know there is such a transporter, which gives NMN the advantage as it’s also a more direct NAD+ precursor.

NAD salvage pathway

Most of the NAD+ precursor research is done with NR and that used to be my primary choice. However, as you can see from the image above, NMN converts to NAD+ whereas NR must first be converted into NMN before it can be converted into NAD+,10 so it makes more sense to use NMN for NAD+ augmentation.

The image above also shows how niacin (NA) also finds its way to become NAD+. Niacin is also a useful supplement to use in increasing NAD+ levels. You just need to limit the dose to about 25 mg, which most is a dose low enough not to cause any flushing. Higher doses are not likely as effective as NMN and exercise in producing NAD+.

The NMN transporter was discovered11,12 shortly before my interview with David Sinclair, Ph.D., a professor of genetics and co-director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School. Interestingly, NMN is also Sinclair’s favorite NAD+ precursor.

Sinclair is generally acknowledged for bringing the importance of NAD+ to the world with his experiments at MIT in the late ‘90s which connected NAD+ to sirtuin activation. We discuss these issues in “The Revolutionary Science of Aging and Longevity,” the interview from which is embedded above for your convenience.

I believe one of the most effective ways of boosting your NAD+ level is to use NMN in suppository form, as this allows you to avoid most of the methylation of the supplement. Other alternatives include subcutaneous or intranasal administration, all of which are more effective than oral supplements.

Unfortunately, NMN is not sold in suppository form, so you would need to get silicone candy molds and use coconut oil to serve as binder for the NMN. The suppositories would need to be refrigerated as coconut oil tends to melt at 75 degrees Fahrenheit. Additionally, NMN is quite perishable, which is another reason to refrigerate it.

As for the other NAD+ boosters, I do not recommend using high-dose niacinamide because in high doses it inhibits Sirt1, an important longevity protein. As mentioned above, low-dose niacin (vitamin B3) of 25 mg can be used.

Low doses of niacin, along with NMN in suppository form — both of which are precursors to NAD+ — are typically sufficient. As an added boon, raising your NAD+ also appears protective against severe COVID-19, as detailed in “Is Niacin a Missing Piece of the COVID Puzzle?” There are also NAD+ supplements available, but their price tags can be prohibitive.

Lifestyle Strategies Can Address Underlying Cause of Low NAD+

While supplements such as NMN can certainly be helpful, if your NAD is low, your best bet is really to address the underlying cause. The good news is that this can be done through simple lifestyle strategies such as exercise, sauna bathing, fasting, realigning your circadian rhythm and minimizing electromagnetic field (EMF) exposure.

One of the reasons exercise, heat exposure and fasting work to address low NAD+ levels is because they are catabolic stressors that activate AMP protein kinase (AMPK). AMPK, in turn, activates an enzyme called NAMPT, which governs the NAD+ salvage pathway.

Blood flow restriction (BFR) training can be particularly beneficial in terms of exercise. It has been shown to naturally increase your NAD level and is very safe for the elderly. You can learn more about this in “BFR Training for Muscle Mass Maintenance.”

Your circadian rhythm, meanwhile, plays a role because it is controlled by longevity genes called sirtuins, SIRT1 in particular. If your circadian rhythm is misaligned, then sirtuins are not expressed, which in turn inhibits NAMPT, thereby shutting down your NAD+ salvage pathway.

Oxidative stress and inflammation also use up and deplete NAD+, and exercise, sauna and fasting all help to reduce these. As a result, less NAD+ is depleted. So, these strategies not only improve your NAD+ production, but also reduce your body’s NAD+ consumption. The end result is a higher NAD+ baseline.

EMF exposure, which is the topic of my book “EMF*D,” is one common source of oxidative stress, so it too increases your NAD+ consumption. It does this by activating PARP, a DNA repairing enzyme. Each time PARP is activated, it uses up 150 molecules of NAD+. Hence, reducing your EMF exposure can also be an important strategy to preserve and protect your NAD+ level.

Your body also uses up NAD+ to detoxify alcohol, so if nightly drinking is part of your routine, consider giving it up. To learn more about how healthy lifestyle strategies such as the ones mentioned here can improve your NAD+ level, consider reading through the paper “Healthy Lifestyle Recommendations: Do the Beneficial Effects Originate from NAD+ Amount at the Cellular Level?”13

NAD+ Is a Crucial Antiaging Component

So, to summarize, raising your NAD+ level and keeping it high has many important health benefits, from supporting mitochondrial function, which is crucial for general health and longevity, to protecting against severe COVID-19 and age-related muscle loss.

The great news is that this can easily be done by implementing the healthy lifestyle strategies reviewed above — exercise, sauna, fasting and recalibrating your circadian rhythm — while simultaneously avoiding things that deplete your body of NAD+, such as EMF exposure and excessive alcohol consumption. On top of that, supplements such as NMN together with normal doses of niacin can help boost your NAD+ in the short term.

Ominous B1 Deficiency Found Throughout Food Chain

Reproduced from original article:

Analysis by Dr. Joseph Mercola      Fact Checked      February 08, 2021

deficiency of thiamine vitamin b1


  • Vitamin B1 (thiamine) is used by nearly all your cells, metabolizing the carbohydrates and lipids in the foods you eat, helping to convert food into energy and boosting the flow of electrolytes in and out of your nerves and muscles
  • Thiamine is important for healthy immune function, and may actually be crucial to protect against infectious respiratory illnesses such as COVID-19
  • While thiamine deficiency is often the result of alcohol misuse, chronic infections, poor nutrition and/or malabsorption, recent research suggests vitamin B1 has dramatically declined throughout the food chain in recent years
  • The transfer of thiamine up the food chain may be blocked by a number of factors, including the overabundance of thiaminase, an enzyme that destroys thiamine. Thiaminase is naturally present in certain microorganisms, plants and fish that have adapted to use it to their advantage
  • Thiamine deficiency has been identified in dozens of animal species and is now suspected of driving declines in wildlife populations across the northern hemisphere. This means our diets are likely to be low in thiamine, thereby raising the risk for thiamine deficiency in the human population

Vitamin B1 (thiamine) is used by nearly all your cells, and helps to metabolize the carbohydrates and lipids in the foods you eat. It also facilitates converting your food into energy and boosting the flow of electrolytes in and out of your nerves and muscles. It’s considered “essential” because your body can’t produce it on its own; it must come from an outside source.

Thiamine is sometimes referred to as an “antistress” vitamin for its positive influence on your central nervous system, and it’s also important for healthy immune function. In addition to nutrients such as zinc and vitamins C and D, vitamin B1 (thiamine) may actually be crucial to protect against infectious respiratory illnesses such as COVID-19.

Thiamine deficiency syndrome (beriberi) has also been implicated in other types of severe infections and bears many similarities to sepsis. This is one of the reasons why thiamine is such an important part of Dr. Paul Marik’s sepsis treatment.1 Sepsis, in turn, is a major contributor in influenza deaths in general, and a primary cause for COVID-19 deaths specifically.

While thiamine deficiency is often the result of alcohol misuse, chronic infections, poor nutrition and/or malabsorption, recent research suggests vitamin B1 availability has dramatically declined throughout the food chain in recent years.2

Lack of Thiamine Is Disrupting Ecosystem

In a January 28, 2021, article in Hakai Magazine,3 Alastair Bland reviews findings showing certain marine ecosystems are being decimated by an apparent lack of thiamine. Problems were noticed in January 2020 at salmon hatcheries in California. Fish were acting disoriented and mortality was surprisingly high.

Initially, they feared a virus might be at play, but after digging through the medical literature, they found research discussing thiamine deficiency in marine life. As noted in the article, vitamin B1 is “a basic building block of life critical to the functioning of cells and in converting food into energy.”

Biologists tested the theory by dissolving thiamine powder into the water, and within hours, nearly all of the fish were acting normally again. Meanwhile, the behavior of fish in an untreated batch continued to decline. As a result of this research, many hatcheries took to applying thiamine, but the underlying problem still remains.

“Since the fish acquire thiamine by ingesting it through their food, and females pass nutrients to their eggs, the troubling condition indicated that something was amiss in the Pacific Ocean, the last place the fish eat before entering fresh water to spawn,” Bland writes, adding:

“California researchers now investigating the source of the salmon’s nutritional problems find themselves contributing to an international effort to understand thiamine deficiency, a disorder that seems to be on the rise in marine ecosystems across much of the planet.

It’s causing illness and death in birds, fish, invertebrates, and possibly mammals, leading scientists from Seattle to Scandinavia to suspect some unexplained process is compromising the foundation of the Earth’s food web by depleting ecosystems of this critical nutrient.”

Click here to learn more

What’s Causing Ecosystem-Wide Thiamine Deficiency?

As explained by Bland, “Thiamine originates in the lowest levels of the food web.” Certain species of bacteria, phytoplankton, fungi and even some plants are responsible for synthesizing thiamine from other precursor compounds.

From there, thiamine makes its way through both the animal and plant kingdoms. All organisms need it. In animals, enzymes interact with thiamine to generate cellular energy. Without sufficient amounts of thiamine, fundamental metabolic processes start to fail, causing neurological disturbances, reproductive problems and increased mortality.

While beriberi has been recognized as a serious health risk in humans for nearly 100 years, and thiamine supplementation has been standard practice for domesticated livestock such as sheep, cattle, mink and goats for several decades,4 the presence in and effect of thiamine deficiency on wildlife wasn’t discovered until the 1990s, when Canadian scientist John Fitzsimons started investigating the decline in Great Lakes trout. Bland writes:5

“Studying lake trout born in captivity, Fitzsimons observed symptoms like hyperexcitability, loss of equilibrium, and other abnormal behavior.

He wondered if a nutritional deficiency was at play, and to test for this he dissolved various vitamin tablets in water and — using trout in different life stages, including fertilized eggs — administered the solutions to the fish, both through injection and baths.

The idea was to see which vitamin, if any, cured the condition. ‘It came down to a range of B vitamins, and it was only the thiamine that was able to reverse the signs I was seeing,’ he says.”

Since the publication of Fitzsimons’ findings in 1995, thiamine deficiency has been identified in dozens of animal species, including birds and moose. While severe deficiency has lethal consequences, sublethal deficiency can have insidiously devastating effects, including:6

  • Lowering strength and coordination
  • Reducing fertility
  • Impairing memory and causing other neurobehavioral deficits.7 In humans, thiamine deficiency has been shown to play a role in cases of delirium. In one study,8 45% of cancer patients suffering from delirium had thiamine deficiency, and 60% recovered when treated with intravenous thiamine
  • Paralysis
  • Loss of vocalization

B1 Deficiency May Be Responsible for Wildlife Declines

Thiamine deficiency is now suspected of driving declines in wildlife populations all across the northern hemisphere.9 Bland cites research showing marine and terrestrial wildlife populations declined by half between 1970 and 2012. Between 1950 and 2010, the global seabird population declined by 70%.10

The transfer of thiamine up the food chain may be blocked by a number of factors, including overfishing. But there’s yet another possibility, and that is the overabundance of thiaminase, an enzyme that destroys thiamine. Thiaminase is naturally present in certain microorganisms, plants and fish that have adapted to use it to their advantage.

While habitat loss and other environmental factors are known to impact biodiversity, these declines are allegedly occurring far faster than can be explained by such factors. Researchers strongly suspect human involvement, but how?

“Scientists are floating various explanations for what’s depriving organisms of this nutrient, and some believe that changing environmental conditions, especially in the ocean, may be stifling thiamine production or its transfer between producers and the animals that eat them,” Bland writes.11

“Sergio Sañudo-Wilhelmy, a University of Southern California biogeochemist, says warming ocean water could be affecting the populations of microorganisms that produce thiamine and other vitamins, potentially upsetting basic chemical balances that marine ecosystems depend on.

‘In different temperatures, different phytoplankton and bacteria grow faster,’ he says. This, he explains, could hypothetically allow microorganisms that do not produce thiamine — but, instead, acquire it through their diet — to outcompete the thiamine producers, effectively reducing thiamine concentrations in the food web.”

The transfer of thiamine up the food chain may be blocked by a number of factors, including overfishing. But there’s yet another possibility, and that is the overabundance of thiaminase, an enzyme that destroys thiamine. Thiaminase is naturally present in certain microorganisms, plants and fish that have adapted to use it to their advantage.

“When larger animals eat prey containing thiaminase, the enzyme rapidly destroys thiamine and can lead to a nutritional deficiency in the predator,” Bland explains. One thiaminase-rich species is an invasive species of herring called alewife, which during the 20th century have spread through the Great Lakes, displacing native species.

This, some researchers believe, has led to chronic and severe thiamine deficiency in larger fish species. “The Great Lakes’ saga illustrates the outsized impact that one single nutrient can have on an entire ecosystem,” Bland writes.

An overabundance of thiaminase-containing species also appears to be responsible for the decline in Sacramento River salmon. In this case, northern anchovy, which is rich in thiaminase, is the suspected culprit.

Unfortunately, few answers have emerged as of yet. Giving thiamine to fish in hatcheries is not a long-lasting solution, because once they re-enter the wild, the deficiency reemerges. One scientist likened the practice to “sending a kid with a fever off to school after giving them a Tylenol.”12

Signs and Symptoms of Thiamine Deficiency

Considering both plants and wildlife are becoming increasingly thiamine-deficient, it’s logical to suspect that this deficiency is becoming more common in the human population as well. Early symptoms of thiamine deficiency include:13,14

  • Fatigue and muscle weakness
  • Confusion and/or memory problems
  • Loss of appetite and weight loss
  • Numbness or tingling in arms or legs

As your deficiency grows more severe, the deficiency can progress into one of four types of beriberi:15

  • Paralytic or nervous beriberi (aka “dry beriberi”) — Damage or dysfunction of one or more nerves in your nervous system, resulting in numbness, tingling and/or exaggerated reflexes
  • Cardiac (“wet”) beriberi — Neurological and cardiovascular issues, including racing heart rate, enlarged heart, edema, breathing problems and heart failure
  • Gastrointestinal beriberi — Nausea, vomiting, abdominal pain and lactic acidosis
  • Cerebral beriberi — Wernicke’s encephalopathy, cerebellar dysfunction causing abnormal eye movements, ataxia (lack of muscle coordination) and cognitive impairments. If left untreated, it can progress to Korsakoff’s psychosis, a chronic brain disorder that presents as amnesia, confusion, short-term memory loss, confabulation (fabricated or misinterpreted memories) and in severe cases, seizures

Thiamine is frequently recommended and given to people struggling with alcohol addiction, as alcohol consumption reduces absorption of the vitamin in your gastrointestinal tract. An estimated 80% of alcoholics are deficient in thiamine and therefore more prone to the side effects and conditions above.16

Thiamine is also very important for those with autoimmune diseases such as inflammatory bowel disease (IBD) and Hashimoto’s (a thyroid autoimmune disorder).17 In case studies,18,19 thiamine supplementation has been shown to improve fatigue in autoimmune patients in just a few days.

Interestingly, in one of these studies,20 which looked at patients with IBD, patients responded favorably to supplementation even though they all had “normal” baseline levels.

The authors speculate that thiamine deficiency symptoms in such cases may be related to enzymatic defects or dysfunction of the thiamine transport mechanism (opposed to being an absorption problem), which can be overcome by giving large quantities of thiamine.

Thiamine in Infectious Disease

As mentioned earlier, thiamine deficiency has also been implicated in severe infections, including COVID-19. In fact, researchers have noted that, based on what we know about B vitamins’ effects on the immune system, supplementation may be a useful adjunct to other COVID-19 prevention and treatment strategies. You can learn more about this in “B Vitamins Might Help Prevent Worst COVID-19 Outcomes.”

More generally, a 2016 study21 in the journal Psychosomatics sought to investigate the connection between thiamine and infectious disease by looking at 68 patients with Korsakoff syndrome.

Thirty-five of them suffered severe infections during the acute phase of the illness, including meningitis, pneumonia and sepsis, making the authors conclude that “Infections may be the presenting manifestation of thiamine deficiency.”

Another study22 published in 2018 found thiamine helps limit Mycobacterium tuberculosis (MTB) by regulating your innate immunity. According to this paper:

“… vitamin B1 promotes the protective immune response to limit the survival of MTB within macrophages and in vivo … Vitamin B1 promotes macrophage polarization into classically activated phenotypes with strong microbicidal activity and enhanced tumor necrosis factor-α and interleukin-6 expression at least in part by promoting nuclear factor-κB signaling.

In addition, vitamin B1increases mitochondrial respiration and lipid metabolism … Our data demonstrate important functions of thiamineVB1 in regulating innate immune responses against MTB and reveal novel mechanisms by which vitamin B1 exerts its function in macrophages.”

Thiamine deficiency is also associated with the development of high fever, and according to a letter to the editor,23 “Is Parenteral Thiamin a Super Antibiotic?” published in the Annals of Nutrition & Metabolism in 2018, thiamine injections are “likely to eradicate microbial infections” causing the fever.

By dramatically increasing susceptibility to infections, thiamine deficiency could potentially have the ability to impact the spread of just about any pandemic infectious disease — including COVID-19.

Are You Getting Enough B Vitamins?

While biologists struggle to find an ecosystem-wide solution for thiamine deficiency in the food chain, the solution for us, in the meantime, may be to make sure we get enough thiamine through supplementation. Evidence suggests thiamine insufficiency or deficiency can develop in as little as two weeks, as its half-life in your body is only nine to 18 days.24

Ideally, you can select a high-quality food-based supplement containing a broad spectrum of B vitamins to avoid creating an imbalance. The following guidelines will also help protect or improve your thiamine status:

Limit your sugar and refined grain intake — As noted by the World Health Organization,25 “Thiamine deficiency occurs where the diet consists mainly of milled white cereals, including polished rice, and wheat flour, all very poor sources of thiamine.”

Simple carbs also have antithiaminergic properties,26 and raise your thiamine requirement for the simple fact that thiamin is used up in the metabolism of glucose.

Eat fermented foods — The entire B group vitamin series is produced within your gut provided you have a healthy gut microbiome. Eating real food, ideally organic, along with fermented foods will provide your microbiome with important fiber and beneficial bacteria to help optimize your internal vitamin B production as well.

Avoid excessive alcohol consumption, as alcohol inhibits thiamine absorption, and frequent use of diuretics, as they will cause thiamine-loss.

Avoid sulfite-rich foods and beverages such as nonorganic processed meats, wine and lager, as sulfites have antithiamine effects.

Correct any suspected magnesium insufficiency or deficiency, as magnesium is required as a cofactor in the conversion of thiamine.

Daily Intake Recommendations

While individual requirements can vary widely, the typical daily intake recommendations for B vitamins are as follows:

Nutrient Supplement Recommendations
Thiamine (B1) Adult men and women need 1.2 and 1.1 mg respectively each day.27 If you have symptoms of thiamine deficiency, you may need higher doses.

Thiamine is water-soluble and nontoxic, even at very high doses, so you’re unlikely to do harm.

Doses between 3 grams and 8 grams per day have been used in the treatment of Alzheimer’s without ill effect.

Riboflavin (B2) Suggested daily intake is about 1.1 mg for women and 1.3 mg for men.28
Niacin (B3) The dietary reference intake established by the Food and Nutrition Board ranges from 14 to 18 mg per day for adults.

Higher amounts are recommended depending on your condition. For a list of recommended dosages, see the Mayo Clinic’s website.29

Vitamin B6 Nutritional yeast (not to be confused with Brewer’s yeast or other active yeasts) is an excellent source of B vitamins, especially B6.30

One serving (2 tablespoons) contains nearly 10 mg of vitamin B6, and the daily recommended intake is only 1.3 mg.31

B8 (inositol/biotin) B8 is not recognized as an essential nutrient and no recommended daily intake has been set. That said, it’s believed you need about 30 mcg per day.32

Vitamin B8 is sometimes listed as biotin on supplements. Brewer’s yeast is a natural supplemental source.33

Folate (B9) Folic acid is a synthetic type of B vitamin used in supplements; folate is the natural form found in foods. (Think: Folate comes from foliage, edible leafy plants.)

For folic acid to be of use, it must first be activated into its biologically active form (L-5-MTHF).

This is the form able to cross the blood-brain barrier to give you the brain benefits noted.

Nearly half the population has difficulty converting folic acid into the bioactive form due to a genetic reduction in enzyme activity.

For this reason, if you take a B-vitamin supplement, make sure it contains natural folate rather than synthetic folic acid.

Nutritional yeast is an excellent source.34 Adults need about 400 mcg of folate per day.35

Vitamin B12 Nutritional yeast seasoning is also high in B12, and is highly recommended for vegetarians and vegans.

One serving (2 tablespoons) provides about 67 mcg of natural vitamin B12.36

Sublingual (under-the-tongue) fine mist spray or vitamin B12 injections are also effective, as they allow the large B12 molecule to be absorbed directly into your bloodstream.

The Overlooked Vitamin That Improves Autoimmune Disease and Autonomic Dysfunction

© February 1st 2021 GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC.
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Posted on: Monday, February 1st 2021 at 4:45 am
Written By: Ali Le Vere, B.S., B.S. – Senior Researcher-Greenmedinfo
This article is copyrighted by GreenMedInfo LLC, 2021

Thiamin may be the missing link to treating autoimmune disease and autonomic dysfunction. Although deficiencies in this vitamin have long been considered eradicated, case studies show supplementation with this nutrient improves fatigue in autoimmune patients in a matter of hours to days

One of the common threads uniting disparate autoimmune disease labels, irrespective of diagnosis, is the debilitating fatigue that plagues patients. Although methylated B vitamins have been given ample fanfare, vitamin B1, or thiamin, has garnered far less attention in communities that emphasize the holistic management of autoimmune disease.

Functions of Thiamin

One of eight essential B vitamins, thiamin is a water-soluble vitamin that functions in the conversion of food into energy (1). The active form of thiamin, known as thiamin pyrophosphate or thiamin diphosphate, is an essential cofactor in both the citric acid cycle and pentose phosphate pathway, two enzyme-mediated pathways of carbohydrate metabolism (1). The citric acid cycle, for example, also known as the Kreb’s cycle, is a central metabolic pathway in the mitochondria that participates in the oxidative degradation of monosaccharides and other nutrients, which generates cellular energy currency in the form of adenosine triphosphate (ATP) to be used in a myriad of energy-demanding cellular reactions (1).

Inhibition of the two main enzymes of the Kreb’s cycle for which thiamin is a cofactor, pyruvate dehydrogenase complex (PDH) and alpha-ketoglutarate dehydrogenase (alpha-KGDH), leads to decreased brain levels of ATP (1). Suppression of brain ATP levels impairs degradation of dopamine in the prefrontal cortex, disrupts synthesis of the nerve-insulating myelin sheath, prevents production of the neurotransmitter acetylcholine, and reduces levels of the major inhibitory neurotransmitter gamma aminobutyric acid (GABA), which collectively leads to delirium, delusions, hallucinations, and cognitive impairment (1).

The transketolase enzyme of the cytosol-based pentose phosphate pathway (PPP), on the other hand, also requires thiamin as a cofactor (1). Transketolase converts glucose-6-phosphate into both ribose-5-phosphate and reduced nicotinamide adenine dinucleotide phosphate (NADPH), the latter of which is required to donate hydrogen atoms in chemical reactions that produce particular neurotransmitters, steroids, amino acids, fatty acids, and the master antioxidant of the body, glutathione (1). Given its centrality to these biochemical pathways which generate energy for the entire organism, the effects of thiamin deficiency are all-encompassing.

The Re-Emergence of Thiamin Deficiency Disorders

The relationship between food and berberi, the classical syndrome of thiamin deficiency, was first discovered by Japanese naval surgeon Takaki in the late nineteenth century, who found that nearly two-thirds of his crew were stricken with berberi after a long voyage. Two years later, when he loaded another warship with dry milk and meat, he noticed that a much smaller percentage of the crew succumbed to berberi, such that “Takaki concluded that the disease was caused by a lack of nitrogenous food in association with excessive intake of non-nitrogenous food” (2).

In addition to impaired reflexes, peripheral neuropathy, edema, cardiovascular abnormalities and hypesthesia, or a diminished capacity for physical sensation, signs of autonomic dysfunction such as sinus tachycardia, vasovagal syncope, mitral valve prolapse, hypotension, sweating, dermographia, and attention deficit are a prominent part of the clinical expression of berberi (2, 3). Other extreme manifestations of thiamin deficiency include Wernicke’s encephalopathy, which includes signs such as ataxia, weakness, paralysis, cognitive impairment, apathy, significant spatial and temporal disorientation, and problems with movement in the muscles around the eyes such as ocular palsies, nystagmus, and opthalmoplegia (1). These symptoms are caused by lesions in brain areas including the hypothalamic nuclei, tectal plate, periventricular nuclei, thalamus, pontine tegmentum, and abducens and oculomotor nuclei, and untreated, lead to coma and death (1).

Korsakoff’s psychosis is often a progression of Wernicke’s encephalopathy (4), and includes symptoms such as amnesia, decreased initiative, and confabulation, which means distorted, fabricated, or misinterpreted memories. Although thiamin deficiency, and its extreme incarnations in particular such as Wernicke’s encephalopathy and Korsakoff’s psychosis, is considered a medical emergency, 80% of the time these diagnoses are made during autopsy (5), mainly due to low index of suspicion, and the nonspecific clinical signs of these syndromes (1).

Although the benefit of thiamin in these classical syndromes of thiamin deficiency, which were recorded as far back as the ninth century, is uncontested, milder forms of thiamin deficiency often elude diagnosis. Marginal thiamin deficiency presents with vague symptomatology, including fatigue, irritability, abdominal pain, frequent headaches, and a decline in growth rate in children (6). The World Health Organization states, in fact, that, thiamin deficiency is a clinical diagnosis confirmed upon improvement with thiamin administration:

The symptoms of mild thiamin deficiency are vague and can be attributed to other problems, so that diagnosis is often difficult…The symptoms of mild thiamin deficiency clinically improve by the administration of thiamin.(7)

In the minds of conventional providers, deficiency diseases have been eradicated in the industrialized world; however, unbeknownst to the medical establishment, it is our Western diets that are facilitating the re-emergence of these diseases considered long-abolished:

Perhaps, in the light of more modern knowledge, it is possible to state that high simple carbohydrate malnutrition can cause symptoms of early beriberi. Since beriberi conjures up an unacceptable concept in the mind of many modern physicians it is probable that it would not be considered in differential diagnosis. It is very likely that many of the poorly understood symptomatology seen today that responds to nutrient therapy is caused by a mixture of marginal classic nutritional diseases, including beriberi, pellagra and scurvy.(2)

Efficacy of Thiamin in Inflammatory Bowel Disease

Especially encouraging are the results of a small open-label pilot study of thiamin use in patients with inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, who presented with fatigue and lingering extra-intestinal symptoms despite their diseases being characterized as quiescent or in remission (8). Patients, all of whom had normal thiamin levels at the commencement of the study, were treated orally with 600 milligrams per day of thiamin, with additional doses in increments of 300 mg per day for those cases in which regression of fatigue was not considered satisfactory, up to a total of 1,500 mg per day (8). In other words, the dose was defined empirically, with calibration based upon subject weight and according to symptomatic remission.

All but two of the twelve patients exhibited a complete regression of fatigue, and in the remaining two, near complete regression was observed (8). Moreover, one hundred percent of patients reported complete regression of symptoms associated with fatigue (8). Impressively, the majority of patients also displayed improvements in intestinal function, with marked reductions in the number of diarrhetic episodes (8).

Notably, in one of the series of case studies presented, fatigue disappeared completely after intramural thiamin injection, and authors mention that “within 20 days, the patient regained complete wellness” (8). This study confirmed findings by Magee and colleagues, who found that consumption of thiamin-rich foods decreases disease activity in patients with ulcerative colitis (9).

Effect of Thiamin in Hashimoto’s Thyroiditis

Another series of case reports published in The Journal of Alternative and Complementary Medicine chronicles the use of thiamin in patients with Hashimoto’s thyroiditis who had persistent symptoms such as fatigue, depression, anxiety, sleep disruption, impaired memory and concentration, dry skin, and cold intolerance despite normal thyroid parameters (10). Patients, all of whom exhibited normal blood levels of thiamin and TPP prior to treatment, were administered either 600 mg per day of oral thiamin or 100 mg per mL of thiamin administered parenterally every four days, depending on weight (10).

In the two patients given oral thiamin, complete regression of fatigue occurred within 3 to 5 days, whereas fatigue regressed within 6 hours in the patient given intramuscular thiamin therapy (10). Although case studies rank low on the hierarchy of evidence-based data, and underscore the need for higher quality research, the mechanism linking functional thiamin deficiency to autoimmune-based fatigue is so plausible that the study authors assert:

While further studies are necessary to confirm our findings, we strongly believe that our observations represent an important contribution to the relief of many patients.(10)

Reasons Underlying Thiamin Deficiency in Autoimmunity

As indicated by the IBD pilot study in which all patients exhibited normal levels prior to treatment, yet still responded favorably to thiamin supplementation, tests of thiamin and thiamin pyrophosphate (TPP), the active form of thiamin, may be of no value in identifying functional thiamin deficiency (8).

Normal serum levels of thiamin and TPP, in fact, indicate normal thiamin absorption by the small intestine (8). Researchers instead attribute the symptoms of thiamin deficiency that appeared in these autoimmune patients in both studies to either structural enzymatic defects or to dysfunction of the vitamin B1 active intracellular transport mechanism from the blood to the mitochondria (8). Administration of large quantities of vitamin B1, on the other hand, is able to circumvent this abnormality:

The administration of large quantities of vitamin B1 orally increases the concentration in the blood to levels in which the passive transport restores the normal glucose metabolism. The glucose metabolism of all organs goes back to normal values and fatigue disappears.(8)

As an alternative explanation, one author in the New England Journal of Medicine proposes that a deficiency in activity of one thiamin transporter can cause another to pick up the slack when high doses of thiamin are administered. This occurs because one member of the solute carrier (SLC) gene family of transporter proteins, which possess structural similarity, can substitute for the function of another.

In other words, at large doses, thiamin can induce expression of the solute carrier gene family member SLC19A2, which encodes the human thiamin-only transporter 1 (hTHTR1), in order to compensate for defects in SLC19A3, which encodes the human thiamin and biotin transporter 2 (hTHTR2) (11). Increasing the concentration of blood thiamin also augments the chances that it crosses the blood brain barrier (BBB) to correct neurological deficits, since thiamin penetration of the BBB occurs via passive diffusion, an energy-independent process, when there is a surplus of thiamin available (12).

Food-Based Sources of Thiamin

Only plants, bacteria, and fungi can synthesize thiamin, so humans must acquire thiamin from external food sources. Because they are nutrient-poor, breads and cereals are oftentimes fortified with thiamin, but ingestion of these foodstuffs for thiamin sufficiency is counter-intuitive, since simple carbohydrates increase the need for thiamin. Although data on thiamin content of foods is limited (13), whole-food sources of thiamin include liver and other sources of offal, meat, pork, poultry, fish, eggs, dried legumes, nuts, and whole grains such as brown rice and bran (2).

Additionally, other plants which have relatively high thiamin content include Nicaraguan cacao, black cohosh, spirulina, string beans, kidney beans, black beans, navy beans, green beans, peas, black-eyed peas, bael fruit, asparagus, macambo, sunflower seed, shepherd’s purse, okra, high mallow, sow thistle, mountain buchu, watercress, and garlic (14). However, cooking and heat-processing of food results in considerable thiamin losses, so preparation methods matter from a thiamin sufficiency perspective (2).

Thiamin Repletion: Correcting the Deficiency

Of note, is that the dose administered in the IBD study is much higher than that which can be obtained from food, and approximately 600-fold higher than the daily recommended intake for men and women older than ten years of age (1). Due to the supra-physiological nature of the dosing regimen, patients should consult with a naturopathic or integrative doctor prior to consuming a dose of this magnitude.

However, the safety profile of thiamin, as observed in the literature, demonstrates that this intervention is benign. Unlike other immunosuppressant drugs often administered for autoimmune diseases, which can be accompanied by catastrophic side effects such as infection and cancer, there are no collateral effects of thiamin administration, even when used at high doses long-term (10).

In fact, thiamin is nontoxic to the body even at excess amounts (15), and doses as high as 3 to 8 grams per day have been used to treat Alzheimer’s disease without adverse effects (8). Only mild tachycardia appeared in one patient in the IBD study, which abated upon reduction of the dose (8).

This safety profile stands in stark contrast to a drug like hydroxychloroquine (Plaquenil), which is often prescribed to improve fatigue in autoimmune diseases such as systemic lupus erythematosus, antiphospholipid syndrome, sarcoidosis, rheumatoid arthritis, and Sjögren’s syndrome, which poses the risk of potentially irreversible retinopathy (16) that may progress to blindness even 7 years after the drug has been discontinued (17). Similarly, newer generation biologic drugs such as antitumor necrosis factor (anti-TNF) therapy and anti-T cell strategies carry risk of autoimmune disease itself, causing the very diseases they are designed to treat in a cruel poetic irony (18).


Other considerations for using thiamin include integrating supplementation with a broad-spectrum low-dose B vitamin formulation to prevent any imbalances in B vitamins. Likewise, another factor often at play is magnesium deficiency, since the conversion process of thiamin to its metabolically active form requires magnesium as a cofactor (19). Therefore, magnesium deficiency should be corrected, since hypomagnesaemia can mimic thiamin deficiency (1).

Although scientists state, “We deem necessary a lifelong use of high doses of thiamin in affected subjects,” researchers are unable to clarify whether the aberration in thiamin transport is secondary to genetic mutations or to an autoimmune-inflammatory process (8), which raises the possibility that resolution of the underlying immune dysregulation, namely, through approaches that restore an evolutionarily appropriate diet and lifestyle template, may negate the need for high-dose thiamin long-term.

Forms of Thiamin

One potential limiting factor of thiamin use is its poor bioavailability and slower absorption as a supplement, which is why high doses of thiamin are prescribed for certain medical conditions (3). To circumvent this issue, researchers have developed fat-soluble derivatives of thiamin called allithiamines. Benfotiamine, one lipophilic derivative of thiamin which readily diffuses through biological membranes, has been shown to have clinical benefit in diabetic vascular complications (3).

Its mechanisms of action includes reduction of advanced-glycation end products (AGEs), highly oxidant compounds with pathogenic significance in aging and chronic disease states (20), and modulation of pathways that play roles in cell survival, death, and repair (3). Impressively, benfotiamine also reduces activation of the nuclear factor kappa beta (NFkB) signaling pathway, the gateway to inflammatory eicosanoid mediators, and mitigates signaling down the arachidonic acid pathway, inhibiting the same cyclooxygenase (COX) enzymes (3) exploited by non-steroidal anti-inflammatory drugs (NSAIDs) without the deleterious side effects.

In addition, benfotiamine has been found to have free radical-scavenging properties via its ability to modulate levels of enzymes involved in endogenous antioxidant defense, such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) (3). Not only that, but benfotiamine reduces activity of glycogen synthase kinase 3 (GSK-3), which is involved in deposition of β-amyloid plaques in the brain in Alzheimer’s disease (3). Proof-of-concept of its neuroprotective abilities have been demonstrated in recent studies showing that benfotiamine reduces plaque accumulation, improves symptomatology (3), and inhibits progression of cognitive impairment in Alzheimer’s disease (21). Therefore, due to its pleiotropic effects, thiamin in this form has the potential to improve a host of chronic, inflammatory, and neurodegenerative conditions.

Removing Anti-Thiamin Agents

Predisposing factors for thiamin deficiency include malnutrition, acquired immunodeficiency syndrome (AIDS), gastrointestinal surgical procedures such as vertical banded gastroplasty, gastric bypass surgery, colectomy, and intragastric balloon, and psychiatric disorders including anorexia nervosa, bulimia, and binge-eating disorders (1). Certain medical conditions, such as pancreatitis, renal disease, thyrotoxicosis, celiac disease, cancer, peptic ulcers, and other gastrointestinal disorders are likewise associated with increased risk of thiamin deficiency (1).

However, chronic alcoholism poses special risk, since it interferes with the rate-limiting step of carrier-mediated thiamin absorption in the duodenum (22), alongside impairing the storage and phosphorylation of thiamin that is essential to its function (1). In addition, thiamin deficiency is under-recognized in obesity and is implicated in the progression of obesity-related chronic disease states (Maguire et al., 2018). Furthermore, people with type 1 and type 2 diabetes have plasma thiamin levels that are 76% and 50% to 75% lower, respectively, than healthy volunteers (24, 25).

Certain dietary factors, such as simple carbohydrates, also have anti-thiaminergic properties (9), which is referred to as high-calorie malnutrition when excessive intake produces thiamin deficiency. Carbohydrates increase the need for the vitamin since thiamin is a major factor in the metabolism of glucose (2). What’s more, polyphenolic compounds present in tea and coffee can inactivate thiamin (2).

Also problematic are sulfiting agents, including sulfites, sulfur dioxide, hydrogen sulfites, and metabisulfites, which are used as food preservatives to prevent microbial growth, food spoilage, and discoloration, and to extend the shelf life of the product (9). Sulfites, which are contained in foods such as wines, lager, non-organic processed meats such as sausage and burgers, sulfited seafoods, and soft drinks from concentrate, are problematic because of their anti-thiamin effects, since thiamin is readily cleaved by the sulfite ion, particularly at a colonic pH (9). The role of sulfites reinforces the thiamin-autoimmune connection, as studies of ulcerative colitis have elucidated a role of sulfited foods in the pathogenesis of the disease, with high sulfite foods producing worse sigmoidoscopy scores (9)—presumably due in part to thiamin depletion.

Therapeutic Potential for Thiamin in Autoimmune Disease

Researchers state that the role of thiamin as a medicinal agent is under-appreciated in Western civilization (26). Although deficiency disorders are considered afflictions of developing societies, the prevalence of subclinical thiamin deficiency has been demonstrated to be on the rise (3). In addition, because a response to thiamin therapy is considered diagnostic of thiamin deficiency, in concert with its excellent safety profile, a trial of thiamin poses little risk. As asserted by researchers in The Journal of Alternative and Complementary Medicine,

Our team is convinced that the fatigue correlated with all autoimmune inflammatory diseases is a manifestation of an intracellular mild thiamin deficiency likely due to thiamin transporter deficiency or to enzymatic dysfunctions.(8)

Not only does thiamin deficiency cause mitochondrial dysfunction, but it also results in oxidative stress, which is central to the pathophysiology and perpetuation of autoimmune disorders. Not only that, but some of the cardinal symptoms of thiamin deficiency are features of autonomic dysfunction, or dysautonomia, which 24% to 100% of autoimmune patients have been shown to experience (27). Therefore, restoration of thiamin status in autoimmune patients has the potential to ameliorate a vast array of symptoms, since the autonomic nervous system is responsible for a diversity of largely unconscious physiological activities including digestion, urination, defecation, heart rate, blood pressure, pupillary response, and sexual arousal.

Lastly, another line of reasoning connecting autoimmunity to thiamin deficiency is postural orthostatic tachycardia syndrome (POTS), a form of dysautonomia with suspected autoimmune etiology that is often comorbid with other autoimmune diseases (28). The symptoms of POTS, which has been shown to respond to thiamin supplementation in some cases (29), resemble berberi.

Given the ubiquity of anti-thiamin agents in the Western diet alongside problems with thiamin transport in autoimmune patients, these preliminary studies raise the possibility of thiamin as a potent therapeutic option for autoimmune disorders alongside a holistic regimen that addresses mindfulness, toxicity, diet, and lifestyle.


  1. Osiezagha, K. et al. (2013). Thiamin deficiency and delirium. Innovations in Clinical Neuroscience, 10(4), 26-32.
  2. Lonsdale, D. (2006). A Review of the Biochemistry, Metabolism and Clinical Benefits of Thiamin(e) and Its Derivatives. Evidence Based Complementary and Alternative Medicine, 3(1), 49-59.
  3. Raj, V. et al. (2018). Therapeutic potential of benfotiamine and its molecular targets. European Review for Medical and Pharmacological Sciences, 22, 3261-3273.
  4. Zubaran, C., Fernandes, J.G., & Rodnight, R. (1997). Wernicke-Korsakoff syndrome. Postgraduate Medical Journal, 73(85%), 27-31.
  5. Thomson, A.D., Guerrini, I., & Marshall, E.J. (2009). Wernicke’s encephalopathy: role of thiamine. Practices in Gastroenterology, 33(6), 21-30.
  6. Shikata, E. et al. (2000). “Iatrogenic” Wernicke’s encephalopathy in Japan. European Neurology, 44(3), 156–161.
  7. World Health Organization, United Nations High Commissioner for Refugees. (1999). Thiamin Deficiency and Its Prevention and Control in Major Emergencies. Retrieved from
  8. Costantini, A., & Pala, M.I. (2013). Thiamin and Fatigue in Inflammatory Bowel Diseases: An Open-label Pilot Study. The Journal of Alternative and Complementary Medicine, 19(8), 704-708.
  9. Magee, E. et al. (2005). Association between diet and disease activity in ulcerative colitis patients using a novel method of data analysis. Nutrition Journal, 4(7).
  10. Costantini, A., & Pala, M.I. (2014). Thiamin and Hashimoto’s Thyroiditis: A Report of Three Cases. The Journal of Alternative and Complementary Medicine, 20(3), 208-2011.
  11. Kono, S. et al. (2009). Mutation in a thiamin-transporter gene and Wernicke’s like encephalopathy. New England Journal of Medicine, 360, 17921.
  12. Thomson, A.D. (2000). Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. Alcohol & Alcoholism, 35(Suppl 1), 2–7.
  13. National Institutes of Health: Office of Dietary Supplements. (2018). Thiamin: Fact Sheet for Professionals. Retrieved from
  14. United States Department of Agriculture, Agricultural Research Service. (1992-2016). Dr. Duke’s Phytochemical and Ethnobotanical Databases. Home Page,
  15. Hope, L.C., Cook, C.C., & Thomson, A.D. (1999). A survey of the current clinical practice of psychiatrists and accident and emergency specialists in the United Kingdom concerning vitamin supplementation for chronic alcohol misusers. Alcohol and Alcoholism, 4(6), 862–867.
  16. Lehne, R.A. (2007). Pharmacology for Nursing Care. St. Louis, Missouri: Saunders-Elsevier Inc.
  17. Abdulaziz, N. et al. (2018). Hydroxychloroquine: balancing the need to maintain therapeutic levels with ocular safety: an update. Current Opinion in Rheumatology, 20(3), 249-255. doi: 10.1097/BOR.0000000000000500.
  18. Chandrashekara, S. (2012). The treatment strategies of autoimmune disease may need a different approach from conventional protocol: A review. Indian Journal of Pharmacology, 44(6), 665-671.
  19. Zieve, L. (1969). Influence of magnesium deficiency on the utilization of thiamin. Annals of the New York Academy of Science, 162(2), 732–743.
  20. Uribarri, J. (2010). Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. Journal of the American Dietetic Association, 110(6), 911-916.e12.
  21. Pan, X. et al. (2016). Long-term cognitive improvement after benfotiamine administration in patients with Alzheimer’s disease. Neuroscience Bulletin, 32, 591-596.
  22. Todd, K.G., Hazell, A.S., & Butterworth, R.F. (1999). Alcohol-thiamin interactions: an update on the pathogenesis of Wernicke encephalopathy. Addiction Biology, 4(3), 261–272.
  23. Maguire, D. et al. (2018). The role of thiamine dependent enzymes in obesity and obesity related chronic disease states: A systematic review. Clinical Nutrition ESPEN, 25, 8-17.
  24. Thornalley, P.J. et al. (2007). High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease. Diabetologia, 50, 2164-2170.
  25. Al-Attas, O.S. et al. (2012). Blood thiamine and its phosphate esters as measured by high-performance liquid chromatography: levels and associations in diabetes mellitus patients with varying degrees of microalbuminuria. Journal of Endocrinology Investigations, 35, 951-956.
  26. Lonsdale, D. (2011). Thiamin(e): The Spark of Life. Water Soluble Vitamins, 199-227.
  27. Stojanovich, L. (2009). Autonomic dysfunction in autoimmune rheumatic disease. Autoimmune Reviews, 8(7), 569-572.
  28. Blitshteyn, S. (2015). Autoimmune markers and autoimmune disorders in patients with postural tachycardia syndrome (POTS). Lupus, 24(13), 1364-1369.
  29. Blishteyn, S. (2017). Vitamin B1 deficiency in patients with postural tachycardia syndrome (POTS). Neurology Research, 39(8), 685-688.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.


Can Carrots Help Combat COVID?

Reproduced from original article:

Analysis by Dr. Joseph Mercola   Fact Checked    January 23, 2021

can carrots help combat covid


  • Scientists studying the relationship between nutrition, your immune system and COVID-19 have found that carrots have a compound that is stable against SARS-CoV-2 proteins
  • Carrots are rich in vitamins A and C; data show a deficiency in vitamin A leads to age-related macular degeneration, cataracts and inhibition of normal apoptosis in bone marrow
  • Beta-carotene helps optimize levels of non-HDL cholesterol and compounds found in carrots help lower the risk of diabetes, heart disease, cancer and metabolic syndrome
  • While the demand for baby carrots is rising in the U.S., it’s wise to steer clear of them as they are usually given a chlorine bath before sale; choose whole, unprocessed, ideally organic, carrots that you can wash, peel and cut yourself

Carrots (Daucus carota) are root vegetables and one of the most popular food ingredients used worldwide. Researchers have found this popular vegetable may hold one key in the fight against COVID-19.1

Historians believe the history of the carrot is somewhat obscured since, initially, carrots and parsnips were used interchangeably and it has been difficult to identify when wild carrots were first cultivated.2

It is believed they originated in Iran and Afghanistan and were popular in ancient Egypt, where the most-used carrot was believed to be purple. English settlers brought the modern-day carrot to Jamestown, Virginia, in 1609, where they spread to South America and then made the jump to Australia.

Wild carrots are still indigenous to Europe, North Africa and Western Asia and appear in temperate regions around the world.3 The modern carrot appeared in the 17th century after selective breeding reduced the wooden core and increased the sweetness.4 But it was only after World War I that carrots became popular in the U.S.

China leads the market for turnips and carrots combined, producing 48.2% of world sales for the two veggies.5 Global production in 2019 was 44.7 million metric tons and the market is expected to continue to grow at 3.4% through 2025. The major challenge during the COVID-19 pandemic has been the impact on the supply chain, which has increased direct farm-to-consumer sales and delayed shipping.

Some Components of Carrots Influence SARS-CoV-2 Proteins

Many scientists have begun studying the relationship between nutrition, your immune system and COVID-19 infection. Since carrots are consumed around the world, scientists at a private institution in Mexico developed a study in which they analyzed the effect retinol RTN from carrots has on amino acids that make up SARS-CoV-2, the virus that causes COVID-19.6

Preformed vitamin A, called retinol, comes only from animal products such as buttercream, cod liver oil, eggs and liver.7 However, carrots contain beta-carotene, which is converted into vitamin A in a range of 3-to-1 or 28-to-1, depending on factors such as thyroid function and zinc levels.

Researchers used the HyperChem molecular modeling software to evaluate electron transfer coefficients of the nutritional compounds found in carrots and the SARS-CoV-2 amino acids. What they found was the interaction between carrot RTN and the virus amino acids was the most stable, concluding that the results of their analysis “may indicate a recommendation to increase carrot consumption to mitigate the effects of COVID-19.”8

They point out that carrots are a rich source of vitamins C and A, as well as energy, fiber, calcium and beta-carotene. In the past researchers have demonstrated carrots have anti-inflammatory properties, anticancer activity and antioxidant activity by scavenging free radicals, which is essential for your immune system.

Their present work looked at the interaction between the amino acids in the COVID-19 coronavirus and multiple components found in carrots. Using chemical quantum analysis, they found RTN was the most stable substance and functioned as an antioxidant agent.

The data showed RTN, with other chemical compounds found in carrots, worked together to fight SARS-CoV-2. Interestingly, when they compared the power of RTN against commonly used allopathic medicines used for COVID-19, including remdesivir, ivermectin, aspirin and favipiravir, the natural substances in carrots appeared to be more powerful.9

Click here to learn more

Retinoids and Carotenoids Support Your Immune Health

While beta-carotene-rich vegetables, such as carrots, are helpful, you absorb more vitamin A from animal-based products. However, John Stolarczyk, from the World Carrot Museum, points out it’s easier to get people to eat carrots than it is to eat liver or cod liver oil:10

“Almost everyone, especially kids, likes carrots, whereas liver is an acquired taste. Carrots are very cheap, (easily stored) and attractively displayed in most stores. Liver looks dreadful.”

For nearly 100 years, scientists have understood that vitamin A is an essential component in your body’s ability to resist infectious disease.11 However, it is only recently that researchers have begun to understand the mechanism vitamin A uses to regulate cell- and humoral-mediated immunity.

This includes the discovery that retinoic acid plays an important role in cell regulation on immunity.12 Retinoic acid helps balance TH17 and T cell regulatory responses, as well as having a therapeutic role in autoimmune diseases. Researchers have found that retinoic deficiency plays an important role in the development of a broad range of autoimmune diseases.13

Your skin is an important part of your immune health, functioning as the front line of defense against bacteria and viruses and other pathogens. Scientists have known that vitamin A plays a unique and vital role in the formation and maturation of epithelial cells.14,15 But this doesn’t happen on just the outside of your body.

Vitamin A also plays an integral role in the production of the mucus layer that lines your respiratory and intestinal tracts and plays a primary role in promoting the secretion of mucin. This is a glycoprotein that plays a central role in limiting infectious disease and in adaptive immunity.16

Researchers have also identified the role it plays in the defense of your oral mucosa and improving the integrity of your intestinal mucosa. In addition to being important to protect your immune system, researchers, using animal models, have found a vitamin A deficiency (VitAD) can result in a:17

“… defect in both T cell-mediated and antibody-dependent immune responses. VitAD can also inhibit the normal apoptosis process of bone marrow cells, which leads to an increased number of myeloid cells in the bone marrow, spleen, and peripheral blood, indicating that VitA is involved in the regulation of homeostasis of bone marrow.”

Beta-Carotene May Help Promote Cholesterol Homeostasis

Cholesterol and beta-carotene have considerable overlapping properties, including transportation facilitated by lipoproteins and the body’s use as precursors for hormones.18 While cholesterol and beta-carotene are present in atherosclerotic plaque lesions, elevated concentrations of beta-carotene are associated with a lower incidence of atherosclerotic cardiovascular disease.

In a study published in the Journal of Nutrition, researchers believe they have shed new light on the interaction between beta-carotene and cholesterol metabolism that has been called a “potential game-changer.”19

After a preclinical study in which they compare the effects of a 10-day diet high in beta-carotene on the plasma cholesterol of beta-carotene oxygenase 1 (BCO1) deficient mice, the research team aimed at determining whether the same BCO1 locus could affect serum cholesterol concentrations in humans.

They evaluated a cohort of college applicants of Mexican ethnicity in the Multidisciplinary Investigation on Genetics, Obesity, And Social Environment. BCO1 is the enzyme that converts beta-carotene into vitamin A.20

Analysis of the animal study showed that the mice without BCO1 had elevated plasma level concentrations of beta-carotene as they could not convert it to vitamin A.21 The higher concentrations were associated with an increase in cholesterol as compared to the wild type mice control, which converted beta-carotene to vitamin A and had lower levels of cholesterol.

Cholesterol changes occurred almost exclusively in non-HDL cholesterol.22 One commentator points out many are deficient in beta-carotene and speculates:23

“… it might be predictable that the observed effect increases with age and that the cholesterol-lowering effect of β-carotene is enhanced on diets rich in carotenoids.

Notably, previous studies linked low vitamin A blood concentrations to coronary events such as myocardial infarction. β-Carotene is a major source of vitamin A, but as recently noted by a conference elucidating the current status of the β-carotene research field, dietary intake is below recommended concentrations of <3 mg/d in many populations.”

More Health Benefits of Carrots and Seed Extract

The flavonoids, vitamins, minerals and carotenoids in carrots all contribute to numerous other health benefits. Data have demonstrated the compounds found in carrots have properties that lower the risk of diabetes, cardiovascular disease, high blood pressure and cancer.24

They also are known for hepatoprotective, renal protective and anti-inflammatory properties. When you develop a habit of including carrots in your daily routine, you enjoy some important health benefits.

Cancer — Data show smokers who eat carrots more than once weekly have a lower risk of lung cancer,25 and a beta-carotene rich diet may help protect against prostate cancer26 and colon cancer,27 and to reduce the risk of gastric cancer.28

Carrots also contain falcarinol, a natural toxin they use against fungal disease, which may stimulate cancer-fighting mechanisms in your body and has demonstrated the ability to reduce the risk of tumors in rats.29

Vision — Carrots have long been associated with good eyesight. Vitamin A deficiency can speed the deterioration of your eyes’ photoreceptors leading to vision problems and night blindness.30 Carrots can also reduce your risk of age-related macular degeneration31 and cataracts.32

Both are eye diseases that get worse over time and may lead to blindness. Additionally, data have shown that women can reduce their risk of glaucoma by 64% when they eat more than two servings of carrots per week.33

Metabolic syndrome — Carrots contain beta-carotene and lycopene, both of which have been associated with lower incidence of metabolic syndrome in middle-aged and elderly men.34 Metabolic syndrome is associated with Type 2 diabetes, heart disease and stroke.

Brain health — Data show middle-aged men and women who eat a high number of root vegetables, such as carrots, show a reduction in cognitive decline.35 Carrot extract has also demonstrated a positive effect on the management of cognitive dysfunction.36

Antiaging effect — Carrots are replete with antioxidants that help reduce the damage caused by free radicals.37 Carrot seeds also have anti-inflammatory properties, which are significant even when compared against drugs like aspirin, ibuprofen and Naproxen.38

Vegetables that are rich in beta-carotene also help prevent premature skin aging. Data also show people with scleroderma, a disorder of connective tissue, had low levels of beta-carotene.39

Choose Your Carrots Carefully

Demand for baby carrots in the U.S. continues to rise as more people are choosing them for snacks over junk foods.40 Baby carrots are made from full-length carrots that are peeled and shaped. Bolthouse Farms and Grimmway Farms are the two leading producers that have focused on advertising campaigns and packaging to improve snack food sales.

However, part of the process of making baby carrots includes a chlorine bath. Grimmway Farms reports they use chlorine on all their baby carrots to prevent food poisoning.41 Chlorine can also be used to extend the shelf life of baby carrots.

Buffing and processing increase the rate at which the carrots begin to deteriorate and develop a white blush on the exterior as the vegetable begins drying out.42 Although the amount of chlorine in each individual baby carrot is minute, it has an additive value to your overall toxic burden.

Additionally, it isn’t the chlorine that causes most problems but, rather, the disinfection byproducts produced when the chlorine interacts with organic matter.43 In this case, the term organic means a carbon-based compound.

Disinfection byproducts are far more toxic than chlorine and are produced in all baby carrots, whether toxic pesticides were used in the growing process or not. Long-term exposure includes excessive free radical formation, which accelerates aging and vulnerability to genetic mutation and cancer.

Scientists are only beginning to understand the long and short-term impact of chlorine base chemicals. Your healthiest option is to grow your own or buy whole, unprocessed, ideally organic carrots and then wash, peel and cut them yourself.

Carrots can stay fresh in the coolest part of your refrigerator for about two weeks when they are wrapped in a paper towel or placed in a sealed bag. Avoid storing them near apples, pears or potatoes since the ethylene gas released from these vegetables and fruit can create a bitter flavor to your carrots.44

If your carrots still have green tops, remove those before storing in the refrigerator since the carrots will wilt faster. However, carrot tops are nutritious and can easily be added to fresh vegetable juice or your salad.


This recommendation on carrots is general and I don’t want you to believe that carrots should be used to treat COVID. It is important to understand that many are unable to effectively convert the carotenoids to the active form retinol that improves immune function.

So if you or anyone you know has an active infection it is FAR better to use retinol. A good form would be emulsified vitamin A. Don’t eat a pound of carrots and think that it will help you fight COVID as it likely won’t. You need the real vitamin A.

– Sources and References

Is Niacin a Missing Piece of the COVID Puzzle?

Reproduced from original article:

Analysis by Dr. Joseph Mercola      Fact Checked      January 20, 2021

what are the benefits of niacin


  • B vitamins may play an important role in COVID-19 prevention and treatment, according to two recent papers
  • Based on B vitamins’ effects on your immune system, immune-competence and red blood cells (which help fight infection), supplementation may be a useful adjunct to other prevention and treatment strategies
  • B vitamins can influence several COVID-19-specific disease processes, including viral replication and invasion, cytokine storm induction, adaptive immunity and hypercoagulability
  • Niacin appears particularly important. According to a recent paper, there appears to be a causative link between low niacin status and SARS-CoV-2 infection
  • SARS-CoV-2’s ability to invade your body is dependent on calcium signaling, which in turn is dependent on the presence of NAADP, which is formed from niacin. NAADP-dependent calcium signaling is responsible both for the inhibition of viral entry into cells and driving the virus out of already infected cells

While vitamins C and D have garnered much attention in the fight against COVID-19, B vitamins can also play an important role, according to two recent papers — niacin (B3) in particular.

The first, “Be Well: A Potential Role for Vitamin B in COVID-19,”1,2,3,4 was published in the February 2021 issue of the journal Maturitas. The paper is the result of a joint collaboration between researchers at the University of Oxford, United Arab Emirates University and the University of Melbourne, Australia.

While no studies using B vitamins have been performed on COVID-19 patients, the researchers stress that, based on B vitamins’ effects on your immune system, immune-competence and red blood cells (which help fight infection), supplementation may be a useful adjunct to other prevention and treatment strategies. As noted by the authors:5

“There is a need to highlight the importance of vitamin B because it plays a pivotal role in cell functioning, energy metabolism, and proper immune function.

Vitamin B assists in proper activation of both the innate and adaptive immune responses, reduces pro-inflammatory cytokine levels, improves respiratory function, maintains endothelial integrity, prevents hypercoagulability and can reduce the length of stay in hospital.

Therefore, vitamin B status should be assessed in COVID-19 patients and vitamin B could be used as a non-pharmaceutical adjunct to current treatments …

Vitamin B not only helps to build and maintain a healthy immune system, but it could potentially prevent or reduce COVID-19 symptoms or treat SARS-CoV-2 infection. Poor nutritional status predisposes people to infections more easily; therefore, a balanced diet is necessary for immuno-competence.”

B Vitamins Play Many Roles in COVID-19 Disease Process

Importantly, B vitamins can influence several COVID-19-specific disease processes, including:6

  • Viral replication and invasion
  • Cytokine storm induction
  • Adaptive immunity
  • Hypercoagulability

The paper goes on to detail how each of the B vitamins can help manage various COVID-19 symptoms:7

Vitamin B1 (thiamine) — Thiamine improves immune system function, protects cardiovascular health, inhibits inflammation and aids in healthy antibody responses. Vitamin B1 deficiency can result in an inadequate antibody response, thereby leading to more severe symptoms. There’s also evidence suggesting B1 may limit hypoxia.
Vitamin B2 (riboflavin) — Riboflavin in combination with ultraviolet light has been shown to decrease the infectious titer of SARS-CoV-2 below the detectable limit in human blood, plasma and platelet products.
Vitamin B3 (niacin/nicotinamide) — Niacin is a building block of NAD and NADP, which are vital when combating inflammation.
Vitamin B5 (pantothenic acid) — Vitamin B5 aids in wound healing and reduces inflammation.
Vitamin B6 (pyridoxal 5′-phosphate/pyridoxine) — Pyridoxal 5′-phosphate (PLP), the active form of vitamin B6, is a cofactor in several inflammatory pathways. Vitamin B6 deficiency is associated with dysregulated immune function. Inflammation increases the need for PLP, which can result in depletion.

According to the authors, in COVID-19 patients with high levels of inflammation, B6 deficiency may be a contributing factor. What’s more, B6 may also play an important role in preventing the hypercoagulation seen in some COVID-19 patients.

Vitamin B9 (folate/folic acid) — Folate, the natural form of B9 found in food, is required for the synthesis of DNA and protein in your adaptive immune response.

Folic acid, the synthetic form typically found in supplements, was recently found8 to inhibit furin, an enzyme associated with viral infections, thereby preventing the SARS-CoV-2 spike protein from binding to and gaining entry into your cells. The research9 suggests folic acid may therefore be helpful during the early stages of COVID-19.

Another recent paper10 found folic acid has a strong and stable binding affinity against SARS-CoV-2. This too suggests it may be a suitable therapeutic against COVID-19.

Vitamin B12 (cobalamin) — B12 is required for healthy synthesis of red blood cells and DNA. A deficiency in B12 increases inflammation and oxidative stress by raising homocysteine levels. Your body can eliminate homocysteine naturally, provided you’re getting enough B9 (folate), B6 and B12.11

Hyperhomocysteinemia — a condition characterized by abnormally high levels of homocysteine — causes endothelial dysfunction, activates platelet and coagulation cascades and decreases immune responses.

B12 deficiency is also associated with certain respiratory disorders. Advancing age can diminish your body’s ability to absorb B12 from food,12 so the need for supplementation may increase as you get older. According to “Be Well: A Potential Role for Vitamin D in COVID-19”:13

“A recent study showed that methylcobalamin supplements have the potential to reduce COVID-19-related organ damage and symptoms. A clinical study conducted in Singapore showed that COVID-19 patients who were given vitamin B12 supplements (500 μg), vitamin D (1000 IU) and magnesium had reduced COVID-19 symptom severity and supplements significantly reduced the need for oxygen and intensive care support.”

Click here to learn more

Niacin — A Missing Piece of the COVID-19 Puzzle?

The second paper,14 “Sufficient Niacin Supply: The Missing Puzzle Piece to COVID-19 and Beyond?” (which is a preprint and has yet to undergo peer review), focuses specifically on niacin (B3), raising the question of whether this vitamin might actually be a crucial player in the COVID-19 disease process. As noted in the abstract:

Definitive antiviral properties are evidenced for niacin, i.e., nicotinic acid (NA), as coronavirus disease 2019 (COVID-19) therapy for both disease recovery and prevention, to the level that reversal or progression of its pathology follows as an intrinsic function of NA supply.

This detailed investigation provides a thorough disentanglement of how the downstream inflammatory propagation of ensuing severe acute respiratory virus 2 (SARS-CoV-2) infection is entirely prohibited or reversed upstream out the body to expeditiously restore health with well-tolerated dynamic supplementation of sufficient NA (i.e., ~1-3 grams per day).”

As noted in this paper, a primary hallmark of COVID-19 pathology is the cytokine storm, which can lead to multiple organ failure and death. Marked elevations in proinflammatory cytokines are to blame for this chain of events, most notable of which are interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1).

If you can decrease and control these damaging cytokines, you stand a good chance of thwarting the cytokine storm and the downstream damage it causes. Nicotinamide adenine dinucleotide (NAD+) plays an important role in this, and niacin is a building block of NAD. As explained in “Be Well: A Potential Role for Vitamin D in COVID-19”:15

“NAD+ is released during the early stages of inflammation and has immunomodulatory properties, known to decrease the pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α. Recent evidence indicates that targeting IL-6 could help control the inflammatory storm in patients with COVID-19.”

Aside from markedly decreasing proinflammatory cytokines, niacin has also been shown to:16

  • Reduce the replication of a number of viruses, including vaccinia virus, human immunodeficiency virus, enteroviruses and hepatitis B virus
  • Reduce neutrophil infiltration
  • Have anti-inflammatory effect in patients with ventilator-induced lung injury

Niacin Modulates the Bradykinin Storm

COVID-19 also triggers bradykinin storms. Bradykinin is a chemical that helps regulate your blood pressure and is controlled by your renin-angiotensin system (RAS). The bradykinin hypothesis provides a model that helps explain some of the more unusual symptoms of COVID-19, including its bizarre effects on your cardiovascular system.

Researchers have discovered SARS-CoV-2 downregulates your body’s ability to degrade or break down bradykinin. The end result is a bradykinin storm, and this appears to be an important factor in many of COVID-19’s lethal effects, perhaps even more so than the cytokine storms associated with the disease. As bradykinin accumulates, the more serious COVID-19 symptoms appear.

Vitamin D has a significant impact on the RAS,17 and can therefore help prevent a bradykinin storm, but niacin also plays an important role. As noted in “Sufficient Niacin Supply: The Missing Puzzle Piece to COVID-19 and Beyond?”:18

“Immediate-release NA [niacin] administration has been reported as highly effective in preventing the lung tissue damage involved in this … pathology. As a matter of fact, authors of a March, 2020, paper19 in Nature for this very reason conclude with suggestion of niacin supplementation to COVID-19 patients as a ‘wise approach.'”

The paper also expounds on the role of NAD+, and why niacin is a useful strategy for boosting NAD+:20

“The major effects of COVID-19 are evidenced to involve tryptophan metabolism and the kynurenine pathway towards depletions of these precursors of NAD+ …

Exclusively sufficient dosage of immediate-release NA — through its processing in the mammalian body to form NAADP [nicotinic acid adenine dinucleotide phosphate, a calcium mobilizer] — leads to an inverse potential energy pump back upstream, from the core up and ultimately out the body, of the downstream ensuing propagation of such inflammatory disease that spreads into the cells.

This is made possible by the capability of NAADP to be readily formed by sufficient NA supply to induce Ca2+ [calcium] channeling back upstream out the body of built-up or ensuing inflammation, representing kinetic energy … that by electron gradient, moves downstream into the body.

Attempting to restore NAD+ with other NAD+-precursors aside from NA (e.g., nicotinamide, nicotinamide riboside, nicotinamide mononucleotide) only actually temporarily and in a sense, artificially, raises NAD+ levels, until they imminently deplete back down with further ensuing inflammation.

NA is in fact the only compound to readily produce NAADP if needed in acidic environments (as is characteristic to ensuing inflammatory disease pathology), which in turn provides a potential energy/H+ pump-out action of its inverse, downstream kinetic (heat) energy inflammation to ultimately restore NAD+ to normal, pre-inflammatory levels, as well as other inflammatorily-depleted cofactors and biochemical pathways towards a more thermodynamically homeostatic health status …

The ‘niacin red flush’ in fact is this thermodynamic exfoliation of ensuing disease, toxins, and (restoration of) free radical-damaged compounds being H+ (potential energy) pumped out the body.

It represents the anti-inflammatory or thermodynamic (i.e., energy transfer-like) therapy in action that only and exclusively sufficient oral intake of immediate-release NA is capable of (readily) accomplishing with potency.”

Recommended Use

The paper21 goes deep into the biochemical aspects of how niacin works in your body, so if you’re interested in that, you may want to read through it. In summary, as it pertains to COVID-19, the important thing to understand is that there appears to be a causative link between low niacin status and SARS-CoV-2 infection.

According to the authors, SARS-CoV-2’s ability to invade your body is dependent on whether calcium signaling can properly proceed, which in turn is dependent on the presence of NAADP. And, as explained in the quoted section above, niacin forms NAADP in your body. NAADP-dependent calcium signaling is responsible both for the inhibition of viral entry into cells and driving the virus out of already infected cells.

And, again, the authors stress that “nothing outside of sufficiently, dynamically supplied niacin is capable of readily leading to the NAADP supply needed in these acidic environments for therapeutic action that counteracts inflammatory disease progression.”

They also point out that the flushing you get from niacin is part of how the niacin drives inflammatory free radicals out of the cells. As you continue to take the supplement at a consistent, sufficiently high dose, that flushing will gradually lessen, which is a sign that your body is reaching a healthy homeostasis.

“This represents perhaps the ideal state that should be worked up to and maintained thereafter — in terms of niacin dosing — to respectively reverse out and prevent inflammation,” the authors state.22

While the flushing can be uncomfortable, the authors stress that it is “indeed safe,” and actually “should be sought when needed for its anti-inflammatory properties.”

Suggested Dosing

As a “health restorative therapy” for those diagnosed with SARS-CoV-2, they recommend starting with a dose of 500 milligrams of immediate-release niacin, two to three times a day, ideally within the first 48 hours of symptom onset. As your flush response lessens, increase your dose to 1,000 mg, two to three times a day.23

“For the subgroup of patients still suffering with high cytokines profiles from deep, remnant damage of previously experienced SARS-CoV-2 infection — termed the ‘long-haulers’ — alleviation from ailment(s) towards complete health restoration to pre-infection state from initiating and maintaining the aforementioned dosage regimen has consistently been reported to assume within two days and to incrementally follow further over the course of weeks.”24

Although the authors suggest you can use niacin prophylactically, using that same dose, I disagree. According to the authors:25

“By readily providing sufficient NAADP, this same NA dosage regimen is capable of serving as prophylaxis, which can be interpreted as the physical/biochemical inability of sufficient progression of SARS-CoV-2 in order to enter into the body and/or thereafter induce replication, infection onset, or disease progression in a previously uninfected host.”

There may be some value to the high doses in acute COVID-19 infections but I am skeptical. I am a huge fan of NAD+ augmentation and have been using it for years. My research suggests you really only need about 25 mg per day of niacin, which will not cause flushing in nearly anyone. I believe most would benefit from taking 25 mg of niacin daily, preferably in a well-balanced B complex, which would have thiamine (B1) that has also been shown to be useful in COVID-19.

Other alternatives to high-dose niacin would be nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), which is my personal favorite. I believe that compounding these into rectal suppositories would avoid most of the methylation of the supplement and supply you with higher NAD+ tissue levels.

Another downside of high-dose niacin is that it breaks down to nicotinamide and in high doses, nicotinamide will inhibit Sirt1, which is an important longevity protein.

Personally, I believe a superior strategy to high-dose niacin in acute COVID-19 would be to use nebulized hydrogen peroxide at 0.1%. I have never seen or heard of this intervention failing in the treatment of COVID-19.

hydrogen peroxide dilution chart

How to Improve Your Vitamin B Status

As a general rule, I recommend getting most if not all of your nutrition from real food. This will work well for most B vitamins, but not if you’re using niacin therapeutically, as described above. For that, you will need to take a supplement.

That said, the list below will show you which foods contain which B vitamins, as well as provide general guidance on dosage if you’re taking a supplement. If you’re trying to improve your vitamin B status, also consider limiting sugar and eating more fermented foods.

The reason for this is because the entire B group vitamin series is produced within your gut, assuming you have healthy gut flora. Eating real food, including plenty of leafy greens and fermented foods, will provide your microbiome with important fiber and beneficial bacteria to help optimize your internal vitamin B production.

Nutrient Dietary Sources Supplement Recommendations
Vitamin B1 Pork, fish, nuts and seeds, beans, green peas, brown rice, squash, asparagus and seafood.26 The recommended daily allowance for B1 is 1.2 mg/day for men and 1.1 mg/day for women.27
Vitamin B2 Eggs, organ meats, lean meats, green vegetables such as asparagus, broccoli and spinach.28 The RDA is 1.1 mg for adult women and 1.3 mg for men.

Your body cannot absorb more than about 27 mg at a time, and some multivitamins or B-complex supplements may contain unnecessarily high amounts.29

Vitamin B3 Liver, chicken, veal, peanuts, chili powder, bacon and sun-dried tomatoes have some of the highest amounts of niacin per gram.30

Other niacin-rich foods include baker’s yeast, paprika, espresso coffee, anchovies, spirulina, duck, shiitake mushrooms and soy sauce.31

The dietary reference intake established by the Food and Nutrition Board ranges from 14 to 18 mg per day for adults.

Higher amounts are recommended depending on your condition. For a list of recommended dosages, see the Mayo Clinic’s website.32

The dosage recommended as an anti-inflammatory, health-restorative therapy in “Sufficient Niacin Supply: The Missing Puzzle Piece to COVID-19 and Beyond?”33 is 500 mg two to three times a day, working your way up to 1,000 mg, two to three times a day as the flushing lessens.

Vitamin B5 Beef, poultry, seafood, organ meats, eggs, milk, mushrooms, avocados, potatoes, broccoli, peanuts, sunflower seeds, chickpeas and brown rice.34 The RDA is 5 mg for adults over the age of 19.

Pantothenic acid in dietary supplements is often in the form of calcium pantothenate or pantethine.35

Vitamin B6 Turkey, beef, chicken, wild-caught salmon, sweet potatoes, potatoes, sunflower seeds, pistachios, avocado, spinach and banana.36,37 Nutritional yeast is an excellent source of B vitamins, especially B6.38

One serving (2 tablespoons) contains nearly 10 mg of vitamin B6.

Not to be confused with Brewer’s yeast or other active yeasts, nutritional yeast is made from an organism grown on molasses, which is then harvested and dried to deactivate the yeast.

It has a pleasant cheesy flavor and can be added to a number of different dishes.

Vitamin B9 Fresh, raw, organic leafy green vegetables, especially broccoli, asparagus, spinach and turnip greens, and a wide variety of beans, especially lentils, but also pinto beans, garbanzo beans, kidney beans, navy and black beans.39 Folic acid is a synthetic type of B vitamin used in supplements; folate is the natural form found in foods.

(Think: Folate comes from foliage, edible leafy plants.)

For folic acid to be of use, it must first be activated into its biologically active form (L-5-MTHF).

Nearly half the population has difficulty converting folic acid into the bioactive form due to a genetic reduction in enzyme activity.

For this reason, if you take a B-vitamin supplement, make sure it contains natural folate rather than synthetic folic acid.

Nutritional yeast is an excellent source.40

Research41 also shows your dietary fiber intake has an impact on your folate status.

For each gram of fiber consumed, folate levels increased by nearly 2%.

The researchers hypothesize that this boost in folate level is due to the fact that fiber nourishes bacteria that synthesize folate in your large intestine.

Vitamin B12 Vitamin B12 is found almost exclusively in animal tissues, including foods like beef and beef liver, lamb, snapper, venison, salmon, shrimp, scallops, poultry, eggs and dairy products.

The few plant foods that are sources of B12 are actually B12 analogs that block the uptake of true B12.

Nutritional yeast is high in B12, and is highly recommended for vegetarians and vegans.

One serving (2 tablespoons) provides nearly 8 mcg of natural vitamin B12.42

Sublingual (under-the-tongue) fine mist spray or vitamin B12 injections are also effective, as they allow the large B12 molecule to be absorbed directly into your bloodstream.