This site presents a natural, science-based approach that supercharges the innate immune system to prevent cold sores. When the virus (HSV-1) that causes cold sores reactivates, a fast innate immune response is crucial. If the innate immune system is not supercharged, the response is slowed, giving the cold sore virus a chance to mass produce at the epithelial layer of cells and create a sore.
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Table of Contents
1. Introduction
2. Background
3. HSV-1 and Immunity
4. Supercharging the Innate Immune Response
5. The Approach (Update on new Vitamin D levels added March, 2015)
6. For More Information
7. Research Updates
8. References
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1. Introduction
Chances are you found your way to this website because you or someone you care about suffers from cold sores. Chances are that you’ve tried products that treat cold sores. There are many products claiming to prevent, cure, and shorten the duration of cold sores. Products that claim to shorten the duration of cold sores when applied to the surface of the skin are usually legitimate. On the other hand, products that claim to cure cold sores and stop them from coming back ever again are probably bogus. Trust me, if there was a cure for cold sores it would have gone to clinical trials and made it out onto the market.
I wish to point out that I am not selling anything nor am I promoting a particular product or company. The purpose of this website is to provide scientific fact-based evidence to help people avoid painful and life-disrupting cold sores. This information is free and made available with no strings attached. So put away your credit card and don’t worry about giving me your name or email address - I won’t ask for them. Before we get into how to prevent cold sores by supercharging the immune system, here is a little information about me and how I became interested in this topic.
I wish to point out that I am not selling anything nor am I promoting a particular product or company. The purpose of this website is to provide scientific fact-based evidence to help people avoid painful and life-disrupting cold sores. This information is free and made available with no strings attached. So put away your credit card and don’t worry about giving me your name or email address - I won’t ask for them. Before we get into how to prevent cold sores by supercharging the immune system, here is a little information about me and how I became interested in this topic.
2. Background
In my work as a senior researcher with a large healthcare organization, I met a cardiologist who was using a surprising therapy to help patients with cardiovascular disease. When I met the same physician a few months later I asked him how the research on the new therapy was coming along. He said that things looked promising. Around the same time I was working with an orthopedics researcher who had just been awarded a grant to investigate the effects of the same therapy on patients recovering from ACL (knee) surgery. The new therapeutic approach was being tested for its ability to reduce post surgery inflammation. Both researchers were using the same therapy to treat two very different conditions. What is this therapy and what does it have to do with cold sores? The therapy is Vitamin D3 (cholecaliciferol). Read on to find out how it can be used to prevent cold sores.
Based on my encounters with the cardiologist and orthopedics reseacher, I decided to investigate Vitamin D3 further. I turned to peer-reviewed medical journals for information. The information on heart and joint benefits were there. What really surprised me, however, was the large amount of recent medical research literature on Vitamin D's immunomodulatory effects, much of it in the past few years. Just this past year a few articles have uncovered the mechanism by which Vitamin D pumps up the innate immune system’s ability to fight off pathogens, including HSV-1. But because most people are Vitamin D deficient, especially during the cold season, they are not benefitting from the positive immunomodulatory effects this vitamin has to offer.
Let’s take a look at how Vitamin D impacts cold sores.
Based on my encounters with the cardiologist and orthopedics reseacher, I decided to investigate Vitamin D3 further. I turned to peer-reviewed medical journals for information. The information on heart and joint benefits were there. What really surprised me, however, was the large amount of recent medical research literature on Vitamin D's immunomodulatory effects, much of it in the past few years. Just this past year a few articles have uncovered the mechanism by which Vitamin D pumps up the innate immune system’s ability to fight off pathogens, including HSV-1. But because most people are Vitamin D deficient, especially during the cold season, they are not benefitting from the positive immunomodulatory effects this vitamin has to offer.
Let’s take a look at how Vitamin D impacts cold sores.
3. HSV-1 and Immunity
The cold sore virus initially gains entrance into the body though contact with the mouth. The most common mode of transmission is kissing, although transmission with HSV-1 can also occur through sharing of utensils, drinking containers, and lip balms, etc. That HSV-1 can be transmitted through an innocent kiss such as from parent to child or a kind gesture like sharing a drink, seems so pernicious. Indeed, the virus has thrived for thousands of years because of humanity’s desire for closeness and affection. It has also thrived because of a lack of knowledge. Additional information on HSV-1 transmission is available on the web. I won’t go into it anymore here. Let's look at why it sticks around and why it causes cold sores.
Once the virus enters the oral cavity through contact, it looks for a place to reproduce. The ideal location for reproduction is the layer of epithelial cells immediately below the layer of dead skin cells (HSV-1 cannot replicate in dead cells). It usually gains access to the epithelial layer through a cut or fissure in the outer skin. Once it reaches the epithelial layer, it begins to multiply. The multiplying virus destroys skin cells causing sores in the mouth or on the lips, however, some people are asymptomatic in that they show no symptoms when first infected. The virus is fairly weak and does not stand a chance against the immune response, this means that, in most cases, after infecting the epithelial layer, the immune system kicks its butt and eventually rids the oral cavity of the virus. If that was all that happened HSV-1 would not be as common as it is today. However, the virus has a trick up its sleeve that keeps it in the game of infecting humans.
During initial infection, some HSV-1 may travel down the axons of sensory neurons and hide out in the sensory neuronal nuclei, near the base of the jaw. There the virus lays dormant (latent), evading detection by the immune system. Once and a while the virus ‘wakes up” and makes a relatively small number of copies. Reactivation of the virus happens when the lips are irritated from too much sunlight, a menstrual cycle, a compromised or distracted immune system (e.g., during a cold), stress, lack of sleep, or nothing at all. The relatively small number of newly replicated HSV-1 travel back down to the lips via the axon of the sensory nerve. When they reach the lip epithelial layer, they begin multiplying rapidly, destroying skin cells. The result? An embarrassing and contagious cold sore.
In my opinion, one of the best ways to prevent a cold sore is by supercharging the innate immune system so that it works faster and with more fire power when HSV-1 becomes reactivated. The innate immune system is our front-line defense against pathogens. It starts the fight against pathogens long before the adaptive immune system ever kicks into action. A fast acting innate immune system is exactly what is needed when it comes to HSV-1. There is a narrow window of opportunity to destroy the reactivated HSV-1 virus while it is traveling to the layer of epithelial cells. And there is a narrow window of opportunity to destroy the virus once it has reached the epithelial layer where it replicates. A supercharged innate immune system can stop it in its tracks or at least minimize the size and duration of a cold sore.
Once the virus enters the oral cavity through contact, it looks for a place to reproduce. The ideal location for reproduction is the layer of epithelial cells immediately below the layer of dead skin cells (HSV-1 cannot replicate in dead cells). It usually gains access to the epithelial layer through a cut or fissure in the outer skin. Once it reaches the epithelial layer, it begins to multiply. The multiplying virus destroys skin cells causing sores in the mouth or on the lips, however, some people are asymptomatic in that they show no symptoms when first infected. The virus is fairly weak and does not stand a chance against the immune response, this means that, in most cases, after infecting the epithelial layer, the immune system kicks its butt and eventually rids the oral cavity of the virus. If that was all that happened HSV-1 would not be as common as it is today. However, the virus has a trick up its sleeve that keeps it in the game of infecting humans.
During initial infection, some HSV-1 may travel down the axons of sensory neurons and hide out in the sensory neuronal nuclei, near the base of the jaw. There the virus lays dormant (latent), evading detection by the immune system. Once and a while the virus ‘wakes up” and makes a relatively small number of copies. Reactivation of the virus happens when the lips are irritated from too much sunlight, a menstrual cycle, a compromised or distracted immune system (e.g., during a cold), stress, lack of sleep, or nothing at all. The relatively small number of newly replicated HSV-1 travel back down to the lips via the axon of the sensory nerve. When they reach the lip epithelial layer, they begin multiplying rapidly, destroying skin cells. The result? An embarrassing and contagious cold sore.
In my opinion, one of the best ways to prevent a cold sore is by supercharging the innate immune system so that it works faster and with more fire power when HSV-1 becomes reactivated. The innate immune system is our front-line defense against pathogens. It starts the fight against pathogens long before the adaptive immune system ever kicks into action. A fast acting innate immune system is exactly what is needed when it comes to HSV-1. There is a narrow window of opportunity to destroy the reactivated HSV-1 virus while it is traveling to the layer of epithelial cells. And there is a narrow window of opportunity to destroy the virus once it has reached the epithelial layer where it replicates. A supercharged innate immune system can stop it in its tracks or at least minimize the size and duration of a cold sore.
4. Supercharging the Innate Immune Response
A lot of dietary and other factors play an important role in regulating the immune response. In looking for a way to effectively supercharge the immune system, I looked for an approach that safely helps the innate immune system to destroy HSV. This approach involves taking immunomodulatory supplements that have been scientifically proven to upregulate the immune system's anti-microbial peptides and virus recognition. Anti-microbial peptides, or AMPs as they are sometimes called, are efficient destroyers of herpetic viruses like HSV-1. When the activity of AMPs is maximized, the immune system is supercharged. To date, the best and safest supplement for boosting AMP activity is Vitamin D3. Vitamin C is also important as it has been shown to enhance immune cells' protection from AMPs. We will take a look at each of these immunity supercharging supplements and how each contributes to the body’s fight against HSV-1, the virus that causes cold sores.
Vitamin D3
Vitamin D3 is a safe and effective supplement for supercharging the innate immune system. Here is how it provides our innate immune cells, the body's first line of defense against pathogens, with the ammunition needed to quickly destroy reactivated HSV-1.
How the Body Processess Vitamin D3 into a Usable Form
After ingesting a Vitamin D3 (cholecaliciferol) supplement, the vitamin is metabolized by the liver into hydroxyvitamin D3 or 25(OH)D. Because 25(OH)D is a stable metabolite, it is used as an indicator of Vitamin D concentrations in the body – it is what the blood test for Vitamin D measures. 25(OH)D is a prohormone that is converted by the kidneys into an active steroidal hormone known as dihydroxyvitamin D3 or 1,25(OH)2D (Calcitriol). The conversion of 25(OH)D into 1,25(OH)2D also takes place in innate immune system and epithelial cells which is good as that is where it is needed the most when it comes to stopping HSV-1. Conversion of 25(OH)D into 1,25(OH)2D in immunity and epithelial cells plays an essential role in halting a reactivated HSV-1 virus.
Here are a few ways in which 1,25(OH)2D triggers the immune system to stop re-activated HSV-1.
1. Virus Recognition
Innate immunity refers to the body’s first line of active defense against pathogens. In this first line of defense there are immune cells called macrophages which are sentinels that seek out and destroy microbes. The macrophages have what are called toll-like receptor (TLR) cells that are activated by microbes. When HSV-1 virus suddenly shows up due to reactivation, it triggers the TLRs in the macrophages which sends a signal to the rest of your immune system that the virus is present and needs to be eliminated. Research shows that 1,25(OH)2D levels play a crucial role in the development of microbe recognition receptors (toll-like receptors or TLR mentioned above) which are responsible for recognizing the virus. When adequate levels of 1,25(OH)2D are present, there are more TLRs and the innate immune system is more adept at recognizing the presence of HSV-1. If 1,25(OH)2D levels are too low, recognition by TLRs is slowed thus delaying the immune response (below) and allowing the virus to "slip in under the radar" so to speak and mass produce at the lip epithelial layer.
2. Virus Killing Peptides
When the toll-like receptor cells have been activated, they trigger the body's macrophages to produce the enzyme know as 1-alpha-hydroxylase (or CYP 27B). This enzyme converts 25(OH)D into active 1,25(OH)2D which in turn activates the macrophage Vitamin D receptor (VDR) which, together with the retinoid X receptor, creates small DNA sequences known as Vitamin D response elements (VDREs). These VDREs then produce a series of molecular interactions that prompt genes to produce antimicrobial peptides (AMPs) that destroy HSV-1. The AMPs are the body's ammunition for destroying HSV-1. Fortunately, macrophages are not the only cells that use 1,25(OH)2D to create AMPs. Skin epithelial cells, the very location where HSV-1 replication occurs, use 1,25(OH)2D in much the same way. When a microbe like HSV-1 is detected, toll-like receptors trigger the epithelial cells to produce enzymes that convert 25(OH)D into 1,25(OH)2D which then activates the epithelial VDR, which in turn activates genes that produce AMPs. The production of AMPs by the macrophages and epithelial skin cells takes place in a matter of a few minutes. If there is sufficient 1,25(OH)2D in the body, adequate amounts of AMPs can be produced to minimize HSV-1 replication. If 1,25(OH)2D levels are low, the production of adequate AMPs is delayed thus allowing HSV-1 time to mass produce at the lip epithelial layer, usually in a couple of hours.
A potent antimicrobial peptide (AMP) produced by microphages and epithelial skin cells is Cathelicidin (LL-37). Cathelicidin is a destroyer of bacteria and enveloped viruses like HSV-1. It is believed to destroy HSV-1 by breaking down its protective envelope and rendering it defenseless. In one study, incubation of Cathelicidin with HSV-1 showed a significant reduction in HSV-1 concentrations. In other words greater amounts of vitamin D lead to more Cathelicidins, and more Cathelicidins lead to more destruction of HSV-1.
It is important to note that macrophages do not stockpile 1,25(OH)2D. They produce an enzyme (CYP 24) that quickly breaks down excess 1,25(OH)2D to prevent toxic buildup in the cell. This means that macrophages rely on current blood serum levels of 25(OH)D for activating a strong immune response against HSV-1. Should 25(OH)D levels drop for a few days and HSV-1 come out of its latent phase during that time period, the immune response will be delayed thus giving a cold sore the chance to grow. Fortunately 25(OH)D has a fairly long half-life, about 12-19 days. This means that it takes about 12-19 days for the body to break down at least half of the serum 15(OH)D. In practical terms this means that someone would have to stop taking D3 for at least 2 weeks before serum 25(OH)D blood levels started falling.
3. Other Boosting Effects on Macrophages
The presence of 1,25(OH)2D has been shown to increase the number of microbe-fighting macrophages by inducing monocytes (a type of white blood cell) to differentiate and form into macrophages. More macrophages means more sentinels to destroy HSV-1. Also, 1,25(OH)2D increases phagocytosis (microbe-eating activity) in macrophages though the production of lysosomal enzymes.
4. Possible Benefits for the Adaptive Immune System
The effects of 1,25(OH)D on adaptive immunity are less well understood. It is believed that 1,25(OH)2D increases the activity of dendritic cells which communicate to the adaptive immune system via the lymph nodes that a microbial infection at the epithelial layer is under way. 1,25(OH)2D is also known to play a role in activating antigen specific killer T-cell division should the innate immune system (e.g., macrophages, epithelial cells) fail to control the infection. Because cold sores are relatively short lived, lasting on average about about 5-10 days, it seems to me that the adaptive system is not particularly involved in fighting off cold sores. The actions of the adaptive system are more slow and specific. I believe that the innate immune system is largely responsible for ridding the body of re-activated HSV-1 cold sore.
How the Body Processess Vitamin D3 into a Usable Form
After ingesting a Vitamin D3 (cholecaliciferol) supplement, the vitamin is metabolized by the liver into hydroxyvitamin D3 or 25(OH)D. Because 25(OH)D is a stable metabolite, it is used as an indicator of Vitamin D concentrations in the body – it is what the blood test for Vitamin D measures. 25(OH)D is a prohormone that is converted by the kidneys into an active steroidal hormone known as dihydroxyvitamin D3 or 1,25(OH)2D (Calcitriol). The conversion of 25(OH)D into 1,25(OH)2D also takes place in innate immune system and epithelial cells which is good as that is where it is needed the most when it comes to stopping HSV-1. Conversion of 25(OH)D into 1,25(OH)2D in immunity and epithelial cells plays an essential role in halting a reactivated HSV-1 virus.
Here are a few ways in which 1,25(OH)2D triggers the immune system to stop re-activated HSV-1.
1. Virus Recognition
Innate immunity refers to the body’s first line of active defense against pathogens. In this first line of defense there are immune cells called macrophages which are sentinels that seek out and destroy microbes. The macrophages have what are called toll-like receptor (TLR) cells that are activated by microbes. When HSV-1 virus suddenly shows up due to reactivation, it triggers the TLRs in the macrophages which sends a signal to the rest of your immune system that the virus is present and needs to be eliminated. Research shows that 1,25(OH)2D levels play a crucial role in the development of microbe recognition receptors (toll-like receptors or TLR mentioned above) which are responsible for recognizing the virus. When adequate levels of 1,25(OH)2D are present, there are more TLRs and the innate immune system is more adept at recognizing the presence of HSV-1. If 1,25(OH)2D levels are too low, recognition by TLRs is slowed thus delaying the immune response (below) and allowing the virus to "slip in under the radar" so to speak and mass produce at the lip epithelial layer.
2. Virus Killing Peptides
When the toll-like receptor cells have been activated, they trigger the body's macrophages to produce the enzyme know as 1-alpha-hydroxylase (or CYP 27B). This enzyme converts 25(OH)D into active 1,25(OH)2D which in turn activates the macrophage Vitamin D receptor (VDR) which, together with the retinoid X receptor, creates small DNA sequences known as Vitamin D response elements (VDREs). These VDREs then produce a series of molecular interactions that prompt genes to produce antimicrobial peptides (AMPs) that destroy HSV-1. The AMPs are the body's ammunition for destroying HSV-1. Fortunately, macrophages are not the only cells that use 1,25(OH)2D to create AMPs. Skin epithelial cells, the very location where HSV-1 replication occurs, use 1,25(OH)2D in much the same way. When a microbe like HSV-1 is detected, toll-like receptors trigger the epithelial cells to produce enzymes that convert 25(OH)D into 1,25(OH)2D which then activates the epithelial VDR, which in turn activates genes that produce AMPs. The production of AMPs by the macrophages and epithelial skin cells takes place in a matter of a few minutes. If there is sufficient 1,25(OH)2D in the body, adequate amounts of AMPs can be produced to minimize HSV-1 replication. If 1,25(OH)2D levels are low, the production of adequate AMPs is delayed thus allowing HSV-1 time to mass produce at the lip epithelial layer, usually in a couple of hours.
A potent antimicrobial peptide (AMP) produced by microphages and epithelial skin cells is Cathelicidin (LL-37). Cathelicidin is a destroyer of bacteria and enveloped viruses like HSV-1. It is believed to destroy HSV-1 by breaking down its protective envelope and rendering it defenseless. In one study, incubation of Cathelicidin with HSV-1 showed a significant reduction in HSV-1 concentrations. In other words greater amounts of vitamin D lead to more Cathelicidins, and more Cathelicidins lead to more destruction of HSV-1.
It is important to note that macrophages do not stockpile 1,25(OH)2D. They produce an enzyme (CYP 24) that quickly breaks down excess 1,25(OH)2D to prevent toxic buildup in the cell. This means that macrophages rely on current blood serum levels of 25(OH)D for activating a strong immune response against HSV-1. Should 25(OH)D levels drop for a few days and HSV-1 come out of its latent phase during that time period, the immune response will be delayed thus giving a cold sore the chance to grow. Fortunately 25(OH)D has a fairly long half-life, about 12-19 days. This means that it takes about 12-19 days for the body to break down at least half of the serum 15(OH)D. In practical terms this means that someone would have to stop taking D3 for at least 2 weeks before serum 25(OH)D blood levels started falling.
3. Other Boosting Effects on Macrophages
The presence of 1,25(OH)2D has been shown to increase the number of microbe-fighting macrophages by inducing monocytes (a type of white blood cell) to differentiate and form into macrophages. More macrophages means more sentinels to destroy HSV-1. Also, 1,25(OH)2D increases phagocytosis (microbe-eating activity) in macrophages though the production of lysosomal enzymes.
4. Possible Benefits for the Adaptive Immune System
The effects of 1,25(OH)D on adaptive immunity are less well understood. It is believed that 1,25(OH)2D increases the activity of dendritic cells which communicate to the adaptive immune system via the lymph nodes that a microbial infection at the epithelial layer is under way. 1,25(OH)2D is also known to play a role in activating antigen specific killer T-cell division should the innate immune system (e.g., macrophages, epithelial cells) fail to control the infection. Because cold sores are relatively short lived, lasting on average about about 5-10 days, it seems to me that the adaptive system is not particularly involved in fighting off cold sores. The actions of the adaptive system are more slow and specific. I believe that the innate immune system is largely responsible for ridding the body of re-activated HSV-1 cold sore.
Vitamin C
We’ve known about Vitamin C’s immune boosting effects for some time. One way Vitamin C strengthens the immune system is by protecting the body’s immune cells (e.g., macrophages, leukocytes, monocytes) from reactive substances (i.e., antimicrobial peptides) that are created by the immune cells to kill pathogens like HSV-1. Immune system cells stockpile Vitamin C so that it is readily available to protect them from their own antimicrobial peptides. In a manner of speaking, vitamin C prevents friendly fire causalities in the immune system. Vitamin C has also been shown to increase production of immune system cells like neutrophils which attack bacteria and viruses. In some studies C has been shown to have direct anti-viral effects; however, the mechanism by which this happens is unclear.
5. The Approach
Disclaimer
I am not rendering professional or medical advice. This information is not intended to prevent, cure, or treat disease. I offer no guarantees that this program will reduce incidences of cold sores. This information is based on current scientific evidence and currently acceptable levels of supplement consumption which may change overtime. Users assume all risks associated with this approach. These supplement levels are for healthy adults only. When in doubt, consult your physician about whether these levels are appropriate for you.
Vitamin D3 (1000 IUs per day. Up to 2000 IUs per day may be appropriate for some healthy adults)
Vitamin D3 is the most important supplement to take when supercharging the innate immune system. Many multivitamins contain only about 400 IU which may be too low for supercharging the immune system thus leaving the immune system short on firepower. 1000 IUs of Vitamin D3 is probably enough to supercharge the innate immune system for most individuals.
Getting too much Vitamin D?
The blood test for Vitamin D checks 25(OH)D levels. Research suggests that 25(OH)D levels that are too low are not good and levels that are too high are not good. In supercharging the immune system, being toward the higher end of normal levels is probably ideal. Check with your physician after taking Vitamin D supplements for a few months to ensure that your levels are not too high. People taking 1000 IU per day are most likely in normal range. People taking between 2000 IUs per day may have higher 25(OH)D levels and thus may want to have their 25(OH)D levels checked to make sure that they are appropriate.
Vitamin D3 warning for people with certain conditions: People with rosacea should consult a doctor before taking Vitamin D supplements. Also, hypercalcemia, a condition where there is too much calcium in the blood, can result when people with primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma take Vitamin D. People with these conditions may develop hypercalcemia and should consult a doctor before increasing vitamin D intake.
Vitamin C (200 mg per day)
For most people, up to 200 mg/day is tolerable. Many multivitamins contain only about 60-100 mg per tablet.
People experiencing diarrhea or gastrointestinal discomfort from taking these supplements should lower their daily intake. People already taking a daily multivitamin should check their current Vitamin D and C intake levels and supplement accordingly to achieve optimum levels. For example, someone taking a daily multivitamin with 500 IU of Vitamin D3 would only need to take an additional 500 IUs of Vitamin D3 to achieve 1000 IUs of Vitamin D3 per day.
Note that it may take up to 3 months for levels of Vitamin D to reach optimal levels in the body. Look for a reduction in colds, the flu, and cold sores after supplementing daily for a few months.
Vitamin E (no longer recommended)
Notwithstanding its benefits to immunity, I cannot recommend high levels of Vitamin E as part of supercharging the immune system because of a recent report in the Journal of the American Medical Association (JAMA), published Fall 2011. In a 7-year study looking at rates of prostate cancer in men taking either 400 IU/day of vitamin E or a placebo, researchers found the opposite of what they expected. 400 IU/day of Vitamin E actually increased the risk of prostate cancer by 17%. Here is a link to a website explaining the Vitamin E study which appeared in JAMA (October 2011) (prostate cancer study). The number one vitamin in supercharging the immune system still appears to be Vitamin D3, and all research points to this vitamin being safe in high doses, so that is good news.
I am not rendering professional or medical advice. This information is not intended to prevent, cure, or treat disease. I offer no guarantees that this program will reduce incidences of cold sores. This information is based on current scientific evidence and currently acceptable levels of supplement consumption which may change overtime. Users assume all risks associated with this approach. These supplement levels are for healthy adults only. When in doubt, consult your physician about whether these levels are appropriate for you.
Vitamin D3 (1000 IUs per day. Up to 2000 IUs per day may be appropriate for some healthy adults)
Vitamin D3 is the most important supplement to take when supercharging the innate immune system. Many multivitamins contain only about 400 IU which may be too low for supercharging the immune system thus leaving the immune system short on firepower. 1000 IUs of Vitamin D3 is probably enough to supercharge the innate immune system for most individuals.
Getting too much Vitamin D?
The blood test for Vitamin D checks 25(OH)D levels. Research suggests that 25(OH)D levels that are too low are not good and levels that are too high are not good. In supercharging the immune system, being toward the higher end of normal levels is probably ideal. Check with your physician after taking Vitamin D supplements for a few months to ensure that your levels are not too high. People taking 1000 IU per day are most likely in normal range. People taking between 2000 IUs per day may have higher 25(OH)D levels and thus may want to have their 25(OH)D levels checked to make sure that they are appropriate.
Vitamin D3 warning for people with certain conditions: People with rosacea should consult a doctor before taking Vitamin D supplements. Also, hypercalcemia, a condition where there is too much calcium in the blood, can result when people with primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma take Vitamin D. People with these conditions may develop hypercalcemia and should consult a doctor before increasing vitamin D intake.
Vitamin C (200 mg per day)
For most people, up to 200 mg/day is tolerable. Many multivitamins contain only about 60-100 mg per tablet.
People experiencing diarrhea or gastrointestinal discomfort from taking these supplements should lower their daily intake. People already taking a daily multivitamin should check their current Vitamin D and C intake levels and supplement accordingly to achieve optimum levels. For example, someone taking a daily multivitamin with 500 IU of Vitamin D3 would only need to take an additional 500 IUs of Vitamin D3 to achieve 1000 IUs of Vitamin D3 per day.
Note that it may take up to 3 months for levels of Vitamin D to reach optimal levels in the body. Look for a reduction in colds, the flu, and cold sores after supplementing daily for a few months.
Vitamin E (no longer recommended)
Notwithstanding its benefits to immunity, I cannot recommend high levels of Vitamin E as part of supercharging the immune system because of a recent report in the Journal of the American Medical Association (JAMA), published Fall 2011. In a 7-year study looking at rates of prostate cancer in men taking either 400 IU/day of vitamin E or a placebo, researchers found the opposite of what they expected. 400 IU/day of Vitamin E actually increased the risk of prostate cancer by 17%. Here is a link to a website explaining the Vitamin E study which appeared in JAMA (October 2011) (prostate cancer study). The number one vitamin in supercharging the immune system still appears to be Vitamin D3, and all research points to this vitamin being safe in high doses, so that is good news.
6. For More Information
For more information on the benefits of Vitamin D, appropriate dosing of Vitamin D, and healthy levels of Vitamin D in the body, visit these sites.
Linus Pauling Foundation
Vitamin D Council
National Institutes of Health
Linus Pauling Foundation
Vitamin D Council
National Institutes of Health
7. Research Updates - check here for recent advances on supercharging the innate immune system to combat HSV-I.
No new updates.
8. References
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Alvarez-Rodriguez, L., Lopez-Hoyos, M., Garcia-Unzueta, M., Amado, J. A., Cacho, P. M., & Martinez-Taboada, V. M. (2012). Age and low levels of circulating vitamin D are associated with impaired innate immune function. Journal of Leukocyte Biology, 91, 829-838.
Beard, J. A., Bearden, A., & Striker R. (2011). Vitamin D and the anti-viral state. Journal of Clinical Virology (in press).
Bosomworth, N.J. (2011). Mitigating epidemic vitamin D deficiency. Canadian Family Physician, 57, 16-20.
Cannell, J. J., et al., (2008). On the epidemiology of influenza. Virology Journal, 5(29).
Correale, J., Ysrraelit, M., & Gaitan, M. I. (2009). Immunomodulatory effects of vitamin D in multiple sclerosis. Brain, 132, 1146-1160.
Gombart, A. F. (2009). Vitamin D antimicrobial peptide pathway and its role in protecting against infection. Future of Microbiology, 4.
Guo C, Rosoha E, Lowry MB, Borregaard N, Gombart AF. (2013). Curcumin induces human cathelicidin antimicrobial peptide gene expression through a vitamin D receptor-independent pathway. Journal of Nutritional Biochemistry, 24(5), 754-759
Guo C, Sinnott B, Niu B, Lowry MB, Fantacone ML, & Gombart AF (2013). Synergistic induction of human cathelicidin antimicrobial peptide gene expression by vitamin D and stilbenoids. Molecular Nutrition and Food Research (http://www.ncbi.nlm.nih.gov/pubmed/24039193).
Lappe, J.M. (2011). The role of vitamin D in human health: A paradigm shift. Journal of Evidence-Based Complementary & Alternative Medicine, 16(1), 58-72.
Melamed, M. L., et al., (2010). Low levels of 25-hydroxyvitamin D in the pediatric populations: prevelance and clinical outcomes. Pediatric Health, 4(1), 89-97.
Rode Von Essen, M., et al., (2010). Vitamin D controls T cell antigen receptor signaling and activation of human T cells. Nature Immunology, 11(4), 344-349.
Schwalfenberg, G. K. (2011). A review of the critical role of vitamin D in the functioning of the immune system and the clinical implications of vitamin D deficiency. Molecular Nutrition and Food Research, 55, 96-108.
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