Vitamin K2
Replies
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https://allergyresearchgroup.com/ARGFocus_201008_VitaminsDAK_web.pdf
@TheDevastator the above PDF article supports your post about balance the fat soluble vitamins. It mentions how vit D and A can be helpful when it comes to cytok ine storm management which can lead to death in cases of COVID-19.
It is 10 years old so when reading it can be helpful to interpolate the article with newer research findings.0 -
Here's some newer research for you vis a vis Vit D and covid 19:The First Randomized Controlled Trial on Vitamin D and COVID-19
The trial was conducted at the Reina Sofía University Hospital in Córdoba, Spain. The trial included 76 patients with COVID-19 pneumonia. Although this is no longer the standard of care, all patients were treated with hydroxychloroquine and azithromycin and, when needed, a broad-spectrum antibiotic. Admission to the ICU was determined by a multidisciplinary committee consisting of intensive care specialists, pulmonologists, internal medicine specialists, and members of the ethics committee.
The patients were randomly allocated to receive or not receive vitamin D in a 2:1 ratio. This resulted in 50 patients in the vitamin D group and 26 patients in the control group.
The Vitamin D Treatment Protocol
The vitamin D was provided as oral calcifediol, also known as calcidiol, 25(OH)D, and 25-hydroxyvitamin D. This is a metabolite of vitamin D that our livers make. It is is the principle form of vitamin D that circulates in the blood, and we use it as a measure of vitamin D status.
Traces of 25(OH)D occur in food, and it is five times as potent as vitamin D. As described on page 255 of the 1997 DRI Report, 25(OH)D is given an international unit (IU) value that equates it to vitamin D. Whereas one microgram (mcg) of vitamin D is 40 IU, 1 mcg of 25(OH)D is 200 IU.
The treatment in this RCT was soft capsules of 532 mcg 25(OH)D on day 1 of admission to the hospital, followed by 266 mcg on days 3 and 7, and then 266 mcg once a week until discharge, ICU admission, or death.
This is equivalent to 106,400 IU vitamin D on day 1, 53,200 IU on days 3 and 7, and 53,200 IU weekly thereafter. If this were given as daily doses, it would be the equivalent of 30,400 per day for the first week, followed by a maintenance dose of 7,600 IU per day.
The vitamin D status of the patients was not measured. However, the average vitamin D status in this region of Spain during the time of year in which the study was conducted is 16 ng/mL. A single dose of 100,000 IU vitamin D tends to raise a 25(OH)D of 10 ng/mL into the 20-30 ng/mL range. My suspicion is that the bolus dosing in the first week brought the patients' vitamin D status into the 30-40 ng/mL range by the end of the week, and that most of the healing took place in the circa 40 ng/mL range.
The Results: Near Abolition of ICU Risk
The results are absolutely stunning. 50% of the control group (13 people) required admission to the ICU. Only 2% of those in the vitamin D group (one person) required admission to the ICU.
Expressed as relative risk, vitamin D reduced the risk of ICU admission 25-fold. Put another way, it eliminated 96% of the risk of ICU admission. Expressed as an odds ratio, which is a less intuitive concept but is often used in statistics because it gives an estimate of the effect of the treatment that would be constant across scenarios with different levels of risk, vitamin D reduced the odds of ICU admission by 98%. Either way, vitamin D practically abolished the need for ICU admission.
This was statistically significant at p<0.001, and the 95% confidence interval was 0.002-0.17. This means that the probability of observing differences this large or greater if there is no true effect of vitamin D is less than one in a thousand, and that the probability is 95% that the true effect lies somewhere between an 83% and a 99.8% reduction int he odds of ICU admission.
No matter how you slice it, the effect of vitamin D is extremely compelling.
Because the study is small, the potential confounding variables were not perfectly evenly distributed between the two groups. There was more high blood pressure in the control group, and there was a borderline greater number of patients with diabetes in the control group. Though not statistically significant, the vitamin D group had more people over the age of 60 and five times as many people with organ transplants or who were otherwise on immunosuppressive drugs. To account for all of these differences, they adjusted for them statistically. In the adjusted model, vitamin D still reduced the odds of ICU admission by 97%, with the 95% confidence interval ranging from a 75% to a 99.7% reduction in the odds.
Did Vitamin D Also Abolish the Risk of Death?
All of the vitamin D patients were discharged without complications. Half the control group was discharged without ICU admission. Among the other half, 11 were eventually discharged from ICU, and 2 died.
Although there were, thankfully, too few deaths to run statistics on, since patients generally would be admitted to the ICU before dying, and since vitamin D nearly abolished the risk of ICU admission, we can infer that in a larger study with more deaths, vitamin D would probably abolish or nearly abolish the risk of death.
Comparison With Observational Studies
These results are consistent with the first observational study on vitamin D, which found that 96% of severe and critical cases occurred at 25(OH)D under 30 ng/mL, whereas 97.5% of mild cases had 25(OH)D above 30 ng/mL.
This study couldn't measure the effect on mortality, but all two deaths were in the control group and the near abolition of ICU risk suggests that death would also be nearly abolished. This is consistent with the second observational study finding that only 4% of those with vitamin D status above 30 ng/mL died, while 88% of those with vitamin D status at 20-30 ng/mL died, and 99% of those with vitamin D status lower than that died.
It is less consistent with the weaker observational studies that came out later. For example, the fourth observational study found that prevalence of 25(OH)D below 20 ng/mL differed across three categories of severity judged by CT scan in males but not females. It is also less consistent with more recent studies in Iran and England. In Iran, 25(OH)D below 30 ng/mL only increased risk of severe infection by 21%, although mortality was roughly cut in half at that level. In England, ICU patients were half as likely to have 25(OH)D above 20 ng/mL as non-ICU patients, and mortality wasn't associated with vitamin D status.
In other words, the first RCT shows the effect of vitamin D is closer to the more extreme estimates of the first observational studies than it is to the more moderate estimates of the more recent studies.
The observational studies on infection risk are weaker than those on severity and mortality (see here, here, here, and here), but this RCT didn't look at infection risk.
The RCT contradicts the findings of the two Mendelian randomization studies. These found either no evidence for causality in the vitamin D/COVID-19 connection, or only weak evidence. However, these studies infer causality by looking at the effect of genetics. Genetics only explain 4.2% of the variation in 25(OH)D and many of the genes involved have non-specific, indirect relationships to vitamin D status. This RCT overwhelmingly takes precedence over the findings of the Mendelian randomization studies.
This Study Is the Single Most Important Vitamin D and COVID-19 Study
Since the first vitamin D study was released as a preprint* on April 23, we have been waiting for data that could settle whether the association between vitamin D and COVID-19 incidence, severity, and mortality is a causal one.
This study settles the question: yes, it is causal.
It is important for scientists to replicate each other's findings. Future studies with more diverse populations may reveal differences in the response between different populations. Future larger studies will more precisely refine the exact effect of vitamin D. Future studies with different dosing protocols, in different contexts (for example, without the use of hydroxychloroquine and azithromycin, or with the administration of other drugs or nutrients) will add nuances to our understanding of the effect of vitamin D.
However, given the degree to which it is nearly entirely harmless, and almost without exception beneficial, to maintain 25(OH)D above 30 ng/mL, it would be irresponsible not to interpret this study as definitive evidence of causality. At an absolute minimum, maintaining vitamin D status in this range should be part of the public health message to reduce COVID-19 risk, and 25(OH)D should be universally screened in all hospitals to be treated in anyone with COVID-19, and should be universally screened in all testing centers when antibodies and PCR testing is done, so that everyone knows not only their COVID-19 exposure but also their vitamin D status. If it's low, they should be given advice on how to bring it back up to normal.
How I've Changed My Position
On March 17, when I released Version 1 of The Food and Supplement Guide for the Coronavirus, I expressed concern that vitamin D might increase infection risk or severity by increasing ACE2, the entryway of SARS-CoV-2, the coronavirus that causes COVID-19, into our cells. In response to the first observational study of vitamin D released on April 23, which I covered in this newsletter on April 24, I released version 3 of the guide on April 28, in which I revised this stance and took the position that 25(OH)D should be maintained at 30-34 ng/mL.
As observational studies accumulated, they converged on the common point that 30-40 ng/mL is the sweet spot where infection risk, severity, and mortality are all lowest, without any risk of getting too much vitamin D.
I remained concerned that there might be some risk of a U-shaped curve, where risk increases at vitamin D levels higher than 40 ng/mL. Evidence for or against this was scant and contradictory. Data from Switzerland provided hints of an increased infection risk above 40 in those under 70 years old, but not in those older than 70. Data from Chicago suggested no difference in infection risk above 40 ng/mL, but it didn't separate the people by age. Data from Israel suggested that 25(OH)D above 53 ng/mL completely abolishes infection risk, but everyone with levels that high was under the age of 50. In the Israeli study, the relevant data were only in the young, and risk seemed abolished. In the Swiss study, the relevant data existed for all ages, and it suggested risk increased in the young. All of these studies concern infection risk, not severity or mortality, they all have too little data at high 25(OH)D levels, and they contradict each other.
While I remain agnostic whether there is some level of vitamin D above which infection risk is increased, the new RCT concerns severity and mortality. Although 25(OH)D levels weren't measured, they must have hit at least 40 ng/mL by the time the patients were released, and they possibly exceeded 50 ng/mL. That they gave these patients such massive doses of vitamin D without measuring their vitamin D levels, and that this nearly abolished the need for ICU admission, suggests that there should be no concern about a U-shaped curve with severity or mortality for short-term dosing of up to 8,000 IU per day over several weeks or for temporarily pushing 25(OH)D above 50 ng/mL during the course of treatment.
Given that observational studies around infection risk can consistently show that it is increased at low vitamin D status but cannot show any consistent picture at high vitamin D status, I am, for now, relieving myself of concern about this U-shaped curve. If high vitamin D status can almost eliminate severity and mortality, the off-chance that in some people at some high level it could increase infection risk should be tolerated.
I get emails from Chris Masterjohn PhD (for @TheDevastator and @GaleHawkins) https://chrismasterjohnphd.com/1 -
canadjineh wrote: »Here's some newer research for you vis a vis Vit D and covid 19:The First Randomized Controlled Trial on Vitamin D and COVID-19
The trial was conducted at the Reina Sofía University Hospital in Córdoba, Spain. The trial included 76 patients with COVID-19 pneumonia. Although this is no longer the standard of care, all patients were treated with hydroxychloroquine and azithromycin and, when needed, a broad-spectrum antibiotic. Admission to the ICU was determined by a multidisciplinary committee consisting of intensive care specialists, pulmonologists, internal medicine specialists, and members of the ethics committee.
The patients were randomly allocated to receive or not receive vitamin D in a 2:1 ratio. This resulted in 50 patients in the vitamin D group and 26 patients in the control group.
The Vitamin D Treatment Protocol
The vitamin D was provided as oral calcifediol, also known as calcidiol, 25(OH)D, and 25-hydroxyvitamin D. This is a metabolite of vitamin D that our livers make. It is is the principle form of vitamin D that circulates in the blood, and we use it as a measure of vitamin D status.
Traces of 25(OH)D occur in food, and it is five times as potent as vitamin D. As described on page 255 of the 1997 DRI Report, 25(OH)D is given an international unit (IU) value that equates it to vitamin D. Whereas one microgram (mcg) of vitamin D is 40 IU, 1 mcg of 25(OH)D is 200 IU.
The treatment in this RCT was soft capsules of 532 mcg 25(OH)D on day 1 of admission to the hospital, followed by 266 mcg on days 3 and 7, and then 266 mcg once a week until discharge, ICU admission, or death.
This is equivalent to 106,400 IU vitamin D on day 1, 53,200 IU on days 3 and 7, and 53,200 IU weekly thereafter. If this were given as daily doses, it would be the equivalent of 30,400 per day for the first week, followed by a maintenance dose of 7,600 IU per day.
The vitamin D status of the patients was not measured. However, the average vitamin D status in this region of Spain during the time of year in which the study was conducted is 16 ng/mL. A single dose of 100,000 IU vitamin D tends to raise a 25(OH)D of 10 ng/mL into the 20-30 ng/mL range. My suspicion is that the bolus dosing in the first week brought the patients' vitamin D status into the 30-40 ng/mL range by the end of the week, and that most of the healing took place in the circa 40 ng/mL range.
The Results: Near Abolition of ICU Risk
The results are absolutely stunning. 50% of the control group (13 people) required admission to the ICU. Only 2% of those in the vitamin D group (one person) required admission to the ICU.
Expressed as relative risk, vitamin D reduced the risk of ICU admission 25-fold. Put another way, it eliminated 96% of the risk of ICU admission. Expressed as an odds ratio, which is a less intuitive concept but is often used in statistics because it gives an estimate of the effect of the treatment that would be constant across scenarios with different levels of risk, vitamin D reduced the odds of ICU admission by 98%. Either way, vitamin D practically abolished the need for ICU admission.
This was statistically significant at p<0.001, and the 95% confidence interval was 0.002-0.17. This means that the probability of observing differences this large or greater if there is no true effect of vitamin D is less than one in a thousand, and that the probability is 95% that the true effect lies somewhere between an 83% and a 99.8% reduction int he odds of ICU admission.
No matter how you slice it, the effect of vitamin D is extremely compelling.
Because the study is small, the potential confounding variables were not perfectly evenly distributed between the two groups. There was more high blood pressure in the control group, and there was a borderline greater number of patients with diabetes in the control group. Though not statistically significant, the vitamin D group had more people over the age of 60 and five times as many people with organ transplants or who were otherwise on immunosuppressive drugs. To account for all of these differences, they adjusted for them statistically. In the adjusted model, vitamin D still reduced the odds of ICU admission by 97%, with the 95% confidence interval ranging from a 75% to a 99.7% reduction in the odds.
Did Vitamin D Also Abolish the Risk of Death?
All of the vitamin D patients were discharged without complications. Half the control group was discharged without ICU admission. Among the other half, 11 were eventually discharged from ICU, and 2 died.
Although there were, thankfully, too few deaths to run statistics on, since patients generally would be admitted to the ICU before dying, and since vitamin D nearly abolished the risk of ICU admission, we can infer that in a larger study with more deaths, vitamin D would probably abolish or nearly abolish the risk of death.
Comparison With Observational Studies
These results are consistent with the first observational study on vitamin D, which found that 96% of severe and critical cases occurred at 25(OH)D under 30 ng/mL, whereas 97.5% of mild cases had 25(OH)D above 30 ng/mL.
This study couldn't measure the effect on mortality, but all two deaths were in the control group and the near abolition of ICU risk suggests that death would also be nearly abolished. This is consistent with the second observational study finding that only 4% of those with vitamin D status above 30 ng/mL died, while 88% of those with vitamin D status at 20-30 ng/mL died, and 99% of those with vitamin D status lower than that died.
It is less consistent with the weaker observational studies that came out later. For example, the fourth observational study found that prevalence of 25(OH)D below 20 ng/mL differed across three categories of severity judged by CT scan in males but not females. It is also less consistent with more recent studies in Iran and England. In Iran, 25(OH)D below 30 ng/mL only increased risk of severe infection by 21%, although mortality was roughly cut in half at that level. In England, ICU patients were half as likely to have 25(OH)D above 20 ng/mL as non-ICU patients, and mortality wasn't associated with vitamin D status.
In other words, the first RCT shows the effect of vitamin D is closer to the more extreme estimates of the first observational studies than it is to the more moderate estimates of the more recent studies.
The observational studies on infection risk are weaker than those on severity and mortality (see here, here, here, and here), but this RCT didn't look at infection risk.
The RCT contradicts the findings of the two Mendelian randomization studies. These found either no evidence for causality in the vitamin D/COVID-19 connection, or only weak evidence. However, these studies infer causality by looking at the effect of genetics. Genetics only explain 4.2% of the variation in 25(OH)D and many of the genes involved have non-specific, indirect relationships to vitamin D status. This RCT overwhelmingly takes precedence over the findings of the Mendelian randomization studies.
This Study Is the Single Most Important Vitamin D and COVID-19 Study
Since the first vitamin D study was released as a preprint* on April 23, we have been waiting for data that could settle whether the association between vitamin D and COVID-19 incidence, severity, and mortality is a causal one.
This study settles the question: yes, it is causal.
It is important for scientists to replicate each other's findings. Future studies with more diverse populations may reveal differences in the response between different populations. Future larger studies will more precisely refine the exact effect of vitamin D. Future studies with different dosing protocols, in different contexts (for example, without the use of hydroxychloroquine and azithromycin, or with the administration of other drugs or nutrients) will add nuances to our understanding of the effect of vitamin D.
However, given the degree to which it is nearly entirely harmless, and almost without exception beneficial, to maintain 25(OH)D above 30 ng/mL, it would be irresponsible not to interpret this study as definitive evidence of causality. At an absolute minimum, maintaining vitamin D status in this range should be part of the public health message to reduce COVID-19 risk, and 25(OH)D should be universally screened in all hospitals to be treated in anyone with COVID-19, and should be universally screened in all testing centers when antibodies and PCR testing is done, so that everyone knows not only their COVID-19 exposure but also their vitamin D status. If it's low, they should be given advice on how to bring it back up to normal.
How I've Changed My Position
On March 17, when I released Version 1 of The Food and Supplement Guide for the Coronavirus, I expressed concern that vitamin D might increase infection risk or severity by increasing ACE2, the entryway of SARS-CoV-2, the coronavirus that causes COVID-19, into our cells. In response to the first observational study of vitamin D released on April 23, which I covered in this newsletter on April 24, I released version 3 of the guide on April 28, in which I revised this stance and took the position that 25(OH)D should be maintained at 30-34 ng/mL.
As observational studies accumulated, they converged on the common point that 30-40 ng/mL is the sweet spot where infection risk, severity, and mortality are all lowest, without any risk of getting too much vitamin D.
I remained concerned that there might be some risk of a U-shaped curve, where risk increases at vitamin D levels higher than 40 ng/mL. Evidence for or against this was scant and contradictory. Data from Switzerland provided hints of an increased infection risk above 40 in those under 70 years old, but not in those older than 70. Data from Chicago suggested no difference in infection risk above 40 ng/mL, but it didn't separate the people by age. Data from Israel suggested that 25(OH)D above 53 ng/mL completely abolishes infection risk, but everyone with levels that high was under the age of 50. In the Israeli study, the relevant data were only in the young, and risk seemed abolished. In the Swiss study, the relevant data existed for all ages, and it suggested risk increased in the young. All of these studies concern infection risk, not severity or mortality, they all have too little data at high 25(OH)D levels, and they contradict each other.
While I remain agnostic whether there is some level of vitamin D above which infection risk is increased, the new RCT concerns severity and mortality. Although 25(OH)D levels weren't measured, they must have hit at least 40 ng/mL by the time the patients were released, and they possibly exceeded 50 ng/mL. That they gave these patients such massive doses of vitamin D without measuring their vitamin D levels, and that this nearly abolished the need for ICU admission, suggests that there should be no concern about a U-shaped curve with severity or mortality for short-term dosing of up to 8,000 IU per day over several weeks or for temporarily pushing 25(OH)D above 50 ng/mL during the course of treatment.
Given that observational studies around infection risk can consistently show that it is increased at low vitamin D status but cannot show any consistent picture at high vitamin D status, I am, for now, relieving myself of concern about this U-shaped curve. If high vitamin D status can almost eliminate severity and mortality, the off-chance that in some people at some high level it could increase infection risk should be tolerated.
I get emails from Chris Masterjohn PhD (for @TheDevastator and @GaleHawkins) https://chrismasterjohnphd.com/
Chris is a sharp guy.
I know some who are not serious about their Vit D levels like I was before I turned 63. When first tested (2013) I was at 22 ng. Several years ago I read about Vit D/ flu shot trial in the UK and in that case the Vit D users had less flu than the ones that only had the protection of a flu shot. What sold me on Vit D and K2 is how it can lower one's heart arteries calcium scores. Now I am trying to decrease calcium deposits in my spine and joints. Now I can open my mouth wide enough to get dental fillings if needed. The AS (Ankylosing Spondylitis) did a number on me when I was eating food and drinks with added any form of any grain which I stopped cold turkey back in 2014 for pain management to avoid starting on Enbrel injections.0 -
https://vitamindwiki.com/Overview+Magnesium+and+vitamin+D#Consumer_Labs_Review_of_Magnesium_-_as_little_as_2_cents_per_200_mg_of_Mg
I found this when doing some reading this morning and ordered two new Mg books and magnesium bar soap that I never knew existed.
The more I read the more I know how much I don't know.0 -
Magnesium bar soap sounds interesting.... would the magnesium stay on your skin long enough for proper absorption? Usually the liquid magnesium-oil-gel suggests leaving it on for a few minutes and only then wiping with a damp cloth to get rid of the salt sticky feeling (if that bugs you.)0
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My two bars were at door just now when I got home and I have the same question.
Some think Mg may enter best through hair follicles so I use a lot of Mg oil starting at my head and working down while hot out of the shower and just leave it on until the next shower. I do wash my hands if I am going to be using my phone screen.
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Thanks for the study, @canadjineh
I feel sorry for the two in the control group that died when vitamin D could have saved them.
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I couldn’t stand Mg oil so I just use mineral drops mostly. Oysters, sesame seeds, and sunflower seeds are all high in magnesium. I’m about 90% carnivore but started eating nuts and seeds again. Epsom salt baths are great as well.0
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I think Chris Masterjohn is really smart but wrong in some things like most gurus.1
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TheDevastator wrote: »I think Chris Masterjohn is really smart but wrong in some things like most gurus.
That is often the case. What do you see Chris is wrong about specifically?0 -
GaleHawkins wrote: »TheDevastator wrote: »I think Chris Masterjohn is really smart but wrong in some things like most gurus.
That is often the case. What do you see Chris is wrong about specifically?
I'd like to check out his diet but it's all behind a paywall. One point is that he thinks the Methionine-Glycine Ratio is so important and that you need collagen. Of course he sells collagen. I think this is easily solved with delicious kielbasa a few times a week if it's even necessary. Maybe it does have some benefit and extra glycine will help certain issues. There is so much information out there to study.
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TheDevastator wrote: »GaleHawkins wrote: »TheDevastator wrote: »I think Chris Masterjohn is really smart but wrong in some things like most gurus.
That is often the case. What do you see Chris is wrong about specifically?
I'd like to check out his diet but it's all behind a paywall. One point is that he thinks the Methionine-Glycine Ratio is so important and that you need collagen. Of course he sells collagen. I think this is easily solved with delicious kielbasa a few times a week if it's even necessary. Maybe it does have some benefit and extra glycine will help certain issues. There is so much information out there to study.
I read Carolyn Dean's, M.D. The Miracle of Magnesium and now I am half way through her 2017 up date called The Magnesium Miracle. It has a lot of good info but it is one big promotion for her line of solutions to health problems. I did order her liquid Mg today because everything the wife tries upsets her. Dean indicates her ReMag is effective as by IV in a hospital setting. One problem I had was she states to not take more than 2,000 units of Vit D3 because it puts a demand for more Mg to get it to work. Did she never think of selling one more of her ReMag to fix that concern?
I just finished Jeff T Bowles 2019 Vit D3 book called The Miraculous Cure for and Prevention of All Diseases What Doctors Never Learned. The Kindle version is more complete with charts and graphs and the hyper links are actually live but it appears to be self published and he was trying to hold down the cost of the paper back. The info is what I was looking for but it is not a smooth read due to the lack of editing. He thinks 2,000 units of D3 is a non starter with 5,000 units as a starting point with cases claiming up to 1 million units. He has a lot of links where doctors are resolving MS side effects with mega doses of D3.
In my case I just read the good, bad and ugly and let my brain sort it out over the coming years.
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https://prnewswire.com/news-releases/doctor-dean-warns-too-little-magnesium-can-affect-heart-health-184276291.html#:~:text=Calcium%20causes%20muscles%20to%20contract,too%20quickly%20(tachycardia).%22
This is the Dr Dean I mentioned above. In reading her last book on the subject this morning she stated calcium build up in the arteries was due to low magnesium levels and by correcting that issue would start to remove that calcium build-up which was news to me. Vitamin D3 and K2 I knew about. Had anyone read this about magnesium levels?0 -
I know that magnesium helps stop calcium buildup in cells. I'm not sure where I read it though. I think it was in the Magnesium Miracle too but that’s not where I first read it.0
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I can't remember which study it was but it mentioned that calcium and magnesium attach to the same receptors in the cells so they can compete with each other. Maybe why the decades of concentration on calcium supplements and focus on 'dairy for your bones' could exacerbate magnesium deficiency. I'm just on my phone at work so I'll check my desktop later....0
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I've also read that with adequate magnesium in a cell, calcium is balanced and extra is forced out. I really would like to remember where that was from though. Dairy is good for the bones as long as they are getting all the other essential minerals but not in excess like a lot of people get.0
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I need to get in the habit of reading books again but it's true that anyone can self publish an eBook nowadays. I have several carnivore books that I've yet to read.1
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"Because calcium is typically an excitatory cofactor, the mineral usually enters a cell only when needed for something specific, like a nervous impulse or a muscle contraction. After such an action occurs, magnesium helps active transporters pump calcium out of a cell."
magnesium.ca/how-magnesium-works/
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https://medicaldialogues.in/diabetes-endocrinology/perspective/vitamin-k2-supplementation-lowers-risk-in-type-2-diabetes-mellitus-review-73072
While some of us use Vit K2 to lower Coronary Artery Calcium Scores K2 seems to perform other health benefits as well.0 -
Raw grass fed cheese is really high in K2 so I’m choosing that. Also I’m addicted to grass fed unsalted butter.2
