For those in Oz, I buy magnesium chloride from Blants in Sydney. They do online too. It comes in a nice tub. I have been sprinkling into my coffee etc and makes water taste a little softer , for want of a better .
(2 of 2) Magnesium is important for many cellular processes. Henry Lahore, in his https://vitamindwiki.com, has a diagram of priorities for health: #1 Healthy food; #2 Exercise; #3 Vitamin D; #4 Magnesium; #5 Omega 3 fatty acids, followed by vitamin K2, boron (https://aminotheory.com/cv19/#08-boron), zinc and iodine. I think this is about right, given the deficiencies in these nutrients in most of the world's population - at least those not living as hunter gatherers. I would would add potassium though this is difficult to supplement in the one or two grams per day quantities we probably need: https://aminotheory.com/cv19/kna/. It is difficult or impossible to obtain this in foods in any reasonable quantities.
I had never heard of low magnesium causing rickets even massive (30 mg a week) vitamin D2 injections. Thanks for citing this article: Reddy and Sivukumar 1974 "Magnesium-Dependent Vitamin-D-Resistant Rickets", the Lancet: https://sci-hub.se/10.1016/S0140-6736(74)91265-3.
I take two of these magnesium chelate tablets a day: https://www.naturesway.com.au/nature-s-way-high-strength-magnesium-250-tablets-one-a-day. Each contains 200 mg magnesium. Magnesium oxide is not very good since it requires a lot of energy to split it into free magnesium - think if the intense light generated when magnesium burns. I used to take magnesium citrate, but this is used, in large quantities, as a laxative.
I looked quickly at the Dai et al. article - but it is complex and I don't have time to understand it properly in the foreseeable future. Suffice to say that magnesium supplementation is generally a good idea, since it is hard to get enough from our current food sources.
You advise against taking vitamin D3 supplements, but your arguments are not at all clear. It is simple: We need 50 ng/mL or more 25-hydroxyvitamin D to be healthy. Foods, vitamin D fortified or not, in any practical quantity, can provide only a small fraction of the vitamin D3 we need to attain this. To attain this level all year round the choice is between substantial UV-B skin irradiation year after year, which damages DNA and so increases the risk of skin cancer, wrinkles etc. or taking vitamin D3 supplements in suitable quantities.
For 70 kg 154 lb body weight without obesity, according to the advise of Prof. Sunil Wimalawansa https://vitamindstopscovid.info/00-evi/#00-how-much, and average vitamin D3 supplemental intake of 0.125 milligrams is sufficient, and can be taken safely without the need for blood tests or medical monitoring. This is 125 millionths of a gram per day, on average. Expressed as IUs, it is 5000 IU, which sounds alarmingly high - especially since Australian retailers are not allowed to sell vitamin D3 capsules containing more than 25 micrograms (1000 IU). Fortunately, eBay and some Australian eBay sellers ignore this and 1.25 mg (50,000 IU) capsules can be purchased with ease. 0.125 mg 5000 IU vitamin D3 a day is a gram every 22 years. Pharma-grade vitamin D3 costs about USD$2.5 a gram, ex-factory. A credit card weighs 5 grams.
What quantities of which foods would a person need to eat per day to attain 200 or 400 mg magnesium?
There is a general argument about nutrients being most helpful and/or best absorbed if they are part of a natural food matrix, rather than in a concentrated form. However, this is a vague objection and doesn't address the need most people have for significant quantities of certain nutrients which are difficult or impossible to obtain in any diet which is practical or available to them.
(1 of 2) I am glad to see a clear distinction between the one hormonal function of circulating calcitriol and the multiple functions of calcitriol as an intracrine or paracrine agent, in and between (respectively) individual cells. The great majority of articles written about the vitamin D compounds fail to do this, mainly because most of the authors have never heard of these signaling systems: https://vitamindstopscovid.info/02-intracrine/.
I have two large, up-to-date, immunology textbooks here (I wish I had time to read them properly). Neither mention vitamin D, intracrine or paracrine signaling in their indexes. Yet, intracrine and sometimes paracrine signaling, both by the intracellular hydroxylation of 25-hydroxyvitamin D to calcitriol, when a cell-type-specific condition is detected in the individual cell, has been elucidated in dendritic cells, macrophages and (in 2022, Chauss et al.) Th1 regulatory lymphocytes. Since many types of cell which are not involved in calcium-phosphate-bone metabolism system are known (by some genetic analysis I don't understand) to also change their cellular behavior in response to calcitriol entering the nucleus, it is reasonable to assume that all these cell types do so for the purposes of intracrine (within the cell) or paracrine (to nearby cells) signaling. Many of these types are immune cells.
So immunology, to the present day, for the great majority of researchers and so for the great majority of medical professionals, is a shadow of its proper self, since these people do not understand an important mechanism by which many types of immune cell respond to their individual circumstances and because they have no idea that most people's immune systems are working very poorly, since most people have only a fraction of the 50 ng/mL 125 nmol/L circulating 25-hydroxyvitamin D which all these cell types (we can reasonably assume) need to run their signaling systems properly.
It is widely reported that the overall activity (in the body, and/or perhaps inside individual cells) of the CYP24A1 enzyme, depends on the level (concentration) of calcitriol. This enzyme irreversibly destroys both 25-hydroxyvitamin D and calcitriol (1,25-dihydroxyvitamin D) by hydroxylating them on the 24th carbon. This enzyme's activity is the primary or sole mechanism by which the body self-limits the level of 25-hydroxyvitamin D. This results in the curved, rather than straight line, relationships between vitamin D3 supplemental intake quantity and circulating 25-hydroxyvitamin D, as seen in, for instance: https://vitamindstopscovid.info/00-evi/#ekwaru.
However, as far as I know - and there is a vast amount of research, which I have only read a small subset of - it is not entirely clear where these enzyme molecule reside and to what extent it is the circulating calcitriol level (which is very low ~~ 0.05 ng/mL, and tightly regulated by the kidneys) modulate their collective activity in limiting the level of circulating 25-hydroxyvitamin D.
I am not sure of the regulatory mechanism either. I recall reading somewhere that it is also affected by the level of circulating 25-hydroxyvitamin D. This would not be surprising, since the calcitriol receptor (known as the "vitamin D receptor") binds weakly to 25-hydroxyvitamin D - and the level of circulating 25-hydroxyvitamin D is 400 to 1500 times the level of circulating calcitriol.
Does the enzyme reside in cells, or in the bloodstream? Where is its production controlled? Its overall ability to 24-hydroxylate these two compounds scales in proportion to the circulating 25-hydroxyvitamin D level, as we can see from the graphs. To what extent this is due to that level directly, as opposed to the modest influence of that level on the level of circulating calcitriol, is not entirely clear - as far as I am aware. I think the truth of the matter is that the 25-hydroxyvitamin D level probably plays the major role in controlling the activity of this enzyme, overall, and perhaps in individual cells. So I assume that the conventional statement that its activity is in proportion to the calcitriol level (in the bloodstream? in cells? which cells?) is far from complete and is probably largely incorrect.
For those in Oz, I buy magnesium chloride from Blants in Sydney. They do online too. It comes in a nice tub. I have been sprinkling into my coffee etc and makes water taste a little softer , for want of a better .
(2 of 2) Magnesium is important for many cellular processes. Henry Lahore, in his https://vitamindwiki.com, has a diagram of priorities for health: #1 Healthy food; #2 Exercise; #3 Vitamin D; #4 Magnesium; #5 Omega 3 fatty acids, followed by vitamin K2, boron (https://aminotheory.com/cv19/#08-boron), zinc and iodine. I think this is about right, given the deficiencies in these nutrients in most of the world's population - at least those not living as hunter gatherers. I would would add potassium though this is difficult to supplement in the one or two grams per day quantities we probably need: https://aminotheory.com/cv19/kna/. It is difficult or impossible to obtain this in foods in any reasonable quantities.
I had never heard of low magnesium causing rickets even massive (30 mg a week) vitamin D2 injections. Thanks for citing this article: Reddy and Sivukumar 1974 "Magnesium-Dependent Vitamin-D-Resistant Rickets", the Lancet: https://sci-hub.se/10.1016/S0140-6736(74)91265-3.
I take two of these magnesium chelate tablets a day: https://www.naturesway.com.au/nature-s-way-high-strength-magnesium-250-tablets-one-a-day. Each contains 200 mg magnesium. Magnesium oxide is not very good since it requires a lot of energy to split it into free magnesium - think if the intense light generated when magnesium burns. I used to take magnesium citrate, but this is used, in large quantities, as a laxative.
I looked quickly at the Dai et al. article - but it is complex and I don't have time to understand it properly in the foreseeable future. Suffice to say that magnesium supplementation is generally a good idea, since it is hard to get enough from our current food sources.
The "sweet spot" for 25-hydroxyvitamin D level (as measured in "vitamin D" blood tests) is widely thought to be 20 to 30 ng/mL (50 to 75 nmol/L). But leading researchers have been calling for 40 to 60 ng/mL to be the target, since 2008: https://www.grassrootshealth.net/project/our-scientists/ and again this year: https://www.grassrootshealth.net/scientists-call-daction-public-health-2024/. It is easy to see why, once it is understood that the immune system's ability to protect against bacterial infections degrades the further below 50 ng/mL the circulating 25-hydroxyvitamin D level is: https://jamanetwork.com/journals/jamasurgery/fullarticle/1782085 https://vitamindstopscovid.info/00-evi/#00-50ngmL.
You advise against taking vitamin D3 supplements, but your arguments are not at all clear. It is simple: We need 50 ng/mL or more 25-hydroxyvitamin D to be healthy. Foods, vitamin D fortified or not, in any practical quantity, can provide only a small fraction of the vitamin D3 we need to attain this. To attain this level all year round the choice is between substantial UV-B skin irradiation year after year, which damages DNA and so increases the risk of skin cancer, wrinkles etc. or taking vitamin D3 supplements in suitable quantities.
For 70 kg 154 lb body weight without obesity, according to the advise of Prof. Sunil Wimalawansa https://vitamindstopscovid.info/00-evi/#00-how-much, and average vitamin D3 supplemental intake of 0.125 milligrams is sufficient, and can be taken safely without the need for blood tests or medical monitoring. This is 125 millionths of a gram per day, on average. Expressed as IUs, it is 5000 IU, which sounds alarmingly high - especially since Australian retailers are not allowed to sell vitamin D3 capsules containing more than 25 micrograms (1000 IU). Fortunately, eBay and some Australian eBay sellers ignore this and 1.25 mg (50,000 IU) capsules can be purchased with ease. 0.125 mg 5000 IU vitamin D3 a day is a gram every 22 years. Pharma-grade vitamin D3 costs about USD$2.5 a gram, ex-factory. A credit card weighs 5 grams.
What quantities of which foods would a person need to eat per day to attain 200 or 400 mg magnesium?
There is a general argument about nutrients being most helpful and/or best absorbed if they are part of a natural food matrix, rather than in a concentrated form. However, this is a vague objection and doesn't address the need most people have for significant quantities of certain nutrients which are difficult or impossible to obtain in any diet which is practical or available to them.
(1 of 2) I am glad to see a clear distinction between the one hormonal function of circulating calcitriol and the multiple functions of calcitriol as an intracrine or paracrine agent, in and between (respectively) individual cells. The great majority of articles written about the vitamin D compounds fail to do this, mainly because most of the authors have never heard of these signaling systems: https://vitamindstopscovid.info/02-intracrine/.
I have two large, up-to-date, immunology textbooks here (I wish I had time to read them properly). Neither mention vitamin D, intracrine or paracrine signaling in their indexes. Yet, intracrine and sometimes paracrine signaling, both by the intracellular hydroxylation of 25-hydroxyvitamin D to calcitriol, when a cell-type-specific condition is detected in the individual cell, has been elucidated in dendritic cells, macrophages and (in 2022, Chauss et al.) Th1 regulatory lymphocytes. Since many types of cell which are not involved in calcium-phosphate-bone metabolism system are known (by some genetic analysis I don't understand) to also change their cellular behavior in response to calcitriol entering the nucleus, it is reasonable to assume that all these cell types do so for the purposes of intracrine (within the cell) or paracrine (to nearby cells) signaling. Many of these types are immune cells.
So immunology, to the present day, for the great majority of researchers and so for the great majority of medical professionals, is a shadow of its proper self, since these people do not understand an important mechanism by which many types of immune cell respond to their individual circumstances and because they have no idea that most people's immune systems are working very poorly, since most people have only a fraction of the 50 ng/mL 125 nmol/L circulating 25-hydroxyvitamin D which all these cell types (we can reasonably assume) need to run their signaling systems properly.
It is widely reported that the overall activity (in the body, and/or perhaps inside individual cells) of the CYP24A1 enzyme, depends on the level (concentration) of calcitriol. This enzyme irreversibly destroys both 25-hydroxyvitamin D and calcitriol (1,25-dihydroxyvitamin D) by hydroxylating them on the 24th carbon. This enzyme's activity is the primary or sole mechanism by which the body self-limits the level of 25-hydroxyvitamin D. This results in the curved, rather than straight line, relationships between vitamin D3 supplemental intake quantity and circulating 25-hydroxyvitamin D, as seen in, for instance: https://vitamindstopscovid.info/00-evi/#ekwaru.
However, as far as I know - and there is a vast amount of research, which I have only read a small subset of - it is not entirely clear where these enzyme molecule reside and to what extent it is the circulating calcitriol level (which is very low ~~ 0.05 ng/mL, and tightly regulated by the kidneys) modulate their collective activity in limiting the level of circulating 25-hydroxyvitamin D.
I am not sure of the regulatory mechanism either. I recall reading somewhere that it is also affected by the level of circulating 25-hydroxyvitamin D. This would not be surprising, since the calcitriol receptor (known as the "vitamin D receptor") binds weakly to 25-hydroxyvitamin D - and the level of circulating 25-hydroxyvitamin D is 400 to 1500 times the level of circulating calcitriol.
Does the enzyme reside in cells, or in the bloodstream? Where is its production controlled? Its overall ability to 24-hydroxylate these two compounds scales in proportion to the circulating 25-hydroxyvitamin D level, as we can see from the graphs. To what extent this is due to that level directly, as opposed to the modest influence of that level on the level of circulating calcitriol, is not entirely clear - as far as I am aware. I think the truth of the matter is that the 25-hydroxyvitamin D level probably plays the major role in controlling the activity of this enzyme, overall, and perhaps in individual cells. So I assume that the conventional statement that its activity is in proportion to the calcitriol level (in the bloodstream? in cells? which cells?) is far from complete and is probably largely incorrect.
What I could understand is fascinating! Question:! Do you do private consults? Regardless, thank you!