Not dead yet!
Well-Known Member
I found something really good about vitamin D, thought I'd share. It plays a huge role in autoimmune disease and in the body's ability to fight germs.
Many pathogens actually deactivate the *receptor* for Vitamin D so that the immune system is lulled into complacency and doesn't fight.
We are too concerned about D2/D3 forms of the vitamin and not concerned enough about the effect on the receptor.
If I take a huge dose of D3 (30,000 IU or more), I get anxiety and a surge of adrenaline that lasts about 4 hours. Not as bad as people with mental illness, but noticeable. People with mental illness might describe it as causing "mania" and it may last for months. So it isn't true that there is no side effect. It's just that the side effect is mental health related and we know that gets a blanket of silence in medicine.
When I looked at why that is happening (since my body can make that much in a single visit to the beach), I finally found information about activating and inactivating the Vitamin D *receptor* which is distinct from active/inactive Vitamin D itself. It's starting to sound a lot like the Thyroid issues with active and inactive T3 and how one can inactivate the other by occupying the receptor. But it turns out, Vitamin D can occupy that receptor too. Since many people take both, it might explain why the body has such trouble with thyroid meds being ineffective for some people.
This article has some good background if anyone needs more help with Vitamin D levels, https://mpkb.org/home/pathogenesis/vitamind/metabolism Note: I didn't spend a lot of energy vetting the foundation or the website, but it looked like good info.
I'll add a few quotes that I think help:
"The simplistic first-order mass-action model used to guide the early vitamin studies has given way to a more complex description of action. When active, the Vitamin D nuclear receptor (VDR) affects transcription of at least 913 genes and impacts processes ranging from calcium metabolism to expression of key antimicrobial peptides. "
"one of the hallmarks of chronic inflammatory disease: a low 25-D and a high 1,25-D" -- so check your recent test results! Many doctors have checked these levels in me, but have never said this to me, so they don't know.
"The body controls activity of the VDR through regulation of the vitamin D metabolites. 25-hydroxyvitamin D (25-D) antagonizes or inactivates the Receptor while 1,25-dihydroxyvitamin D (1,25-D) agonizes or activates the Receptor. " -- I always think, "to what end is it activated/deactivated?" If there may be any useful result of having it inactive, then don't assume that active is always good.
"Epstein-Barr virus (EBV) – shown to downregulate expression of the VDR (and by the VDR) by a factor of about five, inducing “eventual immortalization”29) A 2011 paper further showed that a EBV not only down-regulates expression of the VDR protein itself, but also acts to block transcription by the VDR.30)"
"Molecular modeling data show that at high levels, 1,25-D not only binds the VDR but also has a strong affinity for other key receptors that control the body's major hormonal systems including those that regulate the body's sex, thyroid, and adrenal hormones. As 1,25-D rises, it pushes out the molecules that are meant to control these receptors. Compromising these receptors can disrupt the body's ability to regulate temperature, libido, and any number of other functions.[table of affinities needed] Indeed, in the human brain, the VDR tends to be most common in the hypothalamus, which is responsible for these functions."
"1,25-D has a very high affinity for the alpha thyroid nuclear receptor (ThRa) having a Kd value of 8.41. Normally levels of the endogenous ligand for ThRa known as T3 (which has a Kd 7.20 for ThRa) keep 1,25-D out of the binding pocket, but as 1,25-D rises due to VDR dysregulation it starts to proportionately displace T3 and block transcription by ThRa. "
There are many quotes that tempted me, especially when they talk about Borrellia (Lyme) and how it deactivates the receptor so it can grow. If this interests you, you might want to read further.
And there is a paper called "Vitamin D the Alternative Hypothesis" --
[article=http://autoimmunityresearch.org/transcripts/AR-Albert-VitD.pdf]Recent vitamin D studies seem to address two broad observations
regarding 25-D. First, serum levels of 25-D tend to be significantly
lower in patients with autoimmune disease [13]. Second, subjects
given vitamin D, even in controlled studies, often seem to have lower
rates of autoimmune disease and fewer markers of inflammation [14].
These observations have led people to assume that supplemental
vitamin D is beneficial, because it decreases inflammation and
autoimmune disease symptoms. Therefore, many researchers
suggest, some more strongly than others, that regular and systematic
supplementation with vitamin D alleviates autoimmune disease
[9].
We will call this view the deficiency/disease model. However, these same
observations can be interpreted differently. Low 25-D levels in autoimmune
disease may be a result of the disease process itself, and the drop
in inflammation among individuals taking the secosteroid may stem
from its ability to slow immune function. We will call this view
the alternate model.
Efforts to determine which of these models is correct must examine how 25-
D affects the VDR[/article]
So there's a lot more to this than meets the eye. In particular it's sad that calcitrol is not over the counter yet it has rare side effects. But also sad that its immune suppressive effects aren't even mentioned and I bet people who take it don't even know. I read several inserts for calcitrol and it lists rare side effects. Not one of them mentions immune suppression or infections. Yet prednisone is full of such warnings.
Many pathogens actually deactivate the *receptor* for Vitamin D so that the immune system is lulled into complacency and doesn't fight.
We are too concerned about D2/D3 forms of the vitamin and not concerned enough about the effect on the receptor.
If I take a huge dose of D3 (30,000 IU or more), I get anxiety and a surge of adrenaline that lasts about 4 hours. Not as bad as people with mental illness, but noticeable. People with mental illness might describe it as causing "mania" and it may last for months. So it isn't true that there is no side effect. It's just that the side effect is mental health related and we know that gets a blanket of silence in medicine.
When I looked at why that is happening (since my body can make that much in a single visit to the beach), I finally found information about activating and inactivating the Vitamin D *receptor* which is distinct from active/inactive Vitamin D itself. It's starting to sound a lot like the Thyroid issues with active and inactive T3 and how one can inactivate the other by occupying the receptor. But it turns out, Vitamin D can occupy that receptor too. Since many people take both, it might explain why the body has such trouble with thyroid meds being ineffective for some people.
This article has some good background if anyone needs more help with Vitamin D levels, https://mpkb.org/home/pathogenesis/vitamind/metabolism Note: I didn't spend a lot of energy vetting the foundation or the website, but it looked like good info.
I'll add a few quotes that I think help:
"The simplistic first-order mass-action model used to guide the early vitamin studies has given way to a more complex description of action. When active, the Vitamin D nuclear receptor (VDR) affects transcription of at least 913 genes and impacts processes ranging from calcium metabolism to expression of key antimicrobial peptides. "
"one of the hallmarks of chronic inflammatory disease: a low 25-D and a high 1,25-D" -- so check your recent test results! Many doctors have checked these levels in me, but have never said this to me, so they don't know.
"The body controls activity of the VDR through regulation of the vitamin D metabolites. 25-hydroxyvitamin D (25-D) antagonizes or inactivates the Receptor while 1,25-dihydroxyvitamin D (1,25-D) agonizes or activates the Receptor. " -- I always think, "to what end is it activated/deactivated?" If there may be any useful result of having it inactive, then don't assume that active is always good.
"Epstein-Barr virus (EBV) – shown to downregulate expression of the VDR (and by the VDR) by a factor of about five, inducing “eventual immortalization”29) A 2011 paper further showed that a EBV not only down-regulates expression of the VDR protein itself, but also acts to block transcription by the VDR.30)"
"Molecular modeling data show that at high levels, 1,25-D not only binds the VDR but also has a strong affinity for other key receptors that control the body's major hormonal systems including those that regulate the body's sex, thyroid, and adrenal hormones. As 1,25-D rises, it pushes out the molecules that are meant to control these receptors. Compromising these receptors can disrupt the body's ability to regulate temperature, libido, and any number of other functions.[table of affinities needed] Indeed, in the human brain, the VDR tends to be most common in the hypothalamus, which is responsible for these functions."
"1,25-D has a very high affinity for the alpha thyroid nuclear receptor (ThRa) having a Kd value of 8.41. Normally levels of the endogenous ligand for ThRa known as T3 (which has a Kd 7.20 for ThRa) keep 1,25-D out of the binding pocket, but as 1,25-D rises due to VDR dysregulation it starts to proportionately displace T3 and block transcription by ThRa. "
There are many quotes that tempted me, especially when they talk about Borrellia (Lyme) and how it deactivates the receptor so it can grow. If this interests you, you might want to read further.
And there is a paper called "Vitamin D the Alternative Hypothesis" --
[article=http://autoimmunityresearch.org/transcripts/AR-Albert-VitD.pdf]Recent vitamin D studies seem to address two broad observations
regarding 25-D. First, serum levels of 25-D tend to be significantly
lower in patients with autoimmune disease [13]. Second, subjects
given vitamin D, even in controlled studies, often seem to have lower
rates of autoimmune disease and fewer markers of inflammation [14].
These observations have led people to assume that supplemental
vitamin D is beneficial, because it decreases inflammation and
autoimmune disease symptoms. Therefore, many researchers
suggest, some more strongly than others, that regular and systematic
supplementation with vitamin D alleviates autoimmune disease
[9].
We will call this view the deficiency/disease model. However, these same
observations can be interpreted differently. Low 25-D levels in autoimmune
disease may be a result of the disease process itself, and the drop
in inflammation among individuals taking the secosteroid may stem
from its ability to slow immune function. We will call this view
the alternate model.
Efforts to determine which of these models is correct must examine how 25-
D affects the VDR[/article]
So there's a lot more to this than meets the eye. In particular it's sad that calcitrol is not over the counter yet it has rare side effects. But also sad that its immune suppressive effects aren't even mentioned and I bet people who take it don't even know. I read several inserts for calcitrol and it lists rare side effects. Not one of them mentions immune suppression or infections. Yet prednisone is full of such warnings.