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No-Vit D, No-B Vit Thus Autoimmune and lousy sleep!

Another interesting article popped out of the AI selected articles:
Vitamin D deficiency changes the intestinal microbiome reducing B vitamin production in the gut. The resulting lack of pantothenic acid adversely affects the immune system, producing a “pro-inflammatory” state associated with atherosclerosis and autoimmunity. [2016]
Vitamin D blood levels of 60-80 ng/ml promote normal sleep. The present study was undertaken to explore why this beneficial effect waned after 2 years as arthritic pain increased. Pantothenic acid becomes coenzyme A, a cofactor necessary for cortisol and acetylcholine production. 1950s experiments suggested a connection between pantothenic acid deficiency, autoimmune arthritis and insomnia. The B vitamins have been shown to have an intestinal bacterial source and a food source, suggesting that the normal intestinal microbiome may have always been the primary source of B vitamins. Review of the scientific literature shows that pantothenic acid does not have a natural food source, it is supplied by the normal intestinal bacteria.
Three months of vitamin D plus B100 resulted in improved sleep, reduced pain and unexpected resolution of bowel symptoms. These results suggest that the combination of vitamin D plus B100 creates an intestinal environment that favors the return of the four specific species, Actinobacteria, Bacteroidetes, Firmicutes and Proteobacteria that make up the normal human microbiome.​
This lead to some related articles (also old)
It was found that the time after which changes in vitamin levels developed as well as the intensity of changes differ, depending on the experimental model used, but the sequence of vitamin disappearance from the organism is always the same. The first to disappear were vitamins B1, followed by vitamin B6 and pantothenic acid.
Changes in the levels of certain vitamins from B group under conditions of vitamin deficiency. 1976
Bottom Line
From the above we see a cascade starting with deficient Vitamin D
  1. Reduced Vitamin D
  2. Reduced Thiamine (B1)
  3. Reduced pyridoxine (B6)
  4. Reduced Pantothenic Acid (B5)
  5. eventually reduced Cobalamin (B12)
    1. ” affect VB12 level, indirectly, by reducing 25(OH)D level in middle aged women. ” [2018]
For CFS specifically we have Ana Dorothea Hoeck’s research
How much vitamin D should you take for a healthy microbiome?
The last post, we found that research had found the vitamin D was the key component for a cascade that influenced B Vitamins, sleep and some digestive issues. This post will try to address the issue of vitamin D dosage.
On my old web site, I had done several posts on Vitamin D (from 2005-2006) – with links to PubMed articles.
In this post, I will jump to the bottom line fast (if you want more detail, see above).
Target Level
  • “The patients with optimal vitamin D status [25(OH)D ≥75 nmol/l] ” [2016]
  • “Serum iPTH held a stable plateau level at 36 pg/ml as long as serum 25(OH)D values were higher than 78 nmol/l (31 ng/ml), but increased when the serum 25(OH)D value fell below this. ” [1997]
  • “Evidence is reviewed that shows that serum 25(OH)D3 concentrations of < 80 nmol/L are associated with reduced calcium absorption, osteoporosis, and increased fracture risk.” [2004]
  • In my posts from a decade ago, I created this chart using an image from an article from [2004]
Functional indices of vitamin D status and ramifications of vitamin D deficiency.
My suggested target level is 120 nmol/l. 50% above the level that issues start.
How much to take?
This is easy if you know your current level due to a chart from 2004,

Connie M Weaver and James C Fleet, Vitamin D requirements: current and future
Am J Clin Nutr 2004;80(suppl):1735S–9S
Find the best match in the chart. I will take the high lighted one:
  • Actual reading: 66 nmol/l
  • Chart target: 80 nmol/l
  • Difference: 14 nmol/l
  • Amount to take: 1371 IU
  • So: 1371 IU/14 = 100 IU for each number below. Since our goal is 120 nmol/l, (120-66) * 100 = 5,400 IU/day
A reader indicated their level was 18 nmol/l. this becomes (120-18) * 100 = 12,000 IU/day.
Bottom Line
The numbers above are from the literature assuming no complicating factors such as those listed below.
In these cases the dosages may need to be up to 10x more.

Any process resulting in malabsorption of intestinal fat may impair the absorption of vitamin D. In one study, absorption of tritium-labeled (3H)-vitamin D in normal subjects ranged from 62.4% to 91.3% of the initial oral dose (10). In patients with celiac disease, biliary obstruction absorption and chronic pancreatitis, absorption fell to 50%, < 28% and < 18% of the oral dose, respectively. In each case, impaired vitamin D absorption correlated with the degree of steatorrhea. Other conditions in which vitamin D absorption is impaired include liver failure (see below), cystic fibrosis, Crohn’s disease, and gastric bypass. Individuals taking bile acid-binding medications (such as colestyramine and colestipol for hypercholesterolemia) will also have impaired vitamin D absorption
Factors Influencing Vitamin D Status (2011)
The proper process is simple: Get your base line, do the computed amount above for 3 months, measure again. According to the literature you should be at the desired level by then. If you are 10% below, increase the dosage by 10%. This is the only way to estimate the degree of malabsorption.


The first study seems to have made two contradictory hypotheses.

One is that humans supplied the intestinal microbiome with vitamin D and they supplied us with B vitamins.

But another hypothesis (made in the study objectives) is "that vitamin D replacement slowly induced a secondary pantothenic acid deficiency", implying that if you supplement with vitamin D to correct a deficiency, you may also need to supplement pantothenic acid/B vitamins.

The paper also made the suggestion "that the normal intestinal microbiome may have always been the primary source of B vitamins". I would be very interested to see some evidence for this suggestion.
@Lassesen, you took down your site where you talked about boron. Can you publish the study again where it shows raising temperature in cold ME/CFS patients?

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