Be Wary Of Vitamin D Supplementation

[Sourdoughbanana]

By the way, there is a book on Amazon by Jeff Bowles


Tanning is associated with optimal vitamin D status (serum 25-hydroxyvitamin D concentration) and higher bone mineral density | The American Journal of Clinical Nutrition | Oxford Academic

half an hour per week, now that's way too much IMO. 5 minutes do the job.

https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2133.2011.10697.x

 

[lacto man]

I know the source might not be the best (seems to come from the Paleo/Primal community). Found it an interesting read nonetheless:
Why I don’t take vitamin D supplements

The main argument being that oversupplementation of any nutrient/vitamin can desensitize the body in its capacity to generate its own.

I find the theory interesting because increasingly I see frequent eating and overeating as a stress for the body. Eating all day long requires the body to work at digesting food more frequently. The organs are kept busy defending against outside stressors (food) and trying to restore balance after the nutrient intake. There might not be much time left for the repair work to take place.

Your body doesn't produce Vitamin D. It MUST be consumed.

 

[somuch4food]

Vitamin D is a vitamin A antagonist. Vitamin A is essential in ceruloplasmin generation. Ceruloplasmin is essential to control Iron and the oxidative stress (chronic inflammation) it generates.

Interesting article and same view on iron as Ray Peat:
MAG-pie Alert!… #13 TOXICITY OF IRON: If the Sun is the “center” of our Universe, I’m coming to regard Ceruloplasmin as the “Sun” of our universe of metabolic activity.

 

[somuch4food]

Your body doesn't produce Vitamin D. It MUST be consumed.

What about vitamin D synthesis from the sun?

BTW, vitamin D is an hormone. That is enough to make me cautious of taking hugh dose of it.

 

[Zpol]

Dr. Peat has recommended that I try to attain 50 and 80 ng/ml Vitamin D (blood serum). I have severe autoimmune disease and intestinal inflammation, I am trying to determine the best supplement amount plus UVB exposure combination. I came across this excerpt posted by @Amazoniac ...

"Of clinical importance, the cellular phosphorus burden induced by excessive vitamin D supplementation might contribute to the cellular pathology, even when serum vitamin D levels show hypovitaminosis D status. A wide range of cellular pathology is attributed to cellular phosphorus burden, including necrosis, apoptosis and senescence [47-53]. Available evidences suggest that phosphorus toxicity is a stealth biochemical stress factor that needs greater recognition by researchers and nutrition boards [54]."

This is of great concern to me since I already have high phosphorus and slightly high blood calcium, plus have symptoms of kidney/gallbladder stones and magnesium deficiency. The majority of calcium I get is via supplement (can't have dairy as it flares up psoriasis).
In fact, too high phosphorus to Calcium ratio is one of the biggest underlying issues in degenerative disease today, and Dr. Peat discusses it frequently. There appears to be a giant contradiction here.

@burtlancast I haven't heard of the Coimbra protocol till today and I'm looking into it, but one thing I see is that the older testimonials are only about 5 yrs old and although they do seem miraculous, it seems the problems of too much Vit. D supplementing is cumulative and may take many more years to affect the organs and by then it may be too late to fix the damage. Here's more from the abstract @Amazoniac posted...

"It is likely that calcium and phosphorus dysregulation, induced by exogenous vitamin D supplementation, may lead to tissue and organ damages, even without developing hypervitaminosis D. It is needed to be emphasized that, because of tight homeostatic control of calcium and phosphorus, when hypercalcemia and/or hyperphosphatemia is apparent following vitamin D supplementation, the process of tissue and/or organ damage might already have been started."​

Here's the link to the abstract again...
Can adverse effects of excessive vitamin D supplementation occur without developing hypervitaminosis D?

I can only access the abstract so I imagine there's more information that would be relevant.

@burtlancast Have you any information on if the Coimbra protocol addresses this possibility? Or can you direct me to any helpful information on this? I'm trying to be as informed as possible on this.

Edit... I suppose the blood tests he recommends (PTH, phosphorus, etc) would determine if the the imbalance is occurring, but what if someone already has high PTH and hypercalcemia, calcification. I guess this where you'd have to see a certified doctor, I can't find anything more on the topic beside what was already discussed on this forum.

 

[burtlancast]

@burtlancast I haven't heard of the Coimbra protocol till today and I'm looking into it, but one thing I see is that the older testimonials are only about 5 yrs old and although they do seem miraculous, it seems the problems of too much Vit. D supplementing is cumulative and may take many more years to affect the organs and by then it may be too late to fix the damage. Here's more from the abstract @Amazoniac posted...

"It is likely that calcium and phosphorus dysregulation, induced by exogenous vitamin D supplementation, may lead to tissue and organ damages, even without developing hypervitaminosis D. It is needed to be emphasized that, because of tight homeostatic control of calcium and phosphorus, when hypercalcemia and/or hyperphosphatemia is apparent following vitamin D supplementation, the process of tissue and/or organ damage might already have been started."​

Here's the link to the abstract again...
Can adverse effects of excessive vitamin D supplementation occur without developing hypervitaminosis D?

I can only access the abstract so I imagine there's more information that would be relevant.

@burtlancast Have you any information on if the Coimbra protocol addresses this possibility? Or can you direct me to any helpful information on this? I'm trying to be as informed as possible on this.

Edit... I suppose the blood tests he recommends (PTH, phosphorus, etc) would determine if the the imbalance is occurring, but what if someone already has high PTH and hypercalcemia, calcification. I guess this where you'd have to see a certified doctor, I can't find anything more on the topic beside what was already discussed on this forum.

Dr Coimbra has 15 years of practice in high Vit D therapy: he hasn't lost a single patient yet to my knowledge.
Some of them have been taking these high dosages for that long.

This is a therapy strictly for auto immune diseases and never/ever to be taken on your own: otherwise healthy people only need 10.000 UI/day.

There are now 120 doctors in all the parts of the world that have treated 4500 patients.

 

[Zpol]

Dr Coimbra has 15 years of practice in high Vit D therapy: he hasn't lost a single patient yet to my knowledge.
Some of them have been taking these high dosages for that long.

This is a therapy strictly for auto immune diseases and never/ever to be taken on your own: otherwise healthy people only need 10.000 UI/day.

There are now 120 doctors in all the parts of the world that have treated 4500 patients.

Indeed that is impressive, and not to be discounted. I'm going to bring this information to my FM doctor next time i see him.
I am trying to reconcile in my brain, Dr. Peat's recommendations on calcium intake and the clear benefit of high Vit D for treatment of AI disease.
This thread has provided lots of good information on the topic however I still don't understand completely. Vitamin D resistance... is certainly a new one I'll have to look into.
I'm aware of Dr. Coimbra's stance on lower calcium intake in relation to Vit. D but I'd be interested to know Dr. Peat's ideas on the same topic and vice versa.

... A thought... perhaps using Calcium Acetate concurrently with higher Vit. D intake would help keep phosphate low.

 

[HDD]

I posted this in another thread but thought it might be good to have it here. Ray Peat sent this to me when I was inquiring about vitamin D.

J Steroid Biochem Mol Biol. 2016 Dec 21. pii: S0960-0760(16)30356-9.

Results of daily oral dosing with up to 60,000 international units (iu) of vitamin D3 for 2 to 6 years in 3 adult males.

McCullough P1, Amend J2.

In the 1930's and 1940's, vitamin D was reported to be an effective treatment for a number of diseases, including asthma, psoriasis, rheumatoid arthritis, rickets and tuberculosis. High doses were used, 60,000 to 300,000 IU a day for asthma, and 200,000 to 600,000 IU a day for rheumatoid arthritis. Toxicity from hypercalcemia occurred after prolonged oral dosing with these supraphysiologic doses. Assays for measuring vitamin D in the blood were not available, and blood levels of vitamin D associated with hypercalcemia were unknown. A 2011 report on vitamin D toxicity showed that hypercalcemia resolved when 25-hydroxyvitamin D (25OHD) blood levels dropped below 400ng/ml in 2 patients with blood levels ranging from 645ng/ml to 1220ng/ml after accidental ingestion of massive doses of vitamin D. We now know that vitamin D is made in the skin in amounts ranging up to 25,000 IU a day with exposure to UVB radiation. There is little data on the safety and blood levels of 25OHD and calcium after prolonged daily intake of amounts of vitamin D in this range. In this report, one subject took increasing daily doses of vitamin D3 for 6 years starting in April 2009: 6500 IU for 6 months; increasing to 10,000 IU for 13 months; 20,000 IU for 24 months; 40,000 IU for 12 months; 50,000 IU for 10 months, and 60,000 IU since October 2014. 25OHD blood levels were 28, 81, 204, 216, 225, 166, and 218ng/ml. Subject 2 began 10,000 IU in Nov 2011, increased to 20,000 IU in Feb 2014, 25,000 IU in June 2014, and 30,000 IU in Oct 2014, and then decreased to 20,000 IU in June 2015. 25OHD blood levels were 96.6, 161.1 and 106.9ng/ml. He reported marked clinical improvement in his asthma. Subject 3 started on daily 10,000 IU in Sept 2013, increasing to 20,000 IU on Nov 2013. 25OHD blood levels were 31.4, 102, 164, 148, and 143ng/ml. No one developed hypercalcemia or any adverse events. The major finding of this case series is prolonged daily dosing of vitamin D3 with doses of 10,000 to 60,000 IU was safely tolerated.

 

[burtlancast]

W-O-W.

 

[Zpol]

I posted this in another thread but thought it might be good to have it here. Ray Peat sent this to me when I was inquiring about vitamin D.

J Steroid Biochem Mol Biol. 2016 Dec 21. pii: S0960-0760(16)30356-9.

Results of daily oral dosing with up to 60,000 international units (iu) of vitamin D3 for 2 to 6 years in 3 adult males.

McCullough P1, Amend J2.

In the 1930's and 1940's, vitamin D was reported to be an effective treatment for a number of diseases, including asthma, psoriasis, rheumatoid arthritis, rickets and tuberculosis. High doses were used, 60,000 to 300,000 IU a day for asthma, and 200,000 to 600,000 IU a day for rheumatoid arthritis. Toxicity from hypercalcemia occurred after prolonged oral dosing with these supraphysiologic doses. Assays for measuring vitamin D in the blood were not available, and blood levels of vitamin D associated with hypercalcemia were unknown. A 2011 report on vitamin D toxicity showed that hypercalcemia resolved when 25-hydroxyvitamin D (25OHD) blood levels dropped below 400ng/ml in 2 patients with blood levels ranging from 645ng/ml to 1220ng/ml after accidental ingestion of massive doses of vitamin D. We now know that vitamin D is made in the skin in amounts ranging up to 25,000 IU a day with exposure to UVB radiation. There is little data on the safety and blood levels of 25OHD and calcium after prolonged daily intake of amounts of vitamin D in this range. In this report, one subject took increasing daily doses of vitamin D3 for 6 years starting in April 2009: 6500 IU for 6 months; increasing to 10,000 IU for 13 months; 20,000 IU for 24 months; 40,000 IU for 12 months; 50,000 IU for 10 months, and 60,000 IU since October 2014. 25OHD blood levels were 28, 81, 204, 216, 225, 166, and 218ng/ml. Subject 2 began 10,000 IU in Nov 2011, increased to 20,000 IU in Feb 2014, 25,000 IU in June 2014, and 30,000 IU in Oct 2014, and then decreased to 20,000 IU in June 2015. 25OHD blood levels were 96.6, 161.1 and 106.9ng/ml. He reported marked clinical improvement in his asthma. Subject 3 started on daily 10,000 IU in Sept 2013, increasing to 20,000 IU on Nov 2013. 25OHD blood levels were 31.4, 102, 164, 148, and 143ng/ml. No one developed hypercalcemia or any adverse events. The major finding of this case series is prolonged daily dosing of vitamin D3 with doses of 10,000 to 60,000 IU was safely tolerated.

Nice! Thanks! Although I do know several people with autoimmune disease who are on Vit D therapy who do have hypercalcemia. My friend who has MS is taking huge doses of vitamin d as prescribed by her VA doctor and she is struggling with hypercalcemia rather significantly.
With this information I think we can conclude that high Vit D supplementation does not cause the calcium to phosphate disregulation, rather something else is causing it and also needs to be addressed (i.e. estrogen, PUFA, mineral imbalance, etc, you know usual suspects).

 

[HDD]

@Zpol I was dx with MS in 1988 and I currently have no symptoms. I have baked in the sun consistently since I was aware of the vitamin D connection to MS. However, my worst symptoms were hormonally related. Most likely high estrogen and low thyroid. Is your friend with MS following any of Peat’s other recommendations for MS?

 

[Zpol]

@Zpol I was dx with MS in 1988 and I currently have no symptoms. I have baked in the sun consistently since I was aware of the vitamin D connection to MS. However, my worst symptoms were hormonally related. Most likely high estrogen and low thyroid. Is your friend with MS following any of Peat’s other recommendations for MS?

She does not follow all of Dr. Peats suggestions, some but not all. Her biggest problem now is also estrogen, and dealing with no gallbladder. We live in Wisconsin and getting enough sunlight is a big issue.

 

[HDD]

She does not follow all of Dr. Peats suggestions, some but not all. Her biggest problem now is also estrogen, and dealing with no gallbladder. We live in Wisconsin and getting enough sunlight is a big issue.

Considering I live and grew up in Florida near the beach, I didn’t fit the geographical profile for MS. Peat has said, iirc, thyroid and vitamin D are parallel? I believe my underlying cause was hypothyroidism and getting a lot of sun probably was a huge factor in the course of my illness. The only other thing that triggered serious symptoms besides the estrogen surge at ovulation, was the Paleo diet, when I consumed a lot of pork and pork fat that I had avoided for years.

 

[Zpol]

thyroid and vitamin D are parallel

hmm.. I don't know if I understand all the implications of this but I do believe thyriod supp's could help my friend but the VA will only give her T4. She doesn't eat pork but she eats out at restaurants a lot so I know she's getting too much PUFA.
She was exposed to high amounts of carbon monoxide in the Navy, I think it was the ultimate trigger.
(It's sad the health care our veterans get)

 

[HDD]

This is the clip where he says thyroid and vitamin D are parallel.

 

[InChristAlone]

I've been Dr. Garrett Smith brainwashed. I haven't supplemented it since he came out saying it raises calcium in the hair thus slowing metabolism (and mine shows high calcium). He is also now completely against all forms of vitamin A because of Grant.

 

[Amazoniac]

Are you actually getting paid to post this by any chance? Perhaps you work for Zeus, which in turn works for Michael Holick, which in turn works for the vitamin D industry, which in turn is run by someone with a villain moustache that profits on conventional medical treatments, which Hugh happens to be involved, with finally both of them working for Mon and santo.

Ahaa! You may all be thinking that I have wented insane there, but fasting your seat belts for the following:

Glyphosate | VitaminDWiki

• Glyphosate [glahy-fos-eyt] is associated with many health problems
• Glyphosate reduces Vitamin D by both reducing CYP27A1 gene and reducing many minerals needed by Vitamin D - VitaminDWiki suspects that Glyphosate is responsible for 10-20% of the decreased Vitamin D getting to cells
• Glyphosate is the only acknowledged active component of Roundup - However, Roundup is 125X more deadly to human cells than Glyphosate
• Many countries now ban Glyphosate including all of the European Union as of Oct 25, 2017 - It is still not banned in the US
• A crop can be called organic even if Roundup was used to dry it wheat, oats, beans, lentil, sunflower, soy, rapeseed oil, etc
• You can compensate for Glyphosate by increasing your intake of Vitamin D, Magnesium, Boron, and Omega-3

--
Vitamin D (978-0-12-381978-9) - David Feldman

Chapter 72 []
Hypercalcemia Due to Vitamin D Toxicity​

"The most common etiology of vitamin D toxicity is inadvertent or improper oral use of pharmaceutical preparations. Excessive ingestion of vitamin D (usually greater than 10 000 IU daily; see below) can cause vitamin D intoxication that is recognized by markedly elevated levels of 25(OH)D (usually >150 ng/ml) in association with levels of 1,25(OH)2D that are only slightly elevated. Hyperphosphatemia typically accompanies the hypercalcemia [1-3]. The hyperphosphatemia can be a clue to the etiology of the hypercalcemia as due to vitamin D toxicity since PTH and PTHrP-related disorders usually are associated with reduced serum phosphate or frank hypophosphatemia."

"Hypervitaminosis D has been associated with drinking milk when inadvertently fortified with massive concentrations of vitamin D. One investigation of eight patients manifesting symptoms of nausea, vomiting, weight loss, hyperirritability, or failure-to-thrive revealed markedly elevated mean concentrations of 25(OH)D of 293 +- 174 ng/ml [3]. Analysis of the milk production facility at the local dairy revealed excessive vitamin D fortification of milk with up to 245 840 IU per liter (232 565 IU of vitamin D3 per quart). Usual fortification of milk in the USA and Canada is 400 IU per quart. Milk is not fortified with vitamin D in most other parts of the world. Generally, milk is the only dairy product that is fortified with vitamin D in the USA. Some yogurts in the USA, however, are now fortified with vitamin D. In addition to milk, vitamin D fortification of natural foods includes certain breakfast cereals, pasta, baked goods, fats, and orange juice [11]."

"[..]vitamin D supplementation in PHPT [Primary Hyperparathyroidism] seems to be well tolerated and does not lead, in general, to worsening hypercalcemia or hypercalciuria."

"Two small well-conducted clinical trials by Heaney et al. [31] and Barger-Lux et al. [32] showed that vitamin D3 10 000 IU daily for 8 and 20 weeks, respectively, did not cause an increase in serum calcium or any adverse effects in the combined cohort of 26 healthy men. In these subjects, mean 25(OH)D levels rose to 85 ng/ml (n=10) and 88 ng/ml (n=16) in the two studies [!!], respectively."

"Individuals manifest wide variations both in their response to hypercalcemic doses of vitamin D and in the duration of the effect. This variation in individual responsiveness might reflect differences in intestinal absorption and vitamin D metabolism, in the concentration of free vitamin D metabolites, in the rate of degradation of the metabolites and conversion to inactive metabolites, and in the capacity of storage sites for 25(OH)D [34]. Factors that enhance susceptibility to vitamin D toxicity and hypercalcemia include increased dietary calcium intake, reduced renal function, coadministration of vitamin A, and granulomatous disorders such as sarcoidosis that render subjects more sensitive to vitamin D (see Chapter 45) [2]. Hypercalciuria in hypervitaminosis D usually presents earlier than hypercalcemia, but it is easily missed for the obvious reason that urinary calcium is not routinely measured."

"Vitamin D toxicity may occur in patients due to any one of the three forms of vitamin D, namely, the vitamin D parent compound, 25(OH)D, or 1,25(OH)2D. Multiple factors may influence susceptibility to vitamin D toxicity and include the concentration of the vitamin D metabolite itself, vitamin D receptor (VDR) number, activity of 1a-hydroxylase, the metabolic degradation pathway, and the capacity of the vitamin-D-binding protein (DBP). Vitamin D2 or D3 toxicity is more difficult to manage than toxicity due to its metabolites 25(OH)D or 1,25(OH)2D. In part, this is due to the extensive lipid solubility of the parent compound in liver, muscle, and fat tissues and corresponding large storage capacity. As a result, the half-life of vitamin D ranges from 20 days to months. In contrast, the biological half-life of the less lipophilic compound 25(OH)D is shorter, approximately 15 days [175]. The biological half-life of the least lipophilic compound 1,25(OH)2D, is much shorter, approximately 15 hours [176]. In general, duration of toxicity is related to the half-life of the vitamin D compound. Thus, the hypercalcemia of parent vitamin D overdose can theoretically last for as long as 18 months, long after dosing is discontinued, because of its slow release from fat deposits. Overdosage of 25(OH)D can persist for weeks also, but excessive 1,25(OH)2D toxicity is more rapidly reversed because 1,25(OH)2D is not stored in appreciable amounts in the body [80]."

"Unlike 1,25(OH)2D whose production is tightly regulated in the kidney, the production of 25(OH)D is not tightly controlled by the liver. The high capacity for 25-hydroxylation of vitamin D in the liver as well as loose regulation at this site allows for massive amounts of 25(OH)D to be generated from large amounts of vitamin D. Thus, excessive concentrations of 25(OH)D are typically measured in vitamin D toxicity. Hypercalcemia appears to result only when 25(OH)D concentrations are consistently above 150 ng/ml (375 nmol/l) in normal individuals [2,178]. As would be expected, PTH levels are suppressed in this form of hypercalcemia. In the setting of toxicity due to overadministration of 1,25(OH)2D3, the active metabolite itself is responsible for the hypercalcemia [179]."

"Regulation of cellular VDR numbers is believed to be an important mechanism by which cellular responsiveness to 1,25(OH)2D is modulated, because the biological activity of 1,25(OH)2D is proportional both to tissue VDR number and concentration of 1,25(OH)2D. Increased VDR concentrations imply enhanced tissue responsiveness to 1,25-dihydroxyvitamin D, whereas decreased receptor numbers indicate reduced tissue responsiveness."

"Goff et al. [183] also demonstrated that endogenously produced 1,25(OH)2D3 has a different effect than exogenous administration of 1,25(OH)2D3 on tissue VDR content. Rats fed a calcium-restricted diet resulting in “nutritional” hyperparathyroidism achieved a similar increase in endogenous 1,25(OH)2D3 concentration as rats administered exogenous 1,25(OH)2D3. However, calcium-restricted rats failed to upregulate VDR content in the duodenum or kidney, presumably a consequence of the negative control of VDR by PTH [184]."

"Evidence suggests that in parent vitamin D toxicity, target tissues are responding to high concentrations of 25(OH)D, not 1,25(OH)2D. Concentrations of 1,25(OH)2D are typically only slightly increased, if at all. The hypercalcemia is due to the effects of pharmacologically high levels of 25(OH)D, even though in physiological settings, 25(OH)D is relatively weak. At high concentrations, 25(OH)D can compete for binding at VDR sites, and thereby produce biological effects similar to those of 1,25(OH)2D on intestine and bone [185]. Beckman and colleagues [186] suggested, furthermore, that hypervitaminosis D, like excessive exogenous 1,25(OH)2D, is associated with homologous upregulation of intestinal VDR. Their investigation demonstrated that supraphysiological amounts of vitamin D2 or vitamin D3 administered to rats at doses of 25 000 IU daily for 6 days resulted in increasing plasma 25(OH)D concentrations with significant upregulation of intestinal VDR concentration and hypercalcemia. Plasma 1,25(OH)2D levels were not altered substantially."

"Some investigators have suggested that toxic effects of excessive concentrations of 25(OH)D may result from PTH suppression and downregulation of 1a-hydroxylase with increased concentrations of 25(OH)D. PTH and 1,25(OH)2D have known reciprocal actions on 1a-hydroxylase and 24-hydroxylase activities. PTH stimulates 1a-hydroxylase activity and downregulates 24-hydroxylase activity; 1,25(OH)2D, on the other hand, downregulates 1a-hydroxylase activity and stimulates 24-hydroxylase activity."

Refer to this:
Be Wary Of Vitamin D Supplementation​

"Beckman and colleagues [187] studied the effects of an excess of vitamin D3 and dietary calcium restriction on tissue 1a-hydroxylase and 24-hydroxylase activity in rats. Four groups of rats with different dietary calcium and vitamin D3 concentrations were studied (normal calcium, NC; low calcium, LC; and the excess vitamin D groups with normal or low calcium, NCT and LCT). The data showed that in the setting of a calcium-restricted diet, a nutritional hyperparathyroidism ensued. Under conditions of excess vitamin D3 at doses of 75 000 IU per week and on a calcium-restricted diet, elevations in PTH facilitated the elimination of 25(OH)D3 through its metabolism to 1,25(OH)2D3 and/or degradation to 24,25(OH)2D3. The elevation in PTH was accompanied by increased activation of renal 1a-hydroxylase activity, lower concentrations of 25(OH)D3, increased activation of intestinal 24-hydroxylase activity, and lower renal VDR content compared to the normal calcium group. In contrast, the normal calcium diet in the vitamin D3 excess group contributed to the toxicity by virtue of suppressed PTH concentrations resulting in downregulation of renal 1a-hydroxylase and decreased 24-hydroxylase activity, and, thus, higher 25(OH)D3 concentrations. On the other hand, dietary calcium restriction in the setting of vitamin D3 excess seemed to be protective, providing less biological stimulation due to higher PTH concentrations with reduced VDR, increased activation of both 1a-hydroxylase and 24-hydroxylase activities, greater reductions in 25(OH)D3 concentrations, and lower concentrations of total calcium resulting in a less toxic state. So the low-calcium diet protects, not only by contributing to less hypercalcemia, but also by facilitating metabolic pathways of vitamin D inactivation."

Lack of calcium is so effective in elevating P and T and H that it prevents (to a certain degree) its suppression from massive vit D doses.​

"Others have proposed that inhibition of the enzymes that degrade the vitamin D metabolites may have a role in the pathogenesis of hypervitaminosis D. 1,25(OH)2D is a known regulator of its own catabolism and an inhibitor of its synthesis. In the kidney, intestine, and other targets 1,25(OH)2D induces the enzyme 24-hydroxylase. This enzyme initiates a catabolic cascade that ultimately causes side chain oxidation, cleavage, and metabolic elimination of both 1,25(OH)2D and 25(OH)D, and it accounts for 35-40% of the catabolism of 1,25(OH)2D [188]. The remainder of the metabolic degradation is due to other side chain oxidations and biliary clearance. Reinhart and Horst [189] initially proposed that blunting of the catabolic pathway of 1,25(OH)2D3 with high concentrations of 24,25(OH)2D3 in rat cells would competitively inhibit further inactivation of 1,25(OH)2D3, resulting in an accumulation of 1,25 (OH)2D3 and toxicity."

"24-Hydroxylation is important in the inactivation of both 1,25(OH)2D3 and 25(OH)D3, and in the kidney is largely regulated inversely by 1a-hydroxylation [190]."

"Through inhibition of intestinal 24-hydroxylase activity, calcitonin could be associated with reduced turnover and catabolism of 25(OH)D3, thereby potentiating its toxicity. Thus, increased expression of 24-hydroxylase activity in cases of pharmacological amounts of 25(OH)D3 may be an important mechanism to counteract vitamin D toxicity."

"The clinical manifestations of vitamin D toxicity result from hypercalcemia and reflect the essential role of calcium in many tissues and targets, including bone, the cardiovascular system, nerves, and cellular enzymes. Initial signs and symptoms of hypervitaminosis D may be similar to other hypercalcemic states and include generalized weakness and fatigue. Central nervous system features may include confusion, difficulty in concentration, drowsiness, apathy, and coma [202]. Neuropsychiatric symptoms include depression and psychosis, which resolve following improvement of the hypercalcemia."

"Hypercalcemia can affect the gastrointestinal tract and cause anorexia, nausea, vomiting, and constipation. It can also induce hypergastrinemia. There is no evidence that peptic ulcers are more common in any other form of hypercalcemia. Rarely, pancreatitis may be a presentation of either acute or chronic hypercalcemia."

Some of these are very common in Coimbra's protocol.​

"In the heart, hypercalcemia may shorten the repolarization phase of conduction reducing the Q-T interval on the electrocardiogram (EKG). EKG changes in vitamin D toxicity have been mistaken for myocardial ischemia [203]. A more accurate EKG indication of the level of hypercalcemia is the Q-T interval corrected for rate. Bradyarrhythmias and first-degree heart block have been described, but are rare. Hypercalcemia may potentiate the action of digitalis on the heart [204]."

"Kidney function is affected because high concentrations of calcium alter the action of vasopressin on the renal tubules. The net result is reduced urinary concentrating ability and a form of nephrogenic diabetes insipidus. This usually presents as polyuria, but rarely is the volume as high as that associated with central diabetes insipidus. Symptoms may include polydipsia, which is an expected consequence of polyuria. Hypercalciuria is one of the earliest signs of vitamin D toxicity and precedes the occurrence of hypercalcemia."

"The initial hypercalciuria may be ameliorated as renal failure progresses because of reduced calcium clearance. The pathophysiology of hypercalcemia can be rapidly worsened when dehydration develops. When reduced renal blood flow occurs, less calcium is presented to the renal glomerulus, and hypercalcemia can rapidly progress. Renal impairment from the hypercalcemia is reversible if of short duration. Chronic, uncontrolled hypercalcemia can lead to deposition of calcium phosphate salts in the kidney and permanent damage with eventual nephrocalcinosis. In an investigation of vitamin-Dinduced nephrocalcinosis, Scarpelli and colleagues [205] noted that cell damage, specifically in mitochondria, preceded intracellular calcium deposition. The hypercalcemia induced in rats by excessive vitamin D administration caused mitochondrial swelling, cell injury, and subsequent calcification."

"Ectopic soft tissue calcification can be a particular problem in hypervitaminosis D. The tendency towards soft tissue calcification is compounded by the combination of hypercalcemia and hyperphosphatemia, often exceeding the solubility product of the two ions [206-208]. In rats exposed to excessive vitamin D, Hass and colleagues demonstrated that the pathological processes of vitamin D toxicity were related to dosage, length of time between doses, and duration of exposure [209]."

"Bone mineral density can be decreased due to excessive bone resorption [207,212], changes which can be reversed when vitamin D levels return to normal [213]."

"A reduction in oxalate intake [in these states] may [] be advisable, so as to prevent an increase in oxalate absorption and hyperoxaluria, which may increase the risk of kidney stone formation, despite a reduction in urinary calcium excretion [215]."

"Glucocorticoids have proved to be particularly effective in vitamin D intoxication, granulomatous diseases, and lymphoma (see also Chapter 45). The precise mechanism of action of glucocorticoids in calcium homeostasis is not known. Nonetheless, they are useful because they (1) directly inhibit gastrointestinal absorption of calcium by decreasing the synthesis of calcium-binding protein (calbindin-D) and may downregulate intestinal VDR [215c] and decrease active transcellular transport [216], (2) increase urinary excretion of calcium [217], and (3) may alter hepatic vitamin D metabolism to favor the production of inactive vitamin D metabolites, resulting in lower concentrations of 25(OH)D [218]. Evidence also suggests that they may increase the degradation of 1,25(OH)2D at the receptor sites [219]. Glucocorticoids may also limit osteoclastic bone resorption [220]. Institution of glucocorticoid therapy results in prompt decline of the circulating 1,25(OH)2D concentrations within 3 to 4 days [80]. Patients with non-hematological malignancies and those with primary hyperparathyroidism do not usually respond to glucocorticoids."​

--
- High-Dose Vitamin D: Helpful or Harmful?
- Is High Dose Vitamin D [Clearly] Harmful?

 

[Zpol]

This is the clip where he says thyroid and vitamin D are parallel.

thanks for the link! I listened the whole broadcast. At the very end Dr Peat really wanted to continue what he was saying about Vit D receptors, the host said they talk more about it on another show. Haven't found that show yet. I'll have to look through the transcripts.

Thanks @Amazoniac ! Wow! In regards Vit D absorbtion, Chris Masterjohn did some research in this area.
He mentions the importance of vitamin K in the process. It's a very interesting presentation on the ''vitamin D paradox" as he calls it.

 

[REOSIRENS]

Dr Coimbra has 15 years of practice in high Vit D therapy: he hasn't lost a single patient yet to my knowledge.
Some of them have been taking these high dosages for that long.

This is a therapy strictly for auto immune diseases and never/ever to be taken on your own: otherwise healthy people only need 10.000 UI/day.

There are now 120 doctors in all the parts of the world that have treated 4500 patients.

I take 20 000ui( vitamin d) almost everyday and don't have problems with it... But I take 25 000 UI of retinol everyday as well

 

[Amazoniac]

All credit to the cool author of 'Vitamin D Wiki'. I don't mean that the person has slow metabolism.

- All-Source Basal Vitamin D Inputs Are Greater Than Previously Thought and Cutaneous Inputs Are Smaller

(the original was edited with red)
nmol/L ÷ 2.5 = ng/mL
Length wasn't specified, higher doses can become a problem over time.​

- Vitamin D and mental health in children and adolescents

(this is not found in the link, it was based on it)
The lower the dose, the more time it takes to catch up.​

- Vitamin D status indicators in indigenous populations in East Africa

Chart by 'Vitamin D Council':