Vitamin D Is As Bad In Excess As It Is In Deficiency

[faramir]

About a year ago I started experiencing terrible symptoms of worsening inflammation. My joints were painful, my cognition and physical coordination began to decline. Finally my eyes became very bloodshot(scary!). I din't know what was wrong and thought I might be having a relapse of a mild case of chikungunya that I had experienced earlier. By chance, I looked closely at my bottle of vitamin d and noticed it was 10,000mg! I know! It was crazy that I didn't notice it before but there it was. I was taking one daily, very faithfully for probably 4 or 5 months. I immediately began to research the signs of vitamin d toxicity and my symptoms matched. Of course, I stopped taking it immediately and the symptoms began to diminish and finally disappeared. After a few weeks I took a 1000mg dose just to check and the joint pain came back that day! Knowing that it's stored in the body, I've been hesitant to take anymore for now. I may retest taking 1000mg at a later time.

I have been applying Ray Peat's advice for about 6 years now. Included in my supplementation regime was taking 1000mg of Vitamin D3 daily, along with my vitamin e, aspirin and k.

I just wanted to share my experience as an anecdote, but I found some info that seems to back my experiences:

How A Vitamin D Test Misdiagnosed African-Americans

Here's a section from the article:
The 25-hydroxy form is tightly bound to a protein, and as a result, bone cells, immune cells and other tissues that need vitamin D can't take it up. It has to be converted by the kidneys into a form called 1,25-dihydroxyvitamin D.

For Caucasians, blood levels of 25-hydroxyvitamin D are a pretty good proxy for how much of the bioavailable vitamin they have. But not for blacks.


HEALTH
Medical Panel: Don't Go Overboard On Vitamin D
That's because blacks have only a quarter to a third as much of the binding protein, Thadhani says. So the blood test for the 25-hydroxy form is misleading. His study finds that because of those lower levels of the protein, blacks still have enough of the bioavailable vitamin, which explains why their bones look strong even though the usual blood tests say they shouldn't.

"The conclusion from this study is that just because your total levels are low, it doesn't mean we need to replace vitamin D" using supplements, Thadhani says. The study was published Wednesday in the New England Journal of Medicine.

i meant iu"s not mg, sorry

 

[Platinum]

wow, I converted my 87 ng/mL into nmol/L and got 217!

So I have a question, since the study says 50-60 nmol (and 60 is 24ng/mL) was associated with lowest mortality, how did we end up believing at least 50 ng/mL was ideal? And, couldn't this partly be explained by the low intakes of K2 in the general population? Obviously high D3 without K2 can cause calcification, but K2 prevents that.

 

[Giraffe]

"...RESULTS: During follow-up (median, 3.07 yr), 15,198 (6.1%) subjects died. A reverse J-shaped association between serum level of 25(OH)D and mortality was observed. A serum 25(OH)D level of 50-60 nmol/liter was associated with the lowest mortality risk. Compared to 50 nmol/liter, the hazard ratios (95% confidence intervals) of all-cause mortality at very low (10 nmol/liter) and high (140 nmol/liter) serum levels of 25(OH)D were 2.13 (2.02-2.24) and 1.42 (1.31-1.53), respectively. Similarly, both high and low levels of albumin-adjusted serum calcium and serum PTH were associated with an increased mortality, and secondary hyperparathyroidism was associated with higher mortality (P < 0.0001)."

There is a letter to the editor regarding this study, which says that the J-shaped 25-hydroxyvitamin D concentration-cardiovascular disease mortality relation is very likely due to starting vitamin D supplementation late in life

 

[haidut]

There is a letter to the editor regarding this study, which says that the J-shaped 25-hydroxyvitamin D concentration-cardiovascular disease mortality relation is very likely due to starting vitamin D supplementation late in life

Interesting, thanks. It seems that now even the Endocrine Society recommends about 2,000 IU vitamin D3 daily, which matches with Ray's recent interviews mentioning the Vitamin D Council recommendations of 2,000 - 3,000 IU daily. Given that they recently revised the upper limit for TSH to be at 3.5, little by little medicine quietly aligns with Peat.
"...So far, there is little evidence for a U- or J-shaped 25(OH)D concentration-health outcome relation for either CVD incidence or all-cause mortality rate based on meta-analyses of observational studies (6, 7). Thus, it appears safe to follow the guidelines of The Endocrine Society for a daily vitamin D3 requirement of 1500–2000 IU/d or upper limit of 4000 IU/d"

 

[Agent207]

There is a letter to the editor regarding this study, which says that the J-shaped 25-hydroxyvitamin D concentration-cardiovascular disease mortality relation is very likely due to starting vitamin D supplementation late in life

Good point. I wonder when people will learn to watch out about studies of vitD levels done through d3 supplements. It has NOTHING to do with levels from uvb. Even good initial feelings from oral d3 could be by immunosuppressive effect.

The body counts on several feedback systems to fine tuning metabolites levels for homeostasis. Forcing d3 levels by brute force is increasing the risk for a mess; the higher the dose and longer term, the bigger the chances for it.

Obviously the supplement industry is taking profit from this generalized situation caused by lack of proper sunlight exposure.

 

[Giraffe]

Good point. I wonder when people will learn to take care about studies of vitD levels done through d3 supplements.

You have not read the letter.

My explanation for the J-shaped relation is that those with high 25(OH)D concentrations very likely started to take vitamin D supplements late in life. Two papers from the JCEM support my explanation (2, 3). Cross-sectional studies of frailty were conducted on both elderly men and women in the United States. For men, the odds ratio of the baseline frailty score decreased monotonically from a 25(OH)D concentration of 4 to 58 ng/mL (2). However, for women, the odds ratio of baseline frailty score decreased from 6 to 24 ng/mL then increased from 24 to 60 ng/mL (3). The most likely explanation for the disparate findings is that women in the United States are much more likely to be advised by their physicians to start taking vitamin D after about age 50 years than are men. Starting so late in life cannot erase the adverse effects of low 25(OH)D concentrations earlier in life related to many adverse health conditions that take years to develop.

 

[Agent207]

You have not read the letter.

Yes I did.

Why so the different outcomes between 50nmol/L group and the 140nmol/L one? Did the 50nmol group have proper 25OH levels during early life, while the 140nmol group didn't?

 

[Giraffe]

Why so the different outcomes between 50nmol/L group and the 140nmol/L one? Did the 50nmol group have proper 25OH levels during early life, while the 140nmol group didn't?

It's the patients at high risk that are advised to supplement vitamin D?

 

[WestCoaster]

Isn't one of the functions (or sole function) of Vitamin D to pull calcium from the stomach and place it in the blood? So if this is the case, then obviously having too much vitamin D will place too much calcium in the blood possibly causing calcification issues somewhere. But in order for that calcium to be used as needed, you need some level of PUFA to make it happen (hence the Omega 6/3 ratio. Some fat is needed. So if this is indeed how it works, for one to follow a low or very low PUFA diet, they better go easy on the calcium and vitamin D supplements, or perhaps risk calcification. Perhaps this is why we see in real milk (meaning milk that hasn't been skimmed of any fat), contain high amounts of calcium, vitamin D, and fat.

It's kind of interesting to think about.

 

[Waynish]

I don't have time to read this thread now, but it seems implied that this is about supplemental Vitamin D. I don't think this can happen being in the sunlight - which has different metabolic pathways of production anyway. Therefore, that's the pathway - with necessary precautions - that should be promoted for the increase of the 25-hydroxy vitamin D indicator.

 

[Peater Piper]

It may still be possible to make too much D from sunlight alone. There was the Israeli lifeguard study where their serum D was in the 50's ng/ml, and they had a 20x higher risk of kidney stones than the general population.

 

[InChristAlone]

It may still be possible to make too much D from sunlight alone. There was the Israeli lifeguard study where their serum D was in the 50's ng/ml, and they had a 20x higher risk of kidney stones than the general population.

I don't know about that, that would imply the body just keeps making vitamin D when exposed to too much sun. I think our body is more intelligent than that.

 

[johnwester130]

It needs vitamin k2.

5 drops k2 on the wrist

1 drop vitamin d on the wrist

liver for vitamin a

 

[Amazoniac]

Vitamin D, Essential Minerals, and Toxic Elements: Exploring Interactions between Nutrients and Toxicants in Clinical Medicine

"One point of note is that adequate 25(OH)D3 is associated with improved absorption of essential elements including calcium, magnesium, iron, phosphate, zinc, and copper [12]. What has largely been forgotten, however, is that higher levels of 25(OH)D3 have been linked to enhanced absorption of toxic elements such as aluminum, cadmium, cobalt, and lead as well as radioactive isotopes including cesium and radioactive strontium [12]."

"It is also well recognized that bioaccumulation of such toxic metals in turn appears to disrupt physiological functioning of vitamin D within the body. For example, accrual of lead or cadmium diminishes the activity of vitamin D, by blocking the normal renal synthesis of active 1,25-dihydroxyvitamin D [12]."

"Most toxic elements and compounds tend to sequester in tissues and may not be evident on blood or urine testing [49]. Lead, for example, may be abundant in bone and brain where it tends to accumulate, with potentially little evidence of such accrual with blood or urine testing [50]."

"It is also evident that vitamin D does not act solely in isolation. Impaired vitamin D functioning and insufficient levels of essential minerals can have synergistic and cumulative adverse action on biological function with significant pathophysiological impact. For example, vitamin D metabolism is dependent on sufficient magnesium as a cofactor for vitamin D to bind to its transport protein and for this vitamin to convert into the active form via hydroxylation in renal and hepatic sites [51]. Furthermore magnesium deficiency may upregulate the 24(OH)ase enzyme in the kidney resulting in catabolism of active vitamin D [51]."

"While no more than 800 mg of calcium a day may be required when vitamin D levels are adequate, the typical diet in North America may be inadequate to supply even this limited amount [60]. Furthermore, as is noted in Table 1, toxic metals may impair calcium uptake resulting in deficiency states."

Vitamin D, Essential Minerals, and Toxic Elements: Exploring Interactions between Nutrients and Toxicants in Clinical Medicine

 

[ecstatichamster]

good find.

Ray has said he uses around 1500mg to 2000mg calcium per day I believe.

I think the problem with just D3 is you need all the oil solubles, especially K2...I think high calcium consumption my PROTECT against uptake of the bad metals mentioned in this review.

 

[raypeatclips]

The study said that vitamin D levels above 100nmol/L were associated with higher risk from CVD and stroke. I don't have access to the study so I don't know what the mortality was from in the low ranges. Presumably, the higher than optimal vitamin D levels probably caused arterial calcification, and the lower ones increased PTH. The study abstract says both calcium and PTH were factors influencing all-cause mortality. Since low calcium was also associated with mortality, I suspect this is due to kidney disease as it is the main cause of low serum calcium.

http://www.sciencedaily.com/releases/20 ... 105222.htm
A reverse J-shaped association of all-cause mortality with serum 25-hydroxyvitamin D in general practice: the CopD study. - PubMed - NCBI
A Reverse J-Shaped Association Between Serum 25-Hydroxyvitamin D and Cardiovascular Disease Mortality: The CopD Study. - PubMed - NCBI

"...RESULTS: During follow-up (median, 3.07 yr), 15,198 (6.1%) subjects died. A reverse J-shaped association between serum level of 25(OH)D and mortality was observed. A serum 25(OH)D level of 50-60 nmol/liter was associated with the lowest mortality risk. Compared to 50 nmol/liter, the hazard ratios (95% confidence intervals) of all-cause mortality at very low (10 nmol/liter) and high (140 nmol/liter) serum levels of 25(OH)D were 2.13 (2.02-2.24) and 1.42 (1.31-1.53), respectively. Similarly, both high and low levels of albumin-adjusted serum calcium and serum PTH were associated with an increased mortality, and secondary hyperparathyroidism was associated with higher mortality (P < 0.0001)."

This study has confused me. I originally believe your first line was referring to 100 ng/ml which, of course is high, with the current recommendations being 50 ng/ml. But it was referring to nmol/L with 40 ng/ml levels. Surely this can't be higher risk that someone with extremely low vitamin d? Yes the second study says lowest risk was the 70 nmol/L group, (28 ng/ml) What is happening here?

 

[Waynish]

Haven't had time to read it yet... Does this study imply *why* those serum 25(OH)D levels were present? We know D is stored, so isn't it possible that during stress more is used?

 

[Travis]

I think an commonly-overlooked problem with taking vitamin D pills is that you are throwing it directly at the organ most responsive to it—the intestines, the target organ, where vitamin D is normally used to modulate calcium uptake. I read a study showing that topical absorption achieved nearly the same plasma levels, with about the same dose required.

I bought some vitamin D pills in olive oil, and now I'm just putting them on the skin—on the belly. I'm not sure why I chose this location exactly . . .

. ..but it works. I feel better than when I took it orally. It's certainly more natural to have vitamin D percolating through the skin than through the intestines, where it could perhaps cause too great a calcium absorption and throwing-off mineral balance.

I think it's important to make this distinction. This could be the best way to explain why doses far smaller than the summertime daily skin production rate can have side-effects.

Exposing your skin for a short time will make all the vitamin D your body can produce in one day. In fact, your body can produce 10,000 to 25,000 IU of vitamin D in just a little under the time it takes for your skin to begin to burn. ―Vitamin D Council (was it Cannell himself or an anonymous writer? It doesn't say.)

Really? I never felt hypercalcified in July—in the sun, with my 100,000 IU vitamin D sunlight–skin-megadose. But with doses as little as 5,000 IU is feel like an old man with creaky hypercalcified joints (Ohhw! My back.)

 

[ddjd]

Is Vitamin A the best thing for counteracting any excess vitamin D?

 

[kayumochi]

D3 has been nothing but a blessing to me. 110 ng/ml was the highest I recorded and didn't sense any side effects. Years back, when I was deficient, it was one respiratory infection after another ...

BTW, some MS patients are achieving remission with mega high doses of D3.