RRM wrote:Kasper wrote:- Serum PTH×25(OH) D levels in 393 healthy adolescent females (12–18 years).
The data suggested that the change in the slope of the plot for serum 25(OH)D from negative to positive occurred at 90 nmol/l.
- Guillemant and colleagues found that when 25(OH) levels fell below 83 nmol/l when assayed using the CPB method, the increase in PTH concentration accelerated
- Chapuy and colleagues [14] reported that in French adults (35–60 years), serum PTH levels were stable at a 25(OH)D concentration of 78 nmol/l (CPB assay)
Ah, this is more like it!
I will look into these studies when i have some time.
Hmm. Found some more info on this issue, and lower levels.
Dose response to vitamin D supplementation in postmenopausal women: a randomized trial.
"[The] RDA [is] defined as meeting the needs of 97.5% of the population for vitamin D(3)".
"A vitamin D(3) dosage of 800 IU/d increased serum 25-(OH)D levels to greater than 50 nmol/L (> 20 ng/ml) in 97.5% of women;
however, a model predicted the same response with a vitamin D(3) dosage of 600 IU/d."
"The dose response was curvilinear and tended to plateau at approximately 112 nmol/L in patients receiving more than 3200 IU/d of vitamin D(3)."
So, here the maximum was about 112 nmol / L.
Vitamin D status in healthy Indians aged 50 years and above.
"PTH levels started rising at vitamin D level < 30 ng/ml (75 nmol/L).
However, more than 50% of subjects with severe Vitamin D deficiency (< 20 ng/ml or < 50 nmol/L) had PTH levels within normal range.
So, from these studies we may conclude that what officially constitutes as a severe vitamin D deficiency, may for some in practise not be a deficiency at all,
which makes sense, because the RDA has to meet the requirements for 97.5% of the population.
Whats also interesting:
"Normal bone mass was observed in only 18.6% of study subjects" (first study above)
Whereas their osteoporotic fractures rates are lower than in the Netherlands.
Moreover, what oficially constitutes a vitamin D deficiency, may not be so at all.
Very often there are no deficiency symptoms or adverse health effects at all,
and even PTH levels may get adjusted despite (too) low vitamin D levels:
Factors associated with elevated or blunted PTH response in vitamin D insufficient adults.
"
Our results indicate that during vitamin D insufficiency, factors other than calcium and vitamin D may modify PTH response".
In rickets patients, PTH is
extremely high:
"Mean (SD) PTH level was 23.59 (19.03) pmol/L in the rachitic group and 1.9 (1.05) pmol/L in controls" Al-Mustafa ZH et al
and yet, 10% of them dont lack sunexposure.
25% of them had vitamin D levels greater than 20 nmol/L.
And even in secondary HPTH its not a clear case.
Causes of secondary hyperparathyroidism in a healthy population: the Tromsø study.
"serum 25-hydroxyvitamin D levels were significantly lower in the secondary hyperparathyroid (SHPT) group but only in nonsmokers..."
"in most subjects with SHPT all tests were within the normal range, and the cause is therefore probably a combination of several factors".
Logically,
how much vitamin D is needed, is also debatable:
Regulation of PTH secretion by 25-hydroxyvitamin D and ionized calcium depends on vitamin D status: a study in a large cohort of healthy subjects.
"Our results indicated that PTH levels were highly conditioned by those of 25OHD in subjects with 25OHD values lower than 16.35 ng/mL"[/i] (
40.9 nmol/L)
High prevalence of vitamin D deficiency in the sunny Eastern region of Saudi Arabia: a hospital-based study.
"Serum 25(OH)D levels ...were low [10.1 (SD 4.6) ng/mL and 9.9 (SD 4.5) ng/mL respectively] (25 nmol/L).
When subjects with elevated PTH levels were excluded, serum 25(OH)3 levels were still in the deficiency range."
Serum parathyroid hormone in healthy Japanese women in relation to serum 25-hydroxyvitamin D.
"Intact PTH increased with age" ... "there is no association between serum 25(OH)D and PTH levels in this Japanese population,
supporting a cutoff level of 25(OH)D less than 37.5 nmol/L for the elevated PTH level."
The 25(OH)D/PTH threshold in black women.
"Black women have lower 25-hydroxyvitamin D [25(OH)D] and higher PTH than white women".
"Black women (14.8 ng/ml = 37 nmol/L) have an increase in serum PTH at a lower 25(OH)D level than white women (23,6 ng/ml = 59 nmol/L)."
Optimal vitamin D status and serum parathyroid hormone concentrations in African American women.
"breakpoint between (16 and 20 ng/ml) 40 nmol/L and 50 nmol/L for serum 25(OH)D."
Prevalence of vitamin D deficiency among adult population of Isfahan City, Iran.
[ii]"the cut-off point of serum 25-OHD was determined to be 30 ng/mL" (
75 nmol/L)"[/i]
Reference range for serum parathyroid hormone
"Serum PTH was significantly higher in black study subjects than in white study subjects"
Vitamin D status in a sunny country: where has the sun gone?
"After the winter, median s25(OH)D was 21.4 ng/mL and 77.4% of the population presented hypovitaminosis D. ...
Significant increase in s25(OH)D was verified after summer [10.6 (3.7-19.3 ng/ml); p<0.001]...
We also observed a significant decrease in hyperparathyroidism prevalence (20.8% vs. 4.9%; P<0.0001)."
Effect of different dress style on vitamin D level in healthy young Orthodox and ultra-Orthodox students in Israel.
"
PTH was normal in 87% of vitamin D-deficient subjects from Yeshiva-A and Yeshiva-C (mean age 20), compared to 52% of Yeshiva-B students (mean age 33)."
Assessment of vitamin D status in healthy children and adolescents living in Tehran and its relation to iPTH, gender, weight and height.
"
Severe [vitamin D] deficiency was detected in 25% of subjects, deficiency in 27% and insufficiency in 26%...
The subjects did not have any signs or symptoms of rickets....
The curve of iPTH began to rise when 25(OH)D reached 75 nmol/L"
Predictors of vitamin D status and its association with parathyroid hormone in young New Zealand children
"
When 25(OH)D concentrations were >60-65 nmol/L, a plateau in PTH was evident."
Prophylactic vitamin D in healthy infants: assessing the need.
"breast-fed infants aged 3 months had the lowest value (20.2 ng/mL)" (50.5 nmol/L)
"
The clinical relevance of these findings is probably negligible because serum 25OHD levels spontaneously increased with age and were not associated with high serum PTH."
Even consuming only 2.25 ug/day, being indoors most of the day, some individuals will still not have inadequate blood vitamin D. (not that we recommend it!)
Prevalence of hypovitaminosis D and folate deficiency in healthy young female Austrian students in a health care profession.
"
Mean daily ingestion of vitamin D was 2.25 μg/day .... 6.9% had hypovitaminosis D (25-OH-vitamin D(3) <30 nmol/L) and 89.3% were vitamin D insufficient (<75 nmol/L)."
This one is 'funny':
Impact of two regimens of vitamin D supplementation on calcium - vitamin D - PTH axis of schoolgirls of Delhi.
"Despite supplementation with 60,000 IU of Vitamin D₃(monthly or two-monthly), only 47% were vitamin D sufficient at the end of one year."
Kasper wrote:Both skin types show that there is a mechanism which makes sure vitamin D production in the skin is stopped at a certain level.
"Stopped"? At what level?
You really mean as in: "no further increase
whatsoever"?
Any evidence to back this up?
(or do you mean "plateau on average at...")
Kasper wrote:RRM wrote:Kasper wrote:To estimate the circulating 25(OH)D concentrations prevalent in humans of the late Paleolithic period, we need to focus on people in sun-rich environments who regularly expose most of their skin surface to the sun.
Nonsense. In Europe, vast areas of land were covered by thick forests.
The Paleolithic period ends around 10,000 BP.
The last glacial period was the most recent glacial period within the current ice age occurring from approximately 110,000 to 10,000 BP.
Ecological zones in Europe at the last glacial maximum, ca 18,000 BP, are estimated to look like this:...
...Only at some coastal regions, we see a lot of forest.
In the last Paleolithic period, the ice was retreating.
The forests came back.
From 18,000 BP to 10,000 BP a lot of forest may have grown.
But if you still insist that there was little forest in Europe around 10,000 BP anyway,
then lets look a little further in the history of evolution of mankind in Europe (as we are both white europeans).
What we see then (until very recently), is a lot of forest, covering vast areas of land.
Hence much less UVB exposure.
So, again, to even estimate UVB exposure in the evolution of white europeans, is pure speculation,
and very much depends on what period of time in history is the subject of our speculations.
Most forest in europe originated after the last glacial period. First signs of agriculture are around the same period.
It's more likely that our DNA adopted to agriculture, than it adopted to living predominantly in thick forests width limited UVB exposure.
Huh?
Are you really claiming that since 10,000 BP there were no hunter gatherers in Europe anymore?
Only farmers?
Kasper wrote:RRM wrote:On most days, the sun may have been blocked by clouds, dont you think?
According to you: "Cloud cover reduces UV levels, but not completely; you [can] get burned on a cloudy day."
So, much less UVB exposure.
I don't think that on MOST days the sun was blocked, but I don't know the climate back than.
Wise words, acknowledging another point of speculation in this issue.
Kasper wrote:Of course, its speculation. In some sense, that's what all science is.
It's about making the best guess (model)
In this case, there is too much speculation, which makes it very unconvincing.
I dont think that guessing is good enough.
So, we better stick to the more scientific way to determine the required level of a vitamin.
(by establishing the levels of deficiency / insufficiency / sufficieny via the presence/absence of deficiency symptoms)
"Serum 25-hydroxyvitamin D (25-[OH]D) is considered the best biomarker of clinical vitamin D status".
Gallagher JC et al
Indirect sunlight can also damage the skin.
Of course, if you expose yourself too long, but with direct sun exposure, it happens much faster.
So, if you want to minimize UVB induced damage, i advice to avoid direct sun exposure.