Is Vitamin D Supplementation Even Neccessary

cinderella

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Joined
Oct 29, 2016
Messages
753
Most GPs need to re-attend medical school. In addition to its role in pregnancy prolactin is well-known as both acute and chronic stress biomarker.
Prolactin - Wikipedia
"...Levels can rise after exercise, high-protein meals, minor surgical procedures,[23] following epileptic seizures[24] or due to physical or emotional stress.[25][26] In a study on female volunteers under hypnosis, prolactin surges resulted from the evocation, with rage, of humiliating experiences, but not from the fantasy of nursing.[26"

Acute psychological stress increases plasma levels of cortisol, prolactin and TSH. - PubMed - NCBI
Chronic sustained stress increases levels of anterior pituitary prolactin mRNA. - PubMed - NCBI

Maybe you can politely show these links to your GP and ask that you want yours tested together with cortisol since you are under stress??
Thank you so much for this @haidut
It's a brilliant idea. I will do that!
 

Amazoniac

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- Considering the potential benefits as well as adverse effects of sun exposure: Can all the potential benefits be provided by oral vitamin D supplementation?

"It is important to note that vitamin D is not the only pathway whereby UVR exposure might have beneficial effects on human health. Indeed, both MS and type 1 diabetes are more common in those with fair skin (Ziegler et al., 1990; Harrison’s Online, 2004)—a phenotype associated with rapid vitamin D synthesis under UVB irradiation (compared to darker skin) (Clemens et al., 1982). Similarly, MS and type 1 diabetes are uncommon in those with deeply pigmented skin (Harrison’s Online, 2004)—although people with darker skin residing in higher latitude regions are more likely to have vitamin D deficiency than people with lighter skin (Ponsonby et al., 2002). And there may be critical periods in life where adequate UVR exposure is important, e.g. to risk of MS."

"Some possible pathways for beneficial effects of UVR exposure that are likely to be independent of vitamin D synthesis are described below:
  • Direct immunosuppression by UVR: Both UVA and UVB have direct immunosuppressive effects in humans (Halliday et al., 2004). UVB appears to upregulate secretion of TNF-a, IL-10 and T regulatory cells, providing both local and systemic immunosuppression (Ponsonby et al., 2005). T regulatory cells may be particularly important in removing self-reactive T cells that have escaped clonal deletion in the thymus (Sakaguchi et al., 2001), and thus in protecting against the development of autoimmune diseases (Sakaguchi et al., 2001; Rutella and Lemoli, 2004; Ponsonby et al., 2005).
  • Immunosuppression due to inhibition of melatonin production: Melatonin is synthesized from tryptophan via serotonin by the pineal gland under the influence of the dark/light cycle, with increased melatonin output over night (approximately 10 fold increase) (Liebmann et al., 1997). Suppression of melatonin secretion is particularly responsive to shorter wavelength blue light (460 nm) (Lockley et al., 2003) and brighter light intensity (Reiter, 1992). Melatonin secretion is associated with increased serum levels of Th-1 cytokines (Maestroni, 2001), and may play an adverse role in autoimmune diseases (due to Th-1 upregulation) (Maestroni, 2001). However, animal evidence suggests that melatonin may slow the progression of some cancers (Liebmann et al., 1997). Serotonin (an intermediate in melatonin synthesis) turnover is also positively associated with the duration and intensity of bright sunlight, and seasonal affective disorder may be related to a lowered turnover of brain serotonin during winter (Lambert et al., 2002). Suppression of melatonin secretion occurs predominantly in response to photoreception in the eye. A recent study has however suggested that the skin may contain UVR-sensitive extraretinal photoreceptors that can upregulate circadian clock genes and thus contribute to circadian rhythm modulation (Kawara et al., 2002) and suppression of melatonin (Brainard et al., 1994). In this way, skin exposure to UVR may modulate melatonin secretion and related cellular immune function.
  • Calcitonin gene related peptide (CGRP): CGRP is a potent vasodilator and immunomodulator found in cutaneous nerve fibres, in close association with Langerhans cells (LCs) (Seiffert and Granstein, 2002). CGRP release following UVR irradiation inhibits production of IL-2, TNF-a and IFN-g, stimulates production of IL-10 in macrophages and may inhibit antigen presentation by LCs. Even at non-erythemal doses, CGRP release is associated with impairment of induction of immunity and the development of specific immunological tolerance (Seiffert and Granstein, 2002).
  • Alpha melanocyte stimulating hormone (a-MSH): UVB irradiation stimulates the production of a-MSH from keratinocytes and melanocytes and upregulation of MC1R mRNA expression and MSH binding activity. a-MSH stimulates melanocytes via activation of the MC1R receptor to proliferate and to produce melanin (Scott et al., 2002; Pichler et al., 2004). MC1R is thus a primary regulator of melanin synthesis; allelic variants of MC1R are over-expressed in individuals with red hair and poor tanning ability and result in loss of function of the receptor (Scott et al., 2002). a-MSH modulates the function of MC1R-expressing antigen presenting cells and monocytes, inhibits T cell production of proinflammatory cytokines such as IFN-g and antagonizes the effects of IL-6 and IL-1 (Seiffert and Granstein, 2002). IL-10 production by monocytes and keratinocytes is upregulated and this may account for induction of hapten-specific tolerance and systemic immunosuppression (Luger et al., 2003).
  • Other mechanisms: the neuropeptide Substance P, released from cutaneous sensory nerve fibres following UV irradiation, induces lymphocyte proliferation and chemotaxis; nitric oxide, co-located with substance P and CGRP in cutaneous sensory nerves may contribute to local immunosuppression. UVR-induced DNA damage and other UVR-related changes can deplete Langerhan’s cells (Halliday et al., 1998; Aubin, 2003) and also impair their antigen-presenting function (Aubin, 2003)."
"Excessive doses may cause toxicity. But even modest levels within the normal range may be associated with an increased risk of prostate cancer (Tuohimaa et al., 2004)."​

- Nature vs. Supplements: The Controversy Surrounding Vitamin D

__
- Vitamin D Supplement Warning
- Supplementing for Low Vitamin D? Not So Fast (same author)

__
@Janelle525 @Travis
 
Last edited:

cinderella

Member
Joined
Oct 29, 2016
Messages
753
- Considering the potential benefits as well as adverse effects of sun exposure: Can all the potential benefits be provided by oral vitamin D supplementation?

"It is important to note that vitamin D is not the only pathway whereby UVR exposure might have beneficial effects on human health. Indeed, both MS and type 1 diabetes are more common in those with fair skin (Ziegler et al., 1990; Harrison’s Online, 2004)—a phenotype associated with rapid vitamin D synthesis under UVB irradiation (compared to darker skin) (Clemens et al., 1982). Similarly, MS and type 1 diabetes are uncommon in those with deeply pigmented skin (Harrison’s Online, 2004)—although people with darker skin residing in higher latitude regions are more likely to have vitamin D deficiency than people with lighter skin (Ponsonby et al., 2002). And there may be critical periods in life where adequate UVR exposure is important, e.g. to risk of MS."

"Some possible pathways for beneficial effects of UVR exposure that are likely to be independent of vitamin D synthesis are described below:
  • Direct immunosuppression by UVR: Both UVA and UVB have direct immunosuppressive effects in humans (Halliday et al., 2004). UVB appears to upregulate secretion of TNF-a, IL-10 and T regulatory cells, providing both local and systemic immunosuppression (Ponsonby et al., 2005). T regulatory cells may be particularly important in removing self-reactive T cells that have escaped clonal deletion in the thymus (Sakaguchi et al., 2001), and thus in protecting against the development of autoimmune diseases (Sakaguchi et al., 2001; Rutella and Lemoli, 2004; Ponsonby et al., 2005).
  • Immunosuppression due to inhibition of melatonin production: Melatonin is synthesized from tryptophan via serotonin by the pineal gland under the influence of the dark/light cycle, with increased melatonin output over night (approximately 10 fold increase) (Liebmann et al., 1997). Suppression of melatonin secretion is particularly responsive to shorter wavelength blue light (460 nm) (Lockley et al., 2003) and brighter light intensity (Reiter, 1992). Melatonin secretion is associated with increased serum levels of Th-1 cytokines (Maestroni, 2001), and may play an adverse role in autoimmune diseases (due to Th-1 upregulation) (Maestroni, 2001). However, animal evidence suggests that melatonin may slow the progression of some cancers (Liebmann et al., 1997). Serotonin (an intermediate in melatonin synthesis) turnover is also positively associated with the duration and intensity of bright sunlight, and seasonal affective disorder may be related to a lowered turnover of brain serotonin during winter (Lambert et al., 2002). Suppression of melatonin secretion occurs predominantly in response to photoreception in the eye. A recent study has however suggested that the skin may contain UVR-sensitive extraretinal photoreceptors that can upregulate circadian clock genes and thus contribute to circadian rhythm modulation (Kawara et al., 2002) and suppression of melatonin (Brainard et al., 1994). In this way, skin exposure to UVR may modulate melatonin secretion and related cellular immune function.
  • Calcitonin gene related peptide (CGRP): CGRP is a potent vasodilator and immunomodulator found in cutaneous nerve fibres, in close association with Langerhans cells (LCs) (Seiffert and Granstein, 2002). CGRP release following UVR irradiation inhibits production of IL-2, TNF-a and IFN-g, stimulates production of IL-10 in macrophages and may inhibit antigen presentation by LCs. Even at non-erythemal doses, CGRP release is associated with impairment of induction of immunity and the development of specific immunological tolerance (Seiffert and Granstein, 2002).
  • Alpha melanocyte stimulating hormone (a-MSH): UVB irradiation stimulates the production of a-MSH from keratinocytes and melanocytes and upregulation of MC1R mRNA expression and MSH binding activity. a-MSH stimulates melanocytes via activation of the MC1R receptor to proliferate and to produce melanin (Scott et al., 2002; Pichler et al., 2004). MC1R is thus a primary regulator of melanin synthesis; allelic variants of MC1R are over-expressed in individuals with red hair and poor tanning ability and result in loss of function of the receptor (Scott et al., 2002). a-MSH modulates the function of MC1R-expressing antigen presenting cells and monocytes, inhibits T cell production of proinflammatory cytokines such as IFN-g and antagonizes the effects of IL-6 and IL-1 (Seiffert and Granstein, 2002). IL-10 production by monocytes and keratinocytes is upregulated and this may account for induction of hapten-specific tolerance and systemic immunosuppression (Luger et al., 2003).
  • Other mechanisms: the neuropeptide Substance P, released from cutaneous sensory nerve fibres following UV irradiation, induces lymphocyte proliferation and chemotaxis; nitric oxide, co-located with substance P and CGRP in cutaneous sensory nerves may contribute to local immunosuppression. UVR-induced DNA damage and other UVR-related changes can deplete Langerhan’s cells (Halliday et al., 1998; Aubin, 2003) and also impair their antigen-presenting function (Aubin, 2003)."
"Excessive doses may cause toxicity. But even modest levels within the normal range may be associated with an increased risk of prostate cancer (Tuohimaa et al., 2004)."​

- Nature vs. Supplements: The Controversy Surrounding Vitamin D

__
- Vitamin D Supplement Warning
- Supplementing for Low Vitamin D? Not So Fast (same author)

__
@Janelle525 @Travis
Countries With The Highest Rates Of Diabetes
 

sugarbabe

Member
Joined
Sep 13, 2012
Messages
3,339
- Considering the potential benefits as well as adverse effects of sun exposure: Can all the potential benefits be provided by oral vitamin D supplementation?

"It is important to note that vitamin D is not the only pathway whereby UVR exposure might have beneficial effects on human health. Indeed, both MS and type 1 diabetes are more common in those with fair skin (Ziegler et al., 1990; Harrison’s Online, 2004)—a phenotype associated with rapid vitamin D synthesis under UVB irradiation (compared to darker skin) (Clemens et al., 1982). Similarly, MS and type 1 diabetes are uncommon in those with deeply pigmented skin (Harrison’s Online, 2004)—although people with darker skin residing in higher latitude regions are more likely to have vitamin D deficiency than people with lighter skin (Ponsonby et al., 2002). And there may be critical periods in life where adequate UVR exposure is important, e.g. to risk of MS."

"Some possible pathways for beneficial effects of UVR exposure that are likely to be independent of vitamin D synthesis are described below:
  • Direct immunosuppression by UVR: Both UVA and UVB have direct immunosuppressive effects in humans (Halliday et al., 2004). UVB appears to upregulate secretion of TNF-a, IL-10 and T regulatory cells, providing both local and systemic immunosuppression (Ponsonby et al., 2005). T regulatory cells may be particularly important in removing self-reactive T cells that have escaped clonal deletion in the thymus (Sakaguchi et al., 2001), and thus in protecting against the development of autoimmune diseases (Sakaguchi et al., 2001; Rutella and Lemoli, 2004; Ponsonby et al., 2005).
  • Immunosuppression due to inhibition of melatonin production: Melatonin is synthesized from tryptophan via serotonin by the pineal gland under the influence of the dark/light cycle, with increased melatonin output over night (approximately 10 fold increase) (Liebmann et al., 1997). Suppression of melatonin secretion is particularly responsive to shorter wavelength blue light (460 nm) (Lockley et al., 2003) and brighter light intensity (Reiter, 1992). Melatonin secretion is associated with increased serum levels of Th-1 cytokines (Maestroni, 2001), and may play an adverse role in autoimmune diseases (due to Th-1 upregulation) (Maestroni, 2001). However, animal evidence suggests that melatonin may slow the progression of some cancers (Liebmann et al., 1997). Serotonin (an intermediate in melatonin synthesis) turnover is also positively associated with the duration and intensity of bright sunlight, and seasonal affective disorder may be related to a lowered turnover of brain serotonin during winter (Lambert et al., 2002). Suppression of melatonin secretion occurs predominantly in response to photoreception in the eye. A recent study has however suggested that the skin may contain UVR-sensitive extraretinal photoreceptors that can upregulate circadian clock genes and thus contribute to circadian rhythm modulation (Kawara et al., 2002) and suppression of melatonin (Brainard et al., 1994). In this way, skin exposure to UVR may modulate melatonin secretion and related cellular immune function.
  • Calcitonin gene related peptide (CGRP): CGRP is a potent vasodilator and immunomodulator found in cutaneous nerve fibres, in close association with Langerhans cells (LCs) (Seiffert and Granstein, 2002). CGRP release following UVR irradiation inhibits production of IL-2, TNF-a and IFN-g, stimulates production of IL-10 in macrophages and may inhibit antigen presentation by LCs. Even at non-erythemal doses, CGRP release is associated with impairment of induction of immunity and the development of specific immunological tolerance (Seiffert and Granstein, 2002).
  • Alpha melanocyte stimulating hormone (a-MSH): UVB irradiation stimulates the production of a-MSH from keratinocytes and melanocytes and upregulation of MC1R mRNA expression and MSH binding activity. a-MSH stimulates melanocytes via activation of the MC1R receptor to proliferate and to produce melanin (Scott et al., 2002; Pichler et al., 2004). MC1R is thus a primary regulator of melanin synthesis; allelic variants of MC1R are over-expressed in individuals with red hair and poor tanning ability and result in loss of function of the receptor (Scott et al., 2002). a-MSH modulates the function of MC1R-expressing antigen presenting cells and monocytes, inhibits T cell production of proinflammatory cytokines such as IFN-g and antagonizes the effects of IL-6 and IL-1 (Seiffert and Granstein, 2002). IL-10 production by monocytes and keratinocytes is upregulated and this may account for induction of hapten-specific tolerance and systemic immunosuppression (Luger et al., 2003).
  • Other mechanisms: the neuropeptide Substance P, released from cutaneous sensory nerve fibres following UV irradiation, induces lymphocyte proliferation and chemotaxis; nitric oxide, co-located with substance P and CGRP in cutaneous sensory nerves may contribute to local immunosuppression. UVR-induced DNA damage and other UVR-related changes can deplete Langerhan’s cells (Halliday et al., 1998; Aubin, 2003) and also impair their antigen-presenting function (Aubin, 2003)."
"Excessive doses may cause toxicity. But even modest levels within the normal range may be associated with an increased risk of prostate cancer (Tuohimaa et al., 2004)."​

- Nature vs. Supplements: The Controversy Surrounding Vitamin D

__
- Vitamin D Supplement Warning
- Supplementing for Low Vitamin D? Not So Fast (same author)

__
@Janelle525 @Travis
Yes sunlight exposure would help prevent autoimmune problems from excessive vitamin A.
 

Amazoniac

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- UV exposure inhibits intestinal tumor growth and progression to malignancy in intestine-specific Apc mutant mice kept on low vitamin D diet

"Our study provides the first experimental proof that physiologically relevant, moderate UV irradiation can reduce the load of primary intestinal tumors. This reduction can at least in part be explained by an increase in vitamin D status, as we observed a comparable reduction in tumor load by vitamin D supplementation causing a similar increase in vitamin D status. However, a reduction in malignant progression and growth of adenocarcinomas could not be attributed to vitamin D (in contrast to Ref. 20) as these effects were only observed with moderate UV exposure and not with dietary vitamin D supplementation."

"Although the daily UV exposures produced on average vitamin D statuses comparable to those attained with dietary vitamin D supplementation, only UV exposure impacted malignant progression of the intestinal tumors in the present experiment. Hence, UV exposure appeared to affect tumor progression independently from vitamin D production. Although this finding was statistically significant, the group sizes were rather small, and further experimental corroboration is, therefore, desirable. Remarkably, we found no correlation between individual vitamin D statuses and total tumor loads. We cannot exclude that the measured statuses were not completely representative for each individual mouse, as the statuses may have varied in the course of the experiment. However, we also did not find a gender difference in tumor loads after UV exposure, despite the difference in 25(OH)D levels between males and females. The underlying mechanism of this additional vitamin D-independent UV effect is unclear, but it is reminiscent of such an effect in an experimental mouse model of multiple sclerosis.33 It could be an immunosuppressive effect or it could, for example, be related to UV-induced degradation of folic acid in superficial blood vessels in the skin.34"

"Apperly36 already described in 1941 a negative association between solar UV radiation and cancer mortality, which was confirmed more recently in multiple observational epidemiological studies.23 Garland and Garland1 proposed that the decrease in mortality from colon cancer with increasing ambient UV radiation may be mediated by vitamin D. Here, we experimentally proved for the first time the causality of such a relationship between moderate UV exposure and primary intestinal tumors in mice. The UV-induced reduction in intestinal cancer in mice could at least in part be attributed to vitamin D. However, we also found a reduced progression to malignancy caused by UV exposure which appeared not to be attributable to vitamin D. This latter finding provides experimental support for the hypothesis posed by van der Rhee et al.23 that the protective effect of sunlight may not be mediated by vitamin D alone. Evidently, this additional effect of UV exposure needs further study. As epidemiologic data suggest that our results can be translated to colon cancer in humans, our findings lend support to stimulation of regular moderate sun exposures to lower the risk of colorectal cancers."​

- Ultraviolet radiation inhibits mammary carcinogenesis in an ER negative murine model by a mechanism independent of vitamin D3
 
Joined
Sep 30, 2018
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307
Just go tan 3-5' per week, whatever that doesn't give the slightest burn.

I like this method:
Indoor Tanning For Vitamin D - The Tanning Blog

After having identified the best tanning bed for you according to the UVB selection described above, you ask for the normal session-time for cosmetic tanning in that bed according to your skin-type. Then you cut that time in half.

Following the advice above, you will get enough UVB for creating 10,000 to 15,000 IU vitamin D from one session and you will have absolutely ZERO risk of burning.

one session per week works. Kept my levels above 60 ng/mL last winter in Canada. Type 3 skin, never went above 7'
 

Amazoniac

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Sep 10, 2014
Messages
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Not Uganda
There are claims that vit D have a threshold for affecting calcium adsorption, it's questioned below. How it changes mineral metabolism in the body is not being considered. Extra vit D helps, but doesn't seem to be the best solution for lack of calcium in the diet.

- No vitamin D threshold for calcium absorption: why does this matter? (check out ref. #4 as vvc11)

"Previously, it was suggested that there was a threshold for maximal calcium absorption at a serum 25(OH)D concentration of 80 nmol/L (32 ng/mL), with a steep increase starting from 28 nmol/L (3)."

"In the study by Aloia et al (4), the FCA response to multiple doses of supplemental vitamin D3 was measured for the first time by using the more precise dual-isotope method (4). This trial, which reported a baseline 25(OH)D concentration of 63 nmol/L, found no threshold for calcium absorption at the various doses of vitamin D supplementation. Specifically, after 8 wk, the researchers found increases of 3.9%, 5.0%, and 6.7% in FCA [financial conduct authority] in response to 800, 2000, and 4000 IU vitamin D3/d, respectively, by using a 300-mg Ca load. The placebo group without any supplementation decreased FCA by 2.6%. There are at least 2 reasons why these findings are important. First, whereas some available evidence seemed to have suggested that there was no serum 25(OH)D threshold for FCA (5, 6), only a dose-response study can definitively prove this. Second, the decrease in the placebo group is not surprising given that typical dietary vitamin D intake is low in this group of women (2, 5) who tend to take a small amount of supplements before entering a trial (2). The decrease in FCA underscores the need for adequate vitamin D in maintaining calcium absorption.

Additional information is available from 2 other recent double-blind controlled studies that used vitamin D3 supplementation in postmenopausal women with adequate calcium intake (5, 7). In the Gallagher et al (7) study, multiple doses of vitamin D3 were used from 400 to 4800 IU/d, and findings showed that there was a 6% increase in FCA by using the single-isotope method and a low calcium carrier load (100 mg). These findings are consistent with the Aloia et al study, which showed a 6.7% increase in FCA when women were supplemented with 4000 IU/d and given a 300-mg Ca load (4). In our laboratory (5), we used a similar dual stable-isotope method with a 300-mg carrier Ca load and a similar baseline serum 25(OH)D concentration in postmenopausal women. In [our] study, vitamin D3 intake increased from 400 to 2500 IU/d, and there was a 3.7% increase in FCA. The slightly greater increase in FCA of 5% in the Aloia et al study using nearly identical methods may be explained by an absence of any vitamin D supplementation in the control group (4). In addition, an earlier study (6) administered a large dose of vitamin D2 (50,000 IU/d) to postmenopausal women for 15 d. This study used dual stable isotopes and found a 3% increase in FCA compared with baseline. The effect of vitamin D2 supplementation on FCA has not been found in studies that used smaller daily doses of vitamin D2 (ie, 1000 IU/d) (8, 9), possibly because of its shorter half-life compared with vitamin D3. Overall, there is an increase in calcium absorption with higher vitamin D3 intakes in adults and no threshold."

"[..]if the intake of calcium is at 1000 mg/d, a 3.7–6.7% increase in absorption with 2000–4000 IU/d would provide an additional 37–67 mg Ca/d, which is similar to that found in 0.25 cup of milk or 1 ounce of almonds[*]. Thus, taking high doses of vitamin D is an efficient way to maintain calcium balance."​

[*] Why Ray Recommends Eating Lots Of Calcium

@Shaman
 

haidut

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Mar 18, 2013
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USA / Europe
There are claims that vit D have a threshold for affecting calcium adsorption, it's questioned below. How it changes mineral metabolism in the body is not being considered. Extra vit D helps, but doesn't seem to be the best solution for lack of calcium in the diet.

- No vitamin D threshold for calcium absorption: why does this matter? (check out ref. #4 as vvc11)

"Previously, it was suggested that there was a threshold for maximal calcium absorption at a serum 25(OH)D concentration of 80 nmol/L (32 ng/mL), with a steep increase starting from 28 nmol/L (3)."

"In the study by Aloia et al (4), the FCA response to multiple doses of supplemental vitamin D3 was measured for the first time by using the more precise dual-isotope method (4). This trial, which reported a baseline 25(OH)D concentration of 63 nmol/L, found no threshold for calcium absorption at the various doses of vitamin D supplementation. Specifically, after 8 wk, the researchers found increases of 3.9%, 5.0%, and 6.7% in FCA [financial conduct authority] in response to 800, 2000, and 4000 IU vitamin D3/d, respectively, by using a 300-mg Ca load. The placebo group without any supplementation decreased FCA by 2.6%. There are at least 2 reasons why these findings are important. First, whereas some available evidence seemed to have suggested that there was no serum 25(OH)D threshold for FCA (5, 6), only a dose-response study can definitively prove this. Second, the decrease in the placebo group is not surprising given that typical dietary vitamin D intake is low in this group of women (2, 5) who tend to take a small amount of supplements before entering a trial (2). The decrease in FCA underscores the need for adequate vitamin D in maintaining calcium absorption.

Additional information is available from 2 other recent double-blind controlled studies that used vitamin D3 supplementation in postmenopausal women with adequate calcium intake (5, 7). In the Gallagher et al (7) study, multiple doses of vitamin D3 were used from 400 to 4800 IU/d, and findings showed that there was a 6% increase in FCA by using the single-isotope method and a low calcium carrier load (100 mg). These findings are consistent with the Aloia et al study, which showed a 6.7% increase in FCA when women were supplemented with 4000 IU/d and given a 300-mg Ca load (4). In our laboratory (5), we used a similar dual stable-isotope method with a 300-mg carrier Ca load and a similar baseline serum 25(OH)D concentration in postmenopausal women. In [our] study, vitamin D3 intake increased from 400 to 2500 IU/d, and there was a 3.7% increase in FCA. The slightly greater increase in FCA of 5% in the Aloia et al study using nearly identical methods may be explained by an absence of any vitamin D supplementation in the control group (4). In addition, an earlier study (6) administered a large dose of vitamin D2 (50,000 IU/d) to postmenopausal women for 15 d. This study used dual stable isotopes and found a 3% increase in FCA compared with baseline. The effect of vitamin D2 supplementation on FCA has not been found in studies that used smaller daily doses of vitamin D2 (ie, 1000 IU/d) (8, 9), possibly because of its shorter half-life compared with vitamin D3. Overall, there is an increase in calcium absorption with higher vitamin D3 intakes in adults and no threshold."

"[..]if the intake of calcium is at 1000 mg/d, a 3.7–6.7% increase in absorption with 2000–4000 IU/d would provide an additional 37–67 mg Ca/d, which is similar to that found in 0.25 cup of milk or 1 ounce of almonds[*]. Thus, taking high doses of vitamin D is an efficient way to maintain calcium balance."​

[*] Why Ray Recommends Eating Lots Of Calcium

@Shaman

Thanks. Have you seen anything on optimal ratio of vitamins K/D when used as a supplement?
 

Amazoniac

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Joined
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Messages
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1. Is Vitamin D Supplementation Even Neccessary
2. Is Vitamin D Supplementation Even Neccessary
3. Is Vitamin D Supplementation Even Neccessary


Expanding the list before I lose them:

- Exposure to Ultraviolet Radiation in the Modulation of Human Diseases
- Sun Exposure and Its Effects on Human Health: Mechanisms through Which Sun Exposure Could Reduce the Risk of Developing Obesity and Cardiometabolic Dysfunction
- Systematic Review of the Effects of Ultraviolet Radiation on Markers of Metabolic Dysfunction

- Immune System Modulation Produced by Ultraviolet Radiation
- The suppressive effects of ultraviolet radiation on immunity in the skin and internal organs: Implications for autoimmunity
- Exposure to UV Wavelengths in Sunlight Suppresses Immunity. To What Extent is UV-induced Vitamin D3 the Mediator Responsible?
- Mechanisms by Which UV Radiation, a Natural Component of Sunlight, Suppresses the Immune Response
- Sunlight Effects on Immune System: Is There Something Else in addition to UV-Induced Immunosuppression?

- Can Skin Exposure to Sunlight Prevent Liver Inflammation?

- Narrowband UVB Phototherapy for Clinically Isolated Syndrome: A Trial to Deliver the Benefits of Vitamin D and Other UVB-Induced Molecules

- Sunlight: For Better or For Worse? A Review of Positive and Negative Effects of Sun Exposure
- Multifaceted pathways protect human skin from UV radiation

- Moderate UV Exposure Enhances Learning and Memory by Promoting a Novel Glutamate Biosynthetic Pathway in the Brain
 

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda
- Vitamin D: Beyond Metabolism

"The article explores how vitamin D interacts with another light sensitive vitamin, folic acid, and how these 2 vitamins might influence long-term biological effects (the evolution of skin pigmentation),2,3 as well as shorter “lifecycle” timeframe effects on clinical phenotypes of relevance to human health and well-being.4"

"That vitamin D is an important regulator of many processes within the cell may well be reflected in its ancient origins. It is certainly interesting to speculate that its physiologic role has evolved to counter the challenges faced by evolutionary advancement, particularly of homeostatic iCa2+ control in organisms that left ancient, calcium-replete oceans to reestablish their lineage in calcium-deplete terrestrial ecosystems.1 It has been estimated that vitamin D photosynthesis has occurred in marine phytoplankton for 500 million years and that terrestrial vertebrates have been generating de novo vitamin D for the latter 70% of this same time frame.5 A full vitamin D endocrine system that deploys a specific VDR nuclear receptor and cytochrome P450 enzymes, and which is regulated by calciotropic hormones and vitamin D binding protein, is only found in vertebrates. The origins of this area of metabolism may therefore relate to archaic xenobiotic P450-related detoxification pathways and have been driven by the need to handle the challenges of higher gravity in a calcium-deplete terrestrial environment.6"

"Some terrestrial vertebrates provide adjustments to this process to counter the effects of fur or feathers. Often, vitamin D is generated from 7-dehydrocholesterol in oils secreted onto fur or feathers by the skin. The 7-dehydrocholesterol is spread during preening, allowing vitamin D photosynthesis. The micronutrient is then consumed during grooming.8 Interestingly, one mammal that has no source of vitamin D available to it is the subterranean naked mole rat (Heterocephalus glaber). Levels of 1,25(OH)2D3 are undetectable and supplementation studies have led to speculation that continuously growing incisors act as a mineral dump to assist tight regulation of iCa2+ and phosphorus. Such vitamin D–independent mechanisms of regulating iCa2+ are thus well adapted to an environment devoid of sunlight,7 although they are unusual in nature."


It was a lack of sunlight that was first attributed to the deficiency syndrome of vitamin D in children. Inadequate bone calcium causes rachitic deformities,9 and as early as the mid-17th century rickets was recognized as a discrete phenomenon arising due to urbanization of England’s population, and the associated atmospheric pollution (smoke and smog) that hampered seasonal vitamin D synthesis at northerly latitudes.10 By the 20th century, further industrialization and migration to high latitudes both in Western Europe and the United States saw the creation and proliferation of urban slums and burgeoning atmospheric pollution with overcrowding and impoverished lifestyles adding to UV-R deprivation. As a consequence of this anthropogenic vitamin D–restricting environment, a high prevalence of rickets (under-mineralization of bone) developed among infants.

So how does the atmosphere influence the quality of light/UV-R needed for vitamin D synthesis, and does it have adverse effects on related vitamins? UV-A is more efficient at penetrating both ozone and human skin than UV-B or UV-C.2,11–14 Additionally, factors such as photoperiod (day length) and total solar irradiance (TSI) are important factors to consider, along with those alluded to above. It is particularly interesting to recognize the impact that solar eruptions can have, and their contribution to TSI. These phenomena lead to ionized particles (solar storms) affecting power grids, satellites, and communications. Understandably, much work has focused on the impact of these dramatic solar events on human infrastructure, but very little research has looked at the effects on human biology.

TSI, which increases with sunspot activity,11 is a balance between sunspot-related magnetic influences that shield the solar plasma and highly energetic faculae that surround sunspots. UV-A and to a lesser extent UV-B are likely to be a highly relevant component of the TSI. This is important not only in the context of vitamin D stability and photodegradation but also in maintaining folate stability: Folate has been shown to exhibit an important relationship with UV-R. It is now believed that dermal exposure to UV-A radiation promotes photolytic degradation of folate, lowering systemic vitamin status,2,15,16 work now strongly supported by a recent Australian study.17"

"While vitamin D is usually discussed in terms of photosynthesis, it is also degraded by UV-R. Vitamin D3 synthesized by the action of UV-B can be degraded by UV-A after as little as 10 minutes of nontropical sun, although the rate of loss is lower in winter.2,7 This previtamin D3 photo-isomerization prevents vitamin D toxicity, but means that UV-A degrades "vitamin" D3 at times of the year when there is inadequate UV-B to photosynthesize calciol in the skin7 and hence generate biologically active 1,25(OH)2D3. 1,25(OH)2D3, the main form of vitamin D, is itself UV-A labile and has a short half-life of 15 hours in the circulation.7,18–20 By contrast, 25(OH)D3 has a half-life of around 14 days in the circulation, although limited fat and muscle storage also occurs (half-life 60 days).20 Despite these additional stores, they may be inadequate for lean people when UV-B photosynthesis of the vitamin is absent.21"

"[..]an environment-pigmentation coefficient exists in which melanized skin at high latitudes may limit vitamin D synthesis, while light pigmentation at equatorial latitudes might lead to photolysis of folate—both of which are phenomena with negative attributes."

"Recent research highlights an interesting biological contradiction. UV light is a well-established carcinogen, yet Fell and colleagues29 have provided evidence that UV-seeking behavior is addictive and that UV addiction is mediated by the hedonic action of beta-endorphin and anhedonic effects of withdrawal."

"The major elements of vitamin D metabolism beyond its photosynthesis are shown in Figure 2."

"Vitamin D does not fit the classic definition of a vitamin, as the most important source of this steroid pro-hormone is via endogenous synthesis in the skin following UV exposure. However, it is not the only light-sensitive vitamin, although arguably it is one of the most important. Other vitamins that are also sensitive to and/or transduce light signals include folic acid, "vitamin" A, riboflavin (vitamin B2), and niacin (vitamin B3). In some cases light transduction by these vitamins plays a major role in regulating circadian rhythm.16,39"

"Cryptochromes are blue-light photoreceptors that are central to generating circadian oscillations in animals and plants. They occur in the ganglion cell layer of the retina and transmit/transduce light stimuli to the master circadian clock, which in humans is located in the suprachiasmatic nucleus. It has been shown that purified human cryptochrome 2 (hCRY2) exhibits fluorescence properties consistent with the presence of both flavin (vitamin B2) and folate cofactors,40 although evidence of photoreception in mammalian cryptochromes remains indirect.41 CRY1 and CRY2 are 73% homologous in all organisms and absorb light in the 350 to 450 nm wavelength range. Most often, the folate cofactor is 5,10-methenyl-H4folate, and the flavin vitamer is flavin adenine dinucleotide (FAD). In this relationship, the folate vitamer functions as a light-catching antenna whereas FAD facilitates the subsequent redox reaction. Basically, exposure to blue-light photons excites 5,10-methenyl-H4folate, and an electron is then transferred to the reduced catalytic flavin (FADH−) and then on to CRY1 or CRY2.39,42 Interestingly, in plants, folate vitamer–containing cryptochromes regulate blue-light dependent growth, while in bacteria, insects, and amphibians they stimulate enzymes that repair UV-induced DNA damage. In mammals, they regulate the circadian clock."

"Although "vitamin" A interacts with opsin proteins in circadian photoreception,39 and is obviously critical in vision, it is now thought that cryptochromes are the major mammalian circadian photoreception system. Additionally, while systemic folate is sensitive to UV exposure on the skin, and is easily degraded, the opposite is true of vitamin D, which requires UV for its synthesis. This diametrically opposed effect of UV light may have played a significant role in evolutionary processes (see below)."

"While "vitamin" D is the first vitamin that most people bring to mind when nutrients are discussed in the context of sunlight, and for good reason, it is not the only nutrient of significance. Niacin as NAD(P)(H) is also closely linked to human biology via UV exposure. A niacin deficiency or poor NAD status leads to dermal sun sensitivity, reflecting a poor cellular response to UV exposure (ie, sunlight dermatitis in the deficiency disease, pellagra). Indeed, NAD deficiency leads to genomic instability and may enhance cancer development. In keratinocytes, NAD deficiency promotes photodamage. This stems from both poly(ADP-ribose) polymerases and sirtuins being inhibited by a lack of NAD+. A lack of this important vitamin-related substrate for these enzymes leads to unrepaired photolytic damage to DNA and promotes cell death. Furthermore, the rapid depletion in NAD due to increased poly(ADP-ribose) polymerase activity following genomic damage (UV damage/mycotoxins, etc) has long been seen as one of the potential mechanisms of apoptosis,43 with a variety of deleterious effects in play such as delayed DNA excision repair, a build-up of single and double strand breaks, chromosome breakage, telomere erosion, and malignancy.44"

"After "vitamin" D, "vitamin" A is perhaps the second "vitamin" people tend to associate with light. However, in truth both preformed and pro-"vitamin" A carotenoids fall into this category. The role of 11-cis-retinaldehyde in vision as a prosthetic group for the opsin protein is well established: The protein–"vitamin" complex forms rhodopsin (visual purple), which following UV exposure leads to isomerization of the 11-cis-"vitamer" into the all-trans-retinaldehyde. The associated conformational changes in the opsin protein subsequently lead to a GTP-transduced closing of a sodium channel and a visual signal to the brain. What is perhaps less well recognized is that skin carotenoids derived from our diet also have an important light-related role in protecting us from photo-oxidative damage resulting from UV exposure.45 This effect varies across our bodies."

"Evidence is also emerging that a novel endocrine axis involving "vitamin" A in its retinoic acid "vitamer" form is regulated by photoperiod and melatonin, suggesting new contributors in the photoperiodic neuroendocrine response.47 In a recent review, Ransom and colleagues examine how retinoic acid regulates several rhythms in brain and body, from circadian to seasonal cycles, both of which are entrained by light/photoperiod.48"

"Of course, "vitamin" A and "vitamin" D interact as nuclear cofactors (heterodimerization of VDR-RXR) making it difficult to consider either "vitamin" in isolation. In fact, the best way to summarize "vitamin" D as being the most significant of all light-sensitive vitamins [too many vitamins in a paragraph, enough] is to draw attention to the fact that vitamin D signaling is so fundamentally important that irrespective of whether deficiency stems from inherited defects, nutritional deficits, a lack of sunlight, malabsorption, or covert disease, the consequences can be significant and variable across the lifecycle. This is largely because vitamin D signaling is regulated at several levels and is far more complex than a simplistic ligand–receptor–DNA interaction.49"

"Earlier it was suggested that folic acid and vitamin B2 might play a key role in the generation of circadian oscillations, but vitamin D may also be important. The current paradigm for the mammalian circadian clock involves interplay between 2 transcription–translation feedback loops consisting of “clock” genes and their expression products. Feedback loop one involves positive elements, including the transcription factors CLOCK and BMAL1. Following heterodimerization, these transcription factors enter the nucleus and bind the circadian E-box promoter, enhancing transcription of expression products PER1 and PER2 and both CRY1 and CRY2. These products negatively feedback to inhibit their source genes by arresting CLOCK/BMAL1-mediated activation. The second feedback loop initiates Rev-Erba and Rora genes via CLOCK/BMAL1. The expressed protein products of these genes compete for binding at the BMAL1 promoter, forcing a daily rhythm of BMAL1 transcription, terminating this second feedback loop. In this way, clock-controlled gene transcription allows circadian clock outputs to be harmonized. The kinds of outputs related to this process are manifold, but include melatonin production and numerous post-translational modifications such as phosphorylation and ubiquitinization.16,50 It is interesting that vitamin D has now also been related to circadian processes. 1,25(OH)2D3 was found to synchronize circadian clock gene expression in adipose-derived stem cells. Expression of 2 circadian genes, BMAL1 and PER2, in cells containing 1,25(OH)2D3 pointed to a critical role for this vitamin in regulation of the molecular clock.51 These authors further suggest that as circadian rhythm influences many physiological processes in all forms of life, this could be the key to a better understanding of the mechanisms by which 1,25(OH)2D3 mediates its many cellular functions. It is certainly interesting that adult mesenchymal stem cells may be synchronized (entrained) with 1,25(OH)2D3, suggesting a relationships between circadian oscillations and stem cell properties such as pluripotency and proliferation.51"

"From a more mundane food perspective, many micronutrients are light sensitive. Apart from folate, 2 good examples are thiamin (vitamin B1), which can exhibit total loss from bread when freshly baked produce is exposed to light in shop windows [??], and vitamin B2. When vitamin B2 in milk is exposed to sunlight or even fluorescent light, photolysis leads to lumiflavin under alkaline conditions or lumichrome under neutral or acidic conditions. Neither has vitamin activity and they can catalyze peroxidation of lipids and conversion of methionine to methional. Methional confers an off taste or “sunlight” flavor to milk. As a consequence, cartons now have a protective lining to stop B2 photolysis. It would be wrong to omit the many antioxidant vitamins that undoubtedly also help mop up free radicals and mediate cell repair processes following UV-induced DNA damage."

"There is now overwhelming evidence that seasonality derived from planetary rhythm influences all organisms via recognized, putative, and as yet undiscovered cellular and genetic mechanisms. The sun in particular plays a pivotal role in orchestration of the human lifecycle." "The human exposome, which includes all wavelengths of UV-R, photoperiod, diet, and temperature, as well as an almost incalculable number of other environmental factors, has contributed to the evolution of our species." "[..]the genome and environment are tightly interactive soon after conception. We have previously demonstrated this for both folate and vitamin D genes,16,22–24 but it is recognized that UV-R can also attenuate the maternal immune system leading to cytokine production that influences the fetal genome.57"

"Geophysical cycles impart a rhythm to life and are critical to our biology; accumulating evidence indicates season of birth modifies disease risk and life span.57 Two vitamins for which this may most easily be demonstrated are the 2 light-sensitive micronutrients—vitamin D and folate. In the context of folate, schizophrenia and neural tube defects have a similar rhythm of seasonal conception,58 with schizophrenia exhibiting a 5% to 8% bias toward late winter/early spring conception.59 We know that pharmacologic folic acid prevents neural tube defects (NTD), and the key C677T-MTHFR folate-related gene polymorphism has greater prevalence in both NTD60 and schizophrenia.61 Furthermore, maternal oxidant stress inhibits neural tube closure and alters left–right embryonic asymmetry as might occur in the schizophrenic brain.62 Both clinical phenotypes involve concurrent fourth-embryonic week processes sensitive to folate degrading oxidant stress, a likely action of pro-oxidant sunlight action, which has coined the “solstitial” hypothesis, a paradigm linking month of birth to left-handedness and other markers of lateralization.63 However, one of the most interesting phenomena linking folate to seasonality, and one that might be critical in both schizophrenia and neural tube defects, is the recent finding that the day length a woman experiences during the periconceptional period predicts the C677T-MTHFR genotype of her child.22 The biologic mechanism for this is unclear, although UV-A dermal destruction of 5-methyl-H4folate leading to a lower cellular 5,10-methylene-H4folate status15,64 might increase the viability of TT genotype embryos and hence population mutant T-allele frequency."

"A similar story exists for vitamin D, helping account for environment-related disease phenomena. Seasonality at conception is linked to multiple sclerosis,65,66 and month of birth influences immune-mediated disease implicating UV-B and vitamin D as risk factors.67 In this latter report, the risk of immune-mediated disease (Crohn’s disease, rheumatoid arthritis, ulcerative colitis, and lupus) was inversely correlated to second trimester UV-B exposure and third trimester vitamin D status.67 Interestingly, seasonality at conception is also associated with brain tumors in adults,68 expression of biogenic amine-related genes in psychiatric patients,69 and in the development of specific behavioral traits.70 The present authors demonstrate that the longer the photoperiod at conception, the less the likelihood of depression in adulthood,24 a relationship that might potentially be linked to vitamin D."

"The most logical basis for seasonal effects at conception would seem to relate to photoperiod; however, as has been shown, the quanta of solar radiation received could also be a factor: radiation intensity is linked to the solar cycle, with individuals born at the peak of such cycles living 1.5 years less than those born in nonpeak years.57 Additionally, the solar cycle and hence solar irradiance seems to have a direct effect on gene occurrence.23,24"

"Folate is as important to biological processes as vitamin D, and is necessary for both de novo biosynthesis of DNA-thymidylate (dTMP) and methionine derived methyl groups (genomic [CpG] and nongenomic methylation reactions). It is also required for purine synthesis and serine–glycine interconversion as well as histidine catabolism.79 This means a shortage of folate can lead to uracil being misincorporated into the primary base sequence in place of thymine, and hence it can promote DNA fragility. As half our methionine is provided de novo, a folate shortage can also adversely influence the methylome and hence disrupt epigenetic control.80 Dysregulated folate nutrition and/or genetics are now unequivocally associated with neural tube defects (NTD) and many other developmental and degenerative disorders, including cancers, vascular disease, and neuropsychiatric disorders.81"

"Given the critical role that these 2 light-sensitive vitamins play in cell metabolism, recent research opens up some interesting ideas on how environment (UV-R) might alter/modulate the systemic level of these vitamins that are required as cofactors/ligands for key proteins that have variable activity depending on genotype. Where such polymorphic proteins are absolutely critical for early embryo development, it is conceivable that certain “UV-R–vitamin–genotype” combinations might lead to embryo loss. For example, low systemic levels of folate or vitamin D might favor selection of embryos with specific vitamin-related gene variants that have expression products that are more effective at utilizing low vitamin levels."

"It is suggested that depigmentation in Europe occurred as recently as the past 6000 to 12 000 years. The putative selection pressure for this is thought to be vitamin D related, being stimulated by a move away from fishing and hunting that will have provided adequate preformed dietary vitamin D, to a farming culture with fewer sources of preformed dietary vitamin D.82 That is to say, vitamin D was critical to survival and its synthesis had to be accommodated following this cultural shift."

"Detailed molecular mechanisms for the role of vitamin D in human evolution are lacking; however, vitamin D per se is clearly important as a potential target for putative selection processes. Higher follicular fluid and serum calcidiol predicts success of in vitro fertilization,83 while during pregnancy a woman’s calcidiol level jumps 4- to 5-fold to sequester the additional calcium needed for fetal skeletal growth raising potential issues at higher latitudes where maladapted pigmentation profile, sunscreen use, or cultural issues might promote insufficiency.84 Furthermore, vitamin D inadequacy in early life can lead to pelvis malformation and an inability to facilitate normal childbirth.85"

"It is recognized that in northern Scandinavia/Lapland, skin pigmentation is darker than would be predicted.3 The UV-R regime of these latitudes is almost exclusively UV-A throughout the year, with virtually no UV-B apart from a low summer exposure. Thus, habitation at these latitudes without reliance on a vitamin D–rich diet of marine animals would be impossible. Much of the dietary vitamin D stores are found in body fat.109 This supports a possible evolutionary connection between the development of generous subcutaneous fat stores and vitamin D storage in these populations. This may further help explain a link to insulin as alluded to earlier. Ultimately, the selection pressure for depigmentation in these populations is relaxed because of a high vitamin D diet, with darker skin enabling protection from high levels of UV-A as a result of not just direct solar irradiation but also UV reflection from snow and ice.2 Given the global influence of VDR on homeostasis, other, yet to be discovered, critical early life events and evolutionary processes may also be modulated by vitamin D responsive elements. Effects are likely to relate to the functional consequences of different VDR polymorphisms and how the VDR interacts with vitamin D and other skin pigmentation genes.86"​
 
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