Is Vitamin D Supplementation Even Neccessary

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda
The following link is from a Trevor Marshall page shared by @LLight. Given the conditions, I was expecting something worse:

- Normal vitamin D levels can be maintained despite rigorous photoprotection: Six years' experience with xeroderma pigmentosum

"Eight patients with XP were studied (four males and four females; mean age at beginning of the study, 27 years [range, 14-49 years]). They were all the participants in a study of the use of oral isotretinoin for skin cancer prevention.[7] They did not receive supplemental vitamin D or calcium and did not use oral contraceptives. Values of serum calcium, ionized calcium, 25-hydroxyvitamin D (25-OHD), and 1,25-dihydroxyvitamin D (1,25-[OH]2D) and PTH (intact) were assessed from 1989 through 1995. The patients lived throughout the United States from as far south as California to as far north as Wisconsin."

"All eight patients with XP utilized extreme sun protection measures by staying indoors during daylight hours, wearing sun-protective clothing, and applying sunscreens of at least sun protection factor (SPF) 15 each day. They reported daily sunlight exposure averaging 5 minutes or less. Several of the patients had a history of marked sun burning on minimal sun exposure before diagnosis of XE During the course of this study none experienced sunburning."

"The patients reported adequate dietary vitamin D with an estimated mean daily intake of 307 IU (range, 136 to 543 IU). The main source of dietary vitamin D was milk. Two patients reported vitamin D-deficient diets averaging 136 IU/day (patient 3) and 142 IU/day (patient 1). Patient 1 had the lowest mean value of serum 1,25-(OH)2D and had sporadic values at or below the lower limit of "n"or"m"al for both serum 25-OHD and 1,25-(OH)2D (Figs. 2 and 3). Patient 3 had serum vitamin D levels that were similar to other patients who reported a higher vitamin D intake."

Killcidiol:
upload_2020-1-6_8-28-47.png


Killcitriol:
upload_2020-1-6_8-29-1.png

"Low vitamin D levels may be compensated by increasing the levels of PTH. However, the mean intact PTH levels in the seven patients with XP tested was 36.1 ± 3.4 pg/ml ("n"or"m"al range, 10 to 65 pg/ml)."​
 

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda
- Magnesium status and supplementation influence vitamin D status and metabolism: results from a randomized trial

"The aim of this study was to test the hypothesis that magnesium supplementation differentially affects vitamin D metabolism dependent on baseline 25-hydroxyvitamin D [25(OH)D] concentration."

"A number of previous clinical trials conducted in adults consistently indicated that high calcium supplementation increases urinary excretion of magnesium (35–38), whereas magnesium homeostasis is mainly regulated by kidney reabsorption. Thus, individuals with high calcium-to-magnesium intake ratios in their habitual diet are at high risk of magnesium deficiency."

"Two 24-h dietary recalls were performed for all participants at the baseline of the PPCCT [Personalized Prevention of Colorectal Cancer Trial]. Based on their baseline intakes of calcium and magnesium as well as their calcium-to-magnesium intake ratio, each participant was assigned to a customized dose of magnesium supplementation that would reduce the calcium to magnesium intake ratio to ∼2.3, as suggested by several previous studies (23–27)."

"We found that magnesium supplementation interacted with baseline plasma concentrations of 25(OH)D in affecting the concentrations of 25(OH)D3, 25(OH)D2, and 24,25(OH)2D3. We found that magnesium supplementation reduced 25(OH)D3 and 24,25(OH)2D3 when 25(OH)D concentrations were >30 ng/mL, particularly at 50 ng/mL. These findings are novel. However, there was no consistent evidence that magnesium supplementation increased vitamin D metabolite concentrations [i.e., 25(OH)D3 and 24,25(OH)2D3] at lower concentrations. Magnesium supplementation increased 25(OH)D3 when 25(OH)D concentrations were at 30 ng/mL, but not 20 ng/mL, whereas magnesium supplementation did not increase 24,25(OH)2D3. Also, we found that the pattern of the magnesium association was different with 25(OH)D2 and 25(OH)D3."

upload_2020-1-17_20-33-8.png

"The precise molecular mechanism is not clear. One possible explanation is that magnesium supplementation affects both vitamin D–activating enzymes (i.e., CYP27B1 and CYP2R1) and vitamin D–deactivating enzymes [i.e., CYP24A1 and CYP3A4 (Figure 1)]. When baseline 25(OH)D is <30 ng/mL, the activity of CYP3A4 on vitamin D degradation is limited; thus, the relation of magnesium supplementation is primarily with vitamin D synthesis enzymes. When baseline 25(OH)D concentrations are >30 ng/mL, CYP3A4 activity starts to elevate and the activity is further enhanced by magnesium supplementation, which leads to a significant reduction in concentrations of 24,25(OH)2D3. [?] In addition, the reduction in 24,25(OH)2D3 seems stronger than the reduction in 25(OH)D3, indicating that the reduction in 25(OH)D3 could be secondary to the 24,25(OH)2D3 reduction."

upload_2020-1-17_20-33-18.png
 
Last edited:

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda
Wow is heat with UV lamps?

- Factors Influencing Vitamin D Status

"[..]skin temperature plays an important role in cutaneous vitamin D3 synthesis. Conversion of photosynthesized previtamin D3 to vitamin D3 is a temperature-dependent isomerization process (5). The rate of the isomerization reaction correlates directly with skin temperature. A study using the skin of the lizard Iguana iguana, whose rate constant for the isomerization of previtamin D3 to vitamin D3 is similar to that of human skin, showed that isomerization occurs 9-fold more quickly at 25°C than at 5°C [50% of previtamin D3 converted to vitamin D3 (T1/2) in 8 and 72 h, respectively] (42). At 37°C, the T1/2 for the conversion of previtamin D to vitamin D in human skin decreases to 2.5 h (43). Skin temperature at any given location on the surface of the body is dependent on a number of variables, including blood perfusion, thermal conductivity, metabolic activity, insulation by clothing, ambient temperature, air-flow rate, air pressure and humidity (44). Under most normal conditions, human skin temperature is lower than core body temperature and varies between approximately 29°C and 35°C (45). The rate of cutaneous vitamin D synthesis will, in turn, vary as skin temperature fluctuates."​
 

sweetpeat

Member
Joined
Nov 28, 2014
Messages
614
Wow is heat with UV lamps?

- Factors Influencing Vitamin D Status

"[..]skin temperature plays an important role in cutaneous vitamin D3 synthesis. Conversion of photosynthesized previtamin D3 to vitamin D3 is a temperature-dependent isomerization process (5). The rate of the isomerization reaction correlates directly with skin temperature. A study using the skin of the lizard Iguana iguana, whose rate constant for the isomerization of previtamin D3 to vitamin D3 is similar to that of human skin, showed that isomerization occurs 9-fold more quickly at 25°C than at 5°C [50% of previtamin D3 converted to vitamin D3 (T1/2) in 8 and 72 h, respectively] (42). At 37°C, the T1/2 for the conversion of previtamin D to vitamin D in human skin decreases to 2.5 h (43). Skin temperature at any given location on the surface of the body is dependent on a number of variables, including blood perfusion, thermal conductivity, metabolic activity, insulation by clothing, ambient temperature, air-flow rate, air pressure and humidity (44). Under most normal conditions, human skin temperature is lower than core body temperature and varies between approximately 29°C and 35°C (45). The rate of cutaneous vitamin D synthesis will, in turn, vary as skin temperature fluctuates."​
There were some recent threads about how body temps are lower than they used to be. Maybe this is another factor that explains the prevalence of vitamin D deficiency.
 

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda
Regarding nomenclature, for those that haven't read the last part here, killciol, -diol, and -triol have 1, 2, and 3 hydroxyl groups in the molecule. The (OH) that sometimes appears in the (discouraged) terms is representing these in relation to killciol/venom D3, with 'killcidiol/25-hydroxyvenom D3 as 25(OH)D3 (one more at the specified position)' and 'killcitriol/1a,25-dihydroxyvenom D3 as 1a,25(OH)2D3 (two more at the specified positions)'. They just show where and how many hydroxylations more from the original molecule. It's simpler to use the killciol, -diol, and -triol. All deadly, should be regulated as drugs.

Cholesterol is being used interchangeably with 7-dehydrocholesterol [7(DH)C], which is its precursor and the actual source of prekillciol, it goes either path with the one to cholesterol being reversible. As the name implies for the precursor, it has less hydrogens in the molecule compared to cholesterol, and when light cleaves its ring (where the term secosteroid comes from), it turns into prekillciol, which next changes the arrangement influenced by temperature.

- Vitamin D (DRI 1997) | Institute of Medicine

upload_2020-1-27_11-11-5.png


upload_2020-1-27_11-11-10.png

- Benefits Of Vitamin D, Symptoms Of Low D, Tips For Increasing + We Talk Estrogen Dominance W/Jodelle
 

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda
Diurnals, some publications require deciphering, this wased one: a mess.

- Sunlight exposure vs. vitamin D supplementation on bone homeostasis of vitamin D deficient rats

For 42 days (6 weeks); then treatments for 10 days.
  • Sd) D− (0-50 IU/kg diet); Sun*
  • Tt) D− (0-50 IU/kg diet); Sup (+1080 IU x3/10 days)
  • Ct) D− (0-50 IU/kg diet); Ctl
  • Ss) D+ (1000 IU/kg diet); Sun*
  • C ) D+ (1000 IU/kg diet); Ctl+
*"[..]exposed to direct sunrays from 1:30 to 2 pm during May 2015 in Riyadh Saudi Arabia (latitude 24°N). Body hair of the sunlight-exposed rats was not shaved. No forms of sunscreen or protection were used to protect the sun-exposed groups; rather, they were left in an open field in separate cages to reduce thermal exhaustion and sweating [11]."
upload_2020-1-29_9-10-54.png
- Bone - Wikipedia

upload_2020-1-29_9-11-13.png

upload_2020-1-29_9-11-23.png

Makes no sense to change the scale and there's a toxic inconsistency with the trabecular separation, should've been inspected as drugs.
 
Last edited:

sugarbabe

Member
Joined
Sep 13, 2012
Messages
3,339
Diurnals, some publications require deciphering, this wased one: a mess.

- Sunlight exposure vs. vitamin D supplementation on bone homeostasis of vitamin D deficient rats

For 42 days (6 weeks); then treatments for 10 days.
  • Sd) D− (0-50 IU/kg diet); Sun*
  • Tt) D− (0-50 IU/kg diet); Sup (+1080 IU x3/10 days)
  • Ct) D− (0-50 IU/kg diet); Ctl
  • Ss) D+ (1000 IU/kg diet); Sun*
  • C ) D+ (1000 IU/kg diet); Ctl+
*"[..]exposed to direct sunrays from 1:30 to 2 pm during May 2015 in Riyadh Saudi Arabia (latitude 24°N). Body hair of the sunlight-exposed rats was not shaved. No forms of sunscreen or protection were used to protect the sun-exposed groups; rather, they were left in an open field in separate cages to reduce thermal exhaustion and sweating [11]."
- Bone - Wikipedia

View attachment 16524

View attachment 16525

Makes no sense to change the scale and there's a toxic inconsistency with the trabecular separation, should've been inspected as drugs.
Niice. Sunlight FTW.
 

LeeLemonoil

Member
Joined
Sep 24, 2016
Messages
2,451
The Role of Skeletal Muscle in Maintaining Vitamin D Status in Winter. - PubMed - NCBI

Abstract
The status of vitamin D is determined mainly by its formation in skin by the photochemical action of solar UVB light (wavelength 290-320 nm) on the precursor 7-dehydrocholesterol. Because of seasonal variation in intensity of solar UV light, vitamin D status falls in winter and rises in summer. It has been presumed that there is no functional store of vitamin D. Thus, to avoid deficiency, a nutritional supply would be required in winter. However, there is now evidence that the main circulating metabolite of vitamin D, 25-hydroxyvitamin D, accumulates in skeletal muscle cells, which provide a functional store during the winter months. The mechanism is mediated by muscle cell uptake of circulating vitamin D-binding protein (DBP) through a megalin-cubilin membrane transport process. DBP then binds to cytoplasmic actin to provide an array of high-affinity binding sites for 25-hydroxyvitamin D [25(OH)D]. The repeated passage of 25(OH)D into and out of muscle cells would account for its long residence time in blood.


Vitamin D and evolution: Pharmacologic implications. - PubMed - NCBI

Vitamin D3 is produced non-enzymatically when the cholesterol precursor 7-dehydrocholesterol is exposed to UV-B, i.e., evolutionary the first function of the molecule was that of an UV-B radiation scavenging end product. Vitamin D endocrinology started when some 550 million years ago first species developed a vitamin D receptor (VDR) that binds with high affinity the vitamin D metabolite 1α,25-dihydroxyvitamin D3. VDR evolved from a subfamily of nuclear receptors sensing the levels of cholesterol derivatives, such as bile acids, and controlling metabolic genes supporting cellular processes, such as innate and adaptive immunity. During vertebrate evolution, the skeletal and adaptive immune system showed in part interesting synchronous development although adaptive immunity is evolutionary older. There are bidirectional osteoimmune interactions between the immune system and bone metabolism, the regulation of both is under control of vitamin D. This diversity of physiological functions explains the pleiotropy of vitamin D signaling and opens the potential for various pharmacological applications of vitamin D as well as of its natural and synthetic derivatives. The overall impact of vitamin D on human health is demonstrated by the fact that the need for its efficient synthesis served in European hunter and gatherers as an evolutionary driver for increased 7-dehydrocholesterol levels, while light skin was established far later via populations from Anatolia and the northern Caucasus entering Europe 9000 and 5000 years ago, respectively. The later population settled preferentially in northern Europe and we hypothesize that that the introduction of high vitamin D responsiveness was an essential trait for surviving dark winters without suffering from the detrimental consequences of vitamin D deficiency.


Evaluation of a Ultraviolet B Light Emitting Diode (LED) for Producing Vitamin D3 in Human Skin. - PubMed - NCBI

Abstract
AIM:
A commercially available light emitting diode (LED) that transmitted narrow band ultraviolet B (UVB) radiation was evaluated for its efficacy and efficiency to produce vitamin D3 in human skin.

MATERIALS AND METHODS:
Human skin samples were obtained from surgical procedures. The LED had peak emission wavelength of 295 nm. Skin samples were exposed to the UVB-LED for varying times and then were analyzed by high-pressure liquid chromatography (HPLC) to determine the vitamin D3 content.

RESULTS:
There was a statistically significant time- and dose-dependent increase in the percent of 7-dehydrocholesterol that was converted to vitamin D3 in the skin type II samples; 1.3%±0.5, 2.3%±0.6 and 4.5%±1.67 after exposure to 0.75 (11.7 mJ/cm2), 1.5 (23.4 mJ/cm2) and 3 (46.8 mJ/cm2) minimal erythemal doses (MEDs), respectively.

CONCLUSION:
The UVB-LED was effective and efficient in generating vitamin D3 in human skin, in vitro. The amount of vitamin D3 production increased in a dose-dependent fashion with increased UVB energy. UVB-LEDs can be developed for devices that can efficiently produce vitamin D3 in human skin.
 

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda
Venomoids are interconvertible, the formation of venom D from prevenom D doesn't require enzymes, they call the rearragement spontaneous (depending on temperature) and venom D is the favored metabolite. After a comprehensive review of the literature in 10 seconds, the skin temperature is around 34 degrees Celsius. It seems that if reversion of venom D to prevenom occurs on skin, it's modest. Prevenom could be used by those who struggle with the formed toxin for delaying the process (because actual degradation requires light), but given that the transdermal uptake of venom D is already poor, it may not justify. It's possible to ingest one or the other as well, with the same principle applying.

- The antirachitic activity of previtamin D3

upload_2020-5-24_19-49-24.png

- Evaluation of the Effect of Isomerization on the Chemical and Biological Assay of Vitamin D

upload_2020-5-24_19-49-32.png


- Large-Area Coating of Previtamin D3 Based on Roll-to-Roll Processing
 
Last edited:

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda

"Many of the patients with schizophrenia at our clinic had vitamin D deficiency, as has been reported by others. Vitamin D levels were much lower in patients than in members of staff. The difference was 34.2 nmol/L (13.7 ng/mL), which is much larger than the mean difference of 5.91 ng/mL reported in a meta-analysis by Valipour and colleagues (9). The difference remained significant after the exclusion of data for non-Caucasian patients. Thus the difference cannot be explained by skin pigmentation. The patients had higher levels of vitamin D after the sunny months of May and June than in April, and this was especially the case in the Caucasian patients. The non-Caucasian patients appeared not to benefit from sunshine as much as the Caucasian patients, which can be expected, especially in northern countries such as the Netherlands."

"Although patients stayed outdoors on sunny days for significantly longer than the minimum time required for adequate vitamin D synthesis, and although they stayed outdoors significantly longer than staff members, this exposure to daylight was not as beneficial as could be expected, as their vitamin D levels were still lower than normal and lower than those of the staff members. As we know from clinical experience that patients are often scantily clothed compared with members of staff and that they do not use sunscreen, this apparently lower synthesis of vitamin D in the patients remains surprising. We do not know whether this is due to the characteristics of our patient group (severe illness refractory to treatment), and, if so, the direction of the association is unclear. This should be investigated further because vitamin D supplementation might have clinical consequences, by preventing somatic complications and possibly psychiatric complications. Interestingly, earlier studies have reported that vitamin D levels are lower in patients with current psychotic disease (13,14) than in patients in remission (14), which suggests that low vitamin D levels are associated with florid psychotic symptoms."​
 
Last edited:

laleto12

Member
Joined
Nov 1, 2019
Messages
183
"Many of the patients with schizophrenia at our clinic had vitamin D deficiency, as has been reported by others. Vitamin D levels were much lower in patients than in members of staff. The difference was 34.2 nmol/L (13.7 ng/mL), which is much larger than the mean difference of 5.91 ng/mL reported in a meta-analysis by Valipour and colleagues (9). The difference remained significant after the exclusion of data for non-Caucasian patients. Thus the difference cannot be explained by skin pigmentation. The patients had higher levels of vitamin D after the sunny months of May and June than in April, and this was especially the case in the Caucasian patients. The non-Caucasian patients appeared not to benefit from sunshine as much as the Caucasian patients, which can be expected, especially in northern countries such as the Netherlands."

"Although patients stayed outdoors on sunny days for significantly longer than the minimum time required for adequate vitamin D synthesis, and although they stayed outdoors significantly longer than staff members, this exposure to daylight was not as beneficial as could be expected, as their vitamin D levels were still lower than normal and lower than those of the staff members. As we know from clinical experience that patients are often scantily clothed compared with members of staff and that they do not use sunscreen, this apparently lower synthesis of vitamin D in the patients remains surprising. We do not know whether this is due to the characteristics of our patient group (severe illness refractory to treatment), and, if so, the direction of the association is unclear. This should be investigated further because vitamin D supplementation might have clinical consequences, by preventing somatic complications and possibly psychiatric complications. Interestingly, earlier studies have reported that vitamin D levels are lower in patients with current psychotic disease (13,14) than in patients in remission (14), which suggests that low vitamin D levels are associated with florid psychotic symptoms."​
So, there's no cure to low levels of Vitamin D ?
 

Lejeboca

Member
Joined
Jun 19, 2017
Messages
634
The Role of Skeletal Muscle in Maintaining Vitamin D Status in Winter. - PubMed - NCBI

Abstract
The status of vitamin D is determined mainly by its formation in skin by the photochemical action of solar UVB light (wavelength 290-320 nm) on the precursor 7-dehydrocholesterol. Because of seasonal variation in intensity of solar UV light, vitamin D status falls in winter and rises in summer. It has been presumed that there is no functional store of vitamin D. Thus, to avoid deficiency, a nutritional supply would be required in winter. However, there is now evidence that the main circulating metabolite of vitamin D, 25-hydroxyvitamin D, accumulates in skeletal muscle cells, which provide a functional store during the winter months. The mechanism is mediated by muscle cell uptake of circulating vitamin D-binding protein (DBP) through a megalin-cubilin membrane transport process. DBP then binds to cytoplasmic actin to provide an array of high-affinity binding sites for 25-hydroxyvitamin D [25(OH)D]. The repeated passage of 25(OH)D into and out of muscle cells would account for its long residence time in blood.

Extending on this sub-topic to physical excersise:

[non-strenuous] Relationship Between Vitamin D Status, Body Composition and Physical Exercise of Adolescent Girls in Beijing - PubMed

From Results:
After full adjustment for body composition, pubertal stage, physical activity and dietary variables, the most important independent predictors of plasma 25(OH)D concentration were body mass index (BMI) (P<0.001), milk intake (P<0.01), organized sports participation (P<0.05) and total physical activity level (P<0.05), which accounted together for 16.1% of the total variance (Table 3).

upload_2020-6-19_21-52-12.png
^1 % (n)

[strenuous] The Effects of Muscle-Building Exercise on Vitamin D and Mineral Metabolism - PubMed

Abstract

Exercise and muscle strength are important determinants of bone mass. Studies were carried out in normal young adult white males to determine the effects of exercise on vitamin D and mineral metabolism. Fourteen men who had engaged in regular muscle-building exercises for at least 1 year and 14 age-matched controls (age range, 19-36 year) were hospitalized on a metabolic ward and were given a constant daily diet estimated to contain 400 mg of calcium, 900 mg of phosphorus, 110 mEq of sodium, 65 mEq of potassium, and 18 mEq of magnesium. Body weight averaged 78 +/- 3 kg in the exercisers and 72 +/- 2 kg in the controls (NS). Serum calcium, ionized calcium, phosphate, magnesium, somatomedin-C, and immunoreactive parathyroid hormone (PTH) were not different in the two groups, whereas serum Gla-protein (39 +/- 5 vs. 24 +/- 2 ng/ml, p less than 0.01), 25-hydroxyvitamin D (23 +/- 2 vs. 16 +/- 2, p less than 0.05) and 1,25-dihydroxyvitamin D [1,25(OH)2D] (40 +/- 2 vs. 29 +/- 2 pg/ml, p less than 0.01) were higher in the exercisers than in the controls. Urinary calcium, phosphorus, sodium, potassium, creatinine clearance, and norepinephrine were not different in the two groups, whereas urinary magnesium (12.6 +/- 1.0 vs. 9.4 +/- 0.5 mEq/d, p less than 0.01) and urinary cyclic adenosine 3',5'-monophosphate (cyclic AMP) (2.52 +/- 0.19 vs. 1.72 +/- 0.20 nM/dl glomerular filtrate, p less than 0.01) were higher in the exercisers than in the controls.
 

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda
Someone mentioned recently the notion that the skin shouldn't be washed after sun exposure to prevent the loss of toxins. It was challenged here:
- Does Vitamin D created by sun exposure get washed off in the shower?

Here's the abstract of the publication. Apparently, they were working with irradiated fatty compounds on the surface of the skin, and just because some products might possess venomic activity afterwards (prevenom would suffice to transfer from an animal to another, activation doesn't need to happen where it originated), they isn't necessarily dealing with the major pool of toxins..

Mike commented the following:

- Dr. Holick - The Vitamin D Solution "wash"

"This is a myth. When you're exposed to sunlight you make vitamin D in the living cells in your epidermis and therefore cannot wash it off by bathing."​

- Vitamin D - Wikipedia

"Vitamin D is produced [mainly] in the keratinocytes of two innermost strata, the stratum basale and stratum spinosum."​
 
Last edited:

Amazoniac

Member
Joined
Sep 10, 2014
Messages
7,836
Location
Not Uganda

"Although UVA- and UVB-induced pigmentations are visually identical, only UVB-pigmentation results in a protection which is as large as corresponding to a factor of about 2 to 3 against DNA photodamage and erythema.[11,35,36] This protection is equivalent to using a sunscreen with a sun protection factor (SPF) of 2 to 3.[4]"

"There are three phases of tanning: immediate pigment darkening (IPD), persistent pigment darkening (PPD) and delayed tanning (DT).[6,7]
  • IPD occurs during the first minutes of exposure to UVA, and then fades within few hours.[6,8]
  • PPD appears within hours of higher doses of UVA exposure and persist up to several days or weeks.[7,9]
  • DT develops over 3–7 days after UVB exposure, and then remains for weeks.[10]
The mechanisms of UVA- and UVB-induced pigmentation are different.[11] UVA induces IPD and PPD through oxidation of pre-existing melanin or melanogenic precursors.[6] IPD is oxygen dependent, and reactive oxygen radicals are considered to be responsible for this process.[7,12,13] PPD is also due to the upward movement of melanosomes toward the surface of the skin.[10] Persons with lightest skin (skin type I) almost do not tan, while IPD and PPD are strongest in moderately and darkly pigmented skin.[14,15] DT results from synthesis of melanin in the melanocytes, followed by melanin distribution to neighboring keratinocytes.[6,7,10]"

"UVA tanning is not involved in melanin production, nor in photoprotection.[7,11,36] The evolutionary role of IPD still remains unknown. Recently we have proposed that the biological role of IPD is protection of folates against photodegradation, which would be of large evolutionary importance for early hominids.[37] We found that IPD had an absorption spectrum covering a number of endogenous photosensitizers in skin, such as porphyrins and riboflavin.[38]"


"In 1903, Niels Ryberg Finsen was awarded the Nobel Prize 'in recognition of his contribution to the treatment of diseases, especially lupus vulgaris, with concentrated light radiation, whereby he has opened a new avenue for medical science.' Finsen discovered that UV radiation was beneficial in treating lupus vulgaris, a skin condition caused by Mycobacterium tuberculosis. UV radiation was the only effective treatment against tubercle bacilli in the skin before the introduction of antituberculous chemotherapy in the 1950s.[68,69] Finsen believed that UV radiation killed Mycobacterium tuberculosis, but the detailed mechanism of action is not known.[68] In 1958 it was demonstrated that the UV radiation in Finsen's lamps can lead to vitamin D production.[70,71] It has been suggested that increased levels of vitamin D could be involved in bacterial killing, and it was considered as the mechanism of effect of UV therapy on lupus.[70,71] However, a few years ago Wulf's group in Denmark tried to find which wavelengths could be emitted by Finsen's equipment and which mechanisms could lead to the photoinactivation of Mycobacterium tuberculosis.[68] Their experiments have suggested that only glass quartz was used in the treatment. This means that only wavelengths longer than 340 nm (UVA) could be emitted through Finsen's lenses.[68] They have also detected that Mycobacterium tuberculosis contains the water soluble porphyrin coproporphyrin III which has its highest absorption peak at 398 nm (the Soret band).[68] Exposure of coproporphyrin III to UVA and blue light leads to the production of singlet oxygen and the photoinactivation of bacteria in the process known as photodynamic therapy (PDT). A mechanism like that operating in PDT seems to be a most plausible explanation why Finsen's therapy worked.[68]"​


- Valtsu's
Sunlight and health: shifting the focus from vitamin D3 to photobiomodulation by red and near-infrared light

- Acute Ultraviolet Light Exposure and Post-Resistance Exercise Serum Testosterone: A Pilot Study in Older Men
⬑ [12] Influence of ultraviolet irradiation upon excretion of sex hormones in the male
 

Lejeboca

Member
Joined
Jun 19, 2017
Messages
634
A recent study on vit. D high dosage (i.e., higher levels of ~60 ng/mL) to ameliorate frailty in older adults. To quote @Amazoniac , "it seems [...] that aging is a toxin" ;) .

The study deals with rat population that became vit. D insufficient in old age. Contrary to many other studies for chronically vitamin D deficient, the authors don't observe differences in all the frailty assessment parameters: "..to our surprise, in this study, we observed few differences between vitamin D treatment groups for these assessments and others. A possible explanation is that we initiated vitamin D insufficiency in aged mice that were vitamin D sufficient
up until that point in contrast to establishing vitamin D insufficiency at younger ages. The declines
in physical performance due to vitamin D insufficiency may take decades for humans or a year or
more in mice to develop.
"

Vitamin D Insufficiency Reduces Grip Strength, Grip Endurance and Increases Frailty in Aged C57Bl/6J Mice

Abstract: Low 25-OH serum vitamin D (VitD) is pervasive in older adults and linked to functional
decline and progression of frailty. We have previously shown that chronic VitD insufficiency
in “middle-aged” mice results in impaired anaerobic exercise capacity, decreased lean mass, and
increased adiposity. Here, we examine if VitD insufficiency results in similar deficits and greater frailty
progression in old-aged (24 to 28 months of age) mice. Similar to what we report in younger mice, older
mice exhibit a rapid and sustained response in serum 25-OH VitD levels to differential supplementation,
including insufficient (125 IU/kg chow), sufficient (1000 IU/kg chow), and hypersufficient (8000 IU/kg
chow) groups. During the 4-month time course, mice were assessed for body composition (DEXA),
physical performance, and frailty using a Fried physical phenotype-based assessment tool. The 125
IU mice exhibited worse grip strength (p = 0.002) and inverted grip hang time (p = 0.003) at endpoint
and the 8000 IU mice transiently displayed greater rotarod performance after 3 months (p = 0.012),
yet other aspects including treadmill performance and gait speed were unaffected. However, 125 and
1000 IU mice exhibited greater frailty compared to baseline (p = 0.001 and p = 0.038, respectively),
whereas 8000 IU mice did not (p = 0.341). These data indicate targeting higher serum 25-OH vitamin
D levels may attenuate frailty progression during aging.

Some highlights:

  • Body weight: Did not find any statistically significant differences between vitamin D levels
  • Body fat percentage: Was higher for insufficient levels of vitamin D
  • Vit. D hypersufficiency improved balance and coordination but not gait speed
  • A trend towards greater bone density was observed in the 8000 IU [hypersufficient] group, which wasn't seen in prior 4-week long studies, which the authors speculate may be due to a longer supplementation, which is needed to observe greater bone density
From Conclusion:
"This [study] implies that the “osteocentric” serum 25-OH vitamin D goal of >30 ng/mL may be adequate for bone health, but may be suboptimal for other tissues such as muscle and the vestibulocochlear system, whereby vitamin D may mediate balance and coordination in aged mice."
 
Last edited:
Similar threads
Thread starter Title Forum Replies Date
A Does vitamin K supplementation deplete vitamin E? Vitamins 25
R Interesting podcast on dangers of vitamin E supplementation E 2
Mito Vitamin D Supplementation Ameliorates Metabolic Dysfunction in Patients with PCOS D 0
metabolizm Vitamin D Supplementation is Improving my Sleep D 23
Mito Vitamin D Supplementation During Winter: Effects On Stress Resilience D 10
berk Vitamin B6 And Zinc And Supplementation Increase Conversion Of Tryptophan Into Serotonin Scientific Studies 8
L The Effects Of Vitamin D Supplementation On Thyroid Function In Hypothyroid Patients: A Randomized, Scientific Studies 3
Mito Effects Of Vitamin D Supplementation In Older Adults With Alzheimer's Disease: A Randomised, Double- D 5
Mito Effect Of High-Dose Vitamin D Supplementation On Volumetric Bone Density And Bone Strength D 1
ddjd Which Co-factors For Vitamin D Supplementation? Ask For Help or Advice 10
A What Is The Problem With High Dose Vitamin E Supplementation? E 11
S Be Wary Of Vitamin D Supplementation D 218
raypeatclips Vitamin D Supplementation Improves Colon Cancer, Does Not Cause Hypercalemia Scientific Studies 57
P Effect Of Vitamin D Supplementation On Pain: A Systematic Review And Meta-analysis Articles & Scientific Studies 0
Giraffe Levels Of Vitamin-D Metabolites After Supplementation And After UV Radiation Scientific Studies 11
Drareg Role Of Vitamin E Supplementation On Serum Levels Of Copper And Zinc In Hemolytic Anemic Patients Wi Scientific Studies 0
P Can The Wound Healing Process Be Improved By Vitamin Supplementation? Experimental Study On Humans Articles & Scientific Studies 0
John Frusciante Vitamin E and K supplementation Fat-Soluble Vitamins 0
P The Effect Of Vitamin A Supplementation On Thyroid Function In Premenopausal Women Scientific Studies 38
Suikerbuik Prenatal vitamin D3 supplementation suppresses LL-37 peptide Articles & Scientific Studies 9
J Vitamin E Supplementation and Serum Levels E 2
J Vitamin E Supplementation: Effect On Sodium And Vitamin K Requirements? E 9
L High-dose Vitamin K2 Supplementation K 28
haidut Vitamin D can force cancer cells to differentiate back into normal Scientific Studies 0
haidut Oral testosterone + vitamin E may treat NAFLD, NASH, cirrhosis in humans Scientific Studies 2
haidut Glucose + vitamin B3 combo synergistic for treating mitochondrial disease Scientific Studies 1
haidut Nine out of ten COVID-19 deaths may be due to vitamin D deficiency Scientific Studies 6
S Vitamin E overuse? Ask For Help or Advice 9
K Why does vitamin K2 mk4 make my skin dry? K 4
B Tissue concentrations of Menaquinone-4 (Vitamin K2 MK-4) Scientific Studies 0
youngsinatra Can High Vitamin D Compensate Lower Dietary Calcium? Ask For Help or Advice 2
youngsinatra Vitamin D - Don‘t Guess, But Test! Ask For Help or Advice 30
cjm "Vitamin E inhibits the activation of NF‐kB, with the greatest inhibition seen with the succinate form." Scientific Studies 2
Pina Kale Water Vitamin K Content Diet 1
youngsinatra Post Your Experience With Topical Vitamin A Here Metabolism 17
M Do vitamin A supplements deplete vitamin A? Ask For Help or Advice 5
Jon2547 Koncentrated K brand of Vitamin K Vitamins 12
M B-Complex or Bee Pollen supplement? Vitamin A supplement or Cod liver oil? Ask For Help or Advice 3
M Best Vitamin A and Copper supplements? Ask For Help or Advice 38
P High dose vitamin k2 around 45mg makes vericocele vanish Male Issues 7
M Does cooking vegetables destroy their vitamin C? Ask For Help or Advice 11
Ras Vitamin C neutralizes chlorine in water C 1
Quelsatron A very confusing month? (vitamin D, magnesium, liver) Ask For Help or Advice 33
Mauritio Vitamin E succinate decreases melanoma size by 650% in vivo Scientific Studies 42
charlie Vitamin B1 in critically ill patients: needs and challenges Scientific Studies 53
C Vitamin D, daily low dose or infrequent high dose? Vitamins 11
G How relevant are serum vitamin tests? Vitamins 11
D Vitamin D Always High! Blood Work, Labs 13
Q Is Vitamin D induced serotonin syndrome possible? Please hear me out... Ask For Help or Advice 60
T VItamin D Megadose accident, what to do Supplements, Pharmaceutical Drugs 6

Similar threads

Top