Vitamin D - Healing My Skin And My Nervous System

[InChristAlone]

The issue is what happens when there is no sunlight? I'm also very interested in UV light for D too, and have purchased a light, although slightly concerned about skin cancer.

Yeah definitely need some source. If I had to use it I'd use it on the skin.

Don't be afraid of skin cancer you don't need a lot of the UVB to make enough. If it's a strong lamp. I burned myself for the first time with mine a couple weeks ago. It was only like 5-6 mins! I had been doing like 3 or less though. It can penetrate deeper than UVA.

 

[Amazoniac]

A Curriculum For Self-education In Biological Nutrition

"The most common etiology of vitamin D toxicity is inadvertent or improper oral use of pharmaceutical preparations. Excessive ingestion of vitamin D (usually greater than 10 000 IU daily; see below) can cause vitamin D intoxication that is recognized by markedly elevated levels of 25(OH)D (usually >150 ng/ml) in association with levels of 1,25(OH)2D that are only slightly elevated. Hyperphosphatemia typically accompanies the hypercalcemia [1-3]. The hyperphosphatemia can be a clue to the etiology of the hypercalcemia as due to vitamin D toxicity since PTH and PTHrP-related disorders usually are associated with reduced serum phosphate or frank hypophosphatemia. The usual setting of vitamin D toxicity is in its use as a therapy for the hypocalcemic disorders: hypoparathyroidism, pseudohypoparathyroidism, osteomalacia, or renal failure. Ingestion of excessive quantities of 25(OH)D, 1-alpha-hydroxyvitamin D, 1,25(OH)2D, dihydrotachysterol, or exuberant use of the topical calcipotriene (Dovonex) for psoriasis can also cause vitamin D intoxication [4] and are further discussed in the succeeding sections. Health-conscious adults have been reported to ingest large doses of megavitamins from over-the-counter supplements, in amounts that may exceed 2 million IU of vitamin D daily [5]. Cancer patients, in particular, have been observed to consume excess nutritional supplements such as calcium, vitamin D, and shark cartilage [6]. Moreover, individuals have mistakenly ingested ergocalciferol 50 000 IU daily instead of weekly [6a,6b].
An over-the-counter supplement called Soladek(r) has been implicated in vitamin D toxicity in a published case report and our own personal experience. This supplement, readily available in the Dominican Republic and in urban areas such as Manhattan, contains over 500 000 IU of vitamin D3 and 120 000 IU of vitamin A per 5 mg vial. The package label for Soladek(r) lists a number of indications for its use, including “hypo and avitaminosis, rickets, growth, dentition, lactation, fractures, infections, convalescence, protection and regeneration of certain epithelium (bronchial, glandular, ocular, cutaneous), corticotherapy, aging, pregnancy.” In the case report by Leu et al. [7], a 60-year-old female with a medical history significant only for osteoarthritis presented with symptoms of hypercalcemia and a serum calcium of 15.2 ng/dl in the setting of recent Soladek(r) use. Her 25(OH)D was >150 ng/ml and PTH and PTH-RP levels were undetectable. CT of the chest, abdomen, and pelvis, skeletal survey, and bone marrow biopsy were all negative for malignancy. However, colonoscopy revealed an anal squamous cell carcinoma which was resected. The patient’s hypercalcemia resolved after discontinuation of Soladek(r) in addition to treatment with intravenous fluids, intermittent furosemide, and a single dose of pamidronate. In our own case series of nine patients, the majority of patients with hypercalcemia in the setting of Soladek(r) use had a second condition that could have contributed to the development of hypercalcemia. No patient had previously experienced hypercalcemia before ingesting Soladek(r), however, indicating that the secondary condition was likely necessary, but not perhaps sufficient to produce hypercalcemia outside of excessive vitamin D supplementation from Soladek(r). Hypercalcemia resolved in all patients after stopping the preparation [8].
It is commonly perceived that excessive sunlight exposure can be associated with vitamin D toxicity. However, studies have documented that full summerlong unprotected sun exposure cannot raise serum concentrations of 25(OH)D much more than 70-80 ng/l (nl: 30-100) [9,10]. These recent observations help to document the widely held belief that sun alone cannot cause vitamin D toxicity. In situations where there is excessive conversion of 25(OH)D to 1,25(OH)2D such as in sarcoidosis or other granulomatous diseases, however, sun exposure can lead to hypercalcemia. Natural foods, in general, other than fatty fishes, eggs, milk, and liver do not contain much vitamin D. Hypervitaminosis D has been associated with drinking milk when inadvertently fortified with massive concentrations of vitamin D. One investigation of eight patients manifesting symptoms of nausea, vomiting, weight loss, hyperirritability, or failure-to-thrive revealed markedly elevated mean concentrations of 25(OH)D of 293 +- 174 ng/ml [3]. Analysis of the milk production facility at the local dairy revealed excessive vitamin D fortification of milk with up to 245 840 IU per liter (232 565 IU of vitamin D3 per quart). Usual fortification of milk in the USA and Canada is 400 IU per quart. Milk is not fortified with vitamin D in most other parts of the world. Generally, milk is the only dairy product that is fortified with vitamin D in the USA. Some yogurts in the USA, however, are now fortified with vitamin D. In addition to milk, vitamin D fortification of natural foods includes certain breakfast cereals, pasta, baked goods, fats, and orange juice [11]. Since the amount of vitamin D fortification is very modest, these foods are not generally suspected as a cause, bearing in mind of course the rare but important example of inadvertent toxic amounts of vitamin D fortification in milk. Of note, in addition, industrial contamination of table sugar with vitamin D3 and consequent severe vitamin D toxicity (25(OH)D 623 ng/ml) has been reported [12].

Vitamin D2 and vitamin D3, although used interchangeably in the treatment of metabolic bone diseases, may differ in toxic potential at higher doses. Prior research has led to the established view that D3 is more potent and effective than D2. As reported by Armas et al. [13] the potency of vitamin D3 is three times that of D2. These investigators found that D2 has a shorter duration of action and that it accelerates the metabolism of D3 in human subjects. However, controversy exists in the literature and more recently Holick et al. [14] argue that both D2 and D3 are bioequivalent."

"The smallest dose of parent vitamin D (cholecalciferol or ergocalciferol) in healthy adults that can produce toxicity and hypercalcemia is not known, but is clearly much higher than the RDA [30]. The current tolerable upper intake level (UL) recommended by the Food and Nutrition Board is 1000 IU daily for infants 0-6 months of age, 1500 IU daily for infants 6-12 months of age, 2500 IU daily for children 1-3 years of age, 3000 IU daily for children 4-8 years of age, and 4000 IU daily subsequently throughout life. Again, controversy exists regarding these guidelines [17a,17b,17c]. Two small well-conducted clinical trials by Heaney et al. [31] and Barger-Lux et al. [32] showed that vitamin D3 10 000 IU daily for 8 and 20 weeks, respectively, did not cause an increase in serum calcium or any adverse effects in the combined cohort of 26 healthy men. In these subjects, mean 25(OH)D levels rose to 85 ng/ml (n = 10) and 88 ng/ml (n = 16) in the two studies, respectively. A review by Hathcock et al. [33] supports the selection of 10 000 IU daily as the UL based on these studies. Other studies of much shorter duration or concurrent treatment with prednisone and/or sodium fluoride have also shown that higher doses of vitamin D (up to 100 000 IU per day) were well tolerated. However, these vitamin D studies were not considered in their risk assessment due to short study lengths and potential confounders.
Individuals manifest wide variations both in their response to hypercalcemic doses of vitamin D and in the duration of the effect. This variation in individual responsiveness might reflect differences in intestinal absorption and vitamin D metabolism, in the concentration of free vitamin D metabolites, in the rate of degradation of the metabolites and conversion to inactive metabolites, and in the capacity of storage sites for 25(OH)D [34]. Factors that enhance susceptibility to vitamin D toxicity and hypercalcemia include increased dietary calcium intake, reduced renal function, coadministration of vitamin A, and granulomatous disorders such as sarcoidosis that render subjects more sensitive to vitamin D (see Chapter 45) [2]. Hypercalciuria in hypervitaminosis D usually presents earlier than hypercalcemia, but it is easily missed for the obvious reason that urinary calcium is not routinely measured."

"Vitamin D toxicity may occur in patients due to any one of the three forms of vitamin D, namely, the vitamin D parent compound, 25(OH)D, or 1,25(OH)2D. Multiple factors may influence susceptibility to vitamin D toxicity and include the concentration of the vitamin D metabolite itself, vitamin D receptor (VDR) number, activity of 1startswithD-hydroxylase, the metabolic degradation pathway, and the capacity of the vitamin-D-binding protein (DBP). Vitamin D2 or D3 toxicity is more difficult to manage than toxicity due to its metabolites 25(OH)D or 1,25(OH)2D. In part, this is due to the extensive lipid solubility of the parent compound in liver, muscle, and fat tissues and corresponding large storage capacity. As a result, the half-life of vitamin D ranges from 20 days to months. In contrast, the biological half-life of the less lipophilic compound 25(OH)D is shorter, approximately 15 days [175]. The biological half-life of the least lipophilic compound 1,25(OH)2D, is much shorter, approximately 15 hours [176]. In general, duration of toxicity is related to the half-life of the vitamin D compound. Thus, the hypercalcemia of parent vitamin D overdose can theoretically last for as long as 18 months, long after dosing is discontinued, because of its slow release from fat deposits. Overdosage of 25(OH)D can persist for weeks also, but excessive 1,25(OH)2D toxicity is more rapidly reversed because 1,25(OH)2D is not stored in appreciable amounts in the body [80]. The toxicity of either parent vitamin D or 25(OH)D is due to 25(OH)D. [worth monitoring blood levels in higher dosages] In an investigation examining the concentrations of vitamin D3 and its metabolites in the rat as influenced by various intakes of vitamin D3 or 25(OH)D, Shepard and DeLuca found that intakes of vitamin D3, ranging from 1 to 10 000 IU daily (0.65 to 6500 nmol/day), resulted in excessive concentrations of vitamin D3 and 25(OH)D3 but not in 1,25(OH)2D3 [177]. Similarly, increased dosages of 25(OH)D3 ranging from 0.46 to 4600 nmol/day resulted in excessive amounts of 25(OH)D3, but not of vitamin D3 or 1,25(OH)2D3. Unlike 1,25(OH)2D whose production is tightly regulated in the kidney, the production of 25(OH)D is not tightly controlled by the liver. The high capacity for 25-hydroxylation of vitamin D in the liver as well as loose regulation at this site allows for massive amounts of 25(OH)D to be generated from large amounts of vitamin D. Thus, excessive concentrations of 25(OH)D are typically measured in vitamin D toxicity. Hypercalcemia appears to result only when 25(OH)D concentrations are consistently above 150 ng/ml (375 nmol/l) in normal individuals [2,178]. As would be expected, PTH levels are suppressed in this form of hypercalcemia. In the setting of toxicity due to overadministration of 1,25(OH)2D3, the active metabolite itself is responsible for the hypercalcemia [179]."

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

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

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

Kidney function is affected because high concentrations of calcium alter the action of vasopressin on the renal tubules. The net result is reduced urinary concentrating ability and a form of nephrogenic diabetes insipidus. This usually presents as polyuria, but rarely is the volume as high as that associated with central diabetes insipidus. Symptoms may include polydipsia, which is an expected consequence of polyuria. Hypercalciuria is one of the earliest signs of vitamin D toxicity and precedes the occurrence of hypercalcemia. The initial hypercalciuria may be ameliorated as renal failure progresses because of reduced calcium clearance. The pathophysiology of hypercalcemia can be rapidly worsened when dehydration develops. When reduced renal blood flow occurs, less calcium is presented to the renal glomerulus, and hypercalcemia can rapidly progress. Renal impairment from the hypercalcemia is reversible if of short duration. Chronic, uncontrolled hypercalcemia can lead to deposition of calcium phosphate salts in the kidney and permanent damage with eventual nephrocalcinosis.[..]"

Health Effects of Artificial Lights - SCENIHR (light penetration)

 

[InChristAlone]

A Curriculum For Self-education In Biological Nutrition

"The most common etiology of vitamin D toxicity is inadvertent or improper oral use of pharmaceutical preparations. Excessive ingestion of vitamin D (usually greater than 10 000 IU daily; see below) can cause vitamin D intoxication that is recognized by markedly elevated levels of 25(OH)D (usually >150 ng/ml) in association with levels of 1,25(OH)2D that are only slightly elevated. Hyperphosphatemia typically accompanies the hypercalcemia [1-3]. The hyperphosphatemia can be a clue to the etiology of the hypercalcemia as due to vitamin D toxicity since PTH and PTHrP-related disorders usually are associated with reduced serum phosphate or frank hypophosphatemia. The usual setting of vitamin D toxicity is in its use as a therapy for the hypocalcemic disorders: hypoparathyroidism, pseudohypoparathyroidism, osteomalacia, or renal failure. Ingestion of excessive quantities of 25(OH)D, 1-alpha-hydroxyvitamin D, 1,25(OH)2D, dihydrotachysterol, or exuberant use of the topical calcipotriene (Dovonex) for psoriasis can also cause vitamin D intoxication [4] and are further discussed in the succeeding sections. Health-conscious adults have been reported to ingest large doses of megavitamins from over-the-counter supplements, in amounts that may exceed 2 million IU of vitamin D daily [5]. Cancer patients, in particular, have been observed to consume excess nutritional supplements such as calcium, vitamin D, and shark cartilage [6]. Moreover, individuals have mistakenly ingested ergocalciferol 50 000 IU daily instead of weekly [6a,6b].
An over-the-counter supplement called Soladek(r) has been implicated in vitamin D toxicity in a published case report and our own personal experience. This supplement, readily available in the Dominican Republic and in urban areas such as Manhattan, contains over 500 000 IU of vitamin D3 and 120 000 IU of vitamin A per 5 mg vial. The package label for Soladek(r) lists a number of indications for its use, including “hypo and avitaminosis, rickets, growth, dentition, lactation, fractures, infections, convalescence, protection and regeneration of certain epithelium (bronchial, glandular, ocular, cutaneous), corticotherapy, aging, pregnancy.” In the case report by Leu et al. [7], a 60-year-old female with a medical history significant only for osteoarthritis presented with symptoms of hypercalcemia and a serum calcium of 15.2 ng/dl in the setting of recent Soladek(r) use. Her 25(OH)D was >150 ng/ml and PTH and PTH-RP levels were undetectable. CT of the chest, abdomen, and pelvis, skeletal survey, and bone marrow biopsy were all negative for malignancy. However, colonoscopy revealed an anal squamous cell carcinoma which was resected. The patient’s hypercalcemia resolved after discontinuation of Soladek(r) in addition to treatment with intravenous fluids, intermittent furosemide, and a single dose of pamidronate. In our own case series of nine patients, the majority of patients with hypercalcemia in the setting of Soladek(r) use had a second condition that could have contributed to the development of hypercalcemia. No patient had previously experienced hypercalcemia before ingesting Soladek(r), however, indicating that the secondary condition was likely necessary, but not perhaps sufficient to produce hypercalcemia outside of excessive vitamin D supplementation from Soladek(r). Hypercalcemia resolved in all patients after stopping the preparation [8].
It is commonly perceived that excessive sunlight exposure can be associated with vitamin D toxicity. However, studies have documented that full summerlong unprotected sun exposure cannot raise serum concentrations of 25(OH)D much more than 70-80 ng/l (nl: 30-100) [9,10]. These recent observations help to document the widely held belief that sun alone cannot cause vitamin D toxicity. In situations where there is excessive conversion of 25(OH)D to 1,25(OH)2D such as in sarcoidosis or other granulomatous diseases, however, sun exposure can lead to hypercalcemia. Natural foods, in general, other than fatty fishes, eggs, milk, and liver do not contain much vitamin D. Hypervitaminosis D has been associated with drinking milk when inadvertently fortified with massive concentrations of vitamin D. One investigation of eight patients manifesting symptoms of nausea, vomiting, weight loss, hyperirritability, or failure-to-thrive revealed markedly elevated mean concentrations of 25(OH)D of 293 +- 174 ng/ml [3]. Analysis of the milk production facility at the local dairy revealed excessive vitamin D fortification of milk with up to 245 840 IU per liter (232 565 IU of vitamin D3 per quart). Usual fortification of milk in the USA and Canada is 400 IU per quart. Milk is not fortified with vitamin D in most other parts of the world. Generally, milk is the only dairy product that is fortified with vitamin D in the USA. Some yogurts in the USA, however, are now fortified with vitamin D. In addition to milk, vitamin D fortification of natural foods includes certain breakfast cereals, pasta, baked goods, fats, and orange juice [11]. Since the amount of vitamin D fortification is very modest, these foods are not generally suspected as a cause, bearing in mind of course the rare but important example of inadvertent toxic amounts of vitamin D fortification in milk. Of note, in addition, industrial contamination of table sugar with vitamin D3 and consequent severe vitamin D toxicity (25(OH)D 623 ng/ml) has been reported [12].

Vitamin D2 and vitamin D3, although used interchangeably in the treatment of metabolic bone diseases, may differ in toxic potential at higher doses. Prior research has led to the established view that D3 is more potent and effective than D2. As reported by Armas et al. [13] the potency of vitamin D3 is three times that of D2. These investigators found that D2 has a shorter duration of action and that it accelerates the metabolism of D3 in human subjects. However, controversy exists in the literature and more recently Holick et al. [14] argue that both D2 and D3 are bioequivalent."

"The smallest dose of parent vitamin D (cholecalciferol or ergocalciferol) in healthy adults that can produce toxicity and hypercalcemia is not known, but is clearly much higher than the RDA [30]. The current tolerable upper intake level (UL) recommended by the Food and Nutrition Board is 1000 IU daily for infants 0-6 months of age, 1500 IU daily for infants 6-12 months of age, 2500 IU daily for children 1-3 years of age, 3000 IU daily for children 4-8 years of age, and 4000 IU daily subsequently throughout life. Again, controversy exists regarding these guidelines [17a,17b,17c]. Two small well-conducted clinical trials by Heaney et al. [31] and Barger-Lux et al. [32] showed that vitamin D3 10 000 IU daily for 8 and 20 weeks, respectively, did not cause an increase in serum calcium or any adverse effects in the combined cohort of 26 healthy men. In these subjects, mean 25(OH)D levels rose to 85 ng/ml (n = 10) and 88 ng/ml (n = 16) in the two studies, respectively. A review by Hathcock et al. [33] supports the selection of 10 000 IU daily as the UL based on these studies. Other studies of much shorter duration or concurrent treatment with prednisone and/or sodium fluoride have also shown that higher doses of vitamin D (up to 100 000 IU per day) were well tolerated. However, these vitamin D studies were not considered in their risk assessment due to short study lengths and potential confounders.
Individuals manifest wide variations both in their response to hypercalcemic doses of vitamin D and in the duration of the effect. This variation in individual responsiveness might reflect differences in intestinal absorption and vitamin D metabolism, in the concentration of free vitamin D metabolites, in the rate of degradation of the metabolites and conversion to inactive metabolites, and in the capacity of storage sites for 25(OH)D [34]. Factors that enhance susceptibility to vitamin D toxicity and hypercalcemia include increased dietary calcium intake, reduced renal function, coadministration of vitamin A, and granulomatous disorders such as sarcoidosis that render subjects more sensitive to vitamin D (see Chapter 45) [2]. Hypercalciuria in hypervitaminosis D usually presents earlier than hypercalcemia, but it is easily missed for the obvious reason that urinary calcium is not routinely measured."

"Vitamin D toxicity may occur in patients due to any one of the three forms of vitamin D, namely, the vitamin D parent compound, 25(OH)D, or 1,25(OH)2D. Multiple factors may influence susceptibility to vitamin D toxicity and include the concentration of the vitamin D metabolite itself, vitamin D receptor (VDR) number, activity of 1startswithD-hydroxylase, the metabolic degradation pathway, and the capacity of the vitamin-D-binding protein (DBP). Vitamin D2 or D3 toxicity is more difficult to manage than toxicity due to its metabolites 25(OH)D or 1,25(OH)2D. In part, this is due to the extensive lipid solubility of the parent compound in liver, muscle, and fat tissues and corresponding large storage capacity. As a result, the half-life of vitamin D ranges from 20 days to months. In contrast, the biological half-life of the less lipophilic compound 25(OH)D is shorter, approximately 15 days [175]. The biological half-life of the least lipophilic compound 1,25(OH)2D, is much shorter, approximately 15 hours [176]. In general, duration of toxicity is related to the half-life of the vitamin D compound. Thus, the hypercalcemia of parent vitamin D overdose can theoretically last for as long as 18 months, long after dosing is discontinued, because of its slow release from fat deposits. Overdosage of 25(OH)D can persist for weeks also, but excessive 1,25(OH)2D toxicity is more rapidly reversed because 1,25(OH)2D is not stored in appreciable amounts in the body [80]. The toxicity of either parent vitamin D or 25(OH)D is due to 25(OH)D. [worth monitoring blood levels in higher dosages] In an investigation examining the concentrations of vitamin D3 and its metabolites in the rat as influenced by various intakes of vitamin D3 or 25(OH)D, Shepard and DeLuca found that intakes of vitamin D3, ranging from 1 to 10 000 IU daily (0.65 to 6500 nmol/day), resulted in excessive concentrations of vitamin D3 and 25(OH)D3 but not in 1,25(OH)2D3 [177]. Similarly, increased dosages of 25(OH)D3 ranging from 0.46 to 4600 nmol/day resulted in excessive amounts of 25(OH)D3, but not of vitamin D3 or 1,25(OH)2D3. Unlike 1,25(OH)2D whose production is tightly regulated in the kidney, the production of 25(OH)D is not tightly controlled by the liver. The high capacity for 25-hydroxylation of vitamin D in the liver as well as loose regulation at this site allows for massive amounts of 25(OH)D to be generated from large amounts of vitamin D. Thus, excessive concentrations of 25(OH)D are typically measured in vitamin D toxicity. Hypercalcemia appears to result only when 25(OH)D concentrations are consistently above 150 ng/ml (375 nmol/l) in normal individuals [2,178]. As would be expected, PTH levels are suppressed in this form of hypercalcemia. In the setting of toxicity due to overadministration of 1,25(OH)2D3, the active metabolite itself is responsible for the hypercalcemia [179]."

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

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

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

Kidney function is affected because high concentrations of calcium alter the action of vasopressin on the renal tubules. The net result is reduced urinary concentrating ability and a form of nephrogenic diabetes insipidus. This usually presents as polyuria, but rarely is the volume as high as that associated with central diabetes insipidus. Symptoms may include polydipsia, which is an expected consequence of polyuria. Hypercalciuria is one of the earliest signs of vitamin D toxicity and precedes the occurrence of hypercalcemia. The initial hypercalciuria may be ameliorated as renal failure progresses because of reduced calcium clearance. The pathophysiology of hypercalcemia can be rapidly worsened when dehydration develops. When reduced renal blood flow occurs, less calcium is presented to the renal glomerulus, and hypercalcemia can rapidly progress. Renal impairment from the hypercalcemia is reversible if of short duration. Chronic, uncontrolled hypercalcemia can lead to deposition of calcium phosphate salts in the kidney and permanent damage with eventual nephrocalcinosis.[..]"

Health Effects of Artificial Lights - SCENIHR (light penetration)

Yeah, I would not be megadosing vitamin D very much due to these problems.

Thanks for the correction, UVA penetrates deeper.

 

[Blossom]

I went deficient a couple years ago while living at latitude 39 by stopping D supplements. I didn't own a UV light but went to a tanning bed about 2x's per week from late fall through early spring. I got as much sunlight as possible the rest of the year. I have a fair complexion so I should absorb a lot of UV but light alone wasn't enough for me. If I had to do it over I would have tested my levels much sooner instead of assuming they must be fine based on my skin tone and UV exposure. Just sharing my experience.

 

[Tenacity]

I went deficient a couple years ago while living at latitude 39 by stopping D supplements. I didn't own a UV light but went to a tanning bed about 2x's per week from late fall through early spring. I got as much sunlight as possible the rest of the year. I have a fair complexion so I should absorb a lot of UV but light alone wasn't enough for me. If I had to do it over I would have tested my levels much sooner instead of assuming they must be fine based on my skin tone and UV exposure. Just sharing my experience.

Thanks for sharing. Latitude 39 feels like it would be low enough to have a lot of vitamin D produced, but I guess not. I live at latitude 50. Lots of factors can influence vitamin D production, including hormonal status and weight.

 

[Blossom]

Lots of factors can influence vitamin D production, including hormonal status and weight.

Yes, that is so true! I know people with my same skin tone living in the same area that have never supplemented vitamin D and do just fine.

 

[raypeatclips]

I went deficient a couple years ago while living at latitude 39 by stopping D supplements. I didn't own a UV light but went to a tanning bed about 2x's per week from late fall through early spring. I got as much sunlight as possible the rest of the year. I have a fair complexion so I should absorb a lot of UV but light alone wasn't enough for me. If I had to do it over I would have tested my levels much sooner instead of assuming they must be fine based on my skin tone and UV exposure. Just sharing my experience.

How many minutes did you use the sun beds when you went? How deficient were you?

 

[Marcus1000]

Hello,

Since I notice you mention you have the problem called P.O.T.S. (I have this aswell), and I have some succes in improving my situation, I thought I'd share what works for me (after years of experimenting).

I'll try to keep it as concise and to the point as possible.

• Male, early 20s
• HR laying down 80, HR standing 160 (at time of diagnosis), so +80 (which is supposedly very severe for P.O.T.S.)
• Currently with my "methods", HR laying down 45, HR standing <90

Notice this is still in improvement and I am confident I will achieve even better results in the future.

By far the most important factor: Diet.
What makes it by far the worst (I've tested every diet in existance over the years):
High fat, high meat, high protein, low carb sort of thing.

What seems to be the best:

• High carb, low/moderate protein, low fat
• (macronutrient ratios of about 80/13/7)
• Daily fat intake 30 gram, daily protein intake 80 gram, carbs high (~3500 total calories)

(I maintain being very lean on this macronutrient ratio aswell, and it feels instinctively the best food to eat, I'd estimate bodyfat around 8%, caliper reading gave 7,2%, I have completely defined abs with veins visible over them, can pinch about 2mm with bodyfat caliper on lower abs).

Currently I am experimenting with certain things, and having even better results than this.
This is namely, "raw/uncooked foods" (i.e. a LOT of fruits).
For some reason certain things have better results than others, despite similar macronutrient contents.
(I.e. Fruit has much better effect than wheat bread, while wheat bread has better effect than cooked oats)

I keep my protein around 80 grams a day.
This might be considered on the low side, especially since I am lifting weights and doing cardio almost daily.
I am still currently trying to find out a way to increase my protein intake that does not leave me feeling worse.

I do not guarantee this will work, but have read similar testimonies online.
Results for me were noticeable within a day, and kept improving (I am still changing things in my diet biet the macronutrient ratio stays like this).
Things I noticed from diet adjustment:
- Sudden motivation to move around/do things
- Energy increased
- Mental fog reduced
- Heartrate while standing reduced by about 60 within timespan of a few days
- More calm

Another big factor what I notice is, I used to crash severely after meals, with these foods (gorging on tons of fruit) I do not crash at all.

I also can visually see this, when I go to mc donalds and eat a high fat high protein meal for example, my feet go red from blood pooling, and I usually have bad sleep the same day too (wake up constantly/nightmares etc, body is just stressed).

Note that I am still not satisfied with the performance of my organism, but that I am still fine-tuning and evolving.
I went from basically bedridden to studying again and doing exercise nearly daily, so that seems a lot of progress so far to me.

 

[Blossom]

How many minutes did you use the sun beds when you went? How deficient were you?

6-10 minutes in the tanning bed. My level was 19.
They were high uvb beds so maybe it would have been better if I had used the type with higher uva.
Edit: I see where @Janelle525 mentions uvb penetrates deeper!

 

[raypeatclips]

6-10 minutes in the tanning bed. My level was 19.
They were high uvb beds so maybe it would have been better if I had used the type with higher uva.

Why would UVA help increase vitamin D? I thought UVB was the only thing that raised vitamin D? I have just purchased a UVB only bulb, say it ain't so, Blossom.

 

[Blossom]

Why would UVA help increase vitamin D? I thought UVB was the only thing that raised vitamin D? I have just purchased a UVB only bulb, say it ain't so, Blossom.

Yeah, I just edited my post! I guess I made the right choice after all. Sorry for the confusion.

 

[InChristAlone]

6-10 minutes in the tanning bed. My level was 19.
They were high uvb beds so maybe it would have been better if I had used the type with higher uva.
Edit: I see where @Janelle525 mentions uvb penetrates deeper!

Amazoniac corrected me it's UVA that goes deeper, but UVB can still burn quite badly.

 

[Blossom]

Amazoniac corrected me it's UVA that goes deeper, but UVB can still burn quite badly.

Thanks for clarifying!

 

[SB4]

Hello,

Since I notice you mention you have the problem called P.O.T.S. (I have this aswell), and I have some succes in improving my situation, I thought I'd share what works for me (after years of experimenting).

I'll try to keep it as concise and to the point as possible.

• Male, early 20s
• HR laying down 80, HR standing 160 (at time of diagnosis), so +80 (which is supposedly very severe for P.O.T.S.)
• Currently with my "methods", HR laying down 45, HR standing <90

Notice this is still in improvement and I am confident I will achieve even better results in the future.

By far the most important factor: Diet.
What makes it by far the worst (I've tested every diet in existance over the years):
High fat, high meat, high protein, low carb sort of thing.

What seems to be the best:

• High carb, low/moderate protein, low fat
• (macronutrient ratios of about 80/13/7)
• Daily fat intake 30 gram, daily protein intake 80 gram, carbs high (~3500 total calories)

(I maintain being very lean on this macronutrient ratio aswell, and it feels instinctively the best food to eat, I'd estimate bodyfat around 8%, caliper reading gave 7,2%, I have completely defined abs with veins visible over them, can pinch about 2mm with bodyfat caliper on lower abs).

Currently I am experimenting with certain things, and having even better results than this.
This is namely, "raw/uncooked foods" (i.e. a LOT of fruits).
For some reason certain things have better results than others, despite similar macronutrient contents.
(I.e. Fruit has much better effect than wheat bread, while wheat bread has better effect than cooked oats)

I keep my protein around 80 grams a day.
This might be considered on the low side, especially since I am lifting weights and doing cardio almost daily.
I am still currently trying to find out a way to increase my protein intake that does not leave me feeling worse.

I do not guarantee this will work, but have read similar testimonies online.
Results for me were noticeable within a day, and kept improving (I am still changing things in my diet biet the macronutrient ratio stays like this).
Things I noticed from diet adjustment:
- Sudden motivation to move around/do things
- Energy increased
- Mental fog reduced
- Heartrate while standing reduced by about 60 within timespan of a few days
- More calm

Another big factor what I notice is, I used to crash severely after meals, with these foods (gorging on tons of fruit) I do not crash at all.

I also can visually see this, when I go to mc donalds and eat a high fat high protein meal for example, my feet go red from blood pooling, and I usually have bad sleep the same day too (wake up constantly/nightmares etc, body is just stressed).

Note that I am still not satisfied with the performance of my organism, but that I am still fine-tuning and evolving.
I went from basically bedridden to studying again and doing exercise nearly daily, so that seems a lot of progress so far to me.

Hey man, also POTS here. I have found that the higher carb, lower fat I go (even <10% fat) my heart pounding and overall POTS gets way worse. It appears that some POTS people really struggle with glucose control. However at the same time, going keto makes me dramatically worse (I think my body struggles to produce adrenal hormones). So far I do best on just enough carbs to keep me out of keto and the rest fat/protein.

This has seemed to improve when I have messed around with B vitamins (thiamine, and riboflavin in particular). So I do intend to try really high carb again but with very high doses of allithiamine and other b vits.

 

[Marcus1000]

Hey man, also POTS here. I have found that the higher carb, lower fat I go (even <10% fat) my heart pounding and overall POTS gets way worse. It appears that some POTS people really struggle with glucose control. However at the same time, going keto makes me dramatically worse (I think my body struggles to produce adrenal hormones). So far I do best on just enough carbs to keep me out of keto and the rest fat/protein.

This has seemed to improve when I have messed around with B vitamins (thiamine, and riboflavin in particular). So I do intend to try really high carb again but with very high doses of allithiamine and other b vits.

Hi man,

My recommendation is just follow your feelings and what works/doesn't work for you. Don't "force" something on yourself because it is "supposed to work", I did this for a long time and it was very bad for me.
I see a lot of people on a bit higher fat lowerish carb diet claiming to have the same benefit as others have on a high carb low fat diet.
I would assume it simply means different things work for different people, as the old saying goes "one man's meat is another man's poison" I guess.

Avoiding stress of any kind also is very important in my opinion for POTS, be it stress from a non-optimal diet for you, relationship stress, working out too agressively, watching too many scary movies, anything that triggers your adrenalin. I find I do better when I don't "push" myself too hard in the moment, but instead take more time and prevent rushing anything.

On a high fat/protein meal immediately I notice a worsening, if you do not have this then I would assume it just works very well for you.
I've read before online that people get shaky/feel bad on high sugar/high carb foods. This is basically what I have with high fat/protein, become very slow/sluggish/shaky. While with high carbs/sugar I do not crash whatsoever.

 

[2thecloudsabove]

Did you test the new D status once you felt recovered, to know what levels where needed for your issues to be fixed?

 

[Tenacity]

Did you test the new D status once you felt recovered, to know what levels where needed for your issues to be fixed?

I don't feel 'recovered' yet, just massively improved. Given the severity of my condition it's going to take a little while for a full recovery, I suspect. I plan to retest my levels in May.

 

[SB4]

@Marcus1000 Completely agree. Though I will try high carb again in the near future but this time with B vitamins as I am very far from cured woth my current set up.