The Great Vitamin D Experiment; Ongoing II : Countdowns, Buddies & Challenges Forum : Active Low-Carber Forums

#151 ^

Wed, Jul-01-09, 08:02

Wifezilla

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Quote:

This Lere person seems to be intent on hijacking this thread for his anti-vitamin D rants, which is really annoying!!!

I agree. Didn't we have someone droning on and on about the Marshall protocol in the last thread?

I suggest that if you are really concerned about too much vitamin d... START YOUR OWN THREAD.

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#152 ^

Wed, Jul-01-09, 08:14

Demi

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Quote:

Originally Posted by Wifezilla

I suggest that if you are really concerned about too much vitamin d... START YOUR OWN THREAD.

I totally agree

This thread is for those of us who are actually interested in Vitamin D, and not for those who wish to continually engage in anti-D rants.

Quote:

Originally Posted by Lere

Final Word

TG for that!

#153 ^

Wed, Jul-01-09, 08:29

Hutchinson Hutchinson is offline

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Quote:

Originally Posted by Lere

My source re. sunscreen can be found through the links I posted in my first comment, here it is anyway.
http://www.nytimes.com/2009/02/17/h...7real.html?_r=1

YouTube - Skin Cancer/Sunscreen - the Dilemma Wearing sunscreen is a recipe for increasing skin cancer incidence. Watch the video to understand why/how sunscreens do more harm than good.

Quote:

One would need to avoid the shade as well as the sun to lower 'D'

""Dr. Turnbull, working with Dr. Kimlin in Australia, showed that UVB light in the shade is strong enough to activate vitamin D production in the skin. Think of UVB as a ping-pong ball. It bounces off lots of things. When you go into the sun—if the sun is high enough in the sky—UVB light comes through the atmosphere and then starts bouncing around. It bounces at you from the ground, buildings, cars, and even the bottom of clouds. Sitting under a shade tree delivered about half as much UVB as sitting in the direct sun. Furthermore, the damaging UVA radiation under direct sun was three times more than under the shade tree. Sitting in the shade in the summer (and the winter in subtropical and tropical latitudes) is a good way to get vitamin D." (Vitamin D Council)

But most of the readers in this forum don't come from Australia or even the southern hemisphere. We all know the sun shines 10% brighter in the southern hemisphere and Australia has parts that are much nearer the equator. What applies to Australia does not apply in the UK or even Canada.

Quote:

The grassrootshealth trial seems to be well designed, I have read that they suggest 2000 IU a day for those who are trying to raise levels. Some people might be healthier on 2000IU/d - if that meant them reducing from 5000IU /d.

I don't agree at all. I have not seen any convincing evidence that levels above 55ng/mL may be harmful.
While 2000iu/daily is a sensible amount for people to take to avoid deficiency it isn't generally sufficient to attain and maintain a level that allows the body to store D3. As it is those with stored D3 that are most likely to survive a challenge it is safer to suggest 5000iu as basic intake with regular 25(OH)D testing to ensure that at least 50ng/mL is attained and preferably 55ng/mL is maintained.

As D3 depletes in the body at 50% every 3 weeks it is easier to lose D3 than store it so it is better and safer to aim higher rather than lower. The adverse consequences of D3 insufficiency are far more likely and damaging that the remote possibility of excess.

With our money financial accounting we take it for granted that it's easier to manage when there is more coming in daily than is expended daily. Similarly only a fool would suggest it isn't a good idea to have a little reserve of cash stashed away in an instant access account for a rainy day.

Now who is going to suggest that it's a smart idea and healthier to have a lower daily intake of vitamin d than the body ideally uses daily, and who isn't aware of the level at which the body has stored D3 available?

#154 ^

Wed, Jul-01-09, 11:50

Jayppers

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Quote:

Originally Posted by Wifezilla

I agree. Didn't we have someone droning on and on about the Marshall protocol in the last thread?

Yes, Zilla... as a matter of fact, that was me. I assume by your statement that you feel that those discussions points were ill suited for this thread?

I figured if anyone would be able to assist in clarifying inaccuracies in theories presented by the Marshall camp, this group would be best suited; And bringing to light those conclusions I came across that refute some of their theories, that this would be the best place for that, as he directly calls into question the benefit of exogenous D, and claims great harm can be done with such, similarly as Lere is claiming.

Last edited by Jayppers : Wed, Jul-01-09 at 18:02.

#155 ^

Wed, Jul-01-09, 13:44

Jayppers

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Quote:

Or northern states in the United States.

Quote:

...it is easier to lose D3 than store it so it is better and safer to aim higher rather than lower. The adverse consequences of D3 insufficiency are far more likely and damaging that the remote possibility of excess.

Agreed... Vieth points out in one of his excellent, more comprehensive papers that the body's system of managing D is adapted better to dealing with excess vs. insufficiency or deficiency. The PDF I've linked to below provides a great illustration of this point on page four (4).

The Pharmacology of Vitamin D, Including Fortification Strategies

Quote:

Originally Posted by Vieth

If one looks at the system of vitamin D metabolism in Figure 2 from the perspective of a system designed to control something, it becomes clear that this is a system better designed to cope with an abundance of supply, not a lack of it. The flow of vitamin D toward 25(OH)D is remarkably inefficient, with most bypassing it. Furthermore, there is no way to correct for deficiency of vitamin D, other than to redirect utilization of 25(OH)D toward 1,25(OH)2D production, which is the pathway most acutely important for life. That is, when supplies of vitamin D are severely restricted, its metabolism is directed only toward the maintenance of calcium homeostasis. ... The environment under which human vitamin D metabolism was effectively designed was for people without clothing, living at latitudes where UVB intensity was always enough to produce a relative abundance of vitamin D. In contrast, most modern humans cover close to 95 percent of skin surface and avoid sunshine. The vitamin D endocrine/paracrine system is not designed to cope with the lack of vitamin D created by our modern culture of clothing and sun-avoidance. Inadequate supplies of vitamin D limit the paracrine control that many tissues need so they can function properly. As a result, it is possible that what we regard as a modern "normal" prevalence of some of the diseases listed in Table 1 could be reduced substantially if we were to increase our intakes of vitamin D (44-47).

#156 ^

Wed, Jul-01-09, 14:05

Jayppers

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Quote:

Originally Posted by Lere

High vitamin D intake is associated with brain lesions in elderly subjects, possibly as a result of vascular calcification (Payne et al., 2007).

This can be avoided by adequate intakes of the other synergisitic fat soluble nutrients, specifically vitamins A & K2 (the latter being of seemingly greater importance in relation to vitamin D). Even though this is simply a hypothesis paper, this is an example of what I mean when I suggest trying to cast your view beyond more conventional vacuum studies that look at isolated nutrients/elements; The human body is simply not that simplistic.

Vitamin D toxicity redefined: vitamin K and the molecular mechanism.

Quote:

Masterjohn C.
Weston A. Price Foundation, 4200 Wisconsin Ave., NW, Washington, DC 20016, United States. ChrisMasterjohn~gmail.com

The dose of vitamin D that some researchers recommend as optimally therapeutic exceeds that officially recognized as safe by a factor of two; it is therefore important to determine the precise mechanism by which excessive doses of vitamin D exert toxicity so that physicians and other health care practitioners may understand how to use optimally therapeutic doses of this vitamin without the risk of adverse effects. Although the toxicity of vitamin D has conventionally been attributed to its induction of hypercalcemia, animal studies show that the toxic endpoints observed in response to hypervitaminosis D such as anorexia, lethargy, growth retardation, bone resorption, soft tissue calcification, and death can be dissociated from the hypercalcemia that usually accompanies them, demanding that an alternative explanation for the mechanism of vitamin D toxicity be developed. The hypothesis presented in this paper proposes the novel understanding that vitamin D exerts toxicity by inducing a deficiency of vitamin K. According to this model, vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D. This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined. The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect. If animal experiments can confirm this hypothesis, the models by which the maximum safe dose is determined would need to be revised. Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K.

But there's more to this than just a hypothesis. Tufts University explored this possibility and concluded that in fact vitamin A does protect against vitamin D toxicity by curbing excess production of vitamin D-dependent proteins.

9-Cis retinoic acid reduces 1alpha,25-dihydroxycholecalciferol-induced renal calcification by altering vitamin K-dependent gamma-carboxylation of matrix gamma-carboxyglutamic acid protein in A/J male mice.

Quote:

Fu X, Wang XD, Mernitz H, Wallin R, Shea MK, Booth SL.

Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.

Matrix gamma-carboxyglutamic acid protein (MGP), a vitamin K-dependent protein, is involved in regulation of tissue calcification. We previously reported that 9-cis retinoic acid (RA) mitigates 1alpha,25-dihydroxycholecalciferol [1,25(OH)(2)D3]-induced renal calcification in a 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung cancer A/J male mouse model. This raised the question if the mechanism(s) underlying this calcification involves vitamin K. We assessed expression and vitamin K dependent gamma-carboxylation of MGP and vitamin K concentrations [phylloquinone (PK), as well as its conversion product, menaquinone-4 (MK-4)] in tissues obtained from NNK-injected A/J male mice fed 1,25(OH)(2)D3 (2.5 microg/kg diet; D group) +/- RA (15 mg/kg diet) for 20 wk. Renal calcification was only observed in the D group (2/10; 20% of the group). Renal MGP mRNA and uncarboxylated MGP (ucMGP) increased in response to D (P < 0.05) but not in response to RA or RA + D. In contrast, gamma-carboxylated MGP increased to 2.2-fold of the control in response to D+RA (P < 0.05) but not in response to RA or D alone. Although all diets contained equal amounts of PK, the kidney MK-4 concentration was higher in the D group (P < 0.05) and lower in the RA group (P < 0.05) compared with the RA+D or control groups. Renal PK concentrations were lower in the RA and RA+D groups than in the control and D groups (P < 0.05). These data suggest that 9-cis RA mitigated 1,25(OH)(2)D3-induced renal calcification by modifying the 1,25(OH)(2)D3-induced increase in ucMGP. The mechanisms by which 9-cis RA and 1,25(OH)(2)D3 alter vitamin K concentrations warrant further investigation.

The study by Vieth, et al, linked to below, shows that increasing daily intake to 5K IU of D3 per day in nursing home residents resulted in no hypercalcemia and no evidence of any adverse effects, and also resulted in significant gains in bone mineral density and lowered parathyroid hormone (as expected).

Long-term effects of giving nursing home residents bread fortified with 125 microg (5000 IU) vitamin D(3) per daily serving.

Quote:

RESULTS: The initial mean (+/-SD) serum 25(OH)D concentration was 28.5 +/- 10.8 nmol/L. After 12 mo, the 25(OH)D concentration was 125.6 +/- 38.8 nmol/L, and it exceeded 74 nmol/L in 92% of the patients. At every 3-mo follow-up, serum parathyroid hormone was lower than at baseline (P = 0.001). No changes in serum calcium or cases of hypercalcemia were observed at the follow-up assessments. Both mean total urinary calcium and the mean urinary calcium-creatinine ratio increased from baseline at one follow-up time point (P < 0.05). Between baseline and the 12-mo visit, z scores for bone mineral density at the lumbar spine and the hip both increased significantly (P < 0.001). CONCLUSIONS: Fortification of bread with much more vitamin D than used previously produced no evident adverse effects on sun-deprived nursing home residents and improved bone density measures. Fortification of bread with 5000 IU vitamin D(3)/d provided reasonable assurance that vitamin D-deficient older adults attained a serum 25(OH)D concentration greater than the desirable objective of >75 nmol/L.

Quote:

Originally Posted by Lere

No Inuit ever got 5000 IU a day for more than a month; it would only be possible when there was a salmon run.

Vitamin D is not isolated just to salmon. They also consumed seal oil regularly, according to Price, which he reported was the richest source of vitamin A he had come across throughout his travels. I highly doubt that this rich source of vitamin A contained only trivial amounts of vitamin D as well, but this is pure speculation on my part.

Last edited by Jayppers : Thu, Jul-02-09 at 06:40. Reason: Included additional paper references 07/02/09

#157 ^

Wed, Jul-01-09, 20:54

Wifezilla

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LOLOLOL

Sorry about that.

I have a short attention span. I tuned out of the Marshall protocol stuff after the 2nd or third post.

#158 ^

Thu, Jul-02-09, 01:45

Demi

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From The LA Times:

Quote:

Evolution to your rescue -- Q&A with Dr. William Meller

July 1, 2009

When you think of evolution, you probably imagine a fish that becomes a bird that becomes a primate. You might also think back to cavemen, or early ancestors who held answers to our genetic makeup today.

However, when it comes to your health, you might think that medicine has…well, evolved to a point where we, as a species, no longer need to listen to cues from days of old. Modern medicine will fix us.

Dr. William Meller, a board-certified internist who runs a medical practice in Santa Barbara, argues to the contrary. He writes in his new book, "Evolution Rx: A Practical Guide to Harnessing Our Innate Capacity for Health and Healing," that health concerns today are best remedied by listening to our bodies more, and paying attention to evolutionary clues that explain exactly what we should do and how we should take care of ourselves.

“Sunlight is life,” he writes, for example. We know we need the sun to survive, and yet many of us shun it -- it has become a common practice to stay out of the sun as much as possible and lather on sunscreen everywhere we go.

Meller explains that sunlight actually helps us more than it harms, by creating vitamin D and lightening our mood.

“This book is really giving people a touchstone of our own history," he says of his book. "I was trying to get across to the general public to really look at this and be skeptical of their doctor and the alternative stuff.”

Meller also looks at human behavior and explains how evolution causes us to gossip, take risks -- even desire physical symmetry in our partners.

The author took time out to talk about his book.

LAT: In your chapter “Sunrise, Sunset,” you write about people needing sunlight, possibly more than we are getting. What about skin cancer? We are told to stay out of the sun as much as possible.

Meller: This is the dominant, conventional thought pattern: that the sun would kill us if we didn’t block it out, or at least age us faster.

The fear of skin cancer is vastly overblown. Basal cells and squamous cells are directly related to your genetic makeup. Very easy to recognize. They almost never metastasize.

Melanoma -- the one that scares us. That one is keeping us out of the sun. It is directly related to genetics and how much sun exposure we get. It is extremely hard to treat.

But because of this fear of the sun, we absolutely have an epidemic of vitamin D deficiency and osteoporosis. And maybe even depression and other cancers.

Osteoporosis is a huge problem among older, white women because they are staying out of the sun because they don’t want to age faster. Vitamin D packs calcium into your bones. Fifteen minutes, three times a week -- it doesn’t take a lot of sun exposure, and it's really extremely beneficial.

http://latimesblogs.latimes.com/boo...iam-meller.html

You can read the full article here as well, as I’ve also posted it in the main forum: http://forum.lowcarber.org/showthread.php?t=398197

#159 ^

Thu, Jul-02-09, 06:48

Jayppers

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Quote:

I have a short attention span. I tuned out of the Marshall protocol stuff after the 2nd or third post.

No worries here; However, considering the magnitude and potential implications of some of the MP-camp's hypotheses on the subject of vitamin D (especially exogenous D from food & supplements), I would have thought that inquiries and informational posts that were authored in an attempt to draw light to their shortcomings would have been of great interest to anyone currently or planning on supplementing with vitamin D3; Assuming one has taken the time to thoroughly review the MP science and understand their published rational as to why vitamin D is viewed with such disdain in their camp.

#160 ^

Thu, Jul-02-09, 06:56

Zuleikaa

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Adverse effects of bisphosphonates: implications for osteoporosis management.Kennel KA, Drake MT.
Endocrine Research Unit, Mayo Clinic, 200 First St SW, Rochester, MN 55905. drake.matthew~mayo.edu.

Bisphosphonates are widely prescribed and highly effective at limiting the bone loss that occurs in many disorders characterized by increased osteoclast-mediated bone resorption, including senile osteoporosis in both men and women, glucocorticoid-associated osteoporosis, and malignancies metastatic to bone. Although they are generally well tolerated, potential adverse effects may limit bisphosphonate use in some patients. Optimal use of bisphosphonates for osteoporosis requires adequate calcium and vitamin D intake before and during therapy. The World Health Organization fracture risk assessment algorithm is currently available to determine absolute fracture risk in patients with low bone mass and is a useful tool for clinicians in identifying patients most likely to benefit from pharmacological intervention to limit fracture risk. This fracture risk estimate may facilitate shared decision making, especially when patients are wary of the rare but serious adverse effects that have recently been described for this class of drugs.

http://www.ncbi.nlm.nih.gov/pubmed/...Pubmed_RVDocSum

#161 ^

Thu, Jul-02-09, 07:00

Zuleikaa

Finding the Pieces

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The Effect of Vitamin D2 and Vitamin D3 on Intestinal Calcium Absorption in Nigerian Children with Rickets.Thacher TD, Obadofin MO, O'Brien KO, Abrams SA.
Department of Family Medicine, Mayo Clinic, Rochester, Minnesota, USA; Department of Family Medicine, Jos University Teaching Hospital, Jos, Nigeria; Division of Nutritional Sciences, Cornell University, Ithaca, New York, USA; USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine Houston, Texas, USA.

Context: Children with calcium deficiency rickets have high 1,25-dihydroxyvitamin D values. Objective: To determine if vitamin D increased calcium absorption. Design: Experimental study. Setting: Teaching hospital. Participants: 17 children with nutritional rickets. Intervention: Randomized to oral vitamin D3 (n=8) or vitamin D2 (n=9) 1.25 mg. Main outcome measure: Fractional calcium absorption 3 days after vitamin D administration. Results: Mean baseline 25-hydroxyvitamin D concentrations were 20 ng/ml (range 5-31 ng/ml). The increase in 25-hydroxyvitamin D was equivalent after vitamin D3 (29+/-10 ng/ml) or vitamin D2 (29+/-17 ng/ml). Mean 1,25-dihydroxyvitamin D values increased from 143+/-76 pg/ml to 243+/-102 pg/ml (P=0.001), and the increase in 1,25-dihydroxyvitamin D did not differ between vitamin D2 and vitamin D3 (107+/-110 and 91+/-102 ng/ml, respectively). The degree of rise in 1,25-dihydroxyvitamin D was explained almost entirely by the baseline 25-hydroxyvitamin D concentration (r(2)=0.72; P<0.001). Mean fractional calcium absorption did not differ before (52.6+/-21.4%) or after (53.2+/-23.5%) vitamin D, and effects of vitamin D2 and vitamin D3 on calcium absorption were not significantly different. Fractional calcium absorption was not closely related to concentrations of 25-hydroxyvitamin D (r=0.01, P=0.93) or 1,25-dihydroxyvitamin D (r=0.21, P=0.24). The effect of vitamin D on calcium absorption did not vary with baseline 25-hydroxyvitamin D values or with the absolute increase in 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D values. Conclusions: Despite similar increases in 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D with vitamin D2 or vitamin D3, fractional calcium absorption did not increase, indicating that rickets in Nigerian children is not primarily due to vitamin D-deficient calcium malabsorption.

http://www.ncbi.nlm.nih.gov/pubmed/...Pubmed_RVDocSum

#162 ^

Thu, Jul-02-09, 08:37

deb34

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in relation to my post about being surprised that I burned after a short time in the sun, I did research on my two PCOS meds and they both cause sun senstivity!

What do I do now? Do I stay permanently at a higher dose of D3 to counteract some of this? With the occasional A thrown in along with the mag, potassium?

BTW, how do you swim at the beach when you're supposed to be covered up to avoid excess sun? Do you all wear regular clothing when swimming or do you only swim for a few minutes? I'm not keen on sunscreen, as I don't think it's effective if applied after sun exposure?

#163 ^

Thu, Jul-02-09, 08:45

capmikee

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I wear sunscreen when I'm going to be out in the sun significantly more than normal. That amounts to about 7 days out of the year. Last year when I went to the shore I got a pretty painful sunburn and I didn't feel great, even though I did use some sunscreen.

When I'm at the shore I wear a hat and sit under an umbrella or cabana as much as possible. But I swim as much as I feel like. I think the best way to prepare for increased sun exposure is to gradually increase your sun exposure beforehand.

#164 ^

Thu, Jul-02-09, 08:48

PS Diva

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Vitamin D doesn't make me totally immune to the effects of sunburn. I can still burn, it just takes a whole lot longer, and I just don't seem to burn badly anymore. I don't wear sunscreen at all if I am going to be out only for a short time. If I am going to be out in direct sun for a long time, I do apply it, especially in places that tend to burn, like my nose and chest. I just don't reapply it as often as the "experts" recommend. I try not to burn, only tan. And generally I have gotten pretty good at figuring out how much exposure I can handle. Your skin is different, so you have to find your own limits.

#165 ^

Thu, Jul-02-09, 08:56

deb34

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thanks for your "beachtime" recommendations. I'm going to the beach for 2 weeks starting next week. I think I'll take the advice to expose slowly and shortly, then stay in the shade.