J.D. Moyer

sci-fi writer, beat maker, self-experimenter

Vitamin D Revisited

Getting vitamin D the natural way.

Recently a few articles and studies have come to my attention that have expanded my understanding of vitamin D metabolism, and raised a few questions as well. As previous posts on this blog have advocated relatively high doses of vitamin D3 supplementation for various conditions (especially asthma), I think it’s my responsibility to consider and address this new information.

Most notably:

1. A study out of the Netherlands has identified genetic variants that are associated with both low levels of 25-hydroxyvitamin D and increased longevity. This is the opposite finding of what we might expect from many studies that link higher vitamin D to lower levels of disease. So what to make of it?

2. Paul Albert and Amy Proal discuss why they think vitamin D supplements are mostly harmful in this post. If I correctly understand their main argument, they think that vitamin D may have a short-term palliative effect by suppressing immune response and reducing inflammation, but may have long-term negative health effects by allowing chronic bacterial and viral infections to grow and spread in the body.

3. Todd Becker discusses why he doesn’t take vitamin D supplements in this post. He references Albert and Proal’s research, and suggests that vitamin D sensitivity might be downregulated by excessive supplementation. He notes that  the biologically active form of vitamin D (1,25-dihydroxyvitamin D3, or calcitriol) is produced from 25-hydroxyvitamin D by the kidneys, but that most tests only measure 25-hydroxyvitamin D. Some people have low levels of 25-hydroxyvitamin D but adequate or even high levels of calcitriol (the biologically active form of vitamin D).

The Marshall Protocol

Here’s my favorite quote from Albert and Proal’s post re: questioning the consensus on vitamin D:

We suspect that people would be less willing to take extremely large amounts of vitamin D if they were actually told, “We’re giving you high doses of a secosteroid that will adjust your hormonal and immune activity in ways not yet fully understood.”

I completely agree! Any concentrated substance we put into our bodies might end up doing more harm than good. We should be cautious, and always use the minimum effective dose.

But reading further, I learned that Proal and Albert are advocates of the Marshall protocol. The Marshall protocol suggests that certain autoimmune diseases, including sarcoidosis, rheumatoid arthritis, fibromyalgia, and many others, can be cured by lowering vitamin D levels (by avoiding sunlight, food sources, and supplements), taking rounds of low-dose antibiotics, and taking a drug called Benicar.

Trevor Marshall is a former electronic synthesizer designer and custom amp builder for AC/DC. What an interesting guy! At some point Marshall was diagnosed with sarcoidosis, an inflammatory autoimmune disease. He eventually developed the Marshall protocol, and founded the Autoimmunity Research Foundation.

The hypothesis behind the Marshall protocol is that most chronic diseases are the result of chronic bacterial infections, wherein invading bacteria lose their cells walls and congregate into biofilms, thus becoming resistant to both antibiotics and the body’s own immune system (as well as detection by most medical tests).

According to Marshall, these biofilm “L-form” bacterial colonies produce metabolites which bind to vitamin D receptors (VDRs). This interferes with the production of antimicrobial peptides (AMPs), and important part of our immune system that helps destroy bacteria, viruses, and fungi.

Albert and Proal have published a study that suggests that in some people with autoimmune disease, levels of 1,25-dihydroxyvitamin D3 (the biologically active form of vitamin D produced by the kidneys) are elevated, while levels of 25-hydroxyvitamin D (measured by most vitamin D blood tests) are low. They  hypothesize that low vitamin D levels are caused by chronic disease, rather than being a predictor of disease.

Vitamin D levels from Blaney/Albert/Proal’s study.

What to make of this? This is the same graph used by Todd Becker in his post re: why he doesn’t take vitamin D supplements, to support his assertion that biologically active vitamin D (1,25-D) isn’t necessarily correlated with tested vitamin D levels (25-D). What Becker doesn’t mention is that this graph represents only people with autoimmune diseases (like sarcoidosis). And if you look at it, you can see that mostly 25-D and 1.25-D are correlated … there are just a few exceptions in the dark blue area.

Is there an alternate hypothesis to explain why vitamin D might worsen sarcoidosis, and possibly other autoimmune diseases? Yes there is. Enter Dr. John Cannell (excerpted from this post):

Furthermore, it is well known that sunlight can cause high blood calcium in patients with sarcoidosis. In fact, sarcoidosis is one of several granulomatous diseases with vitamin D hypersensitivity where the body loses its ability to regulate activated vitamin D production, causing hypercalcemia.

By “loses its ability to regulate activated vitamin D production,” Cannell is referring to the body making too much 1,25-dihydroxyvitamin D3 from 25-hydroxyvitamin D (in the graph, the people in the “elevated 1,25-D” section).

Whatever the reason, it does seem to make sense for people with sarcoidosis, and possibly other autoimmune diseases, to experiment with lowering vitamin D levels. But there may be dangers to implementing the Marshall protocol. Again, from Cannell:

However, if Dr. Marshall’s principal hypothesis is correct, that low vitamin D levels are the result of disease, then he is saying that cancer causes low vitamin D levels, not the other way around. The problem is that Professor Joanne Lappe directly disproved that theory in a randomized controlled trial when she found that baseline vitamin D levels were strong and independent predictors of who would get cancer in the future. The lower your levels, the higher the risk. Furthermore, increasing baseline levels from 31 to 38 ng/ml (77.5 to 95 nmol/L) reduced incident cancers by more than 60% over a four year period. Therefore, advising patients to become vitamin D deficient, as the Marshall protocol clearly does, will cause some patients to die from cancer.

As you can imagine, Marshall has some problems with Lappe’s research. But Cannell’s interpretation of the available data makes more sense to me.

Here’s another post on the Marshall protocol worth reading.

What About Asthma?

I take up to 20,000IU of vitamin D a week. Taking supplemental vitamin D, along with a mostly paleo diet, keeps me free of asthma symptoms.

Why does vitamin D help asthma?

Is vitamin D actually an immunosuppressant? That would line up with Marshall’s ideas. Maybe vitamin D works by somehow calming down the immune system and making it less reactive or “twitchy.” Proal calls vitamin D a “pallative” and predicts that that anti-inflammatory effects we see from supplemental vitamin D will be followed up by longer-term damage (decades later) from chronic bacterial infections.

But vitamin D can boost the immune system, for example fending off colds and influenza A. This makes sense — adequate vitamin D stimulates vitamin D receptors (VDRs) to produce adequate antimicrobial peptides (AMPs). According to Cannell, the AMPs working by poking holes in the lipoprotein coat that influenza A uses to protect itself. Some folks at MIT actually took pictures of the process!

I don’t know exactly why vitamin D helps asthma, and I’m not sure anyone does at this point. If you know of a good, detailed explanation, please add it in the comments.

Too Much Vitamin D

How much is too much? For myself, I’ve noticed excessive thirst, constipation, and less restful sleep from taking too much vitamin D — symptoms that quickly go away when I cut back. Magnesium can potentially ameliorate these symptoms, but I’ve noticed side effects even when taking vitamin D with magnesium glycinate (a highly absorbable form), and even when supplementing with other fat soluble vitamins (vitamin A and K2).

Some people notice negative effects on much lower doses than the ones I find to be therapeutic. Maybe this has to do with low magnesium, or maybe it has to do with higher conversion rate to the biologically active form of vitamin D by the kidneys.

If you are you in good health without taking vitamin D, and you notice negative effects from taking supplemental vitamin D, then either reduce the dose, or stop taking supplemental vitamin D altogether and just get what you need from regular sun exposure.

Note that washing your skin with soap after sun exposure can prevent the vitamin D precursor that forms on your skin from being absorbed into your bloodstream.

On the other hand, if you get a great deal of sun, don’t think that you’re safe from the possibility of getting too much vitamin D. Skin cancer risks aside, sunbathing has been linked to both worsening sarcoidosis [PDF] and kidney stones.

Just because it’s the “natural” way to get vitamin D doesn’t mean it’s totally safe. Plenty of natural things can kill you (like komodo dragons, and sun-worship).

The Heemst Study, and Klotho Protein

From digging deep into the raw data of my 23andMe.com profile, I know that I carry several variants that are associated with lower levels of vitamin D. Unfortunately, I don’t know how to interpret the raw data related to gene CYP2R1, which, according to the the recent Diana van Heemst study, is related to both low 25-hydroxyvitamin D levels, and longevity.

Van Heemst found that “the offspring of nonagenarians, people over the age of 90, with at least one nonagenarian sibling, had lower levels of vitamin D as well as a lower frequency of common genetic variants in the CYP2R1 gene.

From the same article:

“We speculate that offspring might have a higher expression of the klotho protein, which is hypothesized to be an ‘aging suppressor’ protein,” van Heemst and her team wrote.

What do we know about klotho? In mice, klotho suppresses aging. In humans, klotho expression is related to levels of calcitriol. Specifically:

In humans, a specific genotype of Klotho has been found to be associated with lower Klotho gene expression and a decrease in survival of dialysis patients. The association was more pronounced among patients who were not treated with active forms of vitamin D. [study]

[Thank you to user “little bit” on the 23andme forum for the link]

So maybe the van Heemst nonagenarians express higher klotho, and thus more efficiently convert 25-D (from sunshine and supplemental D3) to 1,25-D (calcitriol, activated vitamin D)?

Equally possible is that I’ve misinterpreted the mechanisms described in the klotho article — feel free to comment if you think I’ve gotten it wrong. I’m not trained in medicine or biology!

I wonder if these “high klotho” folks are also vulnerable to hypercalcemia and/or autoimmune problems if they get too much sun, or take too much supplemental vitamin D.


Unfortunately I don’t have one … just more questions. My advice, if I were a doctor, would remain the same. If you suffer from asthma symptoms, try taking supplemental vitamin D3, up to 5000IU a day, along with magnesium, and see if that improves your condition. Going on some variation of the paleo diet (thus reducing systemic inflammation, reducing gut permeability, and modifying the composition of your gut biome) may also help you, as it helped me.

To this I would add — if you experience negative side effective from taking vitamin D3 along with a chelated form of magnesium (like citrate or glycinate) then reduce the dose of vitamin D and increase the magnesium, or just stop taking vitamin D altogether and get some sun.


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  1. Regarding the Netherlands study:
    The margin of error is greater than the detectable levels of vitamin D (with the testing equipment used), so there are no conclusions that can be made.

    It’s important to pay attention to the methodology. Just because someone is published doesn’t mean they are more intelligent than you or I. Their research should be highly scrutinized since future studies may rely on their findings. This could cause countless man-hours and millions of dollars to be wasted.

    Keep up the good work!

    • Thanks Nekurahn! Can you please expand on your comment? What led you to your conclusion re: the margin of error?

  2. nekurahn

    I found someone who can articulate is much better than I. This is from Gerry K. Schwalfenberg, who is a familiy physician and is associate in some way to the University of Alberta.


    ” Dear Editor:

    The Noordam et al. Study on vitamin D and longevity[1] is interesting in that it presents data that is contrary to most studies in the area of vitamin D, chronic disease and mortality. There are several flaws in the study design making it almost impossible to draw any conclusions from it.

    The study design assumes that serum 25(OH)D levels are mainly the result of genetic rather than environmental, lifestyle and dietary factors. We know this is not true. We know that solar UVB exposure, mainly, and oral intake of vitamin D, in a secondary role, are the main determinants of serum 25(OH)D. As well, there is no reason to believe that nonagenarians would have the same or even similar serum 25(OH)D concentrations as their offspring. As a result, offspring are a poor proxy for serum 25(OH)D in nonagenarian ancestors.

    A study completed in Edmonton reported the main determinant for 25(OH)D was UV exposure or supplementation.[2] The 25(OH)D levels shown by the Noordam study, 64 nmol/L for offspring and 68 nmol/L for controls, would both be considered low and would reflect the average deficiency state in the Canadian population.[2]

    The only way that this study design could have shown a benefit of vitamin D on longevity would be if:

    1. Vitamin D were an extremely strong, perhaps overwhelming determinant of longevity 2. Most of the variation in vitamin D levels in people is due to genetics

    Under these two assumptions, perhaps offspring’s vitamin D level could be a surrogate of the parents. If either of these assumptions are not true, they essentially have no power to see any effect. Difference in vitamin D levels is primarily due to environmental factors such as UVB exposure, food and D3 supplement use. This study essentially does not contribute information to the hypothesis.

    Other key issues:

    – Serum measurement – this study used electrochemiluminescence immunoassays on Cobas e411 analyzer from Roche Diagnostics. This equipment is known to be inconsistent[3] and has been discontinued and replaced with a vitamin D-binding-protein-based assay. Roche no longer uses an immunoassay for their new, much improved 25(OH)D method. A 4 nmol/L difference in vitamin D levels between the offspring group and control is within lab error ranges. There is no mention of an average intrassay coefficient of variation, which would be extremely important when the offspring and control groups’ level of vitamin D differ by a mere 4 nmol/l.

    – The authors show no significant differences in vitamin D intake or sun exposure between the groups, yet the media interpret the paper as suggesting the response to the findings would be to diminish those intakes or exposures

    – PTH levels were similar in both groups, offspring and controls. Considering that PTH levels are also a hallmark of vitamin D deficiency this argues against a clinically relevant difference in vitamin D status.

    – A difference of 4 nmol/L between the offspring group (64 nmol/L) and the control group (68 nmol/L), although statistically different, is only a 6% difference overall and may not play a significant role in producing health outcome differences between the groups

    – It is quite possible that the lower vitamin D level in the offspring may simply reflect selection bias, in that the offspring of nonagenarians may spend more time indoors attending to the greater needs of the nonagenarians.

    – The authors do not present data showing that polymorphisms of the CYP2R1 gene are clinically important overall in determining the serum 25(OH)D concentration.

    – Klotho (an anti-aging gene) and its interaction with vitamin D was mentioned in the article as a possible reason for the results in this study. It is true, that when the Klotho gene is absent, elevated and unregulated levels of active vitamin D (1,25(OH)2D) result in premature aging. However when Klotho is present, which is the norm, active vitamin D up regulates Klotho the anti aging gene[4] resulting in slowing of aging.

    – Another area that was not examined is telomere length. A recent study shows that telomeric aging is significantly reduced by higher levels of vitamin D resulting in the equivalent of a 5-year difference.[5] There would be significant benefit on aging and a reduction of age related diseases.

    The interpretation by the authors in proclaiming “these results cast doubt on the casual nature of previously reported associations between low levels of vitamin D and age-related diseases and mortality” is unwarranted.

    With a recent publication last week on November 1, there are now 24 out of 27 studies showing that higher 25(OH)D levels have statistically favorable outcomes for survival. This is quite the opposite of the conclusions of this study. This recent study published last week shows significant benefit from higher levels of vitamin D on mortality.[6]The lowest quartile of 25(OH)D had an 80% increased risk of mortality compared to the highest quartile! The difference in the level of vitamin D was more than 25nmol/l between these groups or more than 100%. These results are consistent with previous literature and the assay has an average intrassay coefficient of variation of 4.2%. Another such study evaluated the risk of entering a nursing home over a 7- year period of time in healthy outpatients over the age of 65. 25(OH)D levels >75 nmol/l resulted in almost a 4 fold risk reduction compared to those that had levels of 25 nmol./l.[7] The difference in the two groups was more than 50nmol/l or 200%.

    Overall this study is of poor design and it is nearly impossible to draw any kind of conclusion from it adding very little to the literature.


    Dr. Gerry Schwalfenberg MD, CCFP, FCFP Assistant clinical Professor in the Department of Family Medicine, University of Alberta

    1. Noordam R, de Craen AJ, Pedram P, Maier AB, Mooijaart SP, van Pelt J, Feskens EJ, Streppel MT, Slagboom PE, Westendorp RG, et al: Levels of 25-hydroxyvitamin D in familial longevity: the Leiden Longevity Study. CMAJ 2012. 2. Genuis SJ, Schwalfenberg GK, Hiltz MN, Vaselenak SA: Vitamin d status of clinical practice populations at higher latitudes: analysis and applications. Int J Environ Res Public Health 2009, 6:151-173. 3. Wagner D, Hanwell HE, Vieth R: An evaluation of automated methods for measurement of serum 25-hydroxyvitamin D. Clin Biochem 2009, 42:1549-1556. 4. Torres PU, Prie D, Molina-Bletry V, Beck L, Silve C, Friedlander G: Klotho: an antiaging protein involved in mineral and vitamin D metabolism. Kidney Int 2007, 71:730-737. 5. Richards JB, Valdes AM, Gardner JP, Paximadas D, Kimura M, Nessa A, Lu X, Surdulescu GL, Swaminathan R, Spector TD, Aviv A: Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women. Am J Clin Nutr 2007, 86:1420-1425. 6. Signorello LB XH, Cai Q, Cohen SS, Cope EL, Zheng W, Blot WJ: A Prospective Study of Serum 25-Hydroxyvitamin D levels and Mortality Among African Americans and Non-African Americans. American Journal of Epidemiology 2012. 7. Visser M, Deeg DJ, Puts MT, Seidell JC, Lips P: Low serum concentrations of 25-hydroxyvitamin D in older persons and the risk of nursing home admission. Am J Clin Nutr 2006, 84:616-622; quiz 671-612.

    Conflict of Interest:

    None declared

    • Thanks for posting the letter in full. Though the experimenters controlled for environmental factors like diet and sun exposure, that does seem to be a small difference between the offspring and control group (4 nmol/L).

      If you are used to reading 25-D test levels as ng/ml instead of nmol/L (as I am), the offspring (nonagenarian) group levels were 25.6 ng/ml, while the control group was 27.2 ng/ml. Much ado about nothing?

      • nekurahn

        Completely agree.

        Let’s keep in mind that because of the abundance of research pointing to the advantages of Vit D, from a research looking to get published’s standpoint, the incentive to have an somewhat against the grain title or position on the topic becomes attractive. Trying to strand out and all.

        No clue if that’s what happened here, but I find it incredible that someone, anyone, would spend years of their life on a project and not be aware of so many obvious flaws.

  3. And my favorite bit of the letter, re: selection bias, is this:
    “the offspring of nonagenarians may spend more time indoors attending to the greater needs of the nonagenarians.”

  4. Linda Lancione

    oh, what a can of worms . . .

  5. This study found that higher vitamin D intake was associated with lower risk of rheumatoid arthritis:

  6. I recently ran into this issue myself, trying to evaluate the risks/benefits of high-dose Vitamin D (in conjunction with Vitamin A and K2). The short answer is that the Marshall Protocol’s theory does not appear to be valid, even though their protocol will help people with sarcoidosis. I found a post on Paleo Hacks with links to a number of articles discussing the issues with the MP: see http://paleohacks.com/questions/22007/vdr-agonists-vitamin-d-and-the-marshall-protocol/22019#22019.

    In order to understand the main problem with the Marshall Protocol, you need some background on how Vitamin D is metabolized.

    Vitamin D3 from diet or sun is converted into 25(OH)D. 25(OH)D is converted by the kidneys into 1,25(OH)2D, and blood plasma levels of 1,25(OH)2D are primarily used to control blood calcium levels. 25(OH)D is also converted locally within tissues to 1,25(OH)2D, and local usage may well be related to immune activity and local suppression of infection.

    1,25(OH)2D is an extremely potent agonist (activator) for our cell’s vitamin D receptors (VDRs). The mainstream belief is that 25(OH)D is also an agonist, but with greatly reduced effectiveness. So increasing your vitamin D levels then increases 25(OH)D levels and will increase the total stimulation of your VDR receptors, which will upregulate immune response, autophagy, and other beneficial processes.

    The Marshall Protocol believes that 25(OH)D is an antagonist of the VDR receptor, that is, the receptor is blocked by 25(OH)D, and is only stimulated by 1,25(OH)2D (see http://mpkb.org/home/pathogenesis/vitamind/metabolism). This would mean that increasing Vitamin D and 25(OH)D would result in *less* activation of your VDR receptors, which would downregulare your immune system, etc. Because the amount of 1,25(OH)2D in the blood plasma is strictly limited to control calcium levels, it does not increase proportionally to the 25(OH)D increase from high Vitamin D intake, so according to the Marshall Protocol you’ll have more antagonist and not as much more agonist, with a net reduction in Vitamin D activity. Reading through the research that has been done, and looking at real-world results from Vitamin D, this just does not appear to be the case.

    In the mouse, the VDR receptor is activated by both 25(OH)D and 1,25(OH)2D. See http://www.ncbi.nlm.nih.gov/pubmed/19944755 It is also activated by 25(OH)D in human tumor cells. So for the MP to be correctly, our cells would have to work differently than another mammal’s, and normal cells differently than cancer cells. So this is possible, but unlikely.

    All of the other evidence, except for rare cases such as sarcoidosis, supports the case for 25(OH)D stimulating the VDR receptor.

    • Thanks for your comment Tim. I came to the same general conclusion re: the Marshall protocol. At the same time, exploring the issue made me realize how much there still is to learn re: the VDR pathway and optimum vitamin D dose (taking both health status and genetics into account). The cases that *don’t* fit the general “supplemental vitamin D in reasonably high doses is helpful” are interesting to me (even though my own experience has been the opposite — with moderate vitamin D supplementation being extremely helpful).

      Is there a threshold over which 25-D levels trigger VDR desensitization? Certainly we see that with other hormones, like insulin. Insulin is “good” because it controls blood sugar, but too much insulin causes tissues to lose insulin sensitivity.

      The study I linked above showed that higher vitamin D levels are generally linked to lower rheumatoid arthritis, but even vitamin D advocate Dr. Cannell tells a story of a man who experiences R.A. flare-ups when he gets to much sun, and Cannell isn’t sure why (but he doesn’t ignore the data point).

      “Minimum effective dose” is probably a good supplementation strategy for vitamin D, as it is with most everything!

  7. tlundeen

    Yes, I agree with “minimum effective dose”, for sure. All of these things have a hill-shaped benefit/dose relationship, even water is toxic at high intake.

    Your 20,000IU/week is only 3,000/day, which might well be low. Many researchers recommend 4,000-5,000/day for most people; if you check your blood levels you can titrate your dose to get to 40-60 ng/pl which looks optimal for most Caucasians.

    There is a case for short-term high-level Vitamin D supplementation, though, in that it can help the body heal and remodel (in conjunction with Vitamins A and K2 and C). There is a fascinating book by Jeff Bowles at http://www.amazon.com/MIRACULOUS-EXTREMELY-SUNSHINE-EXPERIMENT-ebook/dp/B005FCKN2S/ref=sr_1_2?ie=UTF8&qid=1353693538&sr=8-2&keywords=jeff+bowles, and many anecdotal results that parallel his experience.

    My wife and I have been trying to get our teeth to be healthy with ongoing Vitamin D, A (retinol) and K2 intake, which is supposed to do it! What is finally working for us is to take 2 tsps per day of Green Pasture’s Fermented Skate Liver Oil, which typically has 9,000 IU of Vitamin A retinol, 4,500 IU of Vitamin D, and some unknown levels of MK-5..10. In addition, we take a few mg of MK-4 K2 drops (Thorne Research), plus Vitamin D drops from Pure Encapsulations, getting my total intake to 10,000 IU/day of Vitamin D, my wife’s to 20,000 IU/day. With this food/supplement intake, our teeth are finally smooth and glossy feeling, with no plaque or tartar, the way they are supposed to be… We’re going to try backing off the Vitamin D supplement in the spring, when we can start getting Vit D from the sun again.

    The case of sun exposure flaring up R.A. is interesting. The sun also increases melatonin, maybe it is from that… I suggest that anyone with auto-immune issues should eat an auto-immune-type paleo diet (e.g. 100% grass-fed organic meats, pastured egg yolks from chickens not fed soy or GMO grains, wild-caught fish, lots of veggies, some “safe” starches, no grains, no dairy, no legumes, no nightshades, no nuts, no seeds or seed oils, no fruit, no sweeteners, no processed foods, modest or no olive oil/chicken/duck because they are high omega-6). This diet, plus iodine/selenium to rebuild the thyroid, and enough D/A/K2/C to help heal the gut, clear calcium from soft tissues, and rebuild bones/cartilage, will typically produce excellent results; I would expect that this particular case would be in complete remission with this protocol regardless of sun exposure.

  8. tlundeen

    Re: “Is there a threshold over which 25-D levels trigger VDR desensitization? Certainly we see that with other hormones, like insulin. Insulin is “good” because it controls blood sugar, but too much insulin causes tissues to lose insulin sensitivity.”

    It doesn’t look like this happens with Vit D. As blood levels increase, the conversion from sunlight is reduced, the amount of Vit D3 retained in the body goes down, and the percentage converted to 25(OH)D goes down. So it is not easy to get blood levels of 25(OH)D over 100 ng/pL from just sun exposure, and hard to get over 150 ng/dL from supplements.

    In the case of insulin, there is a “rein” control, with glucagon working as needed to increase blood sugar, and net glucose absorption/production resulting from the net excess of insulin vs glucagon. Insulin resistance usually means that baseline glucagon levels are such that the pancreas can’t produce enough insulin to counter the glucagon headwind (as beta cells die off but their matched alpha cells remain and produce a constant glucagon output regardless of need). I don’t know if high insulin produces insulin resistance or if it is due to chronically high glucose levels; I suspect that it is actually from always having glucose levels over baseline (e.g. constantly having blood glucose over 83 will downregulate the number of insulin receptors). My own experience is that as long as my blood glucose gets to 83 or lower once per day, I don’t see any insulin resistance.

    What’s interesting about my experience is that my pancreas appears to be totally healed; my last blood test showed fasting insulin of 2 and blood sugar of 81, which means that there isn’t any glucagon headwind at all. This means that any beta-cell die-off that I had before has been totally reversed and healed. (People with “insulin resistance” typically have much higher insulin and a matching higher than baseline glucose; we probably should measure fasting glucagon instead of insulin as an indication of health and pancreas status.)

    This doesn’t appear to happen with Vit D, there are no counter-regulatory controls — if Vitamin D levels get too high, then the system will downregulate 1,25(OH)2D production to compensate, and the skin also downregulates D3 production with continuous exposure, to limit it at the source. The Vit D system is optimized for high levels of input, and assumes that changes in Vit D intake happen fairly slowly, as with seasonal changes.

    • nekurahn

      tlundeen, thank you for these insightful posts.

      I would like to add a few points to this discussion.

      First, my personal experience. I do not have access to Vit D from food or the sun, so all of mine comes from supplementation. Taking 10,000 UI per day, I reached 45 ng/ml. I was expecting to get at least 75 ng/ml with that dosage.

      Second, I take Vit A & E as a supplement as well. I had taken them for years and one day realized I had made a terrible mistake. As fat-soluble vitamins, they obviously require fat for absorption, yet I had been taking them by themselves without food. When I added a cube of butter, I saw the difference.

      I suspect that part of the reason why different dosages of Vit D can affect people differently is because of the fat (or lack thereof) consumed with the supplement.

      • tlundeen

        Very good point, thanks!

        Are you taking K2 with your D and A? It is critical for good health — it tells the calcium released by the D and A where to go, to keep your soft tissues and arteries clear of calcium, and builds up your bones instead. Taking K2 will clean out blocked arteries and calcified heart valves. 1-2 g/day of Vitamin C will help this process, and help build stronger bones.

        I don’t take Vit E, because the studies don’t support it; my belief is that you should get this as part of your food. If you are taking E, it looks like the tocotrienols and mixed tocopherols are both important, and not to take very much.

        Paul Jaminet has updated his supplement recommendations, a pretty good list except for omitting the fermented fish oils 🙂 http://perfecthealthdiet.com/recommended-supplements/

  9. A side note here, but related to vitamin D … why are high vitamin A levels associated with higher osteoporosis? Vitamin A works against vitamin D in terms of calcium absorption:

    So to reduce osteoporosis risk, adequate D/sunlight, K2, calcium and magnesium, silica (for bone matrix formation), and not too much A (I doubt beta-carotene is a risk). Too much animal protein is probably also problematic unless overall diet is alkaline (lots of veggies).

    • Vitamin A and D are actually synergistic, but they both need K2 in order to work correctly. Optimal is enough A (retinol), D, and K2 for your body to manage calcium properly. See the book K2 and the Calcium Paradox, highly recommended. Also see Chris Masterjohn’s articles for even more detail.

      From my own experience, taking 10,000 IU of retinol, 5,000 IU of D, and enough K2 made a dramatic difference to my tooth health. My teeth are now smooth and glossy, no plaque or tartar. I get mine from fermented skate liver oil (2 tsp per day), which also provides about 1.5g/day of long-chain omega 3 fats, plus quinones, etc. Also helps boost mood and brain function.

  10. Strela

    The issue most people have with Vitamin D nowadays is twofold:
    1. We invented buildings and spend too much time indoors.
    2. We do not eat foods containing nearly adequate amounts of Vitamin D.
    The Inuit for example could not get their Vitamin D from the sun. Yet these people have always had adequate levels of Vitamin D – how? By consuming the organs and fats of animals such as seals and fish which store high amounts of that Vitamin, typically around 6000 IU per day. Compare that to the amount of Vit.D obtained on SAD.

    Meanwhile we lock up all our poultry and cows in confinement so that they may never see the sun hence they make no Vitamin D.

    The kind of Vitamin D that is obtained from eating animals is in fact D3 and is activated in the liver in the same way as the D generated from the sun under the effect of UVB rays.
    Making people scared of supplementing is ridiculous as the D3 in your supplement (made of sheep wool) is the exact same chemical compound as is found in fish and other animals rich in Vitamin D, it is the backup mechanism for getting it when sun is not available, just as nature intended.

    To further compound the problem is the fact that Vitamin D needs Vitamin A to be safe and work properly, along with Vitamin K2 (and possibly others), both of which are also absent in SAD – what with the scaremongering of Vitamin A toxicity (oh no! Liver!) and grain-fed animals which do not contain K2 in adequate amounts.

    • Thanks for the link Meg. For those of us with overactive immune systems (asthma, in my case), mild suppression of the immune system from high vitamin D supplementation can drastically improve quality of life. Side effects and long-term health concerns are low compared to the alternative (inhaled steroids).

      For people in good health, there’s more reason to be cautious with vitamin D supplements.

    • Thanks from me too, Meg — excellent article, much appreciated.

      One of the things that helps calm down and balance overactive allergies is high-dose probiotics. We like the Advanced Naturals 100billion capsules, and are seeing wonderful things with them. Our 4-year old has stopped grinding his teeth at night after 2 days, my wife’s oral thrush is mostly cleared up (she took 17 capsules, which is 1.7 trillion cfus, her second day on them…), and my sleep/mood is much better.

      One of the leading allergy researchers cured his allergies and asthma by diet changes and probiotics…

  11. wow I will ask a question, when are vitamins and minerals so dangerous we have to be warned against them? really? our bodies are designed for them and knows what to do with them, in fact for me d3 supplementation is the only thing addressing my metabolic syndrome, ashma, chornic infections and ravenous appetite, etc. 40 years of trying to get better has not worked (name the diet or supplement or multivita and I have probably done it) lets not confuse a healing crisis with actually over dosing of nutrients. the only thing I never did was d3 supplementation at all, 2000 per day for several weeks did nothing, neither did 3,000 (fearmongering made me scared to go to high now I know the fear is unfounded just probably something to keep us sick for the drug companies to profit from.) I started at 40,000 iu per day for weeks now I am finally at 20,000 after going down to far when I started to feel better , only to have symptoms return by the way I am a lover of the sun, never use sunscreen am careful not to wash it off and still I got no improvment kept getting sicker and sicker (despite trying to improve my diet dramatically) now the trend has reversed and frankly it has been a total surprise, I actually can take a deep breath when I exercise now, by the way what we term intolerance when we improve our diet and take supplements for nutrients we are not getting enough of may just well be the air sacs getting healed and not a immune suppressive affect at all (like inhalers do) I mean it makes sense to me if oxygen is very damaging to the air sacs they will constrict to protect themselves from all that oxygen but once the saces get the nutrients they need they will work fine. the normal response to adrenalin in a emergency is dilatation of air sacs not constrition. also what we term asthma due to allergies just may be inflammation is needed to protect the airways from all that unbuffered oxygen. (don’t know for sure not an expert just an observation.

    • Hi Roberta — thanks for your comment. I continue to take vitamin D and magnesium to control asthma symptoms. A more-or-less paleo diet and about 4K IU vitamin D/a day continues to work for me. Chemistry is complex and everyone is different!

  12. henry77777

    How long did it take for Vitamin D supplementation to ameliorate asthma symptoms for you?

    • For me most of my symptoms were improved by switching to a mostly paleo diet. It was only later that I realized vitamin D played an important role, so in regards to your question I couldn’t tell you exactly. At times I have stopped taking vitamin D and stopped eating well, and noticed a flare-up in symptoms. In cases like that I usually feel better within a few days of improving my diet and resuming vitamin D supplementation at 3-5KIU per day, usually along with some form of chelated magnesium.

      I would say the response time for vitamin D supplementation would depend on your initial levels, but if you are taking enough for your body size then you may notice results in a just a few days. Bromelain may also help for short-term relief.

  13. simone

    Hi Amy we do not know I’m writing from Italy … I wanted to ask a question, as in many studies highlighted by you and Professor Marshall, it often refers to the Pseudomonas aeruginosa bacterium, especially when it comes to biofilm. Now I wonder, since patients with cystic fibrosis, where they almost always have P.As, within the lungs, how can the Marshall protocol suppress PA,? Marshall’s antibiotics are not indicated for this bacterium. I would love to know what you think Thank you and I hope in a reply:?

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