In the first post in this series, I critiqued the “naked ape hypothesis of optimal serum 25(OH)D,” which I believe influences many researchers to interpret uncertainties in the scientific literature in a way that is biased towards recommendations for high intakes of vitamin D that could be harmful to some people, especially without appropriate attention to the nutrient density and balance of the diet, and to the overall context of a healthy diet and lifestyle.
Now I would like to begin critiquing the use of low 25(OH)D on its own to determine vitamin D status. As the series progresses, I will discuss numerous explanations for low 25(OH)D besides vitamin D deficiency. In this post, I will discuss why a deficient intake of calcium can probably cause low 25(OH)D.
I’ve explained the gist of this post and its bottom line over at the Daily Lipid Video Blog. The details follow.
25(OH)D Is Not a Specific Marker of Vitamin D Status
Although commonly used as one, 25(OH)D is not a specific marker of vitamin D status. 25(OH)D is a compound that we make from vitamin D in our liver. Vitamin D will indeed dose-dependently increase 25(OH)D, but many other factors affect the rate at which 25(OH)D is synthesized, used, or degraded. These include variations in the genetics of vitamin D metabolism, intakes of other nutrients, crisis states such as inflammation, and disease states such as cancer.
Some of the factors that cause low 25(OH)D are bad and some of them are good. While there is likely some critical threshold below which low 25(OH)D almost certainly indicates a major problem, this is not necessarily the case with moderately low 25(OH)D. In order to determine whether moderately low 25(OH)D is a good thing or a bad thing, and in order to understand what, if anything, to do about it, we need to understand why it’s low.
Let’s begin by considering one of the “bad” things that can cause low 25(OH)D besides a deficiency of vitamin D itself: a deficiency of calcium.
Vitamin D Regulates Serum Calcium
In order to understand why a deficiency of calcium can cause low 25(OH)D, we need only consider the most well established and best understood role of vitamin D: to regulate the level of calcium in our blood.
If our blood level of calcium drops for any reason — for example, if we aren’t consuming or absorbing enough calcium from our food — our endocrine system quickly launches a systematic program to bring that level back to normal (1). Our parathyroid glands ramp up their production of parathyroid hormone, which sends a signal to our kidneys to ramp up their conversion of 25(OH)D to calcitriol, the most active form of vitamin D. Calcitriol then increases serum calcium in two ways: preventing loss of calcium in the urine and feces, and extracting calcium from bone.
Or one could splice it three ways: we absorb more calcium from our food, and we lose more from our bones into our blood, but we lose less from our blood into our urine.
Even a slight increase in calcitriol can lead to a big drop in 25(OH)D. This may seem counter-intuitive at first, but it makes more sense if we realize that when we look at the concentration of a compound in the blood, we are taking a static snapshot of a dynamic process. Molecules are always coming and going. As a result, maintaining a constant blood level of a given compound requires a continuous supply of that compound itself. Since calcitriol is made from 25(OH)D, maintaining a given concentration of calcitriol also requires a continuous supply of 25(OH)D.
Calcitriol disappears far more rapidly than 25(OH)D (2). The amount of 25(OH)D that would sustain a certain concentration of itself in the blood for a day would only maintain the same concentration of calcitriol for an hour. So if the body decides to maintain a slightly higher concentration of calcitriol, it would have to levy a much heavier tax on the supply of 25(OH)D.
We should expect, then, that a deficient intake of calcium will lead to increased production of calcitriol, and thereby to depletion of 25(OH)D.
Would an excess of calcium, conversely, cause higher than normal 25(OH)D? Maybe, but not necessarily. While excess calcium would be expected to suppress the production of parathyroid hormone and calcitriol, thereby sparing 25(OH)D, it also elicits additional responses to suppress serum calcium: in response to high levels of calcium, our thyroid glands produce calcitonin, which not only blocks the loss of calcium from bone (1), but appears to stimulate the production of an enzyme that degrades both 25(OH)D and calcitriol to other products generally thought to be inactive (3). Excess calcium could, therefore, have conflicting effects on 25(OH)D, preventing its conversion to calcitriol but increasing its degradation through an alternative pathway, perhaps leading to no net change in 25(OH)D at all.
Overall, then, we would expect that a deficiency in calcium would cause low 25(OH)D, and that correcting the deficiency would normalize the 25(OH)D, but that beyond a certain threshold, increasing calcium intake might not increase 25(OH)D any further.
Let’s take a look at some of the evidence suggesting this is indeed the case.
Calcium Deficiency Depletes 25(OH)D in Rats
In rats, experimental calcium deficiency in the presence of adequate vitamin D caused a more than four-fold elevation of calcitriol and a more than 60 percent drop in 25(OH)D from just under 40 ng/mL to about 15 ng/mL (4) (click to enlarge):
Consistent with the physiology I described above, calcium deficiency also caused a large increase in parathyroid hormone. These findings indicate that, as expected, dietary calcium deficiency causes our parathyroid glands to make more parathyroid hormone, thus increasing the conversion of 25(OH)D to the more active calcitriol. As a result, 25(OH)D tanks.
A similar study came to similar conclusions, but also looked at a number of additional enzymes involved in vitamin D metabolism (5). This study found that calcium deficiency stimulates the production of calcitriol regardless of vitamin D intake, while vitamin D deficiency has no effect on calcitriol levels. When both calcium and vitamin D were adequate, the rats produced more of an enzyme that degrades 25(OH)D. Despite the increase in this enzyme, 25(OH)D was nevertheless highest in that group. This suggests that at least up through the recommended intakes, the predominant effect of calcium is to spare 25(OH)D.
Perhaps with excessive calcium intake, the sparing and degrading effects would balance out differently. If that is the case, it could explain why some human studies described below have had trouble demonstrating an effect of calcium intake on 25(OH)D.
Ambiguous But Supportive Evidence in Humans
To my knowledge, no studies have definitively demonstrated an effect of calcium intake on 25(OH)D in humans. This is most likely because it has hardly been studied rather than because the effect does not exist. Indeed, the basic physiology works the same in humans and rats, and the likelihood that calcium deficiency doesn’t deplete 25(OH)D in humans strikes me as extremely small.
Several randomized controlled trials have failed to show any effect of calcium supplementation on 25(OH)D (6, 7, 8).
Should we have expected them to? Not really. There are some important obstacles to showing this effect in humans, particularly in Americans, who tend to have high calcium intakes, especially the older Americans targeted for calcium supplementation studies who are usually already keeping an eye on their calcium intake.
First, none of these studies were dealing with true calcium deficiency. Before supplementation, mean calcium intakes were roughly 700 mg/day (8), 800 mg/day (7), and 1000 mg/day (6). It may be that calcium intakes lower than these cause drops in 25(OH)D, but that calcium intakes higher than these have little effect on 25(OH)D.
Second, as I am in the process of explaining through this series, many different factors affect 25(OH)D. 25(OH)D levels in these studies were roughly 26 ng/mL (8), 30 ng/mL (7), or unreported (6). Since the individuals in these studies by definition fall both above and below the mean, these studies likely had some individuals who had pretty low 25(OH)D and others who did not. Similarly, while the mean calcium intakes were reasonably adequate there may have been individuals with calcium intakes much lower than the mean. Of those with low 25(OH)D, then, there may have been some individuals whose low 25(OH)D was a result of calcium deficiency, but these individuals could have been few and far between.
The ideal way to test this principle in humans would be to specifically target individuals with low calcium intakes and low 25(OH)D and randomize them to supplementation with calcium or a placebo, but I am not aware of such studies.
Reference 8 nevertheless seems to provide some slightly supportive evidence, statistically underpowered thought it may be (click to enlarge):
As can be seen when comparing the data in the red square to that in the green square, the placebo group had zero people with “sufficient” 25(OH)D, while the calcium supplementation group had five fewer people in the “deficient” and “insufficient” ranges, with those five missing folks being found — score! — in the “sufficient” range.
The evidence is not all that convincing because the difference is not statistically significant and calcium supplementation didn’t seem to help the people who were also getting vitamin D at all, but it is possible that if this study had been much larger or had specifically targeted people with low calcium intake and low 25(OH)D, it would have demonstrated the effect more convincingly.
There is some observational evidence suggesting that one of the reasons rural Indians with abundant sun exposure have such low 25(OH)D is because of low intakes of bioavailable calcium (9). These particular Indians consume diets dominated by cereal grains, with relatively few animal products and vegetables providing only five percent of calories. Cereal grains provide very little calcium but large amounts of phytate, which inhibits the absorption of calcium. As calcium intake increases among these subjects and phytate intake declines, 25(OH)D status improves:
Perhaps one of the reasons that the Maasai and Hadza have considerably higher 25(OH)D status than rural Indians (as discussed in the previous post in this series) despite all three groups being exposed to abundant sunshine is because calcium deficiency is prevalent among neither the Maasai nor the Hadza. The Maasai herd cattle and consume large amounts of dairy products. In addition to animal products, the Hadza consume some 14 percent of their diet as baobab, which some investigators have said is one of the Hadza’s five food groups (10), and which is very rich in calcium (11).
Low 25(OH)D? Check Your Calcium Intake!
Although randomized controlled trials have thus far not provided the definitive evidence that low calcium intake is a cause of low 25(OH)D in humans, this is far more likely to be because no trials have adequately addressed the question than because the interaction does not exist. Experimental evidence in rats has demonstrated the interaction beyond doubt, and the physiology — which very clearly implies the interaction — appears to be, for all relevant intents and purposes, identical between humans and rats. It is thus extremely unlikely in my opinion that low calcium intake is not a cause of low 25(OH)D in humans.
The practical implications are two-fold. First, we are in desperate need of clinical trials to address this question adequately. In the mean time, if someone has low 25(OH)D, they should assess their calcium intake.
Obtaining a bird’s-eye view of one’s calcium intake is relatively easy to do without the help of a professional, any fancy software, or even an internet database. Most Americans and others in modern, industrial society have easy access to just three sets of foods that are rich in highly absorbable and utilizable calcium: dairy products, edible bones, and cruciferous vegetables.
Most people are well aware that dairy products are rich in calcium.
Bone broth is delicious and provides important bone-building trace minerals and amino acids, but it contains relatively little calcium relative to our overall requirement. The soft edible bones in canned fish, however, or, for adventurous eaters, the soft edible knobs on the ends of small chicken bones, are all very rich in calcium.
Calcium is widely distributed in plant foods, but the amounts are often small and in some calcium-rich leafy greens like spinach, the availability is terrible. Calcium absorption from kale, however, is better than that from conventional, commercial milk (12). Numerous cruciferous vegetables provide anywhere from half as much to twice as much absorbable calcium, cup for cup, as commercial milk (13).
As a rule of thumb, then, I would say that if someone has low 25(OH)D and she is eating two to three servings of dairy products or soft, edible bones, or two to three cups of cruciferous vegetables per day (which have their downsides), then calcium deficiency is unlikely to be the explanation. If one is not eating these foods, however, it could very easily be the explanation. In such a case, the person has little to lose and much to gain by including more calcium-rich foods.
Because the calcium content and availability is quite variable even between different cruciferous vegetables, and because many other plant foods contain smaller amounts of calcium that could contribute to the overall intake or, on the other hand, anti-nutrients that could detract from the overall intake, greater attention should be paid to this possibility if someone is attempting to meet their calcium requirement with plant foods alone. If such a person has low 25(OH)D and thinks she is getting enough calcium, she would do well to record her dietary habits, research the relative amounts of calcium and anti-nutrients in the foods she is eating, and consider consulting a registered dietician or another type of professional nutritional consultant.
If poor calcium intake is depleting vitamin D stores and thereby causing low 25(OH)D, throwing extra vitamin D at the problem is not the optimal solution. It will not be the most effective way of normalizing the hormonal milieu or preventing bone loss. Only calcium can correct a calcium deficiency. Throwing a calcium supplement at the problem is not the ideal solution either. Both vitamin D and calcium supplements leave the diet lacking in a broad spectrum of other important nutrients found in dairy products, bones, and leafy greens.
In future posts in this series, I will discuss other potential causes of low 25(OH)D besides poor vitamin D exposure. By the end of the series, I’ll provide a systematic approach for interpreting the likely cause of low 25(OH)D. In the mean time, I’d love to hear your thoughts in the comments!
1. Institute of Medicine (US) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium; Ross AC, Taylor CL, Yaktine AL, et al., editors. Dietary Reference Intakes for Calcium and Vitamin D. Washington (DC): National Academies Press (US); 2011. p. 40. [NCBI Bookshelf]
2. Jones G. Pharmacokinetics of vitamin D toxicity. Am J Clin Nutr. 2008;88(2):582S-6S. [Pubmed]
3. Gao XH, Dwivedi PP, Omdahl JL, Morris HA, May BK. Calcitonin stimulates expression of the rat 25-hydroxyvitamin D3-24-hydroxylase (CYP24) promoter in HEK-293 cells expressing calcitonin receptor: identification of signaling pathways. J Mol Endocrinol. 2004;32(1):87-98. [PubMed]
4. D’Amour P, Rousseau L, Hornyak S, Yang Z, Cantor T. Influence of Secondary Hyperparathyroidism Induced by Low Dietary Calcium, Vitamin D Deficiency, and Renal Failure on Circulating Rat PTH Molecular Forms. Int J Endocrinol. 2011;2011:469783. [PubMed]
5. Anderson PH, Lee AM, Anderson SM, Sawyer RK, O’Loughlin PD, Morris HA. The effect of dietary calcium on 1,25(OH)2D3 synthesis and sparing of serum 25(OH)D3 levels. J Steroid Biochem Mol Biol. 2010;121(1-2):288-92. [PubMed]
6. Elders PJ, Lips P, Netelenbos JC, van Ginkel FC, Khoe E, van der Vijgh WJ, van der Stelt PF. Long-term effect of calcium supplementation on bone loss in perimenopausal women. J Bone Miner Res. 1994;9(7):963-70. [PubMed]
7. McKane WR, Khosla S, Egan KS, Robins SP, Burritt MF, Riggs BL. Role of calcium intake in modulating age-related increases in parathyroid function and bone resorption. J Clin Endocrinol. Metab. 1996;81(5):1699-703. [PubMed]
8. McCullough ML, Bostick RM, Daniel CR, Flanders WD, Shaukat A, Davison J, Rangaswamy U, Hollis BW. Vitamin D status and impact of vitamin D3 and/or calcium supplementation in a randomized pilot study in the Southeastern United States. J Am Coll Nutr. 2009;28(6):678-86. [PubMed]
9. Harinarayan CV, Ramalakshmi, Prasad UV, Sudhakar D, Srinivasarao PV, Sarma KV, Kumar EG. High prevalence of low dietary calcium, high phytate consumption, and vitamin D deficiency in healthy south Indians. Am J Clin Nutr. 2007;85(4):1062-7. [PubMed]
10. Berbesque JC, Marlowe FW, Crittenden AN. Sex differences in Hadza eating frequency by food type. Am J Hum Biol. 2011;23(3):339-45. [PubMed]
11. Prentice A, Laskey MA, Shaw J, Hudson GJ, Day KC, Jarjou LM, Dibba B, Paul AA. The calcium and phosphorus intakes of rural Gambian women during pregnancy and lactation. Br J Nutr. 1993;69(3):885-96. [PubMed]
12. Heaney RP, Weaver CM. Calcium absorption from kale. Am J Clin Nutr. 1990;51(4):656-7. [PubMed]
13. Weaver CM, Heaney RP. 2006. Food sources, supplements, and bioavailability. In: WeaverCM, HeaneyRP, editors. Calcium & human health. Totowa , N.J. : Humana Press. 137 p. [Springer]🖨️ Print post
This is an excellent series. I am looking forward to the next parts.
At last some rationality about vitamin D!
I have been exasperated by the lack of science behind the support for extraordinary levels of supplementation that are often supported by seeminly intelligent people.
Measuring 25OHD is just silly. It is a storage mechanism for excess vitamin D because we cannot readily excrete it. Raising levels of this makes no sense.
Looking forward to part 3. I had a few questions on the calcium and vitD supplementation. Are there downsides to supplementing calcium and vitD together besides the “missed opportunity” of getting the other nutrients that come from the calcium rich foods? Are you mentally differentiating pastured raw milk from factory farmed ultra-pasteurized milk here or is that irrelevant with respect to calcium content? Are all calcium forms equally bioavailable, or are there some forms and co-factors that are preferable?
I hope this request for slightly more detail doesn’t distract from my appreciation of the information in the current form 🙂
Thanks in advance.
JP DC says
One of the keys to health for the body is, the ease at which it can maintain it’s homeostasis or balance in spite of an ever changing environment. Stress in the form of mechanical, emotional or nutritional/chemical continually challenges homeostasis. Using high doses of any isolated substance challenges this balance. One reason drugs have side effects is because they challenge the homeostasis, or in other words they make certain organ systems work hard at detoxification (which uses up valuable resources) but also detracts the organs from contributing to maintaining balance. The drug is a stress to the body which makes it work harder. High dose supplements are also a stress which makes it work harder (just not as hard as a “drug”). The key to health is to make the body’s job easier not harder.
Gary Ogden says
Do you think taking cod liver oil/high vitamin butter oil through the winter for A/D/K2 is sufficient to maintain good status of those vitamins, in a dairy-rich and nutrient dense diet? What about the necessity of taking them during the summer? BTW your Foreword to “Death…” is a fine piece of writing. I had no idea you had literary talent. (You do) Also, I liked the natto in Atlanta, but don’t plan to make a habit of it.
Cory Altabet, DC says
Hi Dr. Masterjohn, many years ago I wrote and article on my my website regarding the issues with oral vitamin d supplement and it role in calcium metabolism. While all my assertions where about the basic calcium metabolism it definitely raises the questions about oral supplement issues. When I saw your series on Vit d I was excited in that I knew it would go way more in depth than my article. Thanks so much for doing this series. Here is the link to my article that explains the potential pitfalls of oral Vit D.
Mary E says
The above is consistent with my experience. I get vitamin D from the sun and cannot tolerate D from supplements or UVB lamps. The amount I get is consistent every year. My 25D usually quickly jumps up to the high 40’s ng/ml from sun exposure. Last summer it was only at 26. I had occasional carpopedal spasms suggestive of tetany, and my parathyroid hormone was below the reference range (I believe from supplementing vitamin A for dangerously low vitamin A per blood test). My 1,25D was at the top of the reference range, 60.5 pg/ml–way too high. I lowered the vitamin A amount, and parathyroid returned to normal. (Never toxic on A per blood tests.) I experienced similarly elevated 1,25D several years ago for another reason, and my 25D was again in the 20’s rather than the usual 40’s.
This is a terrific series, Chris. It’s personally relevant and I’m very interested in learning the other potential causes for low Vitamin D levels. I especially appreciate the effort you make to explain these topics in a way that is understandable to a non-scientist such as myself.
A couple of years ago, my 25(OH)D level was measured at 11 ng/mL, despite my taking 2000 IUs of D3/day during the two or three years preceding the test and getting weekend sun exposure. (My doctor thought that amount of supplementation was too much and wanted to make sure my D level hadn’t gone too high.) At the time, I was eating dairy, sardines or salmon with bones, and plenty of calcium-rich vegetables daily.
But I was also eating a lot of raw seeds and nuts, particularly almonds. Almonds look to be a decent source of calcium, but I’m guessing the calcium and other minerals were less available — or not available at all — due to their phytic acid content. I’ve since taken to soaking and then drying almonds and sunflower seeds in a low heat oven, a la Sally Fallon, in an effort to decrease phytic acid and increase mineral availability.
What I’d like to know, though, if you have the opportunity to respond, is whether the phytic acid and/or other anti-nutrients in grains, nuts, legumes, etc., not only interfere with the bio-availablity of the minerals in those items, but also in the absorption of the minerals in foods eaten along with them?
For example, would eating oatmeal along with sardines keep some or all of the calcium in the bones from being absorbed? Or the calcium in cheese mixed with whole wheat pasta? If that’s the case, then I’m probably not getting nearly as much (absorbable) calcium as I thought I was and the daily menus will have to be adjusted accordingly.
Very interesting, I also once wondered whats up with vitamin d and animals that never go into the sun or eat any vitamin D like bats or deep water fish. Its seems bats are vitamin D deficients but not mineral deficient.
Have you seen this study discussing 25(OH) Vit. D’s apparent anti-carcinogenic effects in vivo (in rats)? Considering how widely useful calcitriol/25(OH) Vit D are in many many metabolic processes – shouldn’t we expect the level(s) to change significantly depending on metabolic issues that may be present?
Looking forward to the rest of the series!
[1a,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis
David I says
A bit off-topic, but your mention of cruciferous veggies and their downsides raised a question in my mind about preparation. All the info I seem to find on vitamins and antinutrients seem to be on steaming vs boiling vs microwaving.
Where does roasting fit into all this? My favorite method for brussels sprouts or cauliflower is 350 F for 20-40 minutes. That to raise the internal temp quite high, but doesn’t drain anything away via cooking water…
Patrick Taylor says
Thanks for your excellent work.
I just got some lab results. My 25(OH)D is a bit low (it’s 22). However, my calcium was also measured and is well within normal range (it’s 9.3 mg/dL). Is that calcium measure a reliable indicator that my calcium intake is probably sufficient and is unlikely the cause of my low 25(OH)D?
Jack Cameron says
The information you have provided debunking the “naked ape theory” of vitamin D has clarified the findings of a couple of studies on vitamin D levels and mortality that found the lowest CVD and all cause mortality at vitamin D levels that are much lower than vitamin D levels widely promoted by the “experts”.
A 2010 study, “Plasma vitamin D and mortality in older men: a community based prospective cohort study”, found the lowest hazard ratio of mortality and cancer incidence when the range of vitamin D was between 18 and 37 ng/ml
A 2008 study “25-hydroxyvitam D levels and risk of mortality in the general population” found the lowest ratio of all cause and CVD mortality in the quartile of vitamin D (3rd highest quartile) with vitamin D levels between 24.4 and 32.1 ng/ml.
The two aforementioned studies kept me from being concerned about achieving the high Vitamin D levels that have been widely promoted. Your explanations given in the series have been very reassuring
Then there is the study about breast cancer and vit D status showing those with the highest concentration were more likely to survive. The last study you cited says that women are more likely to have low D levels.
Gary Via says
I’ve had a comment “awaiting moderation” for nearly a month (posted on Dec. 31).
Do you find my question threatening? Is Trevor Marshall’s work (right or wrong) being censored on your site?
If censorship is not your goal, what exactly is the problem with my comment?
Chris, will topical application of coconut oil on the skin block UV, necessary for Vit D sythesis? thanks
Lauri P says
2 weeks before I gave birth to my daughter I started shuffling my feet when I would get up. I had terribly stiff joints. Moving on to 2 years later I had 3 episodes of pseudo gout and a frozen shoulder due to calcium deposits the Dr. said. Continue with heavy leg symptoms, stiff joint and joint pain. then kidney stone (biggest one they ever saw) Finally found out I was low Vit D at 22. Took supplements felt better, winter came started to have joint pain and hurting legs again and found out back to low D at 25. On supplements again. Any ideas to guide me to what the problem may be?
I haven’t found a proper forum in which to ask this in yet, so I hope it’s okay that I ask the question here:
I’ve been trying to follow a diet of traditional foods for about 3-4 months now and I think I have the most crucial parts down.
You see in Sweden, where I live, proper “oldschool” food is kind of hard to come by. (What with the lobbyism of dairy companies and so on.) But I’ve managed to secure the things that I have found to be the most important.
Now, i eat the same lunch every day because I really don’t care about it, I just want the nutrition. Proper nutrition. It consists of the following:
Natrol Multivitamin (It seems to be the most natural supplement for multivitamins.)
Carlson Labs CLO gelcaps. (Can’t really afford the green pasture CLO Butteroil blend)
Now Foods Vitamin K-2 (Again, can’t afford the butter oil)
Garden of life expeller pressed coconut oil.
Raw Multiple (Compound of dried organs, can’t stand eating liver or brain)
Those are the supplements I’m taking. Now on to the smoothie:
Organic raspberries, frozen.
Organic raw eggs.
Organic Kefir (Not homemade, haven’t found kefir seeds that I want to try yet.)
Raw milk (Managed to find, after 10 hours of searching, an organic dairy farm willing to sell)
Raw honey, locally produced (also very hard to find)
For extra safety of the milk I blend the other ingredients first, then add the milk in a shaker.
Oh, and I shouldn’t forget to tell you. I eat no breakfast, I keep a 12-8 pm (16/8 diet) eating schedule, so I take Garden of Life Primal Defense ultra probiotics in the morning. I do drink coffee every morning at 10, and it’s my only real health crime in the morning.
Now, as I can’t afford the pricier CLO+Butteroil blend, I can’t afford eating only pasturized grass-fed cowmeat, so the dinners are usually just normal, but with low carbohydrate intake. I try buying all the things that aren’t that much more expensive when bought organic (cream, vegetables and so on.)
Is there something crucial I’m missing? I’m a student now which limits my funding for food, but when I start earning money it will get better. So for now, just something that I’m missing.
Also, I have to say, I’m doing this for the future, not because I have any certain issues right now.
All the vitamins are very important for our body to make it healthy. i respect your thought and the way you share this with all of us thanks for sharing this blog with us.
Meg Mangin, RN says
Dr. Masterjohn, Thank you for this excellent article on calcium deficiency as a cause of low 25(OH)D. I look forward to future articles about other potential causes of low 25(OH)D besides poor vitamin D exposure. We sorely need a systematic approach for interpreting the likely cause of low 25(OH)D. You may be interested to read our paper “Inflammation and Vitamin D: the Infection Connection” which was recently published in Inflammation Research. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160567/
so whats the bottom line? increase calcium intake before taking vitamin D supplements?
I drink plenty of fresh raw milk and take cod liver oil, high vitamin butter oil and k2, but my vitamin d is at 29. What can I do to improve my levels and feel better. my ph is also 5 and I’m concerned about this.
what do u mean by ”plenty”? 1 quart/liter per day?
Jimmy Walter says
Have you read Dr Seneff on sunlight vs Vitamin D?
What about the case of someone with hyperparathyroid who presents with low (OH) Vitamin D (But High calcitriol) who obviously has an excess of calcium floating around?
I’ve had this issue for over 20 years but feel great and definitely don’t want to mess with surgery and risk feeling terrible afterwards (As many do).
My theory is hyperparathyroid has some sort of adrenal-thyroid mechanism and can be fixed….naturally….but how?
Budge, I have the same problem. Had an op 20 years ago, (also thyroid cancer) the hyperparathyroidism has come back in 2013. Have only 1 parathyroid left and do not want another operation (which would leave me HYPOparathyroid) I have surfed the internet extensively over the last couple of years, but there is no other solution than surgery. If you were to have any info on HOW, it would be interesting.