If you are you wondering about Vitamin D and Constipation then you've come to the right place. And the answer to your question is that 'Yes', taking vitamin d CAN and does cause constipation despite what your doctor may have told you. There is even a simple solution AND interesting information about your body that you'll learn from this page. Bear with me for a moment because you need to first understand about the relationship between Magnesium and Vitamin D in order in order to understand what is going on here and how you are going to fix this. When vitamin d is taken it requires magnesium- and other nutrients known as 'cofactors'- in order to work properly, and those who have even a subtle magnesium deficiency will then get obvious Signs of Magnesium Deficiency after taking vitamin d. Other problems that vitamin D can cause from lack of magnesium and other cofactors are things like:And many other related issues. Many people will think this is a sign of Overdose on Vitamin D, but it is not.
It's just a sign that you are nutrient deficient, possibly seriously deficient. Constipation is one of these signs of magnesium deficiency and if you are getting constipation from vitamin d, then your body is telling you that you ARE magnesium deficient and that you probably have been for a long long time. Most people who complain of Vitamin D and Constipation have had other health problems related to magnesium deficiency for long periods of time, but they simply didn't realize what they were. So, the solution for most people is to simply follow the instructions on the Magnesium Dosage page and remedy your magnesium deficiency. But do remember that vitamin d also uses up OTHER nutrients too, such as Vitamin K and Vitamin A, and many many people get relief from their Vitamin D Side Effects from taking Vitamin K and Vitamin A as well. Since deficiencies of these nutrients are also rampant in western countries, I NEVER EVER recommend taking large doses of single nutrients, and the best course of action is to take all of the cofactors necessary as 'insurance' against vitamin d side effects.
We've included all of these cofactors into our Vitamin D Absorption Pack for convenience. As you just found out, not getting the necessary cofactors with vitamin d is a recipe for problems- and since you found out that you are deficient in both vitamin D and in magnesium, what OTHER nutrients are you deficient in that will cause even more problems if you 'just' take high doses of magnesium and vitamin d? So, if you are going to correct these two nutrient deficiencies, then you should consider taking a HIGH QUALITY multivitamin supplement such as our Daily Vitamin Supplement that contains Vitamin A, Vitamin K, magnesium and more, or do it right and get the full Vitamin D Absorption Pack for best results and to prevent most side effects. For your next step, go to the Magnesium Dosage page and find out the right dosage of magnesium that is right for you.. Already Answered Questions about Vitamin D Side Effects Click below to see already answered questions about Vitamin D Side Effects.
vitamin D - cause constipation? I am a 79-y/o white female. I never took calcium with vitamin D in the past because of constipation. I have had hypercalcemia in the past anyway, on blood … Does Vitamin D Cause Constipation? SINCE I HAVE BEEN TAKING 2000 IUS OF VTAMIN D 3 (as cholecalciferol) I have become so constipated I have never been constipated.I feel as if I need to … Is Constipation a Side Effect of Vitamin D? My Vitamin D level is 8 ng/ml. My doctor put me on once a week pill 50,000 units plus additional 1,800 by mouth a day and I've been taking it for 5 weeks … Back to Top of Vitamin D and ConstipationBack to Easy Immune Health Home Page 1From the Bone Program Section of Endocrinology, Diabetes, and Metabolism, The University of Chicago, Chicago, IL. 3↵Address correspondence to MJ Favus, The University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637. See corresponding article on page 270. In the United States, the 37% increase in lifetime prevalence of kidney stones in adult women between 1976–1980 and 1988–1994
(1) corresponds to the onset of widespread use of calcium supplements in the prevention of osteoporosis. By the time recruitment into the calcium/vitamin D arm of the Women's Health Initiative (WHI) study was begun in the 1990s, the average total calcium intake of postmenopausal women had reached 1100–1200 mg/d (2). As 65% of participants in each experimental group had a baseline daily calcium intake of ≥800 mg, those randomly assigned to receive an additional 1000 mg of calcium supplements plus vitamin D raised their total calcium intake to at least 1800 mg/d. Whereas new kidney stones were self-reported in participants in both experimental groups, the increase in stone formers was greater among those in the calcium–vitamin D supplementation group (hazard ratio: 1.17; 95% CI: 1.02, 1.34) (2). by Wallace et al (3) published in this issue of the Journal failed to describe demographic characteristics or personal dietary habits that could account for the increased kidney stones.
A small number of prior stone formers were inadvertently included in the study but appear not to have contributed to the excess stone incidence. Neither was there an increase in the frequency of family history of stones among stone formers. Of particular importance was the lack of relation between new stone formation and baseline total calcium intake or calcium supplement use. At baseline, the mean total calcium intake of 1145 mg daily from dietary plus supplement sources did not differ between stone formers and non–stone formers. The increased calcium intake in the calcium–vitamin D supplement arm of the study raised calcium intakes to as high as 2000 mg/d when the 1000 mg calcium supplement was added to baseline calcium intake. Calcium is a major component of 85% of kidney stones, largely as either calcium oxalate or calcium phosphate (4). The single most common cause of calcium oxalate kidney stones is idiopathic hypercalciuria (IH), which is a familial disorder
characterized by life-long hypercalciuria, normal serum calcium in the absence of known systemic causes of hypercalciuria such as sarcoidosis, Cushing syndrome, hyperthyroidism, and Paget disease of bone (5). Ninety percent of IH patients never form a kidney stone, but further increases in urine calcium oxalate supersaturation from calcium supplements would enhance the risk of stone formation. The study did not assess biochemical changes that predispose to stone formation, including urine volume, urine calcium, magnesium, oxalate and citrate excretions, and the ingestion of animal protein and sodium. The new kidney stones are unlikely to be composed of uric acid, because increased calcium excretion would not predispose to uric acid stones. Furthermore, vitamin D intake achieved by vitamin D supplements is insufficient to increase urine calcium excretion. Given the predisposition for IH subjects to form stones, the excess kidney stones in the calcium–vitamin D arm of the trial
could have arisen from inclusion of subjects with IH. Individuals with IH comprise 5–7% of the adult population, and urine supersaturation with respect to calcium and oxalate, calcium phosphate, and uric acid would provide useful data with predictive value regarding risk of stone formation and recurrence. In the absence of laboratory testing, one can only speculate as to the cause of the stones. Nevertheless, the high-calcium supplements plus the habitual dietary and supplemental calcium intakes as identified at baseline would be sufficient to increase kidney stone risk in IH subjects. IH patients are more sensitive to forming stones because relatively small increases in urine calcium increase calcium oxalate supersaturation. the relative risk of new kidney stone formation among women who consumed 1–100 mg supplemental calcium/d compared with women who did not take supplemental calcium was 1.26 (95% CI: 0.79, 2.00) (6). There was no further increase in stone risk among women who consumed >100 mg calcium/d.
The relative risk in women who took supplemental calcium compared with women who did not was 1.20 (95% CI: 1.02, 1.41) (6), which is in close agreement with the 17% increase in new kidney stones in the randomized calcium–vitamin D trial. On the surface, it seems difficult to reconcile the increased kidney stone rates with calcium supplements and the reports that high dietary calcium intake reduces kidney stones (7). The relative risk of kidney stone formation in women in the highest quintile of dietary calcium intake was lowered by 65% (95% CI: 0.50, 0.83) compared with women in the lowest quintile of dietary calcium intake (6). The other extreme of ingesting low calcium to avoid stone recurrence is ineffective in lowering new kidney stone formation because dietary oxalate absorption, urine excretion, and urine calcium oxalate supersaturation increase in the presence of low calcium intake (8). The mechanism whereby dietary calcium intake reduces calcium oxalate kidney stones is through binding of dietary oxalate