What vitamin deficiency causes tendonitis?

The causation test, and vitamin C in the dock

What vitamin deficiency causes tendonitis is a question that assumes its own answer, that some deficiency does, and the honest page tests the assumption rather than picking a vitamin to satisfy it, using the test epidemiologists apply before blaming any exposure for any disease. The test has several criteria. Strength and consistency: is the association between the deficiency and tendonitis large, and does it appear in study after study rather than in one? Dose response: do worse deficiencies produce more tendonitis? Temporality: does the deficiency come before the tendon problem rather than after it, since an injured, inactive person's blood values change for reasons that have nothing to do with cause? Plausibility: is there a mechanism by which the deficiency would damage a tendon? And experiment: when the deficiency is corrected in a trial, does the tendonitis improve or stop occurring? An exposure that passes all of these is a cause; one that passes some is an association worth watching; one that passes none is a shelf story. Vitamin C goes into the dock first because the shelf names it most often, on the reasoning that collagen needs vitamin C and tendons are collagen. The plausibility criterion is passed, since vitamin C is the cofactor for the hydroxylases that fold collagen chains and without it connective tissue fails. Every other criterion fails. Severe vitamin C deficiency causes scurvy, whose signs are bleeding gums, bruising, poor wound healing, fatigue and joint pain from bleeding into joints, a general connective tissue failure that is not tendonitis and is not confined to tendons; scurvy is rare in the UK, confined to very restricted diets, alcohol dependence and some eating disorders, and a reader with patellar tendon pain who eats any fruit or vegetables is not deficient. No study shows a dose response between vitamin C status and tendinopathy, no study shows low vitamin C preceding tendinopathy in otherwise fed adults, and no trial shows that giving vitamin C to a replete person treats or prevents tendonitis; the register's sentence, vitamin C contributes to normal collagen formation for the normal function of cartilage and bones, is a maintenance sentence describing what the vitamin permits, and it is as far as the evidence goes. Vitamin C fails the test as a cause and remains what it always was, a cofactor met from food that the collagen protocol includes because the enzymes need it present.

Vitamin D half passes, the rest fail, and the exposure that passes everything

Vitamin D goes into the dock second and is the only vitamin that comes out with anything, so the honest page is careful about how much. The association criterion is partly met: several observational studies report lower vitamin D levels in groups with rotator cuff tears, rotator cuff tendinopathy and some other tendinopathies than in comparison groups. Consistency is not met: other cohorts find no difference, and reviews describe the evidence as inconsistent and low in quality. Temporality is doubtful, since a person with a painful shoulder does less outdoors and their vitamin D falls as a consequence of the injury rather than a cause of it, and the studies cannot tell the directions apart. Dose response has not been shown. Plausibility is indirect: vitamin D's established role is in muscle function and bone, so a deficient person has weaker muscle around the joint and more load falling on the tendon, a route through the muscle rather than through the tendon's own biology. And the experimental criterion is empty: no randomised trial shows that correcting vitamin D treats tendinopathy or prevents it. So vitamin D half passes, which makes it an association worth a blood test in a UK adult with persistent tendinopathy, because vitamin D insufficiency is common through a UK winter and correcting it at the guidance dose of ten micrograms a day is cheap and right for other reasons, and not a cause, since a reader who corrects it and keeps loading badly will keep the tendonitis. The remaining vitamins, B12, E, K, A and the B group, fail at the first criterion for want of any association with tendonitis in the literature, and the minerals that the connective tissue sentences belong to, copper and zinc, have deficiency states that weaken connective tissue generally and are rare, with no tendonitis link. The exposure that passes every criterion is not a vitamin: it is load rising faster than the tendon can adapt, the association strong and consistent across every tendinopathy studied, the dose response clear in training volume data, the temporality obvious, the mechanism known in tenocyte biology, and the experiment run thousands of times in every rehab clinic where progressive loading treats it; with age, sudden volume or range increases, poor recovery, smoking and fluoroquinolone antibiotics as the accelerators that make the same load injure sooner. The honest page therefore answers the question with no, names vitamin D as the one worth testing, and sends the reader to a physiotherapist for the loading programme that treats the actual cause, adding that a swollen, hot or hour-stiff joint or a tendon that hurts at rest and at night is a doctor's assessment rather than a vitamin's. The worked example is the cofactor pairing stated on its true terms: two capsules, 1200mg hydrolysed type 1 marine collagen with 12mg vitamin C at 15% of its reference value plus zinc, 120 for £16.99 at 28p a day, lab tested and UK made, the vitamin C carrying its collagen formation sentence for cartilage and bones, the collagen below the research band and holding no claim, and nothing on the label about tendonitis, because no vitamin deficiency causes it.

What to check on the label