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Study: Vitamin D Deficiency Leads to Higher Likelihood of Fibromyalgia & Death

A study by K.-C. Hung et al titled “Low vitamin D status and long-term risk of incident fibromyalgia: a propensity score–matched cohort study” published on 24 August 2026 adds to the already large body of evidence that vitamin D is vital to one’s health.


The paper is about 12 pages, including references. The study examined not only fibromyalgia (long-term and widespread pain) but also all-cause mortality.


The study involved a comparison of the vitamin D deficient (VDD) group with serum 25-hydroxyvitamin D concentrations of <20 ng/mL (<50 nmol/L) matched to the control group with concentrations of ≥30 ng/mL (≥75 nmol/L). Those with concentrations of 20.0–29.9 ng/mL, amongst other conditions, were excluded for a clearer comparison.


Each group contained 561,418 individuals with ~67% female. All were adults with at least one vitamin D serum measurement between 1 January 2010 and 31 December 2024. The age at the index date was about 50 years ± 20 years.

Follow-up began 365 days after the index date and continued until the first outcome event, death, last recorded encounter, or 3,650 days after the index date, whichever occurred first.

The following hazard ratios were observed:

  • Fibromyalgia: 1.63 (95% CI: 1.56–1.71)

  • Chronic pain-related diagnosis: 1.30 (95% CI: 1.28–1.31)

  • All-cause mortality: 1.43 (95% CI: 1.41–1.46)

The VDD group is 63% more likely to develop fibromyalgia and 43% more likely to die.


For the chronic VDD group, defined as those with two vitamin D serum measurements of <20 ng/mL within one year, it is not surprisingly worse. The control group is also chronic; that is, with two vitamin D serum measurements of ≥30 ng/mL within one year. Each group contained 116,156 individuals.

  • Fibromyalgia: 1.97 (95% CI: 1.78–2.19)

  • Chronic pain-related diagnosis: 1.65 (95% CI: 1.60–1.70)

  • All-cause mortality: 1.76 (95% CI: 1.70–1.83)


Although the study did not delve into the participants’ personal habits such as physical activity and seasonal variations were not considered, it is at least a large sample with a study window of up to 10 years.


The authors, of course, express caution regarding causality but they nevertheless speculate.

Several mechanisms may plausibly link VDD to pain amplification, although these pathways were not directly assessed in the present study. Vitamin D receptors are expressed in the nervous system and immune cells, and experimental evidence suggests that vitamin D may modulate neuroimmune signaling, microglial activation, oxidative stress, and pro-inflammatory cytokine release relevant to nociceptive processing. Current concepts of fibromyalgia emphasize altered pain processing, including central sensitization, neuroinflammatory and immune activation, impaired descending pain modulation, and altered peripheral sensory input.

Table 2: Association between low vitamin D status and incident fibromyalgia, chronic pain-related diagnoses, all-cause mortality, and control outcomes after propensity score matching.
Table 2: Association between low vitamin D status and incident fibromyalgia, chronic pain-related diagnoses, all-cause mortality, and control outcomes after propensity score matching.

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