23/11/2025
Continuing our theme of crystals, older naturopathic writers often talked about a “uric-acid diathesis,” and crystal “deposits,” and they explicitly linked these to joint troubles that would overlap with what we now call osteoarthritis (OA). For example, Henry Lindlahr, Nature Cure (1922), in the chapter “Acid Diseases” argued that excess uric acid precipitates out of the blood and is “deposited in the tissues,” noting that “the diseases caused by permanent deposits of uric acid in the tissues are called arthritic diseases, because the accumulations frequently occur in the joints.
Alexander Haig (Uric Acid as a Factor in the Causation of Disease) also wrote on this topic in the early 20th century. Although not a naturopath, his uric-acid theory was highly influential in naturopathic circles. He repeatedly associated elevated uric acid with gout, rheumatism/arthritis, and tissue “deposits,” advocating low-purine diets to prevent joint disease.
The language of these writers is pre-modern in that they do not separate OA from gout in the way we do now. But the mechanism they describe—uric-acid precipitation/crystal deposits in and around joints leading to chronic, degenerative joint disease—matches the idea of joint crystals contributing to arthritis. They often imply cartilage/bone changes consistent with osteoarthritic degeneration. Lindlahr’s chapter is the clearest single naturopathic statement tying uric-acid deposition to a joint-centric “arthritic” pathology.
Biomedical scientists now acknowledge the growing body of evidence for a link between uric acid and OA, although it is not as well established as the relationship between uric acid and gout.
Several population studies have shown that people with higher serum uric acid levels are more likely to have radiographic OA, particularly in the knee and hand. Hyperuricaemia is associated with both incident OA (developing OA over time) and progression (faster cartilage loss and worsening symptoms). There is emerging, but still limited, research on whether urate-lowering therapy slows OA progression. Pilot studies are ongoing.
This line of thinking is strongly supported by a recent review of the evidence that argues serum urate (SU, or uric acid in circulation) is not only relevant in gout, but may play broader roles in various musculoskeletal conditions (sarcopenia, OA, intervertebral disc degeneration and osteoporosis).
The authors highlight that in many of these associations causality is not yet proven, and some relationships may be U- or J-shaped (both low and high urate could be harmful) in certain tissues.
The review outlines several ways in which uric acid (or related species) could influence musculoskeletal tissues. These include oxidative stress/reactive oxygen species/mitochondrial dysfunction, inflammation/immune activation and mechanical damage, among others.
The review is comprehensive in integrating clinical association data and mechanistic hypotheses across muscle, bone, cartilage and disc tissues. It brings attention to the possibility that uric acid is a pervasive modulator of musculoskeletal health beyond gout, vindicating the earlier naturopathic writings.
For more information see: https://pubmed.ncbi.nlm.nih.gov/39968300/
