Background/Purpose:          

Current guidelines for gout
management, based in part on epidemiologic data for development of incident
gout, recommend limiting intake of high-purine fish. However, fatty fish also
contain omega-3 polyunsaturated fatty acids (ω-3 FA), which have
been shown to have multiple anti-inflammatory effects including reduction of
NSAID consumption, morning stiffness, and tender joint counts in rheumatoid
arthritis, particularly in early disease. ω-3 FA are known to suppress activation
of the NLRP3 inflammasome in vitro in macrophages, and limit experimental
IL-1beta mediated inflammatory responses in vivo. Since gouty inflammation is
driven by NLRP3 inflammasome-mediated IL-1beta release, we assessed whether ω-3 FA intake is
associated with reduction of acute flares in gout.

Methods:

We
used data from the Boston University Online Gout Study, an internet-based,
case-crossover study conducted from 2003-2012.  Each subject acted as his or
her own control, allowing for elimination of between-person differences.  All
subjects were recruited online and had to report at least one gout attack in
the prior year, with diagnosis confirmed by medical record review. 
Participants logged on to the study website at times of gout attacks (hazard
periods) and every 3 months for 1 year during gout flare-free periods (control
periods) to complete questionnaires regarding exposures (including over-the-counter
medications, supplements, and diet) during the 24 and 48 hours preceding the attack
or control period. We examined the relation of self-reported ω-3 FA-rich supplements
and fish
intake in the prior 48 hours to the risk of recurrent gout attacks using
conditional logistic regression, adjusting for alcohol and total purine intake,
and urate-lowering or flare prophylactic medications (allopurinol, NSAIDs,
colchicine).

Results:

Of the 724 participants who experienced ≥ 1 gout attack
during the study period and completed ≥1 control period questionnaire, 85% met the 1977
Preliminary ACR classification criteria for acute gout.  In the 48 hours prior
to attack, 22% of participants reported some form of FA consumption. Of those,
4.6% reported use of supplements (i.e., “fish oil” supplements, “ω-3 FA”
supplements, or “cod liver oil” supplements) and 19% was from dietary fish. The
adjusted odds ratios (aOR) were 1.01 (95% CI, 0.63-1.60) for all three
supplement types combined and 0.77 (95% CI, 0.61-0.96; p=0.02) for ≥1 ω-3 FA-rich fish
servings, respectively (Table).  For any ω-3 FA-rich supplements or fish
combined, the aOR was 0.78
(95% CI, 0.63-0.97;
p=0.02).

Conclusion:

Dietary ω-3
FA-rich fish consumption had a protective effect for recurrent gout attacks in
the community, whereas ω-3 FA supplementation alone, as taken in
a self-directed manner, did not. Consumption of specific sources of ω-3 FA for gout
flare prevention warrants further study in an adequately powered clinical trial.