06.27.2016
Saturated fats tied to faster symptom worsening
by Wayne Kuznar
Contributing Writer
High intakes of total fat and particularly saturated fatty acids (SFA) increased the rate of structural progression of knee osteoarthritis (OA), whereas high intakes of unsaturated fatty acids appeared to slow the rate of radiographic progression in a prospective observational study.
In examining data from more than 2,000 patients with knee OA who participated in the Osteoarthritis Initiative, researchers led by Bing Lu, MD, MPH, of Brigham and Women’s Hospital in Boston, found more severe joint space narrowing with increasing intake of total fat and SFA, even after adjusting for BMI and other potential confounders.
In contrast, higher intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) were associated with less loss of joint space width.
“Although the potential mechanisms linking dietary PUFA and OA are unknown, there is consistent evidence that PUFAs are directly linked to inflammation via their role as precursors for a family of compounds known as eicosanoids,” the authors wrote online in Arthritis Care & Research. The pathophysiology of OA is now recognized to involve “a complex interplay between articular pro- versus anti-inflammatory mediators,” they added.
The study included 2,092 individuals with medial radiographic knee OA with a Kellgren-Lawrence grade of 2 or 3 in at least one knee, and excluded knees with severe radiographic OA. Their dietary intake of fatty acids was assessed using the Block Brief Food Frequency Questionnaire. Joint space width measured between the medial femur and tibia of the knee on plain posterior-anterior radiographs was used to evaluate radiographic progression.
At baseline, those in the highest quartile of dietary fat intake were more likely to be younger, non-Hispanic black, less educated, depressed, and smokers; have higher body mass index; and have higher intakes of calcium, protein, and total calories compared with the participants in the bottom quartile of total fat intake.
On multivariable analyses, “we observed a significant dose response-relationship between total fat and SFA intakes and joint space width loss.”
As total fat level intake increased from the bottom quartile of intake to the highest, joint space width decreased over 48 months by 0.26 mm, 0.27 mm, 0.31 mm and 0.35 mm, respectively (P=0.02). Joint space narrowing also progressed significantly per quartile of dietary SFA intake: by 0.25 mm, 0.26 mm, 0.33 mm and 0.37 mm, respectively (P<0.01).
In contrast, a significant inverse association was found between joint space width loss and PUFA intake (P=0.02) and the ratio of polyunsaturated to SFA intake (P<0.01).
Participants with higher MUFA intake had less joint space narrowing than those with lower MUFA intake, but this trend did not achieve significance.
No significant interactions were observed between kinds of dietary fats and age, sex, BMI and smoking status.
“Consistent with joint space width analysis, after adjustment for covariates, we found a significant positive association between SFA intake and risk of OA progression,” Lu and colleagues wrote. With increasing quartiles of SFA intake, the odds for OA progression were 1.32 (95% CI 0.95-1.82), 1.59 (95% CI 1.11-2.27), and 1.60 (95% CI 1.02-2.51) compared with the bottom quartile (P=0.03).
Although total fat intake was positively related to OA progression, this relationship was not statistically significant (P=0.29). Participants in the top quartile of MUFA intake had a 25% reduced risk of OA progression compared with those in the bottom quartile (P=0.05).
The association between higher PUFA intake and reduced risk of OA progression was significant. With increasing quartiles of PUFA intake, the odds for OA progression were 1.01 (95% CI 0.79-1.30), 0.67 (95% CI 0.51-0.89) and 0.70 (95% CI 0.53-0.93) compared with the bottom quartile (P<0.01). An inverse relationship was also found between the PUFA:SFA ratio and risk of knee OA progression (P=0.01).
“Our findings add to the literature, showing a positive association of dietary saturated fat with knee OA progression, and potential protective effects of dietary PUFA and MUFA against knee OA progression,” the authors concluded.
Among the limitations, they cited the lack of randomization to dietary exposure group, the possibility of residual confounding and selection bias, self-report of dietary fat exposure at baseline, the potential for obesity and weight change as intermediate factors linking fat intake and outcomes, and the possibility that dietary fat intake may have resulted in index event bias in case-only studies included in the analysis.
Authors report no conflicts of interest.
The study was supported by National Heart, Lung, and Blood Institute.
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