Many people choose low-carbohydrate diets hoping to reduce inflammation. Inflammation is a body process that can lead to heart disease and other health problems. Researchers looked at how two common diets compare. They compared low-carb diets to low-fat diets in a group of 2222 adults. The study tracked specific proteins in the blood that signal inflammation. These include interleukin-6, C-reactive protein, and others like adiponectin and leptin. The participants followed their chosen diets for five and a half months. The results showed no significant difference between the two approaches. Low-carb diets did not outperform low-fat diets in changing these blood markers. This means both diets may have similar effects on these specific inflammation signals. The study did not report safety issues or side effects for either group. However, the researchers note that future trials should explore nutrient quality and how well people stick to the diet. They also suggest looking at the metabolic status of the participants. This review confirms that for these specific markers, the choice between low-carb and low-fat may not matter much.
Low-carbohydrate diets showed no significant difference versus low-fat diets for inflammatory markers in adults over 5.5 monthsLow-carb diets did not beat low-fat diets on inflammation markers in adults
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Key Takeaway
Note that low-carbohydrate diets were not superior to low-fat diets for inflammatory markers in this meta-analysis.
This systematic review and meta-analysis compared low-carbohydrate (LC) diets against low-fat (LF) diets in an adult population. The analysis included 2222 participants and assessed changes in concentrations of interleukin-6, C-reactive protein, tumor necrosis factor-alpha, adiponectin, leptin, and resistin. The follow-up duration was 5.5 months.
The meta-analysis found no significant difference between the two dietary approaches for interleukin-6, with a standardized mean difference of -0.01 and a 95% CI of -0.12 to 0.09. Similarly, C-reactive protein showed no significant difference with an SMD of -0.01 and a 95% CI of -0.11 to 0.09. Tumor necrosis factor-alpha also showed no significant difference with an SMD of -0.03 and a 95% CI of -0.18 to 0.11. Data for adiponectin, leptin, and resistin were not reported for effect size or confidence intervals, yet no significant difference was observed for these markers as well.
Safety data regarding adverse events, serious adverse events, discontinuations, and tolerability were not reported. The authors acknowledge that future trials should explore the influence of nutrient quality, adherence, and metabolic status. Consequently, LC diets were not superior to LF diets in modulating the inflammatory and adipokine profiles in adults.
What this means for you:
Low-carb diets were not better than low-fat diets for inflammation markers in adults. More on Inflammation
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View Original Abstract ↓
Chronic low-grade inflammation is implicated in obesity and related diseases. Dietary composition may modulate inflammatory responses, but the comparative effects of low-carbohydrate (LC) and low-fat (LF) diets remain unclear. We conducted a systematic review and meta-analysis of randomized clinical trials assessing the impact of LC vs LF diets on concentrations of interleukin-6, C-reactive protein, tumor necrosis factor-alpha, adiponectin, leptin, and resistin in adults, to test the hypothesis that LC diets exert beneficial effects on these biomarkers when compared to LF diets. Literature searches were conducted in four databases through June 2025. Two independent reviewers screened and extracted data. Meta-analyses using random-effects models were performed; outcomes were reported as standardized mean differences (SMD) with 95% confidence intervals (CI). Twenty-five studies (n = 2222 participants) met eligibility criteria. Median intervention duration was 24 weeks (range: 8-144). On average, carbohydrate intake accounted for 25.8% of total daily energy intake in LC diets and 54% in LF diets, whereas fat intake averaged 48.6% and 26% of total daily energy intake, respectively. No significant differences were found between LC and LF diets for interleukin-6 (SMD: -0.01; 95% CI: -0.12 to 0.09), C-reactive protein (SMD: -0.01; 95% CI: -0.11 to 0.09), or tumor necrosis factor-alpha (SMD: -0.03; 95% CI: -0.18 to 0.11), nor for adiponectin, leptin, or resistin. Risk of bias was low in most studies. Our results suggest that LC diets were not superior to LF diets in modulating the inflammatory and adipokine profiles in adults. Future trials should explore the influence of nutrient quality, adherence, and metabolic status.
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