Obesity has been linked with elevation of the inflammatory protein, C‐reactive protein (CRP), which increases risk of developing chronic disease. CRP levels less than 1.0 mg/L are associated with a low risk, 1.0 to 3.0 mg/L medium risk, and greater than 3.0 mg/L high risk. Weight loss, specifically loss of abdominal fat, may decrease CRP. Breastfeeding may help reduce CRP. The objective of this study was to determine the effect of weight loss on inflammation in 20 overweight, fully breastfeeding women. Weight, height, waist circumference, and body composition (determined by DXA) were measured at 4 and 20 weeks postpartum. Serum samples were obtained, and concentrations of CRP were measured by ELISA. There was an average (range) loss of weight of ‐4.7 kg (2.8 to ‐11.6 kg), fat mass of ‐4.69 kg (0.45 to ‐13.3 kg), and trunk fat of ‐2.89 kg (0.27 to ‐7.3 kg). There was a non‐significant decrease in CRP from 3.99 to 3.04 mg/L, with 2 participants moving from high to medium risk, and 2 moving from medium to low risk. There was a significant positive association between change in trunk fat and change in CRP (R2=0.20). Also, weight (R2=0.19), fat mass (R2=0.19), and trunk fat (R2=0.24) were significantly positively associated with CRP at endpoint. These results suggest that loss of abdominal fat is associated with a significant reduction of CRP in overweight, fully breastfeeding women and may reduce their risk for chronic disease.

Obesity has been linked with elevation of the inflammatory protein, C‐reactive protein (CRP), which increases risk of developing chronic disease. Weight loss, specifically loss of abdominal fat, may decrease CRP. The Healthy Eating Index (HEI), which measures overall diet quality, may also be associated with CRP levels. These scores are based on the intake of 12 different food components with a maximum score of 100. The objective of this study was to determine the effect of weight loss and dietary quality on CRP in 36 overweight, postpartum (PP) women from two randomized, controlled weight loss trials. Weight, height, and body composition (determined by DXA) were measured at baseline (4‐14 weeks PP) and endpoint (18‐26 weeks PP). Concentrations of CRP were measured by ELISA. HEI scores were calculated from two 24‐hour recalls obtained using the Nutrition Data System for Research. The intervention group lost significantly more weight than the control group (‐6.86 ± 1.04 kg, ‐3.65 ± 1.14 kg, p=0.02). There were no significant differences between groups for CRP or HEI scores. When analyzing data from all participants, there was a significant positive association between change in CRP (‐0.13 ± 0.49 mg/L) and change in weight (R2=0.12) and trunk fat (R2=0.15). Also, while change in HEI scores was not significantly associated with change in CRP, HEI score at baseline (59.9 ± 2.6) tended to be negatively associated with change in CRP (R2=0.09, p=0.09). The relationship between change in trunk fat and change in CRP was strengthened when HEI scores at baseline were added to the model (R2=0.19). These results suggest that loss of total weight and abdominal fat is associated with a reduction of CRP. Diet quality may mediate the relationship seen between body composition and CRP.