Increased lean red meat intake does not elevate markers of oxidative stress and inflammation in humans.

Red meat intake has been associated with increased risk of coronary heart disease and type 2 diabetes, but it remains uncertain whether these associations are causally related to unprocessed lean red meat. It has been proposed that iron derived from red meat may increase iron stores and initiate oxidative damage and inflammation. We aimed to determine whether an increase in unprocessed lean red meat intake, partially replacing carbohydrate-rich foods, adversely influences markers of oxidative stress and inflammation. Sixty participants completed an 8-wk parallel-designed study. They were randomized to maintain their usual diet (control) or to partially replace energy from carbohydrate-rich foods with approximately 200 g/d of lean red meat (red meat) in isoenergetic diets. Markers of oxidative stress and inflammation were measured at baseline and at the end of intervention. Results are presented as the mean between-group difference in change and [95% CI]. Red meat, relative to control, resulted in: higher protein [5.3 (3.7, 6.9) % of energy], lower carbohydrate [-5.3 (-7.9, -2.7)% of energy], and higher iron [3.2 (1.1, 5.4) mg/d] intakes; lower urinary F2-isoprostane excretion [-137 (-264, -9) pmol/mmol creatinine], lower leukocyte [-0.51 (-0.99, -0.02)x10(9)/L] counts, and a trend for lower serum C-reactive protein concentrations [-1.6 (-3.3, 0.0) mg/L, P=0.06]; and no differences in concentrations of plasma F2-isoprostanes [-12 (-122, 100) pmol/L], serum gamma-glytamyltransferase [-0.8 (-3.2, 1.5) U/L], serum amyloid A protein [-1.4 (-3.4, 0.5) mg/L], and plasma fibrinogen concentrations [-0.08 (-0.40. 0.24) g/L]. Our results suggest that partial replacement of dietary carbohydrate with protein from lean red meat does not elevate oxidative stress or inflammation.