Background – Red meat intake has been associated with increased risk of coronary heart disease and type 2 diabetes. The often coupled intake of saturated fat and processing of red meat may be at least partly responsible. Effects of iron derived from red meat to increase iron stores and initiate oxidative damage and inflammation is another possible pathway.
Objective – To determine whether an increase in unprocessed and lean red meat intake, with a concomitant reduction in carbohydrate intake, adversely influences markers of oxidative stress and inflammation.
Design – 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 (protein) in isoenergetic diets. Markers of oxidative stress and inflammation were measured at baseline and at the end of intervention.
Outcomes – Results are presented as the between group difference for protein relative to control. There was a significant decrease in urinary [-137 (-264, -9) pmol/mmol creatinine, P=0.04], but not plasma [-12 (-122, 100) pmol/L, P=0.84] F2-isoprostane concentrations. There was a significant decrease in leucocyte [-0.51 (-0.99,-0.02) X109/L, P=0.04] and lymphocyte [-0.20 (-0.36,-0.05) X109/L, P=0.01] counts, a decrease in plasma high sensitivity C-reactive protein concentrations [-1.6 (-3.3, 0.0) mg/L, P=0.06] of borderline significance, but no significant effect on plasma fibrinogen concentrations [-0.08 (-0.40, 0.24), P=0.63].
Conclusion – Our results do not support the suggestion that an increase in the intake of lean red meat, partially replacing carbohydrate, increases oxidative stress or inflammation.