Normal pregnancy is an insulin-resistant state characterized by intensified fluctuations in maternal fasting and postprandial glycemia, hypertriglyceridemia, and increased insulin secretion.
1 Lactation rapidly lowers maternal circulating triglycerides and glucose, lessens insulin secretion, and mobilizes adipose tissue stores.
2-4 Some longitudinal evidence shows that more favorable metabolic profiles persist postweaning,
5 despite minimal or no weight loss,
6 but biochemical evidence that directly links lactation with long-term diabetes risk is unavailable. Large, prospective epidemiologic studies of middle-aged or older women of northern European or Asian ancestry showed weak to modest relative reductions in diabetes risk of 3% to 15% per year of lactation,
7,8 or 20% for 6 or more months of lactation.
9 All studies relied on self-report of diabetes without biochemical testing or other assessments across the childbearing years or beyond.
7-9 Furthermore, none considered gestational diabetes (GD), a strong risk factor for type 2 diabetes in young women,
10-12 although a retrospective subanalysis among women reporting GD after incident diabetes found no association.
7 Thus, risk estimates may be biased away from the null owing to unmeasured confounding or reverse causation from cardiometabolic risk factors, GD status, perinatal outcomes, and differences in lactation duration among older vs younger women, or biased toward the null by exclusion of high-risk younger women who had transitioned to diabetes many years prior to study baseline. The lack of longitudinal biochemical testing, older age of study participants at baseline, and the inability to evaluate antecedent biochemical and perinatal parameters, including GD status, diminish the validity for this entire body of evidence.