Among 38,564 adult patients with type 1 or 2 diabetes, increasing levels of alcohol consumption predicted lower A1C values through a nadir at consumption of 2–2.9 drinks/day. Ours is the largest study to examine the association between alcohol consumption and glycemic control among diabetes patients. Our results extend the findings of Mackenzie et al.41
who found that alcohol consumption was associated with lower A1C among 1,024 adults with diabetes who participated in Third National Health and Nutrition Examination Survey. Furthermore, a randomized, controlled trial of moderate alcohol consumption among 109 previously abstentious adults with diabetes found that consumption of 13 g of alcohol daily reduced fasting plasma glucose by 9% compared to non-alcohol consuming controls.42
Because of our much larger cohort, we were able to test for different patterns of association by age and type of diabetes and to compare A1C among more precisely defined levels of alcohol consumption.
There are biologically plausible explanations for our findings. Among people without diabetes, moderate alcohol consumption may enhance insulin sensitivity43–51
and has been shown to decrease A1C.52–56
It is plausible that regular, moderate alcohol consumption by people with diabetes similarly enhances insulin sensitivity and improves glycemic control. If this is the case, it might follow that the effect would be greater among type 2 diabetes patients, as they typically have much greater insulin resistance than those with type 1 diabetes; we did not, however, find different patterns of effect by diabetes type in our cohort.
Our study has several limitations. First, as with all human studies of the relationship between alcohol consumption and clinical outcomes, randomization was not possible. However, our rich database allowed us to employ multivariate models that controlled for the affects of a wide array of putative confounding variables. Second, alcohol consumption was assessed at a single point in time. It is possible that lower A1C values among current compared to former drinkers reflect their generally better state of health, as former drinkers include those who stopped drinking because of poor health. Our data do not support this hypothesis, however, as our data allowed us to differentiate former drinkers (among whom we would expect to find those who stopped drinking because of ill health) from lifetime abstainers, and we found that lifetime abstainers had higher A1C values than former drinkers. Third, we rely on self-report of alcohol consumption. If heavy consumers of alcohol underreported their consumption because of their wish not to report socially undesirable behavior, this would have created a conservative bias. Fourth, despite the large study population, our conclusions were limited by the small number of patients reporting higher levels of alcohol consumption. Finally, it is possible that response bias affected our results, as our study cohort composed 41% of the Diabetes Registry. As with other survey studies, respondents tended to be older (although by only 0.3 years) and have higher socioeconomic status than nonrespondents.57–59
However, as our analyses determined associations, rather than prevalence of conditions, the risk of selection bias affecting study conclusions is minimal.60
Furthermore, our finding of similar patterns of association between alcohol consumption and A1C among the cohort of 10,546 patients who had an A1C measured between 1 and 2 years after baseline suggests that our findings are robust. These 10,546, together with the 39,142 patients in our main analysis, comprise 53% of the Diabetes Registry. We have assessed responder bias in our previous research based on survey responders and found no noteworthy selection bias, particularly when assessing statistical associations.26,28
Our study has several strengths. First, we had data to differentiate lifetime abstainers from former drinkers, who include those who stopped drinking because of poor health. We did not observe a clinically meaningful difference in A1C between lifetime abstainers and former drinkers, suggesting that the lower A1C observed among drinkers was because of the effects of alcohol rather than because of the “healthy drinker effect.” Second, the KP membership from which the study population was drawn makes up approximately 30% of the Northern California population and is sociodemographically representative of the general population, giving this study public health relevance and generalizability.20–22,61
Third, we were able to control for a wide variety of potential confounding variables, including diabetes self-care behaviors.62
Fourth, the finding that the inverse relationship between alcohol and A1C persisted during the period 1–2 years after baseline suggests that the relationship is robust.
Our study findings have implications for clinical practice and future research. Half of our study subjects, who are drawn from a population representative of the underlying population, consume alcohol. Both primary care and addiction medicine clinicians are increasingly interested in how substance use and abuse affect the disease course of patients with chronic diseases such as diabetes. Current ADA recommendations call for limiting alcohol consumption by adult diabetes patients to no more than 1 or 2 drinks daily for women and men, respectively.19
Our findings, by demonstrating that moderate alcohol consumption is associated with better glycemic control than abstinence, provide data to support this recommendation. Likely, only meta-analysis will provide more definitive conclusions, as few study populations are as large as ours.
As glycemic control affects incidence of diabetes-related complications, particularly microvascular endpoints, increased understanding of the effects of alcohol consumption on glycemic control may improve the attention that providers pay to assessing alcohol consumption and addressing alcohol use disorders among their diabetes patients. Compared to lifetime abstainers, consumers of 2–2.9 drinks/day had lower A1C by nearly 0.5%. This difference is clinically significant. For example, this is similar to the lowering of A1C obtained with initiation of intensive metformin therapy.63
Furthermore, this may translate into benefits in diabetes-related complications, as a 1% reduction in HbA1c is associated with a 21% reduction of the risk of any diabetes-related endpoint and a 37% reduction in the risk of microvascular complications.64
The mechanisms by which alcohol might affect glycemic control deserve further study. Additionally, research should be directed at assessment of whether the associations between alcohol and glycemic control translate into differential incidence of diabetes complications among patients with different levels of alcohol consumption.