Practice Update: Endocrinology | Volume 1. Number 2. 2016

CARDIOVASCULAR COMPLICATIONS

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EXPERT COMMENTARY Encourage intake of whole, not refined, grains By Dr David Rakel W ith the growing fear of glu- ten, the intake of grains has dropped significantly. Ac-

Whole grain consumption and risk of cardiovascular disease, cancer, and mortality British Medical Journal Take-home message • This meta-analysis of 45 studies evaluated the relative risks of various cardiovascular diseases, cancer, diabetes, respiratory disease, and infectious disease in participants consuming a greater than average amount of whole grain servings per day. The results revealed a reduction in all-cause mortality as well as disease-specific mortality in those participants consuming between 90 g to 225 g of whole grains daily. The most pronounced reduction in relative risk was noted in relation to cardiovascular disease and cancer. • The authors concluded that increased consumption of whole grains reduces the risk for cardio- vascular disease, cancer, diabetes, and several other disease states. Clinicians should convey this information when discussing dietary guidelines with patients. Abstract

cording to this meta-analysis by Aune and colleagues in the BMJ , these foods should be increased. Granted, many people may not be able to tolerate glu- ten, but this evidence would encour- age consumption of other non-gluten grains such as quinoa or amaranth. This meta-analysis of 64 publications found a dose-response effect. Those eating three servings of whole grains daily showed a 19% reduction in coronary artery disease, a 22% reduction in cardiovascular disease, a 15% reduction in total cancer, and a 17% reduction in all-cause mortality. The authors suggest that three servings (90 gms) a day can be achieved with a whole grain fibre cereal in the morning (30 gms) and a piece of whole grain pita bread for dinner (60 gms). The benefits were even greater with 210 to 225 gms/day, which is 7 to 7.5 servings a day. Benefits persisted despite controlling for con- founders such as BMI, smoking, and physical activity. The teaching point here is that the health benefits were fromwhole grains, not processed grains. There was NO benefit correlated with eating refined grains including white rice. So

n=4) for diabetes, 0.74 (0.56 to 0.96; I(2) =0%, n=3) for infectious diseases, 1.15 (0.66 to 2.02; I(2) = 79%, n=2) for diseases of the nervous system disease, and 0.78 (0.75 to 0.82; I(2) = 0%, n = 5) for all non- cardiovascular, non-cancer causes. Reductions in risk were observed up to an intake of 210–225 g/ day (seven to seven and a half servings per day) for most of the outcomes. Intakes of specific types of whole grains including whole grain bread, whole grain breakfast cereals, and added bran, as well as total bread and total breakfast cereals were also associated with reduced risks of cardiovascular disease and/or all-cause mortality, but there was little evidence of an association with refined grains, white rice, total rice, or total grains. CONCLUSIONS This meta-analysis provides further evidence that whole grain intake is associated with a reduced risk of coronary heart disease, cardiovascular disease, and total cancer, andmortality fromall causes, respiratory diseases, infectious diseases, diabetes, and all non-cardiovascular, non-cancer causes. These findings support dietary guidelines that recommend increased intake of whole grain to reduce the risk of chronic diseases and premature mortality. Whole grain consumption and risk of cardio- vascular disease, cancer, and all cause and cause specific mortality: Systematic review and dose-response meta-analysis of prospective studies. BMJ 2016;353:i2716, Aune D, Keum N, Giovannucci E, et al.

OBJECTIVE To quantify the dose-response relation between consumption of whole grain and specific types of grains and the risk of cardiovascular dis- ease, total cancer, and all cause and cause specific mortality. STUDY SELECTION Prospective studies reporting adjusted relative risk estimates for the association between intake of whole grains or specific types of grains and cardiovascular disease, total cancer, all cause or cause specific mortality. DATA SYNTHESIS Summary relative risks and 95% confidence intervals calculated with a random ef- fects model. RESULTS 45 studies (64 publications) were included. The summary relative risks per 90 g/day increase in whole grain intake (90 g is equivalent to three serv- ings – for example, two slices of bread and one bowl of cereal or one and a half pieces of pita bread made fromwhole grains) was 0.81 (95% confidence interval [CI] 0.75–0.87; I(2) =9%, n = 7 studies) for coronary heart disease, 0.88 (0.75 to 1.03; I(2) =56%, n=6) for stroke, and 0.78 (0.73 to 0.85; I(2) =40%, n= 10) for cardiovascular disease, with similar results when studies were stratified by whether the outcome was incidence or mortality. The relative risks for morality were 0.85 (0.80 to 0.91; I(2) = 37%, n = 6) for total cancer, 0.83 (0.77 to 0.90; I(2) =83%, n= 11) for all causes, 0.78 (0.70 to 0.87; I(2) =0%, n=4) for respiratory disease, 0.49 (0.23 to 1.05; I(2) = 85%,

the whole grain bread that leaves a large ball in your closed fist is much better than the white bread that leaves a tiny ball in your closed fist (think cotton candy). One is mainly sugar, the other is sugar, fibre, minerals, and vitamins. We can encourage whole grains even if our patients can’t tolerate gluten. Grains are filled with healthy nutrients and should not be feared. This study supports the intake of three to seven servings daily. I would probably stick with three to five, as calorie restriction has also shown health benefits! Dr David Rakel is Associate Professor at the Department of Family Medicine and Director at the University of Wisconsin Integrative Medicine, University of Wisconsin School of Medicine and Public Health.

EXPERT COMMENTARY Discuss risk in preconception counselling of diabetic women By Dr Gary Webb S ince the early 1970s, Denmark has maintained databases about all of its citizens, inte-

Pre-pregnancy diabetes and risk of congenital heart disease in offspring Circulation Take-home message • This Danish cohort study evaluated the association between mater- nal pre-gestational diabetes and congenital heart disease (CHD) in offspring. The study results support the association between maternal pre-gestational diabetes and CHD in offspring irrespective of diabetes type, maternal age at diabetes onset, and duration of diabetes. The re- searchers did identify a strong association between presence of maternal diabetes complications and increased risk of CHD in offspring compared with those without documented complications (RR, 7.62 and RR, 3.49, respectively; P = 0.0004). • The authors concluded that increased risk for offspring with CHD in mothers with pre-gestational diabetes complications supports the direct association between glucose and development of CHD. Abstract

over a 34-year period (the largest of its kind to date), maternal pre-gesta- tional diabetes was associated with a fourfold increase in the risk of con- genital heart disease (CHD) in the offspring. The increase in CHD risk was stable over time and was similar in women with type 1 and type 2 dia- betes. Pre-gestational acute diabetic complications conferred an almost

eightfold increase in CHD risk compared with risk in nondiabetic women. The offspring of diabetic women had similar risks of most types of congenital heart defects, suggesting that maternal diabetes impacts general cardiac develop- ment very early in embryogenesis. This risk should be included in preconception counselling of dia-

grating health data, medication use, and social, economic, and other data. This must be considered a national treasure. This study is one of a growing number of population- based studies utilizing this data. In this study of 2 million births

duration, and CHD risks associated with type 1 (insulin-dependent) and type 2 (insulin-independent) diabetes did not differ significantly. Persons born to women with previous acute diabetes complications had a higher CHD risk than those exposed to ma- ternal diabetes without complications (RR 7.62, 95% CI 5.23–10.6, and RR 3.49, 95% CI 2.91–4.13, respectively, p = 0.0004). All specific CHD pheno- types were associated with maternal pre-gestational diabetes (RR range: 2.74–13.8). CONCLUSIONS The profoundly in- creased CHD risk conferred by ma- ternal pre-gestational diabetes neither changed over time nor differed by diabetes subtype. The association with acute pre-gestational diabetes complications was particularly strong, suggesting a role for glucose in the causal pathway. Pre-pregnancy diabetes and offspring risk of congenital heart disease: A nationwide cohort study. Circulation 2016 May 10;[Epub ahead of print], Øyen N, Diaz LJ, Leirgul E, et al.

BACKGROUND Maternal diabetes is associated with an increased risk of offspring congenital heart disease (CHD); however, the causal mecha- nism is poorly understood. We further investigated this association in a Dan- ish nationwide cohort. METHODS AND RESULTS In a national cohort study, we identified 2,025,727 persons born in 1978–2011, among them 7,296 (0.36%) persons exposed to maternal pre-gestational diabetes. Pre-gestational diabetes was identified using the National Patient Register and individual-level information on all pre- scriptions filled in Danish pharmacies. Persons with CHD (n = 16,325) were assigned to embryologically-related cardiac phenotypes. The CHD preva- lence in the offspring of mothers with pre-gestational diabetes was 318 per 10,000 live births (n=232), compared with a baseline risk of 80 per 10,000; the adjusted relative risk (RR) for CHD was 4.00 (95% confidence interval (CI) 3.51–4.53). The association was not modified by year of birth, maternal age at diabetes onset, or diabetes

betic women. Unfortunately, diabetic control does not seem to impact the incidence of congenital heart defects in the offspring of diabetic women. Dr Gary Webb is Director of the Cincinnati Adolescent and Adult Congenital Heart Disease Program, and Professor at the Department of Pediatrics, University of Cincinnati Department, Ohio.

VOL. 1 • No. 2 • 2016