Eggs and diabetes: perspectives from clinical studies

Featured article in the Fall 2015 Issue of Nutrition Close-Up; written by Maria Luz Fernandez, PhD

There is a consensus, derived from clinical interventions and epidemiological data over the last 10 years, that eggs do not increase the risk for heart disease in healthy populations.1 It has been demonstrated that eggs: 1) increase both LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C), therefore the LDL/HDL ratio, a key marker of coronary heart disease risk, is maintained; 2) increase the large, less atherogenic LDL particle, known to transport additional antioxidants, in addition to being preferentially removed by the liver; 3) increase the large HDL, a particle that plays a major protective role by removing accumulated cholesterol from macrophages and transporting it back to the liver to be targeted for elimination from the body.2 Thus these established facts support the consensus of the lack of effect of eggs in increasing heart disease risk in non-compromised subjects.

However, uncertainty exists regarding the effects of egg consumption on heart disease in diseased populations with a major emphasis in individuals diagnosed with type-2 diabetes (T2D). While the evidence derived from epidemiological data is controversial,1 there are very few controlled clinical interventions that have been carried out to date to evaluate a cause and effect relationship.

Randomized clinical trials, the gold standard for dietary or drug interventions, can provide a more comprehensive picture on the effects of daily egg consumption on plasma lipids, glucose metabolism, and inflammation in people with T2D. Preliminary studies support the fact that egg intake can reduce inflammation in subjects with metabolic syndrome who are at great risk for diabetes. When compared to egg substitute (lipid-free eggs), whole egg intake resulted in significant decreases in serum amyloid A, an acute phase inflammatory factor associated with HDL, and tumor necrosis factor- alpha (TNF-α), suggesting that eggs have protective effects against inflammation.3

Three trials conducted in diabetic patients have been reported in the last  three years.4-6 One of the trials was a randomized crossover study in which two different breakfasts, either 1 egg/day or 1 cup of oatmeal/day, were consumed for 5 weeks each with a 3-week washout before allocation to the alternate treatment.4 When plasma lipids and parameters of glucose metabolism were compared between breakfasts, no changes in LDL-C, triglycerides, glucose, glycosylated hemoglobin or number of small LDL particles were different between groups. In contrast, TNF-α and AST (a liver enzyme) were reduced during the egg period.4 Another study following a randomized parallel design in which either 2 eggs or lean meat (equivalent in calories) within the context of a high protein-energy restricted diet were fed to T2D patients for 12 weeks, significant decreases were observed in plasma total cholesterol in all subjects, possibly related to weight loss.5 However, only the subjects eating the eggs had significant increases in HDL cholesterol.5 Finally, in a third study involving T2D patients, subjects were divided into two groups consuming either 12 eggs or 2 eggs/week for 3 months.6 No differences in plasma lipids were observed between these two groups, confirming that increased egg consumption does not unfavorably alter plasma lipids in subjects with diabetes.6

A summary of the findings from these studies is presented in Table 1

 table 1

Although it is clear that more clinical trials need to be conducted, evidence from these three dietary interventions is consistent with the fact that egg intake does not alter glucose metabolism or increase the risk for heart disease in patients with diabetes when compared to other foods (lean meat or oatmeal) or with less egg consumption (2 eggs versus 12 eggs/week), supporting the fact that eggs can be part of a healthy diet for individuals with T2D. Further, the additional findings of decreased inflammation in patients with metabolic syndrome3 and diabetic individuals4 supports the fact that eggs are a good choice for patients with diabetes.

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Maria Luz Fernandez, PhD, is a Professor in the Department of Nutritional Sciences at the University of Connecticut in Storrs, CT.

 

Key Messages

  • It has been demonstrated that eggs increase both LDL cholesterol and HDL cholesterol, therefore maintaining the LDL/HDL ratio, a key marker of coronary heart disease risk.
  • Preliminary studies support the fact that egg intake can reduce inflammation in subjects with metabolic syndrome, who are at great risk for diabetes. When compared to egg substitute (lipid-free eggs), whole egg intake resulted in significant decreases in serum amyloid A, and tumor necrosis factor- alpha, suggesting that eggs have protective effects against inflammation.

 

References

  1. Fernandez ML, Andersen CJ. Effects of dietary cholesterol in diabetes and cardiovascular disease. Clinical Lipidology 2014; 9:607-616.
  2. Andersen CJ, Blesso CN, Lee JY, et al. Egg consumption modulates HDL composition and increases the cholesterol accepting capacity of serum in metabolic syndrome. Lipids 2013; 48:557-567.
  3. Blesso CN, Andersen CJ, Barona J, et al. Effects of carbohydrate restriction and dietary cholesterol provided by eggs on clinical risk factors of metabolic syndrome. J Clin Lipidol. 2013; 7:463-471.
  4. Ballesteros MN, Valenzuela F, Robles AE, et al. One egg per day improves inflammation when compared to an oatmeal-based breakfast without increasing other cardiometabolic risk factors in diabetic patients. Nutrients 2015; 7:3449-3463.
  5. Pearce KL, Clifton PM, Noakes M. Egg consumption as part of an energy-restricted high-protein diet improves blood lipid and blood glucose profiles in individuals with type 2 diabetes. Br J Nutr 2011:105:584-592.
  6. Fuller NR, Caterson ID, Sainsbury A et al. The effects of a high-egg diet on cardiovascular risk factors in people with type 2 diabetes: The Diabetes Egg (DIABEGG) study-a 3-mo randomized controlled trial. Am J Clin Nutr 2015: 101:705-713.