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CMHC PULSE

Cardio Metabolic Health Congress – Official Blog

Higher Egg and Cholesterol Consumption Increases Heart Disease and Death Risk

Contrary to 2010 guidelines, the new 2015-2020 Dietary Guidelines for Americans  from the U.S. Department of Health and Human Services no longer limits the consumption of dietary cholesterol, which used to be 300 mg per day, nor does it advise against eating eggs. In fact, the current dietary recommendations include weekly egg consumption as part of a healthy diet. On average, U.S. adults consume an average of 300 mg of dietary cholesterol per day and eat about three or four eggs per week. As the database of clinical research on the connection between high dietary cholesterol levels and heart disease continues to grow, there may be an increased need to reevaluate the current dietary recommendations.

A new Northwestern Medicine study found a link between egg and dietary cholesterol consumption, and a significantly higher risk of cardiovascular disease and death. Evaluating over 30,000 diverse U.S. adults and their diet histories, the research team discovered a correlation between the incidence of heart disease and the eating habits of participants.

Study Findings

Led by Wenze Zhong, the Northwestern team assessed the nutritional patterns of racially and ethnically diverse participants for up to 31 years of follow up and found that eating 300 mg of dietary cholesterol per day was associated with a 17% higher risk of incident cardiovascular disease. An 18% increase in the risk of all-cause deaths was revealed, with cholesterol as the driving factor behind these changes, independent of saturated or dietary fat consumption.

Additionally, the study reported a 6% increased risk of cardiovascular disease associated with high egg consumption as well as a rise of 8% in the risk of all-cause death. Eating three to four eggs per week was enough to raise the risk of these life-threatening consequences, while exercise and overall diet quality had no effect on the association between cholesterol and heart disease.

Eggs and Cholesterol

While eggs are well-known to be high in cholesterol, the notion that they raise the risk of heart disease has been heavily contested over decades. Previous studies have found no link between cardiovascular disease and egg consumption, although most of them had less diverse samples and shorter follow-up times. However, cholesterol, regardless of its source, has been indisputably associated with increased risk of heart disease.

Lowering cholesterol levels is an essential component of maintaining a healthy diet and lowering the risk of heart disease. Eliminating eggs could prove useful as they are notoriously cholesterol-rich; egg yolks themselves are one of the highest sources of most commonly consumed dietary cholesterol, containing up to 186 mg of dietary cholesterol in one large egg.

Recommendations

Based on the study, dietary cholesterol intake should remain low in order to minimize heart disease and death risks. Reducing cholesterol-rich foods such as eggs, red or processed meat, and high-fat dairy products is a key step in maintaining low cholesterol levels.  However, there is no indication that eggs and other high cholesterol foods need to be eliminated entirely, as they are good sources of important nutrients such as essential amino acids and iron.

Opting for egg whites instead of whole eggs, or eating eggs in moderation may be a sufficient preventative measure for some individuals. Adherence to a properly balanced, healthy diet should be recommended to all patients looking to lower their risk of heart disease.

Although the 2015-2020 Dietary Guidelines exclude dietary cholesterol limits, the change does not suggest that this factor is no longer important. Individuals should aim to eat as little dietary cholesterol as possible, while the study findings indicate that the current guidelines may need to be reassessed.

New Metabolic Target to Prevent Heart Failure Identified

The incidence of heart failure is the only form of heart disease that has not decreased in over 30 years, with approximately 550,000 new cases diagnosed in the U.S. per year.  Technological advancements in cardiac devices and improved prevention and treatment methods have diminished the death rate, but cardiovascular disease remains the leading cause of death in the country. A growing need to identify the underlying metabolic causes of heart failure has prompted new studies aimed at developing new therapies for patients and addressing the problem at its earliest stage.

A recent study from researchers at Ohio State University identifies a cardiometabolic process that could prevent and treat heart failure. Led by Dr. Doug Lewandowski, the research team discovered potentially detrimental changes in the heart’s metabolism that occur as a result of chronic stress, long before any physical signs or symptoms of heart failure are present. These first maladaptive changes occur in cardiac cell metabolism as the heart adapts to increased demands; addressing them early could prevent or slow the progression of heart failure.

Lewandowski’s team examined mouse models of heart failure as well as human heart tissue obtained from heart failure patients before and after cardiac assist devices were installed.
The tested mice overexpressed a gene for a protein called ACSL1, known to produce the reactive fat compound acyl-CoA. Upon exposure to conditions that cause heart failure, the mice maintained normal production of acyl-CoA, reducing and/or delaying the extent of heart failure. By maintaining acyl-CoA levels, the hearts were able to maintain the ability to metabolize fat and generate energy. Researchers also found that overexpression of ACSL1 reduces toxic fats, normalizes cell function and reduces the progressive loss of cardiovascular function in mice.

In examining heart failure patients, Lewandowski’s team found that the amount of the reactive fat compound was nearly 60% lower than in those with normal hearts. The decreased levels of acyl-CoA reveal a disruption in the hearts metabolic process, resulting in the creation of toxic fats and cardiac functioning impairment. Failing human hearts with the help of left ventricular assist devices behaved similarly to those of mice, restoring acyl-CoA levels to normal once not overworked.

The recent findings reveal an important relationship between fat metabolism in the heart and its inability to function. Although more research is needed, the team at Ohio State believes that targeting the normalization of acyl-CoA levels has the potential to become an effective method of preventing and treating heart failure. Future cardiometabolic care may include gene and drug therapy, and even dietary modifications aimed at stabilizing acyl-CoA compounds. With the help of advanced imaging, Lewandowski and his team hope to soon track fat metabolism and heart function in greater depth. Further studies will explore how the normalization of acyl-CoA reduces toxic fats and increases protective fats in order to understand how these improvements are achieved, and whether they can be replicated through supplementation with fats, medications, and other compounds.