You’ve probably heard that sugar feeds disease, often cancer, and that inflammation is the root cause of many diseases. But did you know that sugar can also lead to coronary artery disease, which is responsible for nearly half of all deaths in the United States? It’s essential to understand how sugar impacts not only our overall health but also our heart health to manage our diets effectively and protect our well-being.
Macrophages: The Good and the Bad
Coronary artery disease results from plaque buildup in the arteries, impairing the delivery of oxygen-rich blood to your heart. Lipids are a main component of plaque build-up, but plaque also contains immune cells called macrophages. These cells attack and ingest invading bacteria, repair tissue, and clean up debris left after injury or infection.
Macrophages generally fall into two categories:
- M2 macrophages are helpful and oversee tissue repair. They nibble on cellular debris, release factors that encourage new cell growth, and stimulate blood flow.
- M1 macrophages are inflammatory. They attack invaders using biohazardous chemicals called free radicals. They also produce proteins that act both locally and systematically to ramp up the entire immune system to high-alert status, recruiting other immune cells to participate in this unhealthy behavior.
Coronary artery disease patients’ macrophages get so preoccupied with their inflammatory power trip that they neglect their cleanup tasks, allowing plaque to continue building up in arteries. Ongoing inflammation makes plaques increasingly brittle. If a piece of plaque suddenly breaks off and wounds the artery wall, a blood clot can form and lead to a heart attack.
The Role of Sugar in Inflammation
Research from Stanford School of Medicine has shown that glucose, or sugar, can make some macrophages go rogue. A defect in glucose metabolism by immune cells in arterial plaques drives them into a hyper-inflammatory state, ultimately leading to coronary heart disease.
M1 macrophages take up glucose at a higher rate than normal cells, causing them to break it down faster and overheat their mitochondria, which then produce too many free radicals. The excessive free-radical production in patient-derived macrophages is pinned to a faulty overproduction of proteins responsible for importing glucose into cells, such as IL-6, an immune-signaling protein that drives inflammation.
Several interventions, including blocking glucose uptake, sponging up free radicals, and preventing PKM2’s status change, have been proposed to reduce macrophages’ excess inflammatory activity and lead to new therapeutic approaches.
However, before resorting to pharmaceutical interventions, consider taking the first step by reducing the amount of sugar your body needs to process.
The Link Between Sugar Consumption and Heart Disease
Previous studies have shown that individuals who consume more added sugar, especially sugar-sweetened beverages, tend to gain more weight and have a higher risk of obesity, type 2 diabetes, hypertension, and cardiovascular disease. Plaque accumulation can begin early in life, starting as young as 15 years old, and progresses steadily with advancing age.
In the U.S., sugar consumption starts at an early age, even with seemingly healthful foods like juices. However, it’s those hidden added sugars, such as high fructose corn syrup, that can lead to a lifetime of heart trouble and more.
Reducing Sugar Intake to Protect Your Heart
By understanding the role sugar plays in inflammation and coronary artery disease, you can make informed choices about your diet and lifestyle to proactively protect your heart health. Reducing your sugar intake, particularly in the form of added sugars found in processed foods and beverages, is a critical step to preventing disease and promoting overall well-being.
Remember that knowledge is power when it comes to making decisions about your health. By educating yourself on the impact of sugar on our bodies, you can make the necessary changes to your diet and lifestyle to support a healthy heart and a healthier future.
