Atherosclerosis, the underlying cause of most heart attacks and strokes, is a progressive condition involving the build-up of fatty plaques inside arteries. Therapeutic fasting, which involves cycling between periods of eating and not eating, has emerged as a potential lifestyle intervention to improve health. This practice includes regimens like intermittent fasting (IF) or more prolonged periods of calorie restriction. This article examines the scientific evidence to determine if fasting can induce the reversal or stabilization of existing atherosclerotic plaque in human arteries.
What Atherosclerosis Is and Why It Matters
Atherosclerosis is a chronic inflammatory disease where the inner lining of arteries, the endothelium, is damaged, allowing cholesterol-carrying lipoproteins to accumulate. This accumulation triggers an immune response, causing white blood cells, particularly monocytes and macrophages, to infiltrate the arterial wall. These macrophages consume the lipids, transforming into “foam cells,” which form the soft, fatty core of the plaque.
As the plaque grows, it hardens and narrows the artery, restricting blood flow to the heart and other organs. The danger lies not just in the blockage but in the plaque’s instability. If a vulnerable plaque ruptures, it can trigger a blood clot, acutely blocking the artery and leading to a myocardial infarction or an ischemic stroke.
Systemic Effects of Fasting on Cardiovascular Risk Factors
Fasting influences the body’s metabolism in ways that indirectly reduce the overall risk environment for atherosclerosis progression. Periods of fasting consistently lead to improved blood lipid profiles, which are major drivers of plaque formation. Studies show that fasting can significantly reduce plasma triglycerides and very low-density lipoprotein (VLDL) cholesterol, limiting the raw material available for new plaque growth.
Fasting also enhances insulin sensitivity, improving glucose control and reducing the risk of type 2 diabetes, a strong accelerator of atherosclerosis. Fasting is associated with a decrease in systemic markers of chronic inflammation, such as high-sensitivity C-reactive protein (hs-CRP). By lowering these inflammatory signals and improving metabolic parameters, fasting creates an environment less conducive to plaque progression.
Cellular Mechanisms for Plaque Stabilization and Regression
The most compelling evidence for fasting’s impact on established plaque involves specific cellular housekeeping and immune processes within the arterial wall. Fasting triggers autophagy, a mechanism where cells clean out and recycle damaged components. Activating autophagy in macrophages (foam cells) is protective, as it helps these cells clear excess cholesterol and cellular debris, reducing their inflammatory load.
Defective autophagy in macrophages is linked to increased inflammation and the inability to efficiently remove cholesterol, which accelerates plaque growth. Fasting-induced autophagy helps restore this function, reducing the toxic buildup within the plaque’s core.
Fasting influences the phenotype of macrophages within the plaque, promoting a shift away from the pro-inflammatory M1 type toward a more resolving or anti-inflammatory M2-like state. This shift contributes to plaque stabilization, where the fibrous cap covering the fatty core thickens, making the plaque less likely to rupture.
Fasting can reduce the adhesion of monocytes—precursors to macrophages—to the endothelial lining, limiting the recruitment of new inflammatory cells. While these mechanisms show potential for plaque stabilization and regression, much of the specific evidence comes from animal models, such as studies on mice where intermittent fasting has been shown to reduce lesion size and increase plaque stability.
Implementing Fasting Safely and Research Limitations
Different fasting methods, such as time-restricted eating and alternate-day fasting, have been studied for cardiovascular benefits. While some protocols show promise, one animal study using alternate-day fasting aggravated atherosclerosis in a specific mouse model, highlighting that not all regimens are universally beneficial.
For individuals with existing cardiovascular disease or advanced atherosclerosis, fasting should only be attempted under medical supervision. This is especially true for people on medications for diabetes, high blood pressure, or lipid disorders, as fasting can rapidly alter blood sugar and electrolyte levels. The current scientific literature lacks large-scale, long-term human trials using advanced imaging techniques to definitively demonstrate that fasting causes regression of established human plaque.