What Every Clinician Should Know about Ramadan & Intermittent Fasting

Intermittent fasting—defined as alternating between cycles of eating and going without food over a given period of time—has become popular with individuals seeking to lose weight or balance their lifestyle in recent years. During Ramadan (a period based on the Gregorian calendar that changes from year to year), able-bodied Muslims are obligated to observe a fast from dawn to dusk, refraining from food and drink. This year, Ramadan begins at sundown on Sunday, March 10, and ends on April 8 (predicted based on the lunar cycle). Rheumatologists and rheumatology professionals need to be aware of how such fasting could affect their patients.

The Benefits of Fasting

Within medicine and through scientific research, the benefits of fasting have been established, particularly in diabetes and cardiovascular literature. Metabolic dysregulation, such as insulin resistance, hypertension, dyslipidemia and atherosclerosis, has been improved by establishing caloric restriction without malnutrition.

Caloric restriction reduces body weight and increases life expectancy in obese individuals. It has been shown to improve insulin sensitivity, cardiovascular risk factors and mitochondrial dysfunction. Long-term, daily caloric restriction is difficult to adhere to, which is where intermittent fasting has excelled. It has come into favor as an alternative for caloric restriction to achieve the goals of reducing the adverse effects of obesity, insulin resistance and cardiovascular disease by playing a role in reducing systemic inflammation.³

Weight reduction is the main benefit of intermittent fasting. Intermittent fasting has been shown to reduce fasting insulin plasma levels and the overall body inflammatory status by regulating various cytokines that promote inflammatory pathways, which are well established in rheumatic and autoinflammatory conditions. Cytokines, such as the mechanistic target of rapamycin (mTOR), AMP‐activated protein kinase (AMPK) and autophagy, have been shown to be regulated with implementation of intermittent fasting.⁴

During the fed state, signaling pathways for nutrient sensing and cellular growth (e.g., mTOR) are activated. Stress-responsive signaling pathways (e.g., FOXO and AMPK) are activated by fasting, resulting in the protection from cell damage and inhibition of cell proliferation.

An additional mechanism of intermittent fasting is the metabolic switch between fed and fasting states. Fasting, especially repetitive fasting, induces organisms to shift their metabolic phase, which improves metabolic conditions and extends health expectancy.

It has also been reported that fasting optimizes cellular use of fuel sources, favoring ketone bodies and fatty acids over glucose, which ameliorates the blunting of metabolic flexibility observed in obesity and type 2 diabetes mellitus and improves mitochondrial function.