Effect of Intermittent Fasting on Immune Parameters and Intestinal Inflammation

Abstract

Intermittent fasting (IF), including alternate day fasting (ADF) and time-restricted feeding (TRF) or, in humans, time-restricted eating (TRE), has been associated with the prevention and improvement of diseases, including inflammatory bowel disease (IBD). This review summarizes 20 animal and human studies on the influence of IF on intestinal inflammation. In the animal studies, TRF and ADF improved histological scores, inflammatory markers, markers of oxidative stress, and microbiota composition. Apart from the studies on Ramadan fasting, there are no studies on IF in IBD patients, so human studies on IF in healthy people were included. The studies on Ramadan fasting showed almost no effects, but this particular type of fasting is not directly comparable to TRE or ADF. However, TRE and ADF appear to have anti-inflammatory effects in healthy individuals, as they significantly reduce CRP levels and inflammatory markers. TRE also improved the composition of microbiota and the circadian oscillation of clock genes. The beneficial effects of TRE and ADF in healthy people appear to depend on the number of uninterrupted days of fasting, while in animal studies improvements in colitis have been observed regardless of the duration of fasting.

Keywords: alternate day fasting; colitis; immune parameters; inflammation; intermittent fasting; time-restricted feeding.

Figure 1

Effects of fasting on inflammatory signaling intermittent fasting (IF) increases the level of ketone bodies (KB) and inhibits histone deacetylases (HDACs), which promotes the regeneration of the intestinal epithelium. IF also lowers the plasma levels of insulin-like growth factor 1 (IGF-1) and downregulates phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathways. There is an increase in regulatory T cells (Treg) and a reduction in effector T cells, such as T helper cells 1 (Th1) and Th17 cells. IF activates sirtuin 1 (SIRT1) and adenosine monophosphate-dependent kinase (AMPK) through the increase in nicotinamide adenine dinucleotide (NAD⁺) and AMP. NAD⁺, SIRT1, and AMPK can synchronize a circadian rhythm. SIRT1 and forkhead-box O 1/3 (FoxO1/3) inhibit nuclear factor kappa B (NF-κB). The inhibition of NF-κB downregulates pro-inflammatory cytokines such as the tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β). ↑ = upregulation; ↓ = downregulation. The figure was designed with BioRender (https://www.biorender.com; accessed on 27 September 2024).