Therapeutic Potential of Infrared and Related Light Therapies in Metabolic Diseases

Abstract

Infrared and related light therapies are gaining increasing interest due to their potential therapeutic properties in treating various health conditions, particularly metabolic diseases such as insulin resistance and type 2 diabetes. These diseases often coexist with dyslipidemia, obesity, non-alcoholic fatty liver disease, and cardiovascular complications. This review paper analyzes the impact, primarily of far-infrared light therapy (FIR), on improving endothelial function, reducing oxidative stress, and modulating inflammatory responses-key factors in metabolic diseases. Preliminary studies suggest that FIR may improve blood circulation, increase the secretion of VEGF, and enhance insulin sensitivity by alleviating inflammatory states and oxidative damage commonly associated with these diseases. In addition, FIR has been associated with potential benefits in blood pressure regulation and lipid metabolism, which could contribute to reduced cardiovascular risk. However, it is important to acknowledge that most current evidence is derived from preclinical models and small-scale clinical trials, limiting direct applicability to broader patient populations. Moreover, significant variability exists in exposure parameters and treatment protocols across studies. While FIR therapy holds potential as a complementary approach to the conventional management of metabolic diseases, careful monitoring is essential to mitigate potential adverse effects. Further well-designed, large-scale clinical trials are necessary to validate the therapeutic efficacy, optimize treatment parameters, and comprehensively assess the safety profile of FIR interventions in metabolic health.

Keywords: cardiovascular health; far-infrared light therapy (FIR); inflammation; metabolic diseases; non-pharmacological therapies; oxidative stress.

Figure 1

The electromagnetic spectrum and infrared radiation subdivision.

Figure 2

Molecular and cellular mechanisms induced by far-infrared radiation (FIR).

Figure 3

Mechanism of normal insulin action and insulin resistance. The diagram illustrates the differences between normal insulin signaling and the development of insulin resistance, highlighting the roles of pro-inflammatory cytokines, free fatty acids (FFAs), and oxidative stress.

Figure 4

Mechanism of FIR in preserving pancreatic β-Cell mass and function. The figure illustrates the proposed mechanism by which far-infrared radiation protects pancreatic β-cells from dysfunction and apoptosis. FIR stimulates mitochondrial activity, leading to an increased ATP/ADP ratio and a higher NAD⁺/NADH level, which subsequently activates Sirt1. Sirt1 enhances insulin secretion and promotes cell survival through the activation of PLZF and the PI3K/Akt signaling pathway, reducing apoptosis. Additionally, FIR influences intracellular calcium (Ca²⁺) dynamics, further supporting insulin secretion and β-cell function. These mechanisms collectively contribute to the maintenance of β-cell mass and function under metabolic stress.

Figure 5

Pathophysiological mechanism linking obesity, inflammation, and hypertension. The diagram illustrates the pathway through which obesity contributes to the development of hypertension. Increased levels of free fatty acids (FFAs) and glucose lead to the upregulation of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), and fibrinogen. The resulting chronic inflammatory state induces vascular dysfunction and vasoconstriction, ultimately leading to hypertension.