Obesity is a systemic and chronic inflammation, which seriously endangers people\'s health. People tend to diet to control weight, and the short-term effect of dieting in losing weight is significant, but the prognosis is limited. With weight loss and recovery occurring frequently, people focus on weight cycling. The effect of weight cycling on a certain tissue of the body also has different conclusions. Therefore, this article systematically reviews the effects of body weight cycling on the body and finds that multiple weight cycling (1) increased fat deposition in central areas, lean mass decreased in weight loss period, and fat mass increased in weight recovery period, which harms body composition and skeletal muscle mass; (2) enhanced the inflammatory response of adipose tissue, macrophages infiltrated into adipose tissue, and increased the production of pro-inflammatory mediators in adipocytes; (3) blood glucose concentration mutation and hyperinsulinemia caused the increase or decrease in pancreatic β-cell population, which makes β-cell fatigue and leads to β-cell failure; (4) resulted in additional burden on the cardiovascular system because of cardiovascular rick escalation. Physical activity combined with calorie restriction can effectively reduce metabolic disease and chronic inflammation, alleviating the adverse effects of weight cycling on the body.

The aim of this systematic review is to comprehensively assess the weight loss (WL) practices in different combat sports (CS). The review protocol was preregistered with PROSPERO [CRD42023487196]. Three databases were searched (Web of Science, EBSCOhost, and PubMed) until 8 December 2023. Eligible studies had to meet five criteria: they must have been (a) written in English, (b) published in a peer-reviewed journal, (c) used a survey design to investigate the WL practices of CS athletes, and (d) reported the WL methods used by athletes using a five-point scale. Twenty-six studies (3994 participants from 14 CS) were included. This review found that (1) WL is highly prevalent in CS athletes; (2) many CS athletes started losing weight for competition as teenagers two to three times a year; (3) CS athletes usually lose <5% body weight in 7-14 days before competition; (4) increasing exercise and gradually dieting are the most commonly used WL methods; and (5) the influence of scientific practitioners on athletes is negligible. The habitual practices of CS athletes may be relatively harmless, but in some special cases, CS athletes also perform extreme WL practices. Scientific practitioners have little influence on their WL practices, which may form a vicious cycle of non-qualified influence.

BACKGROUND: Obesity is a global public health concern. The goal of this study was to see if eating habits could mediate the relationship between psychological distress and weight maintenance in a population with a history of weight cycling.
METHODS: A 3-month outpatient intervention consisting of a diet and exercise program was provided to 153 participants. Psychological distress, appetite, and behavior were assessed at the beginning and end of the study. Anthropometric measurements were taken at baseline and six months.
RESULTS: After the structural equation model was developed, it was discovered that the psychological status of people with obesity and weight cycling histories correlated with the weight loss outcome effect (three and six months). This effect was mediated by factors related to eating behavior. Associative psychological factors had a direct effect on eating behavior (three months: β = 0.181, 95% CI: 0.055-0.310; six months: β = 0.182, 95% CI: 0.039-0.332) and appetite had a direct effect on eating behavior (three months: β = 0.600, 95% CI: 0.514-0.717; six months: β = 0.581, 95% CI: 0.457-0.713), both of which were significant (p < 0.01). At three months, psychological distress has a more substantial positive impact on weight change, with eating behavior acting as a partial mediator. At six months, there was no support for appetite\'s moderating role in eating behavior.
CONCLUSIONS: The findings suggest that psychological interventions should be strengthened to improve weight loss effectiveness, particularly in participants with a history of weight cycling, making weight loss more complicated and prone to rebound.
BACKGROUND: The study has been registered in Clinical Trials (NCT05311462).

Weight regain subsequent to weight reduction resulting from dietary interventions represents a prevalent phenomenon recognized as \"Yo-yo dieting.\" However, the impact of prolonged Yo-yo dieting on health, especially in relation to the aging process, remains poorly understood. This study aimed to investigate the influence of Yo-yo dieting on the aging process in male Drosophila melanogaster that have been exposed to a high-calorie (HC) diet. Fruit flies were fed with either a consistent HC diet or an alternating regimen of HC and low-calorie diets every 3 days (referred to as \"Yo-yo dieting\") for a total of 24 days. Biochemical assays were utilized to quantify levels of oxidative stress and activities of the mitochondrial respiratory chain complexes. The frozen section staining method was employed to assess the presence of lipid droplets, reactive oxygen species, cellular viability, and mitochondrial abundance in tissues. Additionally, we examined the expression of key regulators involved in mitochondrial dynamics and biogenic signaling pathways. Yo-yo dieting resulted in an extension of the fruit flies\' lifespan, concomitant with reduced body weight, decreased body protein content, and lower triglyceride levels compared to continuous a HC diet feeding. Furthermore, Yo-yo dieting ameliorated impairments in motility and intestinal barrier function. Importantly, it improved mitochondrial function and upregulated the expression of essential mitochondrial fusion proteins, namely mitofusin 1 and mitofusin 2, optic atrophy 1, and peroxisome proliferator-activated receptor-γ coactivator-1α. Therefore, the practice of Yo-yo dieting extends the lifespan of fruit flies by modulating mitochondrial dynamics and the associated biogenic signaling pathways.

Previous studies hardly evaluated the association of variability of body mass index (BMI) or waist circumference with clinical adverse events and investigated whether weight cycling had an effect on the prognosis of patients with heart failure with preserved ejection fraction (HFpEF).
This study was a post-hoc analysis of TOPCAT. Three outcomes were evaluated: the primary endpoint, cardiovascular disease (CVD) death, and heart failure hospitalization. Among them, CVD death and hospitalization were outcomes of heart failure. Kaplan-Meier curves were used to describe the cumulative risk of outcome and were tested using the log-rank test. Cox proportional hazards regression models were used to calculate hazard ratios (HRs) and 95%CIs for outcomes. We also performed a subgroup analysis, and several subgroups were compared.
A total of 3,146 patients were included. In the Kaplan-Meier curves, the coefficients of variation of both BMI and waist circumference were grouped according to quartiles, with the Q4 group having the highest cumulative risk (log-rank P < 0.001). In the coefficient of BMI variation and the outcomes, the HRs for group Q4 of coefficient of variation of BMI were 2.35 (95%CI: 1.82, 3.03) for the primary endpoint, 2.40 (95%CI: 1.69, 3.40) for death, and 2.33 (95%CI: 1.68, 3.22) for HF hospitalization in model 3 (fully adjusted model) compared with group Q1. In the coefficient of waist circumference variation and the outcomes, group Q4 had increased hazard of the primary endpoint [HR: 2.39 (95%CI: 1.84, 3.12)], CVD death [HR: 3.29 (95%CI: 2.28, 4.77)], and HF hospitalization [HR: 1.98 (95%CI 1.43, 2.75)] in model 3 (fully adjusted model) compared with group Q1. In the subgroup analysis, there was a significant interaction in the diabetes mellitus subgroup (P for interaction = 0.0234).
Weight cycling had a negative effect on the prognosis of patients with HFpEF. The presence of comorbid diabetes weakened the relationship between waist circumference variability and clinical adverse events.

As a result of the obesity epidemic, more people are concerned about losing weight; however, weight regain is common, leading to repeated weight loss and weight cycling. The health benefits of early weight loss are nullified by weight regain after weight cycling, which has much more severe metabolic consequences. Weight cycling alters body composition, resulting in faster fat recovery and slower muscle reconstruction. This evident fat accumulation, muscle loss, and ectopic fat deposition destroy the intestinal barrier, increase the permeability of the small intestinal epithelium, and cause the lipotoxicity of lipid metabolites and toxins to leak into extraintestinal tissues and circulation. It causes oxidative stress and hypoxia in local tissues and immune cell infiltration in various tissues, all contributing to the adaptation to this metabolic change. Immune cells transmit inflammatory responses in adipose and skeletal muscle tissue by secreting cytokines and adipokines, which mediate immune cell pathways and cause metaflammation and inefficient metabolic degradation. In this review, we focus on the regulatory function of the immunological microenvironment in the final metabolic outcome, with a particular emphasis on the cellular and molecular processes of local and systemic metaflammation induced by weight cycling-induced changes in body composition. Metaflammation in adipose and muscle tissues that is difficult to relieve may cause weight cycling. As this chronic low-grade inflammation spreads throughout the body, metabolic complications associated with weight cycling are triggered. Inhibiting the onset and progression of metabolic inflammation and enhancing the immune microenvironment of adipose and muscle tissues may be the first step in addressing weight cycling.

UNASSIGNED: In this meta-analysis, we aimed to explore the association between bodyweight cycling (weight fluctuation) and the risk of developing diabetes.
METHODS: We analyzed data from eligible cohort studies that assessed the association between weight cycling in adults and the risk of developing diabetes from online databases PubMed, Cochrane Library and EMBASE databases (1966 to April 2020). We pooled data using relative risks (RRs) with a random effects model.
RESULTS: A total of 14 studies involving 253,766 participants, including 8,904 diabetes events, were included. One study included eight independent reports, resulting in 21 reports in 14 studies. Summary analysis showed that individuals who suffered weight cycling had a higher risk of diabetes (RR 1.23. 95% confidence interval 1.07-1.41; P = 0.003). However, the association between weight cycling and the risk of developing diabetes was not observed in obese participants (body mass index ≥30 kg/m2 ; P = 0.08).
CONCLUSIONS: The present meta-analysis showed that weight cycling was a strong independent predictor of new-onset diabetes. Future studies are required to detect the causal links between weight cycling and the risk of developing diabetes.

Background: The aim of this study was to evaluate associations between body-weight fluctuation and risk of mortality and cardiovascular diseases (CVD). Methods: PubMed, EMBASE databases and Cochrane Library were searched for cohort studies published up to May 20, 2019, reporting on associations of body-weight fluctuation and mortality from all causes, CVD and cancer, as well as morbidity of CVD and hypertension. Summary relative risks (RRs) were estimated using a random-effects model. Results: Twenty-five eligible publications from 23 studies with 441,199 participants were included. Body-weight fluctuation was associated with increased risk for all-cause mortality (RR, 1.41; 95% confidence interval (CI): 1.27-1.57), CVD mortality (RR, 1.36; 95% CI 1.22-1.52), and morbidity of CVD (RR, 1.49, 95% CI 1.26-1.76) and hypertension (RR, 1.35, 95% CI 1.14-1.61). However, there was no significant association between weight fluctuation and cancer mortality (RR, 1.01; 95% CI 0.90-1.13). No evidence of publication bias was observed (all P > 0.05) except for studies on all-cause mortality (Egger\'s test, P = 0.001; Begg\'s test, P = 0.014). Conclusions: Body-weight fluctuation was associated with higher mortality due to all causes and CVD and a higher morbidity of CVD and hypertension.

Impacts of weight cycling on C1q/tumor necrosis factor (TNF)-related protein-3 (CTRP3) expression, adipose tissue inflammation and insulin sensitivity in C57BL/6J mice were evaluated in the current study. A total of 30 male C57Bl/6J mice were divided randomly into three groups; normal control (n=10), high-fat diet (OB, n=10) and weight cycling (WC, n=10), which were fed with high-fat diet in the first and last 8 weeks and regular chow in between. Systemic glucose metabolic status and insulin sensitivity were detected by intraperitoneal glucose tolerance test and hyperinsulinemic-euglycemic clamp, respectively. Blood levels of interleukin (IL)-6 and TNF-α were determined using ELISA. Relative CTRP3, IL-6, TNF-α and glucose transporter (GLUT)4 mRNA expression in adipose tissue was detected using reverse transcription-quantitative polymerase chain reaction assays. Relative CTRP3, phosphatidylinositide 3-kinases (PI3K) and protein kinase B (PKB; Ser473) protein expression were detected by western blot analysis. Area under the curve of glucose and glucose infusion rate of the WC group were significantly increased compared with the OB group (P<0.01). CTRP3 mRNA and protein levels of the WC group were significantly decreased by 20.3 and 23.1%, respectively, compared with the OB group (P<0.01). IL-6 and TNF-α protein plasma levels and gene expression in adipose tissue of the WC group were significantly increased compared with the OB group (P<0.01). Expression and phosphorylation of insulin signaling molecules PI3K and PKB (Ser473), respectively and GLUT4 gene expression in adipose tissue of the WC group were significantly decreased compared with the OB group (P<0.01). In conclusion, weight cycling impaired glucose metabolism and insulin sensitivity by decreasing CTRP3, PI3K, phosphorylated-PKB (Ser473) and GLUT4 expression, and increasing IL-6 and TNF-α levels.