News
Article
Author(s):
Chronic kidney disease has been linked to yo-yo dieting (also known as body-weight cycling) in the general population, which interested investigators in potential links between these weight fluctuations and increased risk of renal events among a population with type 1 diabetes.
Body-weight cycling—more popularly known as yo-yo dieting—may be responsible for greater risks of decreased estimated glomerular filtration rate (eGFR), increased serum creatinine, moderately increased albuminuria, rapid decline in kidney function, and progressing to stage 3 chronic kidney disease (CKD) seen among people living with type 1 diabetes (T1D).
Individuals who have T1D already have elevated mortality rates and impaired vital prognoses, spurred by interactions between diabetic kidney disease and cardiovascular disease, the authors note, but these can be improved with strict glycemic control.
They examined data on 6 years’ worth of body-weight indices for 1432 participants from the Diabetes Control and Complications Trial (NCT00360815), which originally enrolled 1441 participants aged 13 to 39 years, and its posttrial observational follow-up study, Epidemiology of Diabetes Interventions and Complications (NCT00360893). Their findings were published online today in The Journal of Clinical Endocrinology & Metabolism.1 They explain that even after accounting for potential contributions from body mass index and traditional vascular risk factors of decreased glucose tolerance and decreased insulin sensitivity, body-weight cycling maintained its adverse impact on adverse kidney outcomes in patients with T1D.
Variability independent of the mean (VIM) served as the investigators’ primary index for identifying yo-yo dieting patterns, which were noted to be the repeated loss and gaining of weight over several years; the other indices they used were average successive variability (ASV), SD of body-weight measures, and relative ASV. The mean (SD) study follow-up was 21 (4) years, and their 6 criteria for kidney function decline were 40% decline in eGFR from baseline, doubling of baseline serum creatinine, incidence of stage 3 CKD, annual slope of eGFR over time, incidence of moderately increased albuminuria, and incidence of severely increased albuminuria.
Approximately 19% of the study participants (n = 269) experienced a 40% eGFR decline, with the total incidence rate being 9.2 (95% CI, 8.1-10.3) per 1000 person-years. These participants also had higher indices of intraindividual body-weight variability compared with those who did not experience a 40% eGFR decline. Two regression models the authors used resulted in increased risk of this outcome ranging from 16% (P = .02) to 26% (P = .002).
This was seen in 8.6% of the study population (n = 123), at an incidence rate of 3.8 (95% CI, 3.2-4.5) per 1000 person-years. Positive correlations were seen between intraindividual body-weight variability and this outcome. Compared with 40% eGFR decline, these risks were higher under the regression models, ranging from 25% (P = .01) to 35% (P = .0007).
A total of 8.9% of the study population (n = 128) experienced this outcome. The incidence rate was 3.9 (95% CI, 3.3-4.6) per 1000 person-years. The positive correlations with intraindividual body-weight variability were confirmed using Cox proportional hazards, with the elevated risks ranging from 21% (P = .03) to 36% (P = .002) under the regression models.
There were 3 tertiles of mean rates of eGFR change per year: −1.51 (0.06) mL/min/1.73 m2, T1; −1.47 (0.06) mL/min/1.73 m2, T2; and −1.73 (0.06) mL/min/1.73 m2, T3. The associated rapid decline in kidney function, defined by the investigators as an eGFR slope steeper than −3 mL/min/1.73 m2 per year, was seen in 7.1% (n = 102) of the study population. Elevated risks of this outcome ranged from 26% (P = .02) to 55% (P = .002) with the 2 models.
Twenty-six percent (n = 361) and 11.7% (n = 168) had moderately increased albuminuria and severely increased albuminuria, respectively. The corresponding incidence rates were 13.7 (95% CI, 12.3-15.1) and 5.5 (95% CI, 4.7-6.3) per 1000 person-years. Increased risks of moderately increased albuminuria ranged from 3% (P = .60 and P = .64) to 18% (P =.008 and P = .004), and of severely increased albuminuria, from 1% (P = .92) to 36% (P = .001), using the regression models.
Overall, 95 participants died during the follow-up.
“The causes of weight cycling can be multiple and complex, involving genetic, environmental, and pharmacological factors,” the study authors wrote. “In type 1 diabetes, insulin therapy may play a particularly significant role in driving body weight cycling due to the anabolic effects of the hormone.”
They also note potential contributions from behavioral, lifestyle, and dietary influences,2 and that the pathophysiological mechanisms behind the positive correlation between body-weight cycling and kidney disease risk remains poorly understood.1
“Further investigations are needed to clarify the pathophysiological mechanisms behind these associations,” they concluded. “Clinically, strategies aimed at weight reduction in people with type 1 diabetes should focus on promoting long-term weight maintenance, as weight stability may have a positive impact on health outcomes.”
References
1. Camoin M, Mohammedi K, Saulnier PJ, et al. Body-weight cycling and risk of diabetic kidney disease in people with type 1 diabetes in the DCCT/EDIC population. J Clin Endocrinol Metab. Published online February 4, 2025. doi:10.1210/clinem/dgae852
2. Rhee EJ. Weight cycling and its cardiometabolic impact. J Obes Metab Syndr. 2017;26(4):237-242. doi:10.7570/jomes.2017.26.4.237