Across two samples, in both pre- and post-menopausal women, high dietary restraint was linked to shorter leukocyte telomeres. In both samples this effect was independent of BMI, age, perceived stress, and smoking. This report adds to the growing literature on the negative effects of high DR. While DR may to some extent be necessary to maintain weight in the rich food environment of the modern United States, high levels of restraint may be unhealthy, as self-reported dietary restraint has been linked to aberrations in stress and reproductive hormones, greater adiposity, and in some studies, greater levels of life stress [
14–
18]. Here we introduce the possibility that DR may also relate to accelerated aging of the immune system. Identification of lifestyle factors that are linked to telomere maintenance is a nascent field. It was notable that DR had an effect over and above other known effects, such as obesity and stress. Future research should examine whether dietary restraint predicts accelerated telomere shortening prospectively.
There are many potential explanations for why high DR would be negatively associated with TL. Given the cross sectional nature of the study, it is possible that DR may have served as a proxy for an unmeasured third variable that leads to telomere shortening. This study tested several plausible third variables, including emotional eating, external eating, body mass index, and perceived stress, none of which appeared to affect the relationship between DR and TL. Nonetheless, the relationship between DR and TL is likely an indirect relationship that involves a chain of behavioral or biochemical events. Future research should assess additional plausible third variables or mediators of this relationship, such as responsiveness to food cues, dietary habits, early life influences on nutrition, and personality or lifestyle variables.
One might wonder how these findings are related to the literature on caloric restriction. In animal studies, caloric restriction enhances longevity, and delays the onset of the diseases of aging [
37–
39]. Caloric restriction may have similar effects on promoting longevity in humans, in that it improves biomarkers that predict longevity [
39,
40–
42]. The relationship between TL and caloric restriction has not been studied in humans. Caloric restriction may promote TL maintenance by increasing insulin sensitivity, which has been linked to longer telomeres [
43]. Upon superficial examination, our results might appear to contradict the hypothesis that caloric restriction slows aging and telomere shortening in humans. However, caloric intake is not strongly related to DR. Self-reported DR assesses only the intention to reduce caloric intake, not actual restrictive behavior; DR is not consistently associated with weight loss or caloric intake [
2,
4–
7,
20,
44]. Rather, it appears to be related to eating less in controlled conditions, and overeating when self control is challenged, especially if one scores high on the tendency to overeat in response to food cues or emotions [van Strien, 2006}.
The distinction between unhealthy and ineffectual attempts at weight loss, which are frequently reported by chronic dieters, and successful dietary restraint induced by behavioral interventions, which increase well-being and aid weight loss [
6], is important for interpreting our results. We propose that behaviorally successful DR, and the consequent decreases in habitual caloric intake, lowers glucose and insulin levels, distress, and consequently should slow rate of telomeric loss. Free (unrestrained) eaters tend to eat meals more regularly. Conversely, DR, as typically assessed by self-report, is associated with dysregulated patterns of eating (fasting, binging, and purging) [
45]. Frequent missed meals followed by overeating, may cause some ‘metabolic strain,’ in the form of more frequent and greater fluctuations in insulin and glucose levels, and such exposure is hypothesized to accelerate telomeric loss [
46]. These findings therefore call for assessment of eating behaviors in conjunction with self-reported DR, to distinguish “healthy” DR from “unhealthy” DR. Until this research is conducted, we can only speculate about the mechanisms to explain the relationship between self reported dietary restraint and TL in humans.
Additional limitations of these studies include the small sample sizes and exclusive focus on women. Further, in the first study, a subset of the DEBQ was administered over the phone 18 months after the other assessments. Despite these limitations, the results of these two studies were consistent with each other and not explained by obvious confounding factors, such as BMI, age, or reported tendency to overeat in response to stimuli or emotions.
In conclusion, we find that self-reported DR is linked to shortened telomeres. Given the replication across two samples, among pre- and post-menopausal women, the relationship between DR and TL appears to exist at least phenotypically. Findings from this preliminary test of the hypothesis call for experimental and prospective assessment of this relationship to determine if the relationship is causal, and whether it is due to cognitive, behavioral, or physiological pathways.