Chrono-medicine considers circadian biology in disease management, including combined lifestyle and medicine interventions. Exercise and nutritional interventions are well-known for their efficacy in managing type 2 diabetes, and metformin remains a widely used pharmacological agent. However, metformin may reduce exercise capacity and interfere with skeletal muscle adaptations, creating barriers to exercise adherence. Research into optimising the timing of exercise has shown promise, particularly for glycaemic management in people with type 2 diabetes. Aligning exercise timing with circadian rhythms and nutritional intake may maximise benefits. Nutritional timing also plays a crucial role in glycaemic control. Recent research suggests that not only what we eat but when we eat significantly impacts glycaemic control, with strategies like time-restricted feeding (TRF) showing promise in reducing caloric intake, improving glycaemic regulation and enhancing overall metabolic health. These findings suggest that meal timing could be an important adjunct to traditional dietary and exercise approaches in managing diabetes and related metabolic disorders. When taking a holistic view of Diabetes management and the diurnal environment, one must also consider the circadian biology of medicines. Metformin has a circadian profile in plasma, and our recent study suggests that morning exercise combined with pre-breakfast metformin intake reduces glycaemia more effectively than post-breakfast intake. In this review, we aim to explore the integration of circadian biology into type 2 diabetes management by examining the timing of exercise, nutrition and medication. In conclusion, chrono-medicine offers a promising, cost-effective strategy for managing type 2 diabetes. Integrating precision timing of exercise, nutrition and medication into treatment plans requires considering the entire diurnal environment, including lifestyle and occupational factors, to develop comprehensive, evidence-based healthcare strategies.

Common carotid intima-media thickness (ccIMT) progression is a risk marker for cardiovascular disease (CVD), whereas healthy lifestyle habits are associated with lower ccIMT. The objective of the present study was to test whether a healthy lifestyle intervention can beneficially affect ccIMT progression. A community-based non-randomised, controlled lifestyle intervention was conducted, focusing on a predominantly plant-based diet (strongest emphasis), physical activity, stress management and social health. Assessments of ccIMT were made at baseline, 6 months and 1 year. Participants had an average age of 57 years and were recruited from the general population in rural northwest Germany (intervention: n 114; control: n 87). From baseline to 1 year, mean ccIMT significantly increased in both the intervention (0⋅026 [95 % CI 0⋅012, 0⋅039] mm) and control group (0⋅045 [95 % CI 0⋅033, 0⋅056] mm). The 1-year trajectory of mean ccIMT was lower in the intervention group (P = 0⋅022; adjusted for baseline). In a subgroup analysis with participants with high baseline mean ccIMT (≥0⋅800 mm), mean ccIMT non-significantly decreased in the intervention group (−0⋅016 [95 % CI −0⋅050, 0⋅017] mm; n 18) and significantly increased in the control group (0⋅065 [95 % CI 0⋅033, 0⋅096] mm; n 12). In the subgroup, the 1-year trajectory of mean ccIMT was significantly lower in the intervention group (between-group difference: −0⋅051 [95 % CI −0⋅075, −0⋅027] mm; P < 0⋅001; adjusted for baseline). The results indicate that healthy lifestyle changes may beneficially affect ccIMT within 1 year, particularly if baseline ccIMT is high.

This was a longitudinal study utilising the Irish Longitudinal Study on Ageing (n 3849 aged ≥ 50 years) and investigated the relationship between blood plasma folate and B12 levels at baseline (wave 1) and incident depressive symptoms at 2 and 4 years (waves 2 and 3). A score ≥ 9 on the Center for Epidemiological Studies Depression Scale-8 at wave 2 or 3 was indicative of incident depressive symptoms. B12 status profiles (pmol/l) were defined as < 185, deficient low; 185 to < 258, low normal; > 258–601, normal and > 601 high. Folate status profiles (nmol/l) were defined as ≤ 10·0, deficient low; > 10–23·0, low normal; > 23·0–45·0, normal; >45·0, high. Logistic regression models were used to analyse the longitudinal associations. Both B12 and folate plasma concentrations were lower in the group with incident depressive symptoms v. non-depressed (folate: 21·4 v. 25·1 nmol/l; P = 0·0003; B12:315·7 v. 335·9 pmol/l; P = 0·0148). Regression models demonstrated that participants with deficient-low B12 status at baseline had a significantly higher likelihood of incident depression 4 years later (OR 1·51, 95 % CI 1·01, 2·27, P = 0·043). This finding remained robust after controlling for relevant covariates. No associations of folate status with incident depression were observed. Older adults with deficient-low B12 status had a 51 % increased likelihood of developing depressive symptoms over 4 years. The findings highlight the need to further explore the low-cost benefits of optimising vitamin B12 status for depression in older adults.