Photoperiod and metabolic health: evidence, mechanism, and implications.

Circadian rhythms are evolutionarily programmed biological rhythms that are primarily entrained by the light cycle. Disruption of circadian rhythms is an important risk factor for several metabolic disorders. Photoperiod is defined as total duration of light exposure in a day. With the extended use of indoor/outdoor light, smartphones, television, computers, and social jetlag people are exposed to excessive artificial light at night increasing their photoperiod. Importantly long photoperiod is not limited to any geographical region, season, age, or socioeconomic group, it is pervasive. Long photoperiod is an established disrupter of the circadian rhythm and can induce a range of chronic health conditions including adiposity, altered hormonal signaling and metabolism, premature ageing, and poor psychological health. This review discusses the impact of exposure to long photoperiod on circadian rhythms, metabolic and mental health, hormonal signaling, and ageing and provides a perspective on possible preventive and therapeutic approaches for this pervasive challenge.

Dyslipidemia among Patients with Ischemic Stroke in the Department of Medicine of a Tertiary Care Centre: A Descriptive Cross-sectional Study.

Introduction: Stroke is a leading cause of morbidity and disability in Asian population. Dyslipidemia is considered a major risk factor for various cardiovascular diseases. The study aimed to find the prevalence of dyslipidemia among patients with ischemic stroke in the Department of Medicine of a tertiary care centre. Methods: This is a descriptive cross-sectional study conducted among 150 diagnosed cases of ischemic stroke admitted in the Department of Medicine from 1st October, 2020 to 1st October, 2021. The ethical clearance was taken from the Institutional Review Committee (Reference number: 358/2077/78). Fasting blood samples were collected from the patients, serum lipids were measured and atherogenic indices of plasma were calculated. Demographic, anthropometric and cardiovascular risk factors related data were collected. Data were entered in Microsoft Excel 2010 and analysis was using the Statistical Package for the Social Sciences version 22.0. Point estimate at 95% Confidence Interval was calculated along with frequency and proportion for binary data, and mean and standard deviation for continuous data. Results: The prevalence of dyslipidemia among the ischemic stroke patients was 120 (80.00%) (73.60-86.40 at 95% Confidence Interval). High total cholesterol was found in 64 (53.33%) patients, high triglycerides in 70 (58.33%), high low-density lipoprotein cholesterol in 54 (45.00%) and low high-density lipoprotein cholesterol in 51 (42.50%) patients. Conclusions: The prevalence of dyslipidemia among ischemic stroke patients was higher than the studies done in similar settings. Keywords: dyslipidemia; ischemic stroke; lipid; prevalence.

Early or delayed time-restricted feeding prevents metabolic impact of obesity in mice.

Time-restricted feeding (TRF) initiated early during the dark phase prevents the metabolic consequences of a high-fat diet in rodent models. However, the metabolic consequences of delaying the initiation of TRF, akin to breakfast skipping in humans, is unclear. We assigned 8-week-old male C57BL/6J mice (n = 192) to chow or high-fat diet ad libitum (AL) for 4 weeks, before randomization to continue AL or 10 h of TRF, initiated at lights off (TRFe) or 4-h after lights off (TRFd) for a further 8 weeks. Oral glucose tolerance tests (1 g/kg), metabolic monitoring and body composition by echoMRI were performed, and tissues were collected at six time points. TRF reduced weight and fat mass vs AL, with a greater reduction in TRFe vs TRFd. TRF improved glucose tolerance and protected mice from high-fat diet-induced hepatosteatosis vs AL, with no difference between TRFe and TRFd. TRF increased the amplitude of Bmal1, Cry1, Per2, Nampt, and Nocturnin mRNA levels in liver. A phase delay in Bmal1, Cry1, Per2, Reverbα, Nampt, NAD, Sirt1, and Nocturnin was observed in TRFd. Thus, delaying TRF limited the weight benefit and induced a phase delay in the hepatic clock, but improved metabolic health. Allowing more flexibility in when TRF is initiated may increase the translational potential of this dietary approach in humans.

Time-Restricted Eating: Benefits, Mechanisms, and Challenges in Translation.

Eating out of phase with daily circadian rhythms induces metabolic desynchrony in peripheral metabolic organs and may increase chronic disease risk. Time-restricted eating (TRE) is a dietary approach that consolidates all calorie intake to 6- to 10-h periods during the active phase of the day, without necessarily altering diet quality and quantity. TRE reduces body weight, improves glucose tolerance, protects from hepatosteatosis, increases metabolic flexibility, reduces atherogenic lipids and blood pressure, and improves gut function and cardiometabolic health in preclinical studies. This review discusses the importance of meal timing on the circadian system, the metabolic health benefits of TRE in preclinical models and humans, the possible mechanisms of action, the challenges we face in implementing TRE in humans, and the possible consequences of delaying initiation of TRE.

Will Delaying Breakfast Mitigate the Metabolic Health Benefits of Time-Restricted Eating?

Eating out of phase with the biological clock induces circadian misalignment in peripheral organs and impairs glucose tolerance in preclinical models. Time-restricted eating (TRE) is a dietary approach that consolidates energy intake to 6 to 10 hours during the biologically active phase of the day, without necessarily altering diet quality and quantity. TRE induces pleiotropic metabolic benefits in mice, flies, and humans. Most studies have initiated TRE early in the biological morning. This perspective discusses the potential challenges in translating early TRE to the community and considers the potential metabolic consequences of delaying TRE.

Time-Restricted Feeding Improves Glucose Tolerance in Men at Risk for Type 2 Diabetes: A Randomized Crossover Trial.

OBJECTIVE: This study aimed to assess the effects of 9-hour time-restricted feeding (TRF), early (TRFe) or delayed (TRFd), on glucose tolerance in men at risk for type 2 diabetes. METHODS: Fifteen men (age 55 ± 3 years, BMI 33.9 ± 0.8 kg/m2 ) wore a continuous glucose monitor for 7 days of baseline assessment and during two 7-day TRF conditions. Participants were randomized to TRFe (8 am to 5 pm) or TRFd (12 pm to 9 pm), separated by a 2-week washout phase. Glucose, insulin, triglycerides, nonesterified fatty acids, and gastrointestinal hormone incremental areas under the curve were calculated following a standard meal on days 0 and 7 at 8 am (TRFe) or 12 pm (TRFd). RESULTS: TRF improved glucose tolerance as assessed by a reduction in glucose incremental area under the curve (P = 0.001) and fasting triglycerides (P = 0.003) on day 7 versus day 0. However, there were no mealtime by TRF interactions in any of the variables examined. There was also no effect of TRF on fasting and postprandial insulin, nonesterified fatty acids, or gastrointestinal hormones. Mean fasting glucose by continuous glucose monitor was lower in TRFe (P = 0.02) but not TRFd (P = 0.17) versus baseline, but there was no difference between TRF conditions. CONCLUSIONS: While only TRFe lowered mean fasting glucose, TRF improved glycemic responses to a test meal in men at risk for type 2 diabetes regardless of the clock time that TRF was initiated.

Product of serum calcium and phosphorus (Ca × PO4) as predictor of cardiovascular disease risk in predialysis patients.

OBJECTIVES: The mortality rate of chronic kidney disease (CKD) patients is very high due to cardiovascular diseases (CVD) which cannot be fully justified by traditional CVD markers. Since, mineral bone disorder is common in CKD, product of serum calcium and phosphorus (Ca × PO4) can be a predictor of future CVD. So, our study aims to assess the utility of higher Ca × PO4 in prediction of CVD risk in predialysis CKD patients. DESIGN AND METHODS: 150 CKD patients defined by NKF-KDOQI guideline not undergoing dialysis were recruited. Anthropometric and electrocardiographic parameters were recorded. We evaluated CVD risk by: i) Biochemical CVD markers, ii) NCEP ATP III guideline postulated risk factors and iii) Framingham risk scores. RESULTS: Higher Ca × PO4 is associated with presence of Left Ventricular Hypertrophy, oxidative stress, microinflammation, hyperhomocysteinemia, hypercholesterolemia, hypertriglyceridemia and increased LDLc. Compared to cases with Ca × PO4 <55 mg2/dL2, cases with ≥55 mg2/dL2 had relative risk (RR) of 1.82 (95% CI 1.25-2.64) for CVD, 3.24 (95% CI 2.37-4.41) for stroke and 2.43 (95% CI 1.37-4.31) for coronary heart disease (CHD). Moreover, compared to lowest quartile of Ca x PO4, the highest quartile group had RR of 2.13 (95% CI 1.06-4.28) for CVD, 2.61(95% CI 1.80-3.75) for stroke and 2.84 (95% CI 1.15-7.0) for CHD. CONCLUSION: In predialysis patients, higher Ca × PO4 is independent predictor of CVD risk.

Non-high density lipoprotein cholesterol versus low density lipoprotein cholesterol as a discriminating factor for myocardial infarction.

BACKGROUND: Serum total cholesterol (TC) and LDL cholesterol (LDL-C) have been used as major laboratory measures in clinical practice to assess cardiovascular risk in the general population and disease management as well as prognosis in patients. However, some studies have also reported the use of non-HDL cholesterol (non-HDL-C). As non-HDL-C can be calculated by subtracting HDL-C from TC, both of which do not require fasting blood sample in contrast to LDL-C which requires fasting blood sample, we aimed to compare non-HDL-C with LDL-C as a predictor of myocardial infarction (MI). METHODS: This hospital based cross sectional study was undertaken among 51 cases of MI and equal number of controls. MI was diagnosed based on the clinical history, ECG changes and biochemical parameters. 5 mL of fasting blood sample was collected from each research participant for the analysis of lipid profile. Non-HDL-C was calculated by using the equation; Non-HDL-C = TC - HDL-C. Statistical analysis was performed using SPSS 14.0. RESULTS: 42 MI cases were dyslipidemic in contrast to 20 dyslipidemic subjects under control group. The differences in the median values of each lipid parameter were statistically significant between MI cases and controls. The lipid risk factors most strongly associated with MI were HDL-C (OR 5.85, 95% CI 2.41-14.23, P value = 0.000) followed by non-HDL-C (OR 3.77, 95% CI 1.64-8.66, P value = 0.002), LDL-C/HDL-C (OR 3.38, 95% CI 1.44-7.89, P value = 0.005), TC/HDL-C (OR 2.93, 95% CI 1.36-7.56, P value = 0.026), LDL-C (OR 2.70, 95% CI 1.20-6.10, P value = 0.017), TC (OR 2.68, 95% CI 1.04-6.97, P value = 0.042) and Tg (OR 2.54, 95% CI 1.01-6.39, P value = 0.047). Area under the receiver operating curve was greater for non-HDL-C than for LDL-C. Non-HDL-C was also found to be more sensitive and specific than LDL-C for MI. CONCLUSIONS: HDL-C and non-HDL-C are better discriminating parameters than LDL-C for MI. Thus, we can simply perform test for HDL-C and non-HDL-C both of which do not require fasting blood sample rather than waiting for fasting blood sample to measure LDL-C.