Background: Previously we reported severe vitamin D deficiency in a large-scale cohort in Tangshan area in northern China. However, whether vitamin D deficiency is associated with cardiovascular risk factors has not been systematic examined in the cohort. Objective: We aimed to determine the correlation between serum vitamin D status and lipid levels in circulation via an observational study. Methods: Serum 25-hydroxyvitamin D [25(OH)D] was measured. Based on the measurement the subjects were classified into quintiles. Dyslipidemia was defined as having one of the following: elevated serum total cholesterol, LDL cholesterol, triglycerides, or decreased HDL cholesterol, under lipid-control treatment. Results: The study was conducted in a total of 3788 adults in northern China during their routine health examinations. When the highest quintile of the 25(OH)D level was set as reference, the risk of having dyslipidemia increased progressively across the highest to the lowest 25(OH)D with the ORs of 1 (reference), 1.232 (95% CI, 1.005-1.509), 1.235 (95% CI, 1.007-1.513), 1.403 (95% CI, 1.143-1.735) and 1.494 (95% CI, 1.217-1.833), respectively (Ptrend< 0.0001) after adjustment for age. This trend was unchanged after further adjustment for several potential confounders. In linear regression analysis, we found an inverse significant correlation between 25(OH)D and triglycerides (β coefficient=-0.077, p < 0.05), and LDL cholesterol (β coefficient=-0.245, p < 0.05), and positive correlation with HDL cholesterol (β coefficient =0.038, p = 0.018). Conclusion: Vitamin D deficiency is found to be associated with dyslipidemia in a cohort of 3788 subjects. Specifically, serum 25(OH)D is inversely correlated with LDL cholesterol and triglycerides levels, and positively correlated with HDL cholesterol level.

Two large-scale, randomized, double-blind, placebo-controlled trials—REDUCE-IT and STRENGTH—have garnered significant attention in cardiovascular medicine. Both trials aimed to evaluate the effects of prolonged administration of nutritional lipids, specifically omega-3 fatty acids, on major adverse cardiovascular events (MACEs) in high-risk patients undergoing statin therapy. REDUCE-IT used eicosapentaenoic acid (EPA) ethyl ester with mineral oil as a control, while STRENGTH utilized a carboxylic acid formulation of both EPA and docosahexaenoic acid (DHA) with corn oil as a control. Notably, REDUCE-IT demonstrated a reduction in MACE risk with EPA, whereas STRENGTH showed no such benefit with the combination of EPA and DHA. Despite extensive and insightful discussions following the publication of these trials, the underlying reasons for this discrepancy remain elusive. We posit that further investigation into resting heart rate (RHR), heart rate variability (HRV), and ethnic subgroup data—collected but not fully explored—is critical to unraveling the divergent outcomes of the REDUCE-IT and STRENGTH trials. These additional analyses could provide pivotal insights into the mechanisms driving the differential effects of omega-3 fatty acids in high-risk cardiovascular patients. Given that previous discussions have not fully addressed these potential variables, exploring them may illuminate unexplored pathways and offer a deeper understanding of the mechanistic and clinical roles of omega-3 s in cardiovascular health. We hypothesize that by delving into these under-analyzed factors, we can not only clarify the discrepancies between the trials but also advance our broader understanding of cardiovascular nutrition and medicine.

Caloric restriction (CR) or energy restriction, when carefully designed, monitored, and implemented in self-motivated and compliant individuals, proves to be a viable non-pharmacologic strategy for human weight control and obesity management. Beyond its role in weight management, CR has the potential to impede responses involved not only in the pathogenesis of various diseases but also in the aging process in adults, thereby being proposed to promote a healthier and longer life. The core objective of implementing caloric restriction is to establish a balance between energy intake and expenditure, typically involving a reduction in intake and an increase in expenditure—a negative balance at least initially. It may transition toward and maintain a more desired equilibrium over time. However, it is essential to note that CR may lead to a proportional reduction in micronutrient intake unless corresponding supplementation is provided. Historical human case reports on CR have consistently maintained adequate intakes (AI) or recommended dietary allowances (RDA) for essential micronutrients, including vitamins and minerals. Similarly, longevity studies involving non-human primates have upheld micronutrient consumption levels comparable to control groups or baseline measures. Recent randomized controlled trials (RCTs) have also endorsed daily supplementation of multivitamins and minerals to meet micronutrient needs. However, aside from these human case reports, limited human trials, and primate experiments, there remains a notable gap in human research specifically addressing precise micronutrient requirements during CR. While adhering to AI or RDA for minerals and vitamins appears sensible in the current practice, it’s important to recognize that these guidelines are formulated for generally healthy populations under standard circumstances. The adequacy of these guidelines in the setting of prolonged and profound negative energy balance remains unclear. From perspectives of evidence-based medicine and precision nutrition, this field necessitates comprehensive exploration to uncover the intricacies of absorption, utilization, and metabolism and the requirement of each hydrophilic and lipophilic vitamin and mineral during these special periods. Such investigations are crucial to determine whether existing daily dietary recommendations for micronutrients are quantitatively inadequate, excessive, or appropriate when energy balance remains negative over extended durations.

Background: Experimental evidence indicates that oral L-citrulline (L-Cit) may reduce resting blood pressure (BP) as well as BP responses to exercise and cold exposure (non-resting). However, results from human intervention trials are inconsistent. This study aims to summarize the clinical evidence regarding the effects of L-Cit supplementation on brachial systolic blood pressure (SBP), brachial diastolic blood pressure (DBP), in addition to aortic SBP and aortic DBP at rest and non-resting conditions. Methods: Multiple databases including PubMed, Embase, Cochrane library, Web of Science, and Clinical Trials were searched systematically. Randomized controlled trials of human participants were quantitatively meta-analyzed. Results: Fourteen trials contained in eight studies were available for quantitative syntheses for brachial BP. Results showed that L-Cit supplementation significantly reduced both brachial SBP (− 4.490 mmHg, 95% CI: − 7.332 to − 1.648, P = 0.002) and brachial DBP (− 3.629 mmHg, 95% CI: − 5.825 to − 1.434, P = 0.001). Nine of the trials were meta-analyzed for aortic BP which showed that L-Cit intervention significantly reduced aortic SBP (− 6.763 mmHg, 95% CI: − 10.991 to − 2.534, P = 0.002), but not aortic DBP (− 3.396 mmHg, 95% CI: − 7.418 to 0.627, P = 0.098). The observed reducing effects of L-Cit appeared stronger for non-resting than for resting brachial SBP (P for difference = 0.044). Conclusion: L-Cit supplementation significantly decreased non-resting brachial and aortic SBP. Brachial DBP was significantly lowered by L-Cit regardless of resting status. Given the relatively small number of available trials in the stratified analyses and the potential limitations of these trials, the present findings should be interpreted cautiously and need to be confirmed in future well-designed trials with a larger sample size.

Context: Taurine, a sulfur-containing amino acid vital for cardiovascular health, is suggested as a promising intervention for reducing cardiometabolic disease risk. Objective: In this meta-analysis of randomized controlled trials (RCTs) we sought to evaluate the effects of taurine on cardiometabolic risk factors. Data sources: We systematically searched PubMed/MEDLINE, Web of Science, EMBASE, Cochrane Library, and Google Scholar for articles reporting RCTs that investigated the effects of taurine on cardiometabolic risk factors. Data extraction: Data extraction was performed in accordance with the Cochrane and PRISMA guidelines. A random-effects model or a common-effect model was used to calculate mean differences (MDs) or standardized mean differences (SMDs). Data analyses: Thirty-four eligible RCTs were analyzed. Taurine supplementation resulted in significant reductions in fasting blood glucose (MD, −5.90 mg/dL; 95% CI, −9.65 to −2.15), glycated hemoglobin A1c (MD, −0.21%; 95% CI, −0.37 to −0.05), fasting insulin (SMD, −0.55; 95% CI, −0.78 to −0.32), homeostatic model assessment for insulin resistance index (MD, −0.57; 95% CI, −0.74 to −0.40), triglycerides (MD, −14.42 mg/dL; 95% CI, −23.60 to −5.25), total cholesterol (MD, −12.41 mg/dL; 95% CI, −19.10 to −5.71), low-density lipoprotein cholesterol (MD, −5.08 mg/dL; 95% CI, −8.35 to −1.81), systolic blood pressure (MD, −4.38 mmHg; 95% CI, −7.26 to −1.50), diastolic blood pressure (MD, −2.54 mmHg; 95% CI, −3.97 to −1.11), aspartate aminotransferase (MD, −9.65 U/L; 95% CI, −17.39 to −1.90), alanine aminotransferase (MD, −8.26 U/L; 95% CI, −14.81 to −1.70), C-reactive protein (SMD, −1.26; 95% CI, −2.01 to −0.52), tumor necrosis factor-α (MD, −0.35 pg/mL; 95% CI, −0.56 to −0.14), and malondialdehyde (SMD, −1.16; 95% CI, −1.81 to −0.52). Subgroup and dose–response analyses indicated that a daily taurine dose of 1.5-3.0 g was more effective in improving these cardiometabolic risk factors. Specifically, taurine intervention for ≥8 weeks yielded greater improvements in glucose and lipid metabolism, while durations <8 weeks were optimal for managing blood pressure and inflammation. Conclusion: Taurine supplementation may effectively improve cardiometabolic risk factors in adults, underscoring its potential to reduce the incidence of cardiometabolic diseases. Systematic Review Registration: PROSPERO registration No. CRD42024577852.