Adherence to the 2021 dietary guidelines of the European Society of Cardiology on cardiovascular disease prevention in residents of the Pomeranian Voivodeship with increased cardiovascular risk.

INTRODUCTION: Good eating habits can reduce cardiovascular risk. OBJECTIVES: The aim of this work was to verify the compliance with the new European Society of Cardiology (ESC) dietary guidelines in people with increased risk of cardiovascular disease. PATIENTS AND METHODS: The study included 1244 current or former smokers (636 men and 608 women) at a mean (SD) age of 61.6 (6.4) years who volunteered for the MOLTEST BIS lung cancer prevention program. During the program, 49% of the patients were diagnosed with one of the following: arterial hypertension (AH), diabetes mellitus (DM), or coronary artery disease (CAD). The patients with lung cancer were excluded from the study. The participants completed a Food Frequency Questionnaire (FFQ­6) and their food intake was assessed with a 24­hour dietary recall method. RESULTS: Only 2% of the studied individuals declared consuming more than 2 servings of both fruits and vegetables every day, and only 3% of the respondents confirmed daily nut consumption. Most of them weighed too much, consumed too little fiber, and derived too much energy from total and saturated fats. The mean animal to plant protein ratio was higher than recommended, as was the omega­6 to omega­3 fatty acid ratio. Only 40% of the participants with AH, DM, or CAD had a daily cholesterol intake below 200 mg, and in only 12% of them less than 7% of total energy came from saturated fats. CONCLUSIONS: The smokers with increased cardiovascular risk did not comply with the 2021 ESC dietary recommendations. The most common error was inadequate consumption of vegetables, fruits, and nuts.

Inappropriate dietary habits in tobacco smokers as a potential risk factor for lung cancer: Pomeranian cohort study.

OBJECTIVE: Little is known whether diet quality modulates lung cancer risk in smokers. The aim of the study was to assess the dietary habits of a large group of volunteers participating in the lung cancer screening program. METHODS: The 62-item food frequency questionaire was completed by 5997 participants, 127 of whom (2.1%) were later diagnosed with lung cancer. Two approaches were applied to identify dietary habits. The non-healthy diet index was calculated, and a direct analysis of the frequency of consumption was used. A logistic regression analysis was performed to estimate the association between food product intake and the risk of lung cancer. RESULTS: The study population did not follow the Polish nutritional recommendations. They consumed fruits and vegetables too rarely and far too often ate non-recommended foods, such as processed meat, refined products, sugar, sweets, and salty snacks. Participants diagnosed with lung cancer more often consumed low-quality processed meat, red meat, fats, and refined bread and less often whole-grain products, tropical fruits, milk, fermented unsweetened milk drinks, nuts, honey, and wine. The non-healthy diet index score was significantly higher in those with cancer diagnosis compared with those without lung cancer (11.9 ± 5.2 versus 10.9 ± 5.3; P < 0.001). CONCLUSIONS: The surveyed population of smokers did not follow dietary recommendations; there was a particularly high index of an unhealthy diet in by people diagnosed with lung cancer. Prevention programs should be based on encouraging smoking cessation, lifestyle modification, and methods of early detection of lung cancer. Lifestyle modification should include changing eating habits based on a healthy diet, which may be an additional factor in reducing the risk of developing cancer.

Plant-based diets contribute to lower circulating leptin in healthy subjects independently of BMI.

Much research has shown how important role leptin - a hormone secreted by adipose tissue - plays in the regulation of human body weight, mainly due to its appetite-decreasing effects. Under the conditions of energy balance, leptin is an indicator of the amount of triglycerides stored in adipose tissue. In contrast, in a state of hunger or overeating, it acts as an energy balance sensor, and when its level is too high, it fails to reduce food intake, disturbing maintenance of the proper body mass. Recent studies indicate that there is a relationship between a vegetarian diet and the decreased incidence of cardiovascular diseases, certain types of cancer and obesity. It has been noted that people on plant-based diets have lower body weight and percentage of body fat than omnivores. The aim of the study was to analyze the relationship between serum leptin concentrations and the type of diet. The 143 female volunteers on a vegetarian, vegan or omnivore diet were enrolled in the study. All participants had normal body weight (BMI≥18.5<24.9kg/m2). There were statistically significant differences in the serum leptin concentrations of the studied women. Both in the group of vegetarians and vegans circulating leptin was significantly lower (p<0.001) than in the group of omnivores, with the lack of differences in neither BMI nor in body fat content. This suggests that leptin levels are affected not only by the amount of stored fat, but also by the consumed food. This observation indicates the health-promoting properties of plant diets, by influencing circulating leptin.

Dietary Lipids and Dyslipidemia in Chronic Kidney Disease.

The progression of chronic kidney disease (CKD) leads to altered lipid metabolism. CKD patients exhibit high blood triglyceride (TG) levels, reduced concentrations and functionality of high-density lipoproteins (HDL), and elevated levels of atherogenic small, dense, low-density lipoproteins (sdLDL). Disorders of lipid metabolism and other metabolic disturbances place CKD patients at high risk for cardiovascular disease (CVD). Extensive evidence supports the cardioprotective effects of unsaturated fatty acids, including their beneficial effect on serum cholesterol and TG levels. Dietary lipids might therefore be especially important in the nutritional management of CKD. We review current dietary recommendations for fat intake by CKD patients and suggest potential nutritional interventions by emphasizing dietary lipids that might improve the blood lipid profile and reduce cardiovascular risk in CKD.

Multi-omic signatures of atherogenic dyslipidaemia: pre-clinical target identification and validation in humans.

BACKGROUND: Dyslipidaemia is a major risk factor for atherosclerosis and cardiovascular diseases. The molecular mechanisms that translate dyslipidaemia into atherogenesis and reliable markers of its progression are yet to be fully elucidated. To address this issue, we conducted a comprehensive metabolomic and proteomic analysis in an experimental model of dyslipidaemia and in patients with familial hypercholesterolemia (FH). METHODS: Liquid chromatography/mass spectrometry (LC/MS) and immunoassays were used to find out blood alterations at metabolite and protein levels in dyslipidaemic ApoE-/-/LDLR-/- mice and in FH patients to evaluate their human relevance. RESULTS: We identified 15 metabolites (inhibitors and substrates of nitric oxide synthase (NOS), low-molecular-weight antioxidants (glutamine, taurine), homocysteine, methionine, 1-methylnicotinamide, alanine and hydroxyproline) and 9 proteins (C-reactive protein, proprotein convertase subtilisin/kexin type 9, apolipoprotein C-III, soluble intercellular adhesion molecule-1, angiotensinogen, paraoxonase-1, fetuin-B, vitamin K-dependent protein S and biglycan) that differentiated FH patients from healthy controls. Most of these changes were consistently found in dyslipidaemic mice and were further amplified if mice were fed an atherogenic (Western or low-carbohydrate, high-protein) diet. CONCLUSIONS: The alterations highlighted the involvement of an immune-inflammatory response system, oxidative stress, hyper-coagulation and impairment in the vascular function/regenerative capacity in response to dyslipidaemia that may also be directly engaged in development of atherosclerosis. Our study further identified potential biomarkers for an increased risk of atherosclerosis that may aid in clinical diagnosis or in the personalized treatment.

Enhanced cardiac hypoxic injury in atherogenic dyslipidaemia results from alterations in the energy metabolism pattern.

OBJECTIVE: Dyslipidaemia is a major risk factor for myocardial infarction that is known to correlate with atherosclerosis in the coronary arteries. We sought to clarify whether metabolic alterations induced by dyslipidaemia in cardiomyocytes collectively constitute an alternative pathway that escalates myocardial injury. METHODS: Dyslipidaemic apolipoprotein E and low-density lipoprotein receptor (ApoE/LDLR) double knockout (ApoE-/-/LDLR-/-) and wild-type C57BL/6 (WT) mice aged six months old were studied. Cardiac injury under reduced oxygen supply was evaluated by 5 min exposure to 5% oxygen in the breathing air under electrocardiogram (ECG) recording and with the assessment of troponin I release. To address the mechanisms LC/MS was used to analyse the cardiac proteome pattern or in vivo metabolism of stable isotope-labelled substrates and HPLC was applied to measure concentrations of cardiac high-energy phosphates. Furthermore, the effect of blocking fatty acid use with ranolazine on the substrate preference and cardiac hypoxic damage was studied in ApoE-/-/LDLR-/- mice. RESULTS: Hypoxia induced profound changes in ECG ST-segment and troponin I leakage in ApoE-/-/LDLR-/- mice but not in WT mice. The evaluation of the cardiac proteomic pattern revealed that ApoE-/-/LDLR-/- as compared with WT mice were characterised by coordinated increased expression of mitochondrial proteins, including enzymes of fatty acids' and branched-chain amino acids' oxidation, accompanied by decreased expression levels of glycolytic enzymes. These findings correlated with in vivo analysis, revealing a reduction in the entry of glucose and enhanced entry of leucine into the cardiac Krebs cycle, with the cardiac high-energy phosphates pool maintained. These changes were accompanied by the activation of molecular targets controlling mitochondrial metabolism. Ranolazine reversed the oxidative metabolic shift in ApoE-/-/LDLR-/- mice and reduced cardiac damage induced by hypoxia. CONCLUSIONS: We suggest a novel mechanism for myocardial injury in dyslipidaemia that is consequent to an increased reliance on oxidative metabolism in the heart. The alterations in the metabolic pattern that we identified constitute an adaptive mechanism that facilitates maintenance of metabolic equilibrium and cardiac function under normoxia. However, this adaptation could account for myocardial injury even in a mild reduction of oxygen supply.