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We examined the association between plasma antioxidant levels and markers of inflammation, including C-reactive protein (CRP) and fibrinogen (FG) in US adults. National Health and Nutrition Examination Survey participants examined between 2001 and 2002 were included, if data on CRP or FG levels. Serum vitamins A and E, two retinyl esters, and six carotenoids were measured using HPLC with photodiode array detection. Multivariable-adjusted linear regression analyses accounted for the survey design and sample weights. A total of 784 eligible participants were included; 47·5 % (n 372) were men. In multivariable linear regression models, serum α -carotene, trans - β -carotene, cis - β -carotene, β -cryptoxanthin, combined lutein/zeaxanthin, trans -lycopene, retinyl palmitate, α -tocopherol, retinol and 25-hydroxy vitamin D were negatively associated with serum CRP (P <0·001 for all comparisons). Serum α -carotene, trans - β -carotene, cis - β -carotene, combined lutein/zeaxanthin, trans -lycopene, α -tocopherol, retinol and 25-hydroxy vitamin D were negatively associated with serum FG levels (P <0·001 for all comparisons). In the same model, the risk of CVD, defined as CRP levels >3 mg/l, decreased with increasing levels of antioxidants (α -carotene, trans - β -carotene, cis - β -carotene, vitamins A and E). Furthermore, we found a moderate impact of adiposity on the link between antioxidants and CRP. Our results suggest that the lower the antioxidants levels, the higher the inflammatory burden, based on CRP and FG levels. Adiposity moderately affects this association. Furthermore, an inverse relationship between CVD risk and antioxidant levels was observed. This finding suggests that reduced levels of vitamins with antioxidant properties may predispose to increased CVD risk. [ABSTRACT FROM AUTHOR]

Aim: To investigate the association of major dietary patterns with glucose and insulin homeostasis parameters in a large American sample. The association between dietary patterns (DP) derived via principal components analysis (PCA), with glucose/insulin homeostasis parameters was assessed. The likelihood of insulin resistance (IR) across the DPs quarters was also explored. Method: The United States National Health and Nutrition Examination Survey (NHANES) participants during 2005-2012 were included if they underwent measurement of dietary intake as well as glucose and insulin homeostasis parameters. Analysis of covariance (ANCOVA) and adjusted logistic and linear regression models were employed to account for the complex survey design and sample weights. Results: A total of 24,182 participants were included; 48.9% (n = 11,815) were men. Applying PCA revealed three DP (56. 8% of variance): the first was comprised mainly of saturated fat (SFA), total fat, mono-unsaturated fatty acids (MUFA) and carbohydrate (CHO); the second is highly enriched with vitamins, trace elements and dietary fiber; and the third was composed of polyunsaturated fatty acids (PUFA), cholesterol and protein. Among the total population, after adjustment for age, sex, race, C-reactive protein, smoking, and physical activity, glucose homeostasis factors, visceral adiposity index and lipid accumulation product improved across the quarters of the first and third DP; and a reverse pattern with the second DP. The same trend was observed for the non-diabetic subjects. Moreover, subjects with higher adherence to the first and third DP had higher likelihood for developing IR, whereas there was a lower likelihood for the second DP. Conclusion: This study shows that the DP heavily loaded with CHO, SFA, PUFA, protein, total fat and MUFA as well as high-cholesterol-load foods is associated with impaired glucose tolerance; in contrast, the healthy pattern which is high in vitamins, minerals and fiber may have favourable effects on insulin sensitivity and glucose tolerance. [ABSTRACT FROM AUTHOR]

Background and Aims: We evaluated the association of egg consumption with liver tests (LTs) and non-alcoholic fatty liver disease (NAFLD). This relationship is poorly documented., Methods: The National Health and Nutrition Examination Survey (NHANES, 2005-2010) database was used. Analysis of covariance, adjusted linear and logistic regression models were used., Results: Of the 14,369 participants, 46.8% were men and 45.2% had NAFLD. After correction for several variables including: age, gender, race, education, poverty to income ratio, alcohol intake, energy intake, smoking, and physical activity - fatty liver index (FLI), serum aspartate aminotransferase (AST) alanine aminotransferase (ALT) were 36.9, 25.8 (U/L) and 23.9 (U/L), respectively, in the first tertile (T1) reaching 68.7, 34.9 and 36.5, respectively, in the third tertile (T3) (p < 0.001 for all comparisons). In the model with same covariates, there was significant positive linear relationship between FLI (standard β coefficient (β): 0.196), AST (β: 0.099) and ALT (β: 0.112) with egg consumption and participants in the highest tertile (T3) of egg consumption had 11% higher chance of NAFLD compared with T1 (odds ratio: 1.11 and 95% confidence interval: 1.07-1.17). Of note, after more correction for triglycerides, hypertension and diabetes, the significant link between egg consumption and LTs and/or NAFLD attenuated and disappeared., Conclusion: Our findings highlight the adverse role of egg consumption on LTs and likelihood of NAFLD. These associations seem to be attributable to cardio-metabolic risk factors. These findings require confirmation to improve our understanding of the role of egg consumption in the pathogenesis of NAFLD., Competing Interests: Conflict of Interest DPM has given talks and attended conferences sponsored by MSD, AstraZeneca and Libytec. The other authors have no conflict of interest to declare., (Copyright © 2020. Published by Elsevier Ltd.)

Background: The intake of dairy products has been thought to be associated with an increased risk of coronary heart diseases (CHD) and total mortality due to its relatively high content of saturated fat. However, reports on this association particularly among US adults are conflicting and controversial. Therefore, we used data from the 1999-2010 National Health and Nutrition Examination Surveys (NHANES) study to examine whether consumption of total dairy and dairy subgroups was associated with total and cause specific (CHD, cerebrovascular and cancer) mortality. Further we carried out a systematic review and meta-analysis of prospective studies to check for consistency with the NHANES findings., Methods: In the NHANES cohort vital status through December 31, 2011 was ascertained. Cox proportional hazard regression models were used to relate baseline dairy intake with all-cause and cause-specific mortality. For the systematic review PubMed, SCOPUS, Web of Science and Google Scholar databases were searched (up to December 2017). The DerSimonian-Laird method and generic inverse variance methods were used for quantitative data synthesis., Results: In the NHANES data set of 24,474 participants, 3520 deaths occurred during follow-up. In multivariate adjusted Cox models, total mortality risk was lower when comparing the top (Q4) with the lower (Q1) quartiles of total dairy (hazard ratio [HR] 0.98, 95% confidence interval [CI]: 0.95-0.99) and cheese (HR: 0.92, 95% CI: 0.87-0.97) consumption. Using a similar model, we have found a negative association between total dairy and milk consumption with risk of cerebrovascular mortality (HR: 0.96, 95% CI: 0.94-0.98, HR: 0.93, 95% CI: 0.91-0.96, respectively), while milk consumption was associated with increased CHD mortality (HR: 1.04, 95% CI: 1.02-1.06). The meta-analysis with 636,726 participants indicated a significant inverse association between fermented dairy products and total mortality (RR: 0.97, 95% CI: 0.96-0.99), while milk consumption was associated with higher CHD mortality (RR: 1.04, 95% CI: 1.01-1.05). These findings were robust in sensitivity analyses., Conclusions: Among American adults, higher total dairy consumption was associated with lower total and cerebrovascular mortality, while higher milk consumption was associated with higher risk of CHD. These findings do not support dogmatic public health advice to reduce total dairy fat consumption, although the association between milk consumption and CHD mortality requires further study., (Copyright © 2018 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

Serum uric acid (SUA) and apolipoprotein B (apoB) are markers of the risk of morbidity and mortality. However, no study has investigated their role, simultaneously with nutritional factors, on the risk of mortality. We calculated the dietary uricaemia score (DUS) and the dietary atherogenic score (DAS) and evaluated their associations with the risk of all-cause and cause-specific mortality. Data from the NHANES 1999-2010 study were used. Vital status through the 31 December 2011 was ascertained. Reduced rank regression models followed by stepwise linear regression analyses were applied on 39 macro/micronutrients to identify a dietary pattern most predictive of SUA (DUS) and apoB (DAS). Overall, 20,256 participants were included (mean age: 47.5 years; 48.7% men). DUS consists of 14 contributors (eight positive, six negative), whereas DAS consists of 23 contributors (six positive, 17 negative). An increasing risk of cause-specific mortality was found across the quartiles (Q) of DUS, i.e., participants with the highest score of DUS (Q4) had a greater risk of all-cause (hazard ratio (HR): 1.17, 95% confidence interval (CI): 1.07-1.30), cardiovascular disease (CVD) (HR: 1.36, 95%CI: 1.21-1.59) and cancer (HR: 1.06, 95%CI: 1.01-1.14) mortality compared with Q1. Similarly, participants at the highest DAS quartile had 25, 40 and 11% greater risk of all-cause, CVD and cancer mortality, respectively, compared with Q1. For the first time, we reported an underlying shared link between two atherosclerosis factors (SUA and apoB) and nutrients, as well as their joint adverse impact on all-cause and cause-specific mortality.

Background: The health outcomes associated with extremely low or high plasma concentrations of high-density lipoprotein cholesterol (HDL-C) are not well documented mainly because of the small numbers of participants with such values included in the clinical trials., Objective: We prospectively investigated the association between extremely low and high HDL-C with: 1) the risk of overall, coronary heart disease (CHD), cerebrovascular and cancer mortality, and, 2) their link with inflammatory factors., Methods: Analysis was based on subjects ≥18 years old from the National Health and Nutrition Examination Surveys (NHANES). We categorized HDL-C levels as follows: [low HDL-C group ≤30 (extremely low), 30-40 (low), and ≥40 (reference)] [high HDL-C group = 40-80 (reference), 80-100 (high) and ≥100 mg/dl (extremely high). Cox proportional hazard regression models and analysis of covariance accounted for survey design, masked variance and sample weights., Results: After adjustment for age, race and sex, we found that the very low HDL-C category (<30 mg/dl) had a greater risk of total mortality (risk ratio [RR]: 3.00, 95%CI: 2.20-4.09). RR for CHD and stroke mortality was 2.00 and 2.53, respectively; there was no link between cancer and level of HDL-C (p = 0.235). The association between total mortality, CHD and stroke with the level of HDL-C attenuated but remained significant even after adjustment for demographics, dietary, cardiovascular risk factors and treatment for dyslipidemia (all p < 0.001). After adjustments, subjects with extremely high HDL-C levels had a higher risk of mortalities (all p < 0.001). Mexican-American ethnicity, subjects in the low level of HDL-C (30-40 mg/dl) category had higher risk of mortalities than those with a very low level (all p < 0.001). Concentration of C-reactive protein, fibrinogen and white blood count significantly decreased as the level of the HDL-C increased; these findings were robust after adjustment for demographics, dietary, cardiovascular risk factors and treatment for dyslipidemia (all p < 0.001); further subjects with extremely high HDL-C levels have a greater levels of inflammatory factors (all p < 0.001)., Conclusions: Both extremely low and high HDL-C levels were associated with greater risk of mortalities (total, CHD and stroke) and higher level of inflammatory factors, while there was no link between level of HDL-C and risk of cancer. Moreover, we found evidence of an HDL-C paradox in Mexican-American ethnicity participants., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Aims: Relatively little is known about the health outcomes associated with very low plasma concentrations of high-density lipoprotein cholesterol (HDL-C) mainly because of the small numbers of individuals with such extreme values included in clinical trials. We, therefore, investigated the association between low and very low HDL-C concentration at baseline and incident all-cause-mortality, death from malignant disease (i.e. cancer), and with fatal or non-fatal incident coronary heart disease (CHD) in individuals from the Reasons for Geographical And Racial Differences in Stroke (REGARDS) study., Methods and Results: Analysis was based on 21 751 participants from the REGARDS study who were free of CHD, other cardiovascular disease, and cancer at baseline and were categorized by baseline HDL-C into <30 mg/dL (very low), 30-<40 mg/dL (low), and ≥40 mg/dL (reference). A series of incremental Cox proportional hazards models were employed to assess the association between the HDL-C categories and outcomes. Statistical analysis was performed using both complete case methods and multiple imputations with chained equations. After adjustment for age, race, and sex, the hazard ratios (HRs) comparing the lowest and highest HDL-C categories were 1.48 [95% confidence interval (CI) 1.28-1.73] for all-cause mortality, 1.35 (95% CI 1.03-1.77) for cancer-specific mortality and 1.39 (95% CI 0.99-1.96) for incident CHD. These associations became non-significant in models adjusting for demographics, cardiovascular risk factors, and treatment for dyslipidaemia. We found evidence for an HDL paradox, whereby low HDL (30-<40 mg/dL) was associated with reduced risk of incident CHD in black participants in a fully adjusted complete case model (HR 0.63; 95% CI 0.46-0.88) and after multiple imputation analyses (HR 0.76; 95% CI 0.58-0.98). HDL-C (<30 mg/dL) was significantly associated with poorer outcomes in women for all outcomes, especially with respect to cancer mortality (HR 2.31; 95% CI 1.28-4.16) in a fully adjusted complete case model, replicated using multiple imputation (HR 1.81; 95% CI 1.03-3.20)., Conclusion: Low HDL-C was associated with reduced risk of incident CHD in black participants suggesting a potential HDL paradox for incident CHD. Very low HDL-C in women was significantly associated with cancer mortality in a fully adjusted complete case model.

Aims: Familial hypercholesterolaemia (FH) accelerates atherosclerotic cardiovascular disease (ASCVD) and accordingly is the most potent hereditary cause of premature coronary heart disease. The association between telomere length (TL), a biological index of ageing, and FH has not been hitherto investigated. We addressed this question using data from the US National Health and Education National Surveys (NHANES, 1999-2002)., Methods and Results: We included individuals, who had TL measurements (with quantitative polymerase chain reaction method) and a phenotypic diagnosis of FH based on the Dutch Lipid Clinic Network (DLCN) criteria. Sample weights were applied for unequal probabilities of selection, non-response bias, and oversampling by complex sample analysis. The adult prevalence of FH in NHANES was 0.43% [95% confidence interval (95% CI) 0.33-0.57]. The frequencies of probable FH (mean DLCN score: 6.2) and definite FH (mean DLCN score: 8.9) were 0.42% (95% CI 0.32-0.48) and 0.03% (95% CI 0.02-0.06), respectively. Subjects with FH had a higher prevalence of non-communicable diseases (hypertension, diabetes 2 type, and obesity) and early atherosclerosis (2.9% in overall population vs. 42.2% in FH). Overall, the mean TL in the non-FH population was 1.09 (95% CI 1.06-1.12) (T/S ratio) and 1.09 (95% CI 1.03-1.12) [(T/S ratio) for total FH]. Telomere length adjusted for age, sex, race, and body mass index was shorter in FH compared with healthy subjects (FH 0.89, 95% CI 0.84-0.93 vs. healthy: 1.05, 95% CI 0.97-1.11 T/S ratio; P < 0.001). Subjects with longer TL (highest quartile) had 12% less chance of having FH compared with those with TL in the lowest quartile (Q1, 95% CI 0.78-0.93)., Conclusions: These preliminary data suggest an association between TL, an index of biological age, and the presence of FH, the most common inherited cause of premature ASCVD. Given our relatively low sample size, the findings need confirmation in larger studies.

Background and Aims: We investigated the association between Dietary Inflammatory Index (DII ® ) scores and cardio-metabolic risk factors singly and in combination as metabolic syndrome (MetS)., Methods: We used data from participants selected from the US National Health and Nutrition Examination Survey (NHANES). Analyses were restricted to participants with data available on dietary intake, biochemical data, and anthropometric measurements from 2005 to 2012. Statistical analyses used the SPSS ® Complex Samples v22.0 (IBM Corp, Armonk, NY) and accounted for the survey design and sample weights. Energy-adjusted-DII (E-DII ® ) expressed per 1000 kcal was calculated from 24-h dietary recalls. Of the 17,689 participants with evaluable data, 8607 (48.3%) were men. The mean age was 45.8 years in the overall sample, with men being slightly younger than women (44.9 vs. 46.5 years, p = 0.05)., Results: In multivariable-adjusted regression models, the odds of MetS, its components, as well as obesity, and elevated high-sensitivity C-reactive protein (hsCRP) increased across increasing quartiles of E-DII (p < 0.001). In age, sex, race, income-to-poverty ratio-adjusted models, these and other cardiovascular disease risk factors (triglycerides/high density lipoprotein cholesterol (HDL-C) ratio, apolipoprotein (B) and HbA1C) increased across quartiles of the E-DII (all p < 0.001), while HDL-C levels decreased (p < 0.001)., Conclusions: This study suggests associations between MetS, its components, subclinical inflammation, and the DII. These results reinforce the view that diet plays an important role in the occurrence of cardiovascular diseases., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Objective: To explore the association between dietary acid load, potential renal acid load (PRAL) and net endogenous acid production (NEAP), and peripheral arterial disease (PAD) in a national representative sample of American adults., Methods: The National Health and Nutrition Examination Survey (NHANES) database (for 1999-2002) was used. PAD was diagnosed by ankle brachial index assessment. Analysis of covariance was used to examine adjusted mean of different dietary acid load by PAD status; multivariable logistic regression was used to relate dietary acid load with prevalent PAD. Sample weighting was accounted for in all analyses., Results: Of the 4864 eligible participants aged 40-85, 2482 (51.0%) were men, and 269 (5.5%) had PAD. After adjustment for age-, sex-, race-, estimated glomerular filtration rate (eGFR), smoking, dietary fat, carbohydrates, protein, saturated fat, and dietary fiber, and energy intake, body mass index, hypertension, cholesterol, triglyceride and diabetes, estimated glomerular filtration rate, participants with PAD had higher mean of (PRAL: 16.2 vs 9.1mEq/d, NEAP: 56.2 vs 50.1mEq/d, both p<0.001) than PAD-free participants. In logistic regression with same cofounders, the top quarter of PRAL (more acidic) was associated with 31% higher odds of the PAD compared with the bottom quarter (more alkaline) [odds ratio: 1.31, 95% confidence interval: 1.11-1.57]., Conclusion: Our findings, for the first time, suggest that dietary acids load, an index of acid-base balance, is associated with the likelihood of PAD after adjustment for main clinical and anthropometrical confounding factors. These results support the hypothesis that diet plays an important role in chronic disease occurrence., (Copyright © 2018. Published by Elsevier Inc.)

Background and Aims: Conflicting results suggest a link between serum uric acid (SUA), inflammation and glucose/insulin homeostasis; however, the role of adiposity in this relationship is not clear. Therefore, we evaluated the role of different adiposity factors, including central body mass index (BMI), peripheral waist circumference (WC), and visceral adiposity [visceral adipose tissue (apVAT)], on the association between SUA, inflammation and glucose/insulin homeostasis among US adults., Methods: Data were extracted from the 2005-2010 US National Health and Nutrition Examination Surveys. Overall, 16,502 participants were included in the analysis (mean age = 47.1 years, 48.2% men). Analysis of co-variance and "conceptus causal mediation" models were applied, while accounting for survey design., Results: Corrected models showed that subjects with higher SUA levels have a less favorable profile of inflammation and glucose/insulin homeostasis parameters (all p < 0.001). We found that all our potential mediators (BMI, WC and apVAT) had an impact (to various extents) on the link between variables, including serum C-reactive protein (CRP), apolipoprotein-B (apoB), insulin resistance markers, 2-h blood glucose (2hG) and triglyceride, and fasting blood glucose (FBG) (TyG) index (all p < .001), while none of the potential mediators (BMI, apVAT, WC) had an impact on the link between FBG and glycated hemoglobin with SUA (all p > 0.05). We have found that all of our mediators partially mediated the link between inflammation and glucose/insulin homeostasis parameters and SUA. Of note, apVAT fully mediated the association between SUA and 2hG., Conclusions: By applying advanced statistical techniques, we shed light on the complex link of SUA with inflammation and glucose/insulin homeostasis and quantify the role of adiposity factors in that link., (Copyright © 2017. Published by Elsevier B.V.)

Background and Aim: Growing evidence suggests that some of the effects of diet on cardiovascular disease (CVD) occur through mechanisms involving subclinical inflammation. We assessed the relationship between selected dietary constituents and serum high-sensitivity C-reactive protein (hsCRP) concentration in a population-based sample of United States adults., Methods: In this cross-sectional analysis, participants were selected from the US National Health and Nutrition Examination Survey (NHANES) and restricted to those with available data on dietary intake, biochemical and anthropometric measurements from 2001 to 2010. All statistical analyses accounted for the survey design and sample weights by using SPSS Complex Samples v22.0 (IBM Corp, Armonk, NY)., Results: Of the 17,689 participants analysed, 8607 (48.3%) were men. The mean age was 45.8 years in the overall sample, 44.9 in men and 46.5 in women (p = .047). The age-, race-, sex-, energy intake- and body mass index-adjusted mean dietary intakes of total dietary fibre, polyunsaturated fatty-acids, vitamin E, vitamin A, vitamin B6, total folate, vitamin B family, vitamin C, vitamin K, magnesium, iron, copper and potassium monotonically decreased across increasing hsCRP quarters (p < .001 for all), whereas sugar intake increased (p < .001). In analysis of covariance adjusted for potential confounders (age-, race-, sex-, energy intake- and body weight-) hsCRP levels increased across increasing quarters of sugar intake (p < .001)., Conclusions: This study provides further evidence of an association between dietary sugar, polyunsaturated fatty-acids, fibre and antioxidant intake and hsCRP levels, a subclinical inflammation marker. hsCRP concentrations are likely modulated by dietary intake. KEY MESSAGES Serum high-sensitivity C-reactive protein (hsCRP) concentration is positively associated with sugar intake, and negatively with the consumption of minerals, vitamins and polyunsaturated fatty-acids (fruit and vegetables). hsCRP concentrations, and accordingly subclinical inflammation, are likely influenced by dietary intake.

Background: To investigate the association between dietary patterns (DP), plasma vitamins and trans fatty acids (TFAs) with the likelihood of peripheral artery disease (PAD)., Methods: National Health and Nutrition Examination Survey (NHANES) data for the years 1999-2002 were used. PAD was diagnosed by ankle brachial index assessment. Plasma concentrations of vitamins were measured using high performance liquid chromatography. Vitamin D levels were measured by radioimmunoassay. Analysis of covariance, principal components analysis (PCA) and adjusted logistic regression were applied, accounting for the survey design and sample weights., Results: Of the 4864 eligible participants, 2482 (51.0%) were men and 269 (5.5%) had prevalent PAD. PCA uncovered three DPs which accounted for 56.8% of the variance in dietary nutrients consumption including DP1 (fatty acids and cholesterol), DP2 (minerals, vitamins and fiber), and DP3 (polyunsaturated fatty acids [PUFA]). PAD patients had a significantly higher serum concentrations of trans 9-octadecenoic acid and trans 9, trans 12-octadienoic acid as well as lower plasma levels of vitamin D, retinol, retinyl stearate and retinyl palmitate (p < 0.001 for all comparisons). In models adjusted for age, race, diabetes, cholesterol, hypertension, smoking and energy intake, individuals in the highest quartile of the DP1 had higher odds for PAD compared with those in the lowest quartile [(odds ratio (OR): 6.43, 95% confidence interval (CI): 2.00-20.63 p < 0.001], while those in the highest quartile of DP2 and DP3 had lower odds of PAD relative to those in the lowest quartile (OR:0.28, OR:0.44, respectively; p < 0.001 for both comparisons)., Conclusion: We found that quality of diet, plasma vitamins and TFAs are associated with the likelihood of PAD. If confirmed in prospective studies, the possibility that dietary factors, plasma vitamins and TFAs might be valuable for preventing or delaying the clinical progression of PAD, should be investigated in intervention trials.

The prevalence of abdominal aortic aneurysms (AAAs) and AAA-related deaths are steadily declining in some countries as a result of the reduction in smoking rates. It was thus suggested that screening programs that do not target high-risk populations are likely to have very low AAA detection rates. However, this may not apply to other countries that do not exhibit similar reductions in smoking rates. It was assumed that by using the U.S. Preventive Services Task Force screening criteria (men 65-75 years with smoking history) less than 30% of AAAs would be captured. A more extensive scoring system that includes additional risk factors such as the presence of carotid artery or peripheral arterial disease, obesity, hypertension, and so on, may identify almost 90% of AAAs. This article discusses this and other issues on screening, prevention, and treatment of AAAs.

Purpose of Review: To discuss the relevance of triglycerides to cardiovascular disease (CVD) risk., Recent Findings: Triglycerides are a commonly measured component of lipid profiles. Raised triglycerides are a component of the metabolic syndrome and are strongly associated with future risk of diabetes as well as cardiovascular disease. Triglyceride-rich particles form a component of cardiovascular risk above that delineated by low density lipoprotein (LDL) cholesterol. Elevated triglycerides are a marker of atherogenic small dense LDL, excess baseline and residual CVD risk even after statin therapy. Additional methods to lower triglycerides include niacin, fibrates and omega-3 fatty acids. Trials in monotherapy with both niacin and fibrates suggest some benefit in reducing CVD events based on evidence mostly derived from older studies. However, endpoint trials of adding either niacin or fenofibrate to statins have not shown any benefit, except possibly in patients with an increased atherogenic index (triglyceride : HDL-C ratio), or have been underpowered. Trials of omega-3 fatty acids have been performed at doses insufficient to affect lipid profiles in populations with inadequate control of LDL-C but did reduce CVD events., Summary: Further trials of lipid-lowering agents beyond statins will be required in patients with LDL-C adequately controlled on statin therapy.

Many theories aim at explaining the mechanisms of aging and death in humans. Decreased levels of androgens, growth hormone, and insulin-like growth factor accompany natural aging in men. Androgens influence the growth and maturation of men in various stages of their life. The action of androgens is performed by binding or not binding to androgen receptors. However, various actions of androgens were clarified after the discovery and genotyping of the androgen receptor. The influence of androgens on the lipid profile was reported by several researchers. This negative influence of androgens in men and the positive influence of estrogens in women are responsible for the higher impact of atherogenesis in men compared with women. In aging men, this negative influence of androgens on the lipid profile is more pronounced. This review considers the influence of age on lipid metabolism in men., (© The Author(s) 2011)

The metabolic syndrome (MetS) is a cluster of metabolic abnormalities including abdominal obesity, glucose intolerance, hypertension and dyslipidaemia and is associated with an increased risk of vascular events. Since the initial description of the MetS, several expert groups produced different definitions. This variability led to confusion and absence of comparability between studies. Although there is agreement that the MetS is a major public health challenge worldwide and consistent evidence stresses the need for intervention, the definition of the syndrome remains a matter of debate. This review considers the different definitions of the MetS. These include those proposed by the World Health Organisation, the European Group for the Study of Insulin Resistance, the National Cholesterol Education Program Adult Treatment Panel III, the American College of Endocrinology and American Association of Clinical Endocrinologists and the latest International Diabetes Federation definition which includes ethnic-specific waist circumference cut-off points. These definitions share several features but also include important differences; all have limitations. Selected (after a Medline search) studies comparing the different definitions are also considered. There is a need for a standardised definition of the MetS. Furthermore, a definition tailored for children and adolescents is essential. Prospective long-term studies are needed to validate the prognostic power of these definitions. As new information becomes available the definition of the MetS might be further modified.