Erectile dysfunction and cardiovascular risk factors in a Mediterranean diet cohort.

BACKGROUND: Erectile dysfunction affects more than 100 million men worldwide, with a wide variability in prevalence. An overall association of cardiovascular risk factors, lifestyle and diet in the context of ED in a Mediterranean population is lacking. AIM: To assess ED prevalence and associated factors in a Mediterranean cohort of non-diabetic patients with cardiovascular risk factors. METHODS: Observational, cross-sectional study of patients aged over 40 treated at cardiovascular risk units in Catalonia. Anthropometric data, risk factors, lifestyle and diet habits were recorded. ED was assessed using the International Index of Erectile Function. RESULTS: Four hundred and forty patients included, 186 (42.3%) with ED (24.8% mild, 6.8% moderate and 10.7% severe). ED presence and severity were associated with age, obesity, waist circumference, hypertension, antihypertensive treatment and ischaemic disease. Patients with ED were more frequently smokers, sedentary and consumed more alcohol. In multivariate analysis, consumption of nuts (> twice a week) (OR 0.41 (95% CI 0.25 to 0.67) and vegetables (≥ once a day) (OR 0.47 (95% CI 0.28-0,77)), were inversely related to ED. Obesity (as BMI ≥ 30 kg/m(2) ) (OR 2.49 (95% CI 1.48-4.17)), ischaemic disease (OR 2.30 (95% CI 1.22 to 4.33), alcohol consumption (alcohol-units a day) (OR 1.14 (95% CI 1.04 to 1.26), and age (year) (OR = 1.07 (95% CI 1.04-1.10) were directly related to ED. CONCLUSION: Erectile dysfunction is a common disorder in patients treated in lipid units in Catalonia for cardiovascular risk factors. This condition is associated with age, obesity, ischaemic disease and unhealthy lifestyle habits.

Hyperlipoproteinaemia(a) is a common cause of autosomal dominant hypercholesterolaemia.

UNLABELLED: Autosomal dominant hypercholesterolaemia (ADH) are a heterogeneous group of monogenic lipid disorders. The plasma level of lipoprotein(a) (Lp(a)) is a heritable trait associated with increased coronary heart disease (CHD) risk. OBJECTIVE: To evaluate the frequency of elevated Lp(a) as a cause of ADH and the characteristics of subjects with high Lp(a) (hyperLp(a)). MATERIAL AND METHODS: 200 healthy subjects and 933 unrelated Spanish subjects with a clinical diagnosis of ADH who were screened for low-density lipoprotein receptor (LDLR) and apolipoprotein B (APOB) gene mutations. Standard cardiovascular risk factors and blood lipid levels, including Lp(a), were evaluated. HyperLp(a) was defined as Lp(a) levels >or=95th centile of control values. RESULTS: Lp(a) was higher in 263 subjects without LDLR or APOB mutations (nonLDLR/nonAPOB group) than in 670 subjects with mutations (FH group): 40.0 mg/dl (interquartile range (IR) 15.0-89.0) versus 31.0 mg/dl (IR 11.0-73.7) respectively, p = 0.002. HyperLp(a) was present in 23% of ADH subjects (odds ratio (OR) 5.6 (95% CI, 2.9 to 10.7) versus controls) and 29% of nonLDLR/nonAPOB subjects (OR 7.7; 3.9 to 15.4). After adjusting for Lp(a), LDL cholesterol levels were <95th centile in 28 (10.6%) nonLDLR/nonAPOB subjects and in 9 (1.3%) FH subjects. Lp(a) levels were nonsignificantly higher in ADH subjects with early-onset CHD than in those without (43.5 mg/dl, (IR, 12.0-82.0) versus 31.7 mg/dl (11.8-76.5), respectively). CONCLUSIONS: HyperLp(a) is responsible for ADH in approximately 6% of nonLDLR/nonAPOB subjects. HyperLp(a) would not appear to be a risk factor for early-onset CHD in ADH, independently of whether genetic defects have or have not been demonstrated.

Effect of apolipoprotein E polymorphism on renal transplantation.

INTRODUCTION: Dyslipidemia is an important cardiovascular risk factor and is implicated in the pathogenesis of chronic graft failure in renal transplant recipients. Apolipoprotein E (apoE), a hepatic glycoprotein involved in lipid metabolism, has been associated with hypercholesterolemia and premature coronary disease. AIM: This study assessed the impact of apoE polymorphism on the evolution of renal transplant recipients. METHODS: A total of 517 patients (age, 47 +/- 14 years; 62% men), who had undergone renal transplantation at least 12 months before enrollment, were assessed (mean follow-up, 5.4 +/- 2.2 years). ApoE polymorphisms (E2, E3, and E4 alleles) were analyzed using polymerase chain reaction (PCR) using genomic DNA. Donor-recipient clinical variables were assessed using univariate methods and Cox multivariate regression model. RESULTS: Genotype frequency was as follows: E2/E2 <1%, E2/E3 10%, E3/E3 71%, E2/E4 2%, E3/E4 16%, and E4/E4 1%, with no differences between sexes. In the univariate study, E2/E4, E3/E4, and E4/E4 genotypes were related with poorer patient survival (P = .0045). In the multivariate study, the E4 allele was associated with a higher independent risk of graft loss (odds ratio [OR], 3.23; 95% confidence interval [CI], 1.44-7.21; P < .0001) and death of the patient (OR, 16.03; 95% CI, 3.28-75.18; P < .0001), but only in patients older than 60 years of age. In patients with the E4 allele, 45% of deaths were due to cardiovascular causes. CONCLUSIONS: The genetic polymorphism of apoE (E4 allele) has an independent negative impact on patient and graft survival in the long term, particularly in older patients.

Impact of carotid atherosclerosis as assessed by B-mode ultrasonography on the evolution of kidney transplantation.

UNLABELLED: Carotid arteriosclerosis is a marker of cardiovascular risk in the general population. Cardiovascular disease is highly prevalent in kidney transplant recipients. This study analyzed the impact of arteriosclerotic carotid lesions on the evolution of renal transplant recipients. METHODS: This prospective study was performed in 70 patients with renal transplantations (mean age 52 +/- 12 years; 67% men (n = 47). High-resolution B-mode ultrasonography (7.5 MHz) of both carotid arteries was performed at baseline to assess carotid caliber, mean and maximum intima-media thickness (IMT), presence of arteriosclerotic plaques (number and maximum height), and percentage stenosis. We analyzed the impact of carotid arteriosclerosis and various donor-recipient clinical covariables on long-term patient and graft survival. RESULTS: Mean follow-up was 9.7 +/- 2.5 years (2-14). Atheroma plaques were detected in 74% of patients (n = 52). The mean number of plaques was 3.96 +/- 2.88 and maximum plaque height was 2.49 +/- 0.97 mm. IMT was 0.71 +/- 0.21 mm (0.4-1.5) with 27% of patients (n = 19) having an IMT value greater than 0.8 mm. Sonographic signs of occlusion were evident in 13% (n = 9) and the mean occlusion was 33 +/- 11% (range 20%-45%). The presence of plaques was significantly associated with age (P = .002), hypertension and diabetes (P = .016), and hypercholesterolemia (P = .01). There was an association between age and arterial wall thickness (P = .042). Acute rejection was an independent risk factor for graft loss (OR 8.14, P = .003). The multivariate study identified carotid wall thickness as an independent risk factor for patient death (OR 12.7, P = .017). CONCLUSION: Carotid arteriosclerosis is highly prevalent among renal transplant recipients. Carotid lesions were an independent risk factor for long-term patient death. High-resolution ultrasound imaging of the carotid arteries was a useful, noninvasive diagnostic technique for accurate assessment of cardiovascular risk in renal transplant recipients.

¿Presentan los antioxidantes propiedades "protectoras" sobre el tabaquismo? A propósito del estudio HALE / Do antioxidants present protective properties against smoking? With regard to the HALE study

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¿Existe relación entre el colesterol y el deterioro cognitivo? / Does a relationship exist between cholesterol and cognitive deterioration?

La población envejece y, como consecuencia de ello, en las próximas décadas se producirá un incremento espectacular de las enfermedades que se relacionan con la edad. Los procesos neurodegenerativos y la arteriosclerosis serán los fenómenos más prevalentes en esta población. La conservación del árbol vascular y un control adecuado de los factores de riesgo preponderantes pueden disminuir la incidencia de estas enfermedades invalidantes. Diversas investigaciones poblacionales, en animales de laboratorio y en humanos, ofrecen datos esperanzadores sobre el papel que desempeña el colesterol plasmático en el deterioro cognitivo. Los fármacos inhibidores de la HMG-CoA reductasa pueden convertirse, en un futuro no muy lejano, en el tratamiento de elección en pacientes con factores de riesgo vasculares (AU)

Populations age and, as a consequence, in the next few decades there will be a spectacular increase in age-related diseases. Neurodegenerative processes and atherosclerosis will be the most prevalent phenomena in this population. Conservation of the vascular tree and adequate control of the main risk factors could reduce the incidence of these incapacitating diseases. Several population-based studies in laboratory animals and humans provide hopeful data on the role played by plasma cholesterol in cognitive deterioration. In the not too distant future, HMG-CoA reductase inhibitors could become the treatment of choice in patients with vascular risk factors (AU)

Effect of apolipoprotein polymorphisms in renal transplant recipients.

Cardiovascular disease (CVD) is the main cause of mortality among long-term renal transplant recipients (RTR). On the other hand, allograft chronic nephropathy is the primary cause of graft loss among long-term RTR. Hyperlipidemia is a predisposing factor for both conditions. Polymorphisms of the apolipoproteins modulate lipid metabolism. The aim of the study was to evaluate the effect of apo A-I, apo A-IV and apo C-III genotypes on the long-term results of renal transplantation. Clinical assessment (renal allograft and patient survival) and genotyping for apo A-I (+83C/T), apo C-III (Sst I), and apo A-IV (Thr347Ser and Gln360His) polymorphisms were evaluated in 516 kidney transplant patients and correlated with the clinical evolution over 12 months. The distribution of the apo A-I (+83C/T) polymorphisms was: CC 91.9%, CT 7.9%, and TT 0.2%. The apo C-III genotype showed: S1S1 84.4%, S1S2 15.2%, and S2S2 0.4%. The apo A-IV (Pvu II) polymorphism was: GG 82%, GT 18%, and 0% TT. Finally, the frequency of apo A-IV (Hinf I) polymorphism was: AA 69%, AT 27%, and TT 4%. The frequency of polymorphisms was similar between men and women. In conclusion, there was no significant influence of apolipoprotein polymorphisms on renal and patient survival.

Mild hypercholesterolemia is an early risk factor for the development of Alzheimer amyloid pathology.

BACKGROUND: Epidemiologic and experimental data suggest that cholesterol may play a role in the pathogenesis of AD. Modulation of cholesterolemia in transgenic animal models of AD strongly alters amyloid pathology. OBJECTIVE: To determine whether a relationship exists between amyloid deposition and total cholesterolemia (TC) in the human brain. METHODS: The authors reviewed autopsy cases of patients older than 40 years and correlated cholesterolemia and presence or absence of amyloid deposition (amyloid positive vs amyloid negative subjects) and cholesterolemia and amyloid load. Amyloid load in human brains was measured by immunohistochemistry and image analysis. To remove the effect of apoE isoforms on cholesterol levels, cases were genotyped and duplicate analyses were performed on apoE3/3 subjects. RESULTS: Cholesterolemia correlates with presence of amyloid deposition in the youngest subjects (40 to 55 years) with early amyloid deposition (diffuse type of senile plaques) (p = 0.000 for all apoE isoforms; p = 0.009 for apoE3/3 subjects). In this group, increases in cholesterolemia from 181 to 200 almost tripled the odds for developing amyloid, independent of apoE isoform. A logistic regression model showed consistent results (McFadden rho2 = 0.445). The difference in mean TC between subjects with and without amyloid disappeared as the age of the sample increased (>55 years: p = 0.491), possibly reflecting the effect of cardiovascular deaths among other possibilities. TC and amyloid load were not linearly correlated, indicating that there are additional factors involved in amyloid accumulation. CONCLUSIONS: Serum hypercholesterolemia may be an early risk factor for the development of AD amyloid pathology.

Walnut-enriched diet increases the association of LDL from hypercholesterolemic men with human HepG2 cells.

In a randomized, cross-over feeding trial involving 10 men with polygenic hypercholesterolemia, a control, Mediterranean-type cholesterol-lowering diet, and a diet of similar composition in which walnuts replaced approximately 35% of energy from unsaturated fat, were given for 6 weeks each. Compared with the control diet, the walnut diet reduced serum total and LDL cholesterol by 4.2% (P = 0.176), and 6.0% (P = 0.087), respectively. No changes were observed in HDL cholesterol, triglycerides, and apolipoprotein A-I levels or in the relative proportion of protein, triglycerides, phospholipids, and cholesteryl esters in LDL particles. The apolipoprotein B level declined in parallel with LDL cholesterol (6.0% reduction). Whole LDL, particularly the triglyceride fraction, was enriched in polyunsaturated fatty acids from walnuts (linoleic and alpha-linolenic acids). In comparison with LDL obtained during the control diet, LDL obtained during the walnut diet showed a 50% increase in association rates to the LDL receptor in human hepatoma HepG2 cells. LDL uptake by HepG2 cells was correlated with alpha-linolenic acid content of the triglyceride plus cholesteryl ester fractions of LDL particles (r(2) = 0.42, P < 0.05). Changes in the quantity and quality of LDL lipid fatty acids after a walnut-enriched diet facilitate receptor-mediated LDL clearance and may contribute to the cholesterol-lowering effect of walnut consumption.

Substituting walnuts for monounsaturated fat improves the serum lipid profile of hypercholesterolemic men and women. A randomized crossover trial.

BACKGROUND: It has been reported that walnuts reduce serum cholesterol levels in normal young men. OBJECTIVE: To assess the acceptability of walnuts and their effects on serum lipid levels and low-density lipoprotein (LDL) oxidizability in free-living hypercholesterolemic persons. DESIGN: Randomized, crossover feeding trial. SETTING: Lipid clinic at a university hospital. PATIENTS: 55 men and women (mean age, 56 years) with polygenic hypercholesterolemia. INTERVENTION: A cholesterol-lowering Mediterranean diet and a diet of similar energy and fat content in which walnuts replaced approximately 35% of the energy obtained from monounsaturated fat. Patients followed each diet for 6 weeks. MEASUREMENTS: Low-density lipoprotein fatty acids (to assess compliance), serum lipid levels, lipoprotein(a) levels, and LDL resistance to in vitro oxidative stress. RESULTS: 49 persons completed the trial. The walnut diet was well tolerated. Planned and observed diets were closely matched. Compared with the Mediterranean diet, the walnut diet produced mean changes of -4.1% in total cholesterol level, -5.9% in LDL cholesterol level, and -6.2% in lipoprotein(a) level. The mean differences in the changes in serum lipid levels were -0.28 mmol/L (95% CI, -0.43 to -0.12 mmol/L) (-10.8 mg/dL [-16.8 to -4.8 mg/dL]) (P<0.001) for total cholesterol level, -0.29 mmol/L (CI, -0.41 to -0.15 mmol/L) (-11.2 mg/dL [-16.3 to -6.1 mg/dL]) (P<0.001) for LDL cholesterol level, and -0.021 g/L (CI, -0.042 to -0.001 g/L) (P = 0.042) for lipoprotein(a) level. Lipid changes were similar in men and women except for lipoprotein(a) levels, which decreased only in men. Low-density lipoprotein particles were enriched with polyunsaturated fatty acids from walnuts, but their resistance to oxidation was preserved. CONCLUSION: Substituting walnuts for part of the mono-unsaturated fat in a cholesterol-lowering Mediterranean diet further reduced total and LDL cholesterol levels in men and women with hypercholesterolemia.

High-monounsaturated fat, olive oil-rich diet has effects similar to a high-carbohydrate diet on fasting and postprandial state and metabolic profiles of patients with type 2 diabetes.

Whether metabolic control in type 2 diabetes mellitus (DM) is best achieved with the traditional high-carbohydrate (CHO), low-fat diet or a low-CHO, high-fat diet is still controversial. In a randomized crossover study, we compared the effects of a low-fat (30% of daily energy) diet and a high-fat (40% of daily energy), high-monounsaturated-fat diet for 6 weeks each on fasting and postprandial glucose, insulin, and lipoprotein concentrations in 12 patients with well-controlled type 2 DM (fasting blood glucose, 176 +/- 54 mg/dL; hemoglobin A1c, 6.4% +/- 0.7%) and no overt dyslipidemia (serum total cholesterol, 235 +/- 43 mg/dL; triglycerides, 180 +/- 63 mg/dL). Home-prepared foods were used and olive oil was the main edible fat, accounting for 8% and 25% of daily energy requirements in the low-fat and high-fat diets, respectively. For postprandial studies, the same mixed meal containing 36% fat was used in both dietary periods. Body weight and fasting and 6-hour postprandial blood glucose, insulin, and lipoprotein levels were similar after the two diets. The mean incremental area under the curve of serum triglycerides 0 to 6 hours after the challenge meal, adjusted for baseline levels, did not change significantly after the high-fat diet compared with the low-fat diet (1,484 +/- 546 v 1,714 +/- 709 mg x 6 h/dL, respectively, P = .099). Mean postprandial triglyceride levels at 6 hours were increased about 2 times over fasting levels and were still greater than 300 mg/dL after either diet. A diet high in total and monounsaturated fat at the expense of olive oil is a good alternative diet to the traditional low-fat diet for patients with type 2 DM. However, ongoing postprandial hypertriglyceridemia with either diet points to the need for other therapies to decrease triglyceride-rich lipoproteins (TRL) and the inherent atherogenic risk in type 2 diabetics.

Correlation between Apolipoprotein-E polymorphism and Alzheimer's disease pathology.

Alzheimer's disease (AD) and small vessel disease dementia (SVDD) are common causes of dementia. The ApoE genotype has been proposed as a risk factor for AD. The frequency of the three ApoE alleles was correlated with the neuropathological changes of AD (senile plaques, neurofibrillary tangles and amyloid angiopathy) and SVDD (status lacunaris, status cribosus, leucoencephalopathy, micronecrosis and vascular fibrohyalinosis) in order to validate previous ApoE genotyping results in AD and to identify pre-clinical AD. Representative cerebral regions (cortex, gyrus cinguli, putamen, hippocampus, white matter) from 28 AD cases, 7 SVDD and 38 non-neurological controls were studied using classical histological techniques and immunohistochemistry for tau protein and amyloid-beta. The frequency of the ApoE allele 4 was significantly increased not only in AD patients but also in aged controls. However, following a detailed histopathological examination was found 62% of this group to exhibit histological changes associated with AD in limited brain areas (entorhinal region, hippocampus and adjacent temporal cortex or entorhinal region and hippocampus, or only in the entorhinal region), but 87% of these cases were found to be ApoE4 positive. The significant differences found in the distribution of ApoE allele frequencies were more marked when these cases were excluded from the control group and included as AD cases. In contrast, the frequency of the ApoE allele 2 is significantly increased in SVDD patients. Using histological techniques we confirmed the clinical diagnoses of all cases and classified the AD patients according to the severity of cortical pathology related to AD, while re-grouping from the control group those cases which had no clinical history of the disease but exhibited typical AD and SVDD histological lessions which could be considered as "pre-clinical" forms of these diseases.