Linoleic acid intake, plasma cholesterol and 10-year incidence of CHD in 20.000 middle-aged men and women in the Netherlands

We studied the associations of a difference in linoleic acid or carbohydrate intake with plasma cholesterol levels and risk of CHD in a prospective cohort study in the Netherlands. Data on diet (FFQ) and plasma total and HDL-cholesterol were available at baseline (1993–7) of 20 069 men and women, aged 20–65 years, who were initially free of CVD. Incidence of CHD was assessed through linkage with mortality and morbidity registers. During an average of 10 years of follow-up, 280 CHD events occurred. The intake of linoleic acid ranged from 3·6 to 8·0 % of energy (en%), whereas carbohydrate intake ranged from 47·6 to 42·5 en% across quintiles of linoleic acid intake. Linoleic acid intake was inversely associated with total cholesterol and HDL-cholesterol in women but not in men. Linoleic acid intake was not associated with the ratio of total to HDL-cholesterol. No association was observed between linoleic acid intake and CHD incidence, with hazard ratios varying between 0·83 and 1·00 (all P>0·05) compared to the bottom quintile. We conclude that a 4–5 en% difference in linoleic acid or carbohydrate intake did not translate into either a different ratio of total to HDL-cholesterol or a different CHD incidenc

Sources of dietary protein and risk of hypertension in a general Dutch population

Evidence suggests a small beneficial effect of dietary protein on blood pressure (BP), especially for plant protein. We examined the relationship between several types of dietary protein (total, plant, animal, dairy, meat and grain) and the risk of hypertension in a general population of 3588 Dutch adults, aged 26–65 years, who were free of hypertension at baseline. Measurements were done at baseline and after 5 and 10 years of follow-up. Hazard ratios (HR), with 95 % CI, for incident hypertension were obtained in tertiles of energy-adjusted protein, using time-dependent Cox regression models. Models were adjusted for age, sex, BMI, education, smoking, baseline systolic BP, dietary confounders and protein from other sources (if applicable). Mean BP was 118/76 mmHg at baseline. Protein intake was 85 (sd 22) g/d (approximately 15 % of energy) with 62 % originating from animal sources. The main sources of protein were dairy products (28 %), meat (24 %) and grain (19 %). During the follow-up, 1568 new cases of hypertension were identified (44 % of the participants). Energy-adjusted intake of total protein, plant protein and animal protein was not significantly associated with hypertension risk (all HR approximately 1·00, P>0·60). Protein from grain showed a significant inverse association with incident hypertension, with a HR of 0·85 (95 % CI 0·73, 1·00, Ptrend = 0·04) for the upper tertile ( = 18 g/d) v. the lower tertile ( <14 g/d), whereas dairy protein and meat protein were not associated with incident hypertension. In conclusion, higher intake of grain protein may contribute to the prevention of hypertension, which warrants confirmation in other population-based studies and randomised controlled trials

Coronary heart disease risk : family history and gene-environment interaction

The first part of this thesis describes research into lifestyle, genetic, and biological factors that may underlie the increased risk for coronary heart disease (CHD) in individuals with a family history of this disorder. The second part of this thesis describes whether levels of plasma lipids and lipoproteins - which are among the major CHD risk factors - are influenced by the interaction between common gene polymorphisms and lifestyle-related factors. A large cohort study was used to evaluate the association between family history and CHD mortality. The association of a family history with gene polymorphisms, lifestyle-related and biological CHD risk factors, as well as gene-environment interactions were studied cross-sectionally. For this purpose subsamples from a large population-based project (the Cardiovascular Disease Risk Factor Monitoring Project) and the European Atherosclerosis Research Study (EARS) were used.Family history increased the risk for CHD death in men and women. Only a small part was mediated through known CHD risk factors. The most pronounced characteristics of individuals with a family history were the higher levels of total cholesterol and apolipoprotein (apo) B as compared to subjects without a family history. The contribution of lifestyle-related (i.e. modifiable) factors to higher apo B levels in individuals with a family history was small; most of it seemed to be genetically determined. The apo E polymorphism is probably one of the most important genetic factors involved. Besides the apo E4 isoform, the D9N mutation and the N291S mutation in lipoprotein lipase (LPL) were more frequent among subjects with a parental history of premature myocardial infarction. Other gene polymorphisms (LPL S447X, CETP TaqIB and apo CIII SstI) proved to be non-informative.Like family history, genotypes can not be modified. However, the effect of some polymorphisms clearly depended on lifestyle-related factors. A significant interaction between the apo E2 isoform and body mass index was found in EARS as well as in the population-based sample of Dutch origin. Surprisingly, in EARS the association between BMI and apo B levels was more pronounced in E2-carriers compared to subjects with other phenotypes, while in the Dutch sample the association was weaker in apo E2-carriers. Further, a strong interaction between the LPL D9N mutation and physical activity became apparent. Physically inactive carriers of the mutation (n=5) had considerably higher total cholesterol and apo B levels compared to non-carriers, whereas their HDL-cholesterol concentrations were lower. This was not the case for physically active carriers of this mutation (n=10). Our studies also showed that only among moderate alcohol consumers, subjects with the CETP B2B2 genotype presented with higher mean HDL-cholesterol levels compared to subjects with other genotypes. Furthermore, smokers with the apo CIII S1S2 genotype had higher levels of triglycerides and apo B and somewhat lower levels of HDL-cholesterol, compared to smokers with the S1S1 genotype. This was not observed among non-smokers.It is concluded that the underlying mechanisms for the increased risk in individuals with a family history of CHD remain unclear. The risk of CHD is highest in individuals with a family history and unfavorable levels of other CHD risk factors. Therefore, assessing family history is important for risk prediction and prevention, despite the fact that family history by itself cannot be changed. Since little is known about the most useful definition of a family history more large long-term prospective studies are needed. Furthermore, gene-environment interaction implies that a genetic predisposition to unfavorable lipid levels and consequently CHD risk is not in all cases something of which the consequences cannot be influenced. However, our insights into specific gene-environment interactions is limited. More research is needed before our knowledge about gene-environment interactions can be applied for better focusing preventive measures to subgroups in the population that are susceptible to CHD.</p

Tailoring the Implementation of New Biomarkers Based on Their Added Predictive Value in Subgroups of Individuals

Background\ud The value of new biomarkers or imaging tests, when added to a prediction model, is currently evaluated using reclassification measures, such as the net reclassification improvement (NRI). However, these measures only provide an estimate of improved reclassification at population level. We present a straightforward approach to characterize subgroups of reclassified individuals in order to tailor implementation of a new prediction model to individuals expected to benefit from it.\ud \ud Methods\ud In a large Dutch population cohort (n = 21,992) we classified individuals to low (<5%) and high (≥5%) fatal cardiovascular disease risk by the Framingham risk score (FRS) and reclassified them based on the systematic coronary risk evaluation (SCORE). Subsequently, we characterized the reclassified individuals and, in case of heterogeneity, applied cluster analysis to identify and characterize subgroups. These characterizations were used to select individuals expected to benefit from implementation of SCORE.\ud \ud Results\ud Reclassification after applying SCORE in all individuals resulted in an NRI of 5.00% (95% CI [-0.53%; 11.50%]) within the events, 0.06% (95% CI [-0.08%; 0.22%]) within the nonevents, and a total NRI of 0.051 (95% CI [-0.004; 0.116]). Among the correctly downward reclassified individuals cluster analysis identified three subgroups. Using the characterizations of the typically correctly reclassified individuals, implementing SCORE only in individuals expected to benefit (n = 2,707,12.3%) improved the NRI to 5.32% (95% CI [-0.13%; 12.06%]) within the events, 0.24% (95% CI [0.10%; 0.36%]) within the nonevents, and a total NRI of 0.055 (95% CI [0.001; 0.123]). Overall, the risk levels for individuals reclassified by tailored implementation of SCORE were more accurate.\ud \ud Discussion\ud In our empirical example the presented approach successfully characterized subgroups of reclassified individuals that could be used to improve reclassification and reduce implementation burden. In particular when newly added biomarkers or imaging tests are costly or burdensome such a tailored implementation strategy may save resources and improve (cost-)effectivenes

Polarization sensitive optical frequency domain imaging system for endobronchial imaging

A polarization sensitive endoscopic optical frequency domain imaging (PS-OFDI) system with a motorized distal scanning catheter is demonstrated. It employs a passive polarization delay unit to multiplex two orthogonal probing polarization states in depth, and a polarization diverse detection unit to detect interference signal in two orthogonal polarization channels. Per depth location four electro-magnetic field components are measured that can be represented in a complex 2×2 field matrix. A Jones matrix of the sample is derived and the sample birefringence is extracted by eigenvalue decomposition. The condition of balanced detection and the polarization mode dispersion are quantified. A complex field averaging method based on the alignment of randomly pointing field phasors is developed to reduce speckle noise. The variation of the polarization states incident on the tissue due to the circular scanning and catheter sheath birefringence is investigated. With this system we demonstrated imaging of ex vivo chicken muscle, in vivo pig lung and ex vivo human lung specimens

High speed miniature motorized endoscopic probe for optical frequency domain imaging

We present a miniature motorized endoscopic probe for Optical Coherence Tomography with an outer diameter of 1.65 mm and a rotation speed of 3,000-12,500 rpm. This is the smallest motorized high speed OCT probe to our knowledge. The probe has a motorized distal end which provides a significant advantage over proximally driven probes since it does not require a drive shaft to transfer the rotational torque to the distal end of the probe and functions without a fiber rotary junction. The probe has a focal Full Width at Half Maximum of 9.6 μm and a working distance of 0.47 mm. We analyzed the non uniform rotation distortion and found a location fluctuation of only 1.87° in repeated measurements of the same object. The probe was integrated in a high-speed Optical Frequency Domain Imaging setup at 1310 nm to acquire images from ex vivo pig lung tissue through the working channel of a human bronchoscope. © 2012 Optical Society of America

Is uw bemesting optimaal? Meld u nu aan voor een check met BAT!

De Bemestings Analyse Tool BAT analyseert aan het einde van het groeiseizoen de bemesting van elk afzonderlijk perceel en geeft u pasklare adviezen voor de bemesting van het volgende seizoen. Het gebruikt daarbij gegevens die zijn opgeslagen in een bedrijfsmanagementsysteem en vereist daardoor nauwelijks invoer. BAT is ontwikkeld door een samenwerkingsverband tussen het Praktijkonderzoek, het Nutriënten Management Instituut NMI en Agrovision

N-6 and N-3 Fatty Acid Cholesteryl Esters in Relation to Fatal CHD in a Dutch Adult Population: A Nested Case-Control Study and Meta-Analysis

Background: Dietary polyunsaturated fatty acids (PUFA) are inversely related to coronary heart disease (CHD) in epidemiological studies. We examined the associations of plasma n-6 and n-3 PUFA in cholesteryl esters with fatal CHD in a nested case-control study. Additionally, we performed a dose-response meta-analysis of similar prospective studies on cholesteryl ester PUFA. Methods: We used data from two population-based cohort studies in Dutch adults aged 20-65y. Blood and data collection took place from 1987-1997 and subjects were followed for 8-19y. We identified 279 incident cases of fatal CHD and randomly selected 279 controls, matched on age, gender, and enrollment date. Odds ratios (OR) were calculated per standard deviation (SD) increase of cholesteryl ester PUFA. Results: After adjustment for confounders, the OR (95% CI) for fatal CHD per SD increase in plasma linoleic acid was 0.89 (0.74-1.06). Additional adjustment for plasma total cholesterol and systolic blood pressure attenuated this association (OR:0.95; 95% CI: 0.78-1.15). Arachidonic acid was not associated with fatal CHD (OR per SD:1.11; 95% CI: 0.92-1.35). The ORs (95% CI) for fatal CHD for an SD increase in n-3 PUFA were 0.92 (0.74-1.15) for alpha-linolenic acid and 1.06 (0.88-1.27) for EPA-DHA. In the meta-analysis, a 5% higher linoleic acid level was associated with a 9% lower risk (relative risk: 0.91; 95% CI: 0.84-0.98) of CHD. The other fatty acids were not associated with CHD. Conclusion: In this Dutch population, n-6 and n-3 PUFA in cholesteryl esters were not significantly related to fatal CHD. Our data, together with findings from previous prospective studies, support that linoleic acid in plasma cholesteryl is inversely associated with CHD

Single nucleotide polymorphisms (SNPs) involved in insulin resistance, weight regulation, lipid metabolism and inflammation in relation to metabolic syndrome: an epidemiological study

Background: Mechanisms involved in metabolic syndrome (MetS) development include insulin resistance, weight regulation, inflammation and lipid metabolism. Aim of this study is to investigate the association of single nucleotide polymorphisms (SNPs) involved in these mechanisms with MetS. Methods: In a random sample of the EPIC-NL study (n = 1886), 38 SNPs associated with waist circumference, insulin resistance, triglycerides, HDL cholesterol and inflammation in genome wide association studies (GWAS) were selected from the 50K IBC array and one additional SNP was measured with KASPar chemistry. The five groups of SNPs, each belonging to one of the metabolic endpoints mentioned above, were associated with MetS and MetS-score using Goeman's global test. For groups of SNPs significantly associated with the presence of MetS or MetS-score, further analyses were conducted. Results: The group of waist circumference SNPs was associated with waist circumference (P=0.03) and presence of MetS (P=0.03). Furthermore, the group of SNPs related to insulin resistance was associated with MetS score (