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PubMed1984

The combined role of atheroma, cholesterol, platelets, the endothelium and fibrin in heart attacks and strokes.

In 1920 the typical American diet was rich in cholesterol and fat, especially saturated animal fat, with one-third the polyunsaturated vegetable fat as now; yet in that year, death from myocardial infarction (MI) in the United States was so rare that it had no name or medical recognition. In 1960, when MI deaths in the United States had soared to an alarming rate of 600,000, orthodox medicine concluded that cholesterol and saturated animal fat in food caused elevated cholesterol in blood, which caused cholesterol in atheroma, which in turn caused death from MI and strokes. It is suggested that human atheroma is made up mostly of fibers of either collagen or fibrin, smooth-muscle cells or dead smooth-muscle cells, that it contains but little cholesterol, and that it is present in both men and women and in populations having little or no MI as well as in those where MI is the greatest cause of death. It is suggested that MI is largely caused by coronary blood clots formed at the site of a break in the coronary artery endothelium; that the introduction of a new, unnatural dietary fatty acid--trans-trans linoleic acid--in margarine and refined vegetable oils in the 1920s, by inducing a deficiency of beneficial prostaglandin E1 (PGE1) while greatly increasing harmful thromboxane A2 (TXA2), caused vasoconstriction while the clumping of platelets was greatly increased, giving rise to the coronary blood clots that either cause or are part of the fatal process of MI. It is suggested that in fostering the increase of dietary trans-trans linoleic acid in polyunsaturated vegetable fats at the expense of saturated animal fat, orthodox medicine is fostering a principle cause of MI as the cure.

Animals↗
PubMed1999

Optimal macronutrient balance.

There is at present a justifiable debate as to the optimum level of total dietary fat which will reduce the risk of obesity without an elevation of plasma triacylglycerol or a depression of plasma HDL-cholesterol. Total plasma cholesterol and LDL-cholesterol levels are lowered and risk of fatal myocardial infarction is lowered when either saturated or trans-unsaturated fatty acids are replaced isoenergetically by either monounsaturated or polyunsaturated fatty acids. The triacylglycerol-raising and HDL-lowering effects of low-fat high-carbohydrate diets can be overcome with low intakes of n-3 polyunsaturated fatty acids and moderate exercise. Whilst a reduction in dietary fat is being attained in many countries, the reduction is uniform across all fatty acids, leaving dietary fat composition unchanged. The ability of low-fat diets to reduce cholesterol and cause a fall in body weight is not influenced by the carbohydrate ratio starch: sugars in the diet. However, weight-gain susceptibility to high intakes of dietary fat and the plasma cholesterol responsiveness to diet are considerably influenced by common genetic polymorphisms.

Cholesterol↗
PubMed2006

Relationship between crystallization behavior, microstructure, and macroscopic properties in trans containing and trans free coating fats and coatings.

The objective of this study is to gain further understanding into the relationship between crystallization behavior, microstructure, and macroscopic properties in coating fats. The isothermal crystallization behavior of two coating fats (one trans containing and one trans free) was examined, both as pure fats and in coatings, by DSC and microscopy. Furthermore, the hardness of the samples was examined after cooling in a water bath at two different temperatures and at three different storage times. Both fats seemed to show an alpha-mediated beta' crystallization at lower temperatures and a direct beta' crystallization at higher temperatures. The trans free coating fat clearly crystallized faster and in smaller crystals. The hardness was governed not only by the amount of solid fat present in the network but also by the structure of this network. The coating matrix components seem to have a pronounced influence on the microstructure and thus on the macroscopic properties.

Calorimetry, Differential Scanning↗
PubMed2000

Phosphatidylglycerol is involved in the dimerization of photosystem II.

Photosystem II core dimers (450 kDa) and monomers (230 kDa) consisting of CP47, CP43, the D1 and D2 proteins, the extrinsic 33-kDa subunit, and the low molecular weight polypeptides PsbE, PsbF, PsbH, PsbI, PsbK, PsbL, PsbTc, and PsbW were isolated by sucrose density gradient centrifugation. The photosystem II core dimers were treated with phospholipase A2 (PL-A2), which cuts phosphatidylglycerol (PG) and phosphatidylcholine molecules at the sn-2 position. The PL-A2-treated dimers dissociated into two core monomers and further, yielding a CP47-D1-D2 subcomplex and CP43. Thin layer chromatography showed that photosystem II dimers contained four times more PG than their monomeric counterparts but with similar levels of phosphatidylcholine. Consistent with this was the finding that, compared with monomers, the dimers contained a higher level of trans-hexadecanoic fatty acid (C16:1Delta3tr), which is specific to PG of the thylakoid membrane. Moreover, treatment of dimers with PL-A2 increased the free level of this fatty acid specific to PG compared with untreated dimers. Further evidence that PG is involved in stabilizing the dimeric state of photosystem II comes from reconstitution experiments. Using size exclusion chromatography, it was shown that PG containing C16:1Delta3tr, but not other lipid classes, induced significant dimerization of isolated photosystem II monomers. Moreover, this dimerization was observed by electron crystallography when monomers were reconstituted into thylakoid lipids containing PG. The unit cell parameters, p2 symmetry axis, and projection map of the reconstituted dimer was similar to that observed for two-dimensional crystals of the native dimer.

Chromatography, High Pressure Liquid↗
PubMed1983

Influence of trans unsaturated fats on experimental atherosclerosis in rabbits.

To test the effects of trans unsaturated fatty acids (t-FA) on atherosclerosis, lipidemia and enzyme activities, rabbits were fed a semipurified, cholesterol-free diet containing 40% sucrose, 25% casein and 14% fat for 5 months. Two experimental diets provided either 6% (high) or 3.2% (low) t-FA. The control group was fed a fat of composition similar to the two experimental diets but free of t-FA. Serum cholesterol and triglycerides were elevated in the rabbits fed 6% t-FA. Liver glycerides were also elevated in this group. The fatty acids of plasma, erythrocytes, epididymal fat, liver microsomes and liver mitochondria reflected the dietary composition. Levels of aortic atherosclerosis were identical in the three groups. There were no significant differences in activity of five hepatic enzymes: glucose-6-phosphatase (microsomal), fatty acid synthetase (cytosolic), malate dehydrogenase, beta-hydroxybutyrate dehydrogenase and monoamine oxidase (mitochondrial).

Adipose Tissue↗
PubMed1997

Response of low density lipoprotein cholesterol levels to dietary change: contributions of different mechanisms.

In many individuals, LDL-cholesterol levels rise following increased consumption of dietary cholesterol or saturated and trans-monounsaturated fatty acids. In others, a reduction of cholesterogenesis fully compensates for these effects. In responding individuals, much of the increase in LDL-cholesterol observed may result directly from an increase in plasma cholesteryl ester transfer protein activity whose effect is not mediated by hepatic LDL receptors.

Carrier Proteins↗
PubMed2004

Inference for the proportional hazards model with misclassified discrete-valued covariates.

We consider the Cox proportional hazards model with discrete-valued covariates subject to misclassification. We present a simple estimator of the regression parameter vector for this model. The estimator is based on a weighted least squares analysis of weighted-averaged transformed Kaplan-Meier curves for the different possible configurations of the observed covariate vector. Optimal weighting of the transformed Kaplan-Meier curves is described. The method is designed for the case in which the misclassification rates are known or are estimated from an external validation study. A hybrid estimator for situations with an internal validation study is also described. When there is no misclassification, the regression coefficient vector is small in magnitude, and the censoring distribution does not depend on the covariates, our estimator has the same asymptotic covariance matrix as the Cox partial likelihood estimator. We present results of a finite-sample simulation study under Weibull survival in the setting of a single binary covariate with known misclassification rates. In this simulation study, our estimator performed as well as or, in a few cases, better than the full Weibull maximum likelihood estimator. We illustrate the method on data from a study of the relationship between trans-unsaturated dietary fat consumption and cardiovascular disease incidence.

Biometry↗
PubMed2005

The role of diet, exercise and smoking in dyslipidaemia in HIV-infected patients with lipodystrophy.

BACKGROUND: Lipodystrophy in HIV-infected (LDHIV) patients receiving protease inhibitors (PIs) is associated with dyslipidaemia. Whether lifestyle factors play a role in dyslipidaemia in LDHIV subjects on PIs is not well characterized. METHODS: A total of 45 LDHIV male and six LDHIV female patients on PIs were recruited, and data were collected on smoking, exercise, diet (by 3-day food record), and fasting levels of serum lipids and lipoproteins. The relationships between lifestyle factors and metabolic variables were analysed in male patients by Spearman's correlation test and the significant relationships were further analysed by adjusting for age, PI duration, and waist circumference by Spearman's partial correlation test. RESULTS: In men, mean (+/-standard deviation) serum concentrations of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), and non-HDL-C were 212+/-70, 35+/-7.3, 325+/-230 and 169+/-44 mg/dL, respectively. Sixty-seven percent of the men exercised regularly and 31.1% smoked. The reported diet was high in cholesterol (390+/-212 mg) and percentage energy from saturated (12.2+/-3.3%) and trans (2.4+/-1.2%) fats, and low in soluble fibre (6.9+/-2.3 g) compared with recent dietary guidelines. Following adjustments for the confounding variables, percentage energy intake from total protein and animal protein was positively related to TC (r=0.44, P<0.01 and r=0.37, P<0.05, respectively), TG (r=0.40, P<0.01 and r=0.46, P<0.01, respectively) and non-HDL-C (r=0.56, P<0.001 and r=0.49, P<0.01, respectively), that from trans fat was positively related to TG (r=0.34, P<0.05), and soluble fibre was negatively related to non-HDL-C (r=-0.41, P<0.01). Moderate to heavy aerobic exercise tended to be associated with higher HDL-C (r=0.30, P=0.07) whereas smoking was not associated with any of the metabolic variables. CONCLUSIONS: Increased intake of total protein, animal protein and trans fat, and reduced soluble fibre consumption contribute to dyslipidaemia in LDHIV subjects on PIs.

Adult↗
PubMed2006

The elimination of trans fats from spreads: how science helped to turn an industry around.

Mensink and Katan showed in 1990 that trans fats reduce high- and increase low-density lipoprotein cholesterol. Unilever aided this study because the company considered knowledge on trans fats incomplete in spite of their long history of safe use. The decision in 1994 to remove trans fats from Unilever's retail spreads was triggered by media events, but it was built on a solid understanding of the nutritional and technological aspects of trans fats. Over the next 14 years, manufacturers worldwide followed suit. This experience illustrates that food companies need to know about the health effects of their products and how to apply that knowledge.

Dietary Fats, Unsaturated↗
PubMed1996

Cell Envelope Changes in Solvent-Tolerant and Solvent-Sensitive Pseudomonas putida Strains following Exposure to o-Xylene.

Solvent-tolerant and -sensitive Pseudomonas putida strains were studied to determine their cell envelope changes following exposure to o-xylene. Both strains produced trans-unsaturated fatty acids. The tolerant strain showed an increase in total fatty acids, an increase in saturated fatty acids, and modified lipopolysaccharide. It is suggested that these envelope modifications aid in survival at high concentrations of organic solvents.

Journal Article↗
PubMed2004

Dietary hydrogenated fat increases high-density lipoprotein apoA-I catabolism and decreases low-density lipoprotein apoB-100 catabolism in hypercholesterolemic women.

OBJECTIVE: To determine mechanisms contributing to decreased high-density lipoprotein cholesterol (HDL-C) and increased low-density lipoprotein cholesterol (LDL-C) concentrations associated with hydrogenated fat intake, kinetic studies of apoA-I, apoB-100, and apoB-48 were conducted using stable isotopes. METHODS AND RESULTS: Eight postmenopausal hypercholesterolemic women were provided in random order with 3 diets for 5-week periods. Two-thirds of the fat was soybean oil (unsaturated fat), stick margarine (hydrogenated fat), or butter (saturated fat). Total and LDL-C levels were highest after the saturated diet (P<0.05; saturated versus unsaturated) whereas HDL-C levels were lowest after the hydrogenated diet (P<0.05; hydrogenated versus saturated). Plasma apoA-I levels and pool size (PS) were lower, whereas apoA-I fractional catabolic rate (FCR) was higher after the hydrogenated relative to the saturated diet (P<0.05). LDL apoB-100 levels and PS were significantly higher, whereas LDL apoB-100 FCR was lower with the saturated and hydrogenated relative to the unsaturated diet. There was no significant difference among diets in apoA-I or B-100 production rates or apoB-48 kinetic parameters. HDL-C concentrations were negatively associated with apoA-I FCR (r=-0.56, P=0.03) and LDL-C concentrations were negatively correlated with LDL apoB-100 FCR (r=-0.48, P=0.05). CONCLUSIONS: The mechanism for the adverse lipoprotein profile observed with hydrogenated fat intake is determined in part by increased apoA-I and decreased LDL apoB-100 catabolism.

Apolipoprotein A-I↗