| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Elevated low-density lipoprotein cholesterol (LDL-C) enhances pro-erectile neurotransmission in the corpus cavernosum Srilatha, B., P. G. Adaikan, et al. (1999), Int J Impot Res 11(3): 159-65. Abstract: Hypercholesterolaemia is thought to foster atherosclerosis and impotence through its effects on vascular endothelium. In this study, we investigated the pharmacological changes in rabbit corpus cavernosum (CC) secondary to incubation with lysolecithin and hypercholesterolaemia. A daily egg yolk dietary supplement induced gross hypercholesterolaemia in our rabbits. Group A of test animals (n-12) was fed with the yolk content of single egg and group B (n-6), that from two eggs for eight weeks. Serum level estimation revealed a progressive elevation of cholesterol to 15 and 30 times respectively, in the two treated groups as compared to values in the control group (n-6). Early histological manifestations of atherosclerosis were perceived as fat cell lesions in the cavernosum of treated animals. In vitro pharmacological studies on CC strips from both groups of test animals demonstrated a profound accentuation of the contractile responses to noradrenaline and histamine and attenuation of relaxant response to acetylcholine. However, in contrast to single-egg treated group, which demonstrated a reduction in the relaxant response to electrical field stimulation (EFS), there was a marked and statistically significant potentiation of this nitrergic transmission, in the two-eggs group. Prior incubation of CC strips of normolipidaemic rabbits (n-7) with lysolecithin, reproduced similar exaggerated response to EFS. Therefore, from the results of our study, it is concluded that oxidised LDL or its major amphiphile lysolecithin, at some critical level or beyond, may be capable of reverting at least some of the adverse effects of hypercholesterolaemia on erectile function, through its mediating effect on nitrergic transmission. |
| Elevated low-density lipoprotein-cholesterol in women with polycystic ovary syndrome von Eckardstein, S., A. von Eckardstein, et al. (1996), Gynecol Endocrinol 10(5): 311-8. Abstract: Previous studies have indicated that women with the polycystic ovary syndrome (PCOS) are affected by hypertriglyceridemia and low high-density lipoprotein-cholesterol (HDL-C) level. However, most of these studies did not control for confounding factors such as body mass index (BMI) or differences in ethnicity. Therefore, we compared the lipid data for 26 women with PCOS with those for 1428 female control participants of the Prospective Cardiovascular Munster (PRO-CAM) study who did not use hormonal contraceptives and were of similar age. Data were adjusted for age, BMI and ethnicity. Women with PCOS had higher total cholesterol (5.55 +/- 1.24 vs. 4.99 +/- 0.88 mmol/l, p < 0.05) and low-density lipoprotein-cholesterol (LDL-C) levels (3.61 +/- 1.19 vs. 3.08 +/- 0.82 mmol/l, p < 0.05) than the control subjects. Compared with the women in the control population, those with PCOS more frequently had triglyceride levels exceeding 2.3 mmol/l (11.5 vs. 1.6%, p < 0.001), LDL-C levels exceeding 4.2 mmol/l (30.8 vs. 12.1, p < 0.01), and HDL-C levels below 1.2 mmol/l (46.2 vs. 15.3%, p < 0.001). We conclude that dyslipidemia is found more frequently in women with PCOS, independently of the excess weight that is often found in this patient group. |
| Elevated Lp(a) is the most frequent familial lipoprotein disorder leading to premature myocardial infarction in a country with low cholesterol levels Pay, S., N. Ozcan, et al. (1997), Int J Cardiol 60(3): 301-5. Abstract: Disorders of the lipoprotein metabolism are an important cause of premature coronary artery disease and myocardial infarction. Of the genetic lipoprotein disorders, elevation of apoprotein (apo) B containing lipoproteins is the most frequent one in the western population. We aimed to define the prevalence of genetic lipoprotein disorders and other risk factors in a population from a country with a low average cholesterol levels. We examined 48 consecutive patients with premature myocardial infarction below age 55, their 78 siblings and age and body mass index matched controls for familial lipoprotein disorders. The patients with premature myocardial infarction had higher triglyceride, low-density lipoprotein, apo B, lipoprotein (Lp) (a) and lower apo A1 levels then controls (p < 0.05). Of the nonlipid risk factors, 67% smoked, 8% had diabetes mellitus, 17% had hypertension and 58% a family history of premature coronary artery disease. Fifty percent of these patients with premature myocardial infarction had a familial lipoprotein disorder. Familial excess of Lp(a) was the most frequent lipoprotein abnormality present in 16% of the patients followed by familial combined hyperlipidemia. We conclude that, Lp(a) increase was the most frequent familial lipoprotein abnormality in this population. The frequency of familial lipoprotein disorders in this population emphasises the need to screen siblings of patients with premature myocardial infarction. |
| Elevated plasma low-density lipoprotein and high-density lipoprotein cholesterol levels in amenorrheic athletes: effects of endogenous hormone status and nutrient intake Friday, K. E., B. L. Drinkwater, et al. (1993), J Clin Endocrinol Metab 77(6): 1605-9. Abstract: To determine the interactive effects of hormones, exercise, and diet on plasma lipids and lipoproteins, serum estrogen and progesterone levels, nutrient intake, and plasma lipid, lipoprotein, and apolipoprotein concentrations were measured in 24 hypoestrogenic amenorrheic and 44 eumenorrheic female athletes. When compared to eumenorrheic athletes, amenorrheic athletes had higher levels of plasma cholesterol (5.47 +/- 0.17 vs. 4.84 +/- 0.12 mmol/L, P = 0.003), triglyceride (0.75 +/- 0.06 vs. 0.61 +/- 0.03 mmol/L, P = 0.046), low-density lipoprotein (LDL; 3.16 +/- 0.15 vs. 2.81 +/- 0.09 mmol/L, P = 0.037), high-density lipoprotein (HDL; 1.95 +/- 0.07 vs. 1.73 +/- 0.05 mmol/L, P = 0.007), and HDL2 (0.84 +/- 0.06 vs. 0.68 +/- 0.04 mmol/L, P = 0.02) cholesterol. Plasma LDL/HDL cholesterol ratios, very low-density lipoprotein and HDL3 cholesterol, and apolipoprotein A-I and A-II levels were similar in the two groups. Amenorrheic athletes consumed less fat than eumenorrheic subjects (52 +/- 5 vs. 75 +/- 3 g/day, P = 0.02), but similar amounts of calories, cholesterol, protein, carbohydrate, and ethanol. HDL cholesterol levels in amenorrheic subjects correlated positively with the percent of dietary calories from fat (r = 0.42, n = 23, P = 0.045) but negatively with the percent from protein (r = -0.49, n = 23, P = 0.017). Thus, exercise-induced amenorrhea may adversely affect cardiovascular risk by increasing plasma LDL and total cholesterol. However, cardioprotective elevations in plasma HDL and HDL2 cholesterol may neutralize the risk of cardiovascular disease in amenorrheic athletes. |
| Elevated remnant-like particle cholesterol and triglyceride levels in diabetic men and women in the Framingham Offspring Study Schaefer, E. J., J. R. McNamara, et al. (2002), Diabetes Care 25(6): 989-94. Abstract: OBJECTIVE: Remnants of triglyceride-rich lipoproteins are thought to be atherogenic. A new antibody-based assay allows for the isolation of remnant-like particles (RLPs) from plasma or serum, and the subsequent measurement of RLP cholesterol (RLPC) and triglycerides (RLPTGs). We hypothesized that diabetic patients would have higher remnant levels than nondiabetic patients. DESIGN AND METHODS: We compared RLPC and RLPTG levels of diabetic subjects (68 women, 121 men) participating in the Framingham Heart Study with those of nondiabetic subjects (1,499 women, 1,357 men). RESULTS: Mean RLPC values for diabetic women were 106% higher than those for nondiabetic women (0.367 +/- 0.546 mmol/l 14.2 +/- 21.1 mg/dl vs. 0.179 +/- 0.109 mmol/l 6.9 +/- 4.2 mg/dl; P < 0.0001), and RLPTG values for diabetic women were 385% higher than those for nondiabetic women (1.089 +/- 2.775 mmol/l 93.1 +/- 245.6 mg/dl vs. 0.217 +/- 0.235 mmol/l 19.2 +/- 20.8 mg/dl; P < 0.0001). Similar but less striking differences were observed in diabetic men, who had mean RLPC values 28% higher than those seen in nondiabetic men (0.285 +/- 0.261 mmol/l 11.0 +/- 10.1 mg/dl vs. 0.223 +/- 0.163 mmol/l 8.6 +/- 6.3 mg/dl; P < 0.001) and mean RLPTG values 70% higher than those seen in nondiabetic men (0.606 +/- 1.019 mmol/l 53.6 +/- 90.2 mg/dl vs. 0.357 +/- 0.546 mmol/l 31.6 +/- 48.3 mg/dl; P < 0.001). Moreover, diabetic men and women had significantly higher total triglycerides and lower HDL cholesterol levels than nondiabetic subjects. CONCLUSIONS: The data indicate that RLP particles are elevated in diabetic subjects. To achieve optimal reduction of risk for cardiovascular disease, treatment of elevated RLP values, along with the control of LDL cholesterol levels, should be considered. |
| Elevated remnant-like particle cholesterol concentration: a characteristic feature of the atherogenic lipoprotein phenotype Twickler, T. B., G. M. Dallinga-Thie, et al. (2004), Circulation 109(16): 1918-25. |
| Elevated serum cholesterol is a risk factor for both coronary heart disease and thromboembolic stroke in Hawaiian Japanese men. Implications of shared risk Benfante, R., K. Yano, et al. (1994), Stroke 25(4): 814-20. Abstract: BACKGROUND AND PURPOSE: The relation between total serum cholesterol level and thromboembolic or nonhemorrhagic stroke is controversial. The Honolulu Heart Program cohort of Japanese-American men provides data which show that elevated serum cholesterol is an independent predictor of thromboembolic stroke as well as coronary heart disease (CHD). The data are presented to suggest that the association of elevated cholesterol with stroke is sometimes underestimated or underreported partly because of competing or shared risk with CHD, the other major atherosclerotic end point. METHODS: The data are based on 6352 men (aged 51 to 74 years) at baseline examination (1971 to 1974) who were free of clinical CHD and stroke and were followed an average of 15 years for new cases of both end points. Relative risks of serum cholesterol for CHD and thromboembolic stroke were calculated, controlling for other major cardiovascular covariates. RESULTS: There was a continuous and progressive increase in both CHD and thromboembolic stroke rates with increasing levels of serum cholesterol. The relative risk between the highest and lowest quartiles of serum cholesterol was 1.7 (95% confidence interval, 1.4 to 2.0) for CHD and 1.4 (95% confidence interval, 1.1 to 1.9) for thromboembolic stroke. There was a decline in the difference in relative risks between CHD and thromboembolic stroke in older men (aged 60 years and older) compared with younger men (aged younger than 60 years). CONCLUSIONS: These data provide additional evidence that elevated serum cholesterol should be considered a primary risk factor for thromboembolic stroke, presumably through its effect on both coronary and cerebrovascular atherosclerosis. It is suggested that this association is sometimes underestimated or underreported partly because of shared or competing risk with CHD, the clinical manifestation of atherosclerosis that generally occurs earlier in life and with greater frequency than thromboembolic stroke. |
| Elevated serum cholesterol levels in Bangkok children and adolescents Suthutvoravut, U., S. Charoenkiatkul, et al. (1999), J Med Assoc Thai 82 Suppl 1: S117-21. Abstract: Hypercholesterolemia is a major cardiovascular risk factor. This study aimed to assess serum total cholesterol (TC) levels of children and adolescents living in Bangkok, Thailand. During 1995-1997, nonfasting blood samples were obtained from 570 healthy school children and adolescents aged 9-18 years. The mean TC levels ranged from 143-180 mg/dl in males and from 145-202 mg/dl in females. The prevalences of hypercholesterolemia (TC > or = 200 mg/dl) were 12.2 per cent and 20.3 per cent in males and females, respectively. Twenty-eight per cent of males and 26.9 per cent of females had borderline values (TC 170-199 mg/dl). TC inversely correlated with age (r = -0.16, P < 0.01) in males. The findings indicate that notable percentage of these children had elevated cholesterol levels and warrant additional study concerning risk factors and tracking of lipoprotein levels from childhood into adulthood. |
| Elevated serum total and LDL cholesterol in very old patients with Alzheimer's disease Lesser, G., K. Kandiah, et al. (2001), Dement Geriatr Cogn Disord 12(2): 138-45. Abstract: The relationships of serum lipids with Alzheimer's disease (AD) and other dementias in very old patients are not clear. All residents of an academic nursing home were studied clinically for dementia and for serum lipids. All those autopsied over a 7.7-year period had apolipoprotein E (apoE) genotyping and detailed neuropathological examination. Those with pathologically defined criteria for AD (n = 84) were compared to all others who also had clinical dementia but did not show AD changes (n = 22). In contrast to most other reports of serum lipids in very old patients with AD, total cholesterol (TC) and low density lipoprotein cholesterol levels were each significantly higher for those with AD. The lipid-AD associations were progressively stronger with increasing pathological certainty of AD diagnosis. These relationships remained significant after adjustment for apoE genotype and for other known risk factors. The lipid-AD associations in a very old cohort, and prior evidence that elevated TC in middle life is a risk factor for later dementia, prompt consideration of factors associated with lipid metabolism in the development of Alzheimer's dementia. |
| Elevated soluble cellular adhesion molecules in subjects with low HDL-cholesterol Calabresi, L., M. Gomaraschi, et al. (2002), Arterioscler Thromb Vasc Biol 22(4): 656-61. Abstract: The purpose of this study was to investigate whether the expression of cellular adhesion molecules (CAMs) is enhanced in individuals with low HDL cholesterol (HDL-C). Plasma levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin (sE-selectin) were measured in subjects with low (below the 10th percentile for the Italian population), average, or high (above the 90th percentile) HDL-C. Average sICAM-1 and sE-selectin levels were significantly higher in two groups of 65 individuals with low HDL levels, either hyperlipidemic (320.5+/-16.0 and 61.4+/-3.5 ng/mL) or normolipidemic (309.6+/-13.0 and 60.0+/-2.7 ng/mL), than in subjects with average HDL levels, either hyperlipidemic (267.0+/-10.1 and 50.4+/-2.8 ng/mL) or normolipidemic (257.9+/-5.4 and 51.1+/-2.4 ng/mL), or with high HDL levels (254.8+/-10.2 and 52.5+/-3.2 ng/mL). No significant difference was found in the plasma sVCAM-1 concentration. HDL-C was inversely correlated with sICAM-1 and sE-selectin in the low-HDL subjects (r(2)=0.087 and 0.035, P=0.0007 and 0.033, respectively), but not in individuals with normal or elevated HDL-C (r(2)=0.012 and 0.006). A fenofibrate-induced increase of HDL-C in 20 low-HDL subjects was associated with a significant reduction of plasma sICAM-1 and sE-selectin concentrations. An increased CAMs expression may be a mechanism by which a low plasma HDL level promotes atherogenesis and causes acute atherothrombotic events. |
| Elevated total cholesterol in bulimia nervosa Sullivan, P. F., K. A. Gendall, et al. (1998), Int J Eat Disord 23(4): 425-32. Abstract: OBJECTIVE: It has been suggested that total serum cholesterol concentrations are elevated in bulimia nervosa. The objectives of this study were to compare cholesterol concentrations in women with bulimia nervosa with those of depressed women and population norms and to determine the dietary correlates of elevated cholesterol concentrations. METHODS: 126 women with bulimia nervosa and 57 women with major depression participating in clinical trials were studied. Total serum cholesterol concentrations were available for all participants. Prospective 2-week dietary intake analysis was examined for 49 of the bulimic women. RESULTS: Bulimic women had markedly higher total cholesterol concentrations than depressed women and in comparison to consensus recommendations and population norms. This finding remained highly statistically significant after taking into account an array of potential physical and psychopathological covariates. Dietary analysis suggested that increased total cholesterol concentrations were related to cholesterol and fat intake during binge eating, but not during normal eating. DISCUSSION: Bulimic women have higher total cholesterol concentrations that are related to excess cholesterol and fat intake during binge eating. |
| Elevated triglycerides and low HDL cholesterol in transgenic mice expressing human apolipoprotein A-I(Milano) Chiesa, G., L. J. Stoltzfus, et al. (1998), Atherosclerosis 136(1): 139-46. Abstract: In general, plasma concentrations of high density lipoproteins (HDL) are inversely related to the incidence of coronary artery disease. One exception to this trend is individuals with apolipoprotein A-I(Milano) (apo A-IM), a molecular variant of apo A-I, which results in very low plasma apo A-I and HDL-cholesterol levels. Despite these low levels, and other lipoprotein defects, individuals with this mutation have no increased risk for cardiovascular disease. As a first step in proving why apo A-IM carriers appear to be protected from the pro-atherogenic effect of a low HDL, transgenic mice expressing apo A-IM were generated. Mice expressing either wild-type human apo A-I or apo A-IM, together with human apo A-II, were crossed into mice lacking murine apo A-I. Apo A-IM/A-II mice had lower cholesterol and HDL plasma levels compared to apo A-I/A-II mice. Moreover, as in human carriers, apo A-IM mice were characterized by elevated triglyceride plasma levels and by the presence of a population of very small HDL particles. These results indicate that the expression of apo A-IM in a mouse model reproduces the major lipid/lipoprotein abnormalities observed in human carriers. Thus, apo A-IM transgenic mice appear to be a suitable model in which to assess whether the mutation has an anti-atherogenic effect. |
| Elevating high-density lipoprotein cholesterol in apolipoprotein E-deficient mice remodels advanced atherosclerotic lesions by decreasing macrophage and increasing smooth muscle cell content Rong, J. X., J. Li, et al. (2001), Circulation 104(20): 2447-52. Abstract: BACKGROUND: HDL cholesterol levels are inversely correlated with coronary heart disease risk in humans, and in animal studies, HDL elevation decreases formation and progression of foam-cell lesions. The potential for HDL to affect preexisting advanced atherosclerotic lesions is not known. To approach this issue, we used a novel mouse aortic transplantation model. METHODS AND RESULTS: ApoE-deficient (EKO) mice were fed a Western-type diet for 6 months, and thoracic aortic segments containing advanced lesions replaced segments of the abdominal aorta of 4-month-old EKO syngeneic mice not expressing (plasma HDL cholesterol approximately 26 mg/dL) or expressing (HDL approximately 64 mg/dL) a human apoAI (hAI) transgene. Both types of recipients had comparable non-HDL cholesterol levels. Five months after transplantation, mice were killed and grafts analyzed. Compared with lesion area in pretransplant mice (0.14+/-0.04 mm(2), mean+/-SEM), there was progression in the EKO recipients (0.39+/-0.06 mm(2), P<0.01). Compared with EKO recipients, hAI/EKO recipients had retarded progression (0.24+/-0.04 mm(2), P<0.05). Immunostaining for CD68 and other macrophage-associated proteins, monocyte chemoattractant protein-1, acyl coenzyme A:cholesterol acyltransferase, and tissue factor, in lesions of pretransplant and EKO recipient mice showed abundant macrophages. In contrast, compared with any other group, lesional macrophage area in hAI/EKO mice decreased >80% (P<0.003), and smooth muscle cell content (alpha-actin staining) increased >300% (P<0.006). The decrease in macrophages and increase in smooth muscle cells was primarily in the superficial subendothelial layer. CONCLUSIONS: Increasing HDL cholesterol levels in EKO mice retards progression of advanced atherosclerotic lesions and remodels them to a more stable-appearing phenotype. |
| Elevation of 7-dehydrocholesterol concentrations in serum and liver and pericentral peroxisome proliferation in hepatocytes of rats after inhibition of cholesterol biosynthesis by BM 15,766 Weiss, M. C., E. Baumgart, et al. (1995), Berl Munch Tierarztl Wochenschr 108(2): 66-9. Abstract: Sprague-Dawley rats of both sexes were treated for three months with BM 15,766, an inhibitor of cholesterol biosynthesis in conjunction with standard or high-fat and high-cholesterol diets. In serum and livers of all drug-treated rats lowered cholesterol concentration associated with an increase of 7-dehydrocholesterol (7-DHC) was found. Electron microscopy of the liver showed a distinct proliferation of peroxisomes and an increase of dumb-bell shaped mitochondria in the pericentral zone 3. Abnormal-shaped peroxisomes with DAB-negative loops attached to their membranes were found in the intermediate zone 2. These alterations were more accentuated in drug-treated rats fed standard diet, then in treated rats receiving a high-fat and high-cholesterol diet. The observations demonstrate, that the increase of 7-DHC is due to the inhibition of 7-DHC-delta 7-reductase by BM 15.766 and emphasize the zonal heterogeneity of hepatocytes. The relevance of these observations for the investigation of the human Smith-Lemli-Opitz syndrome, in which also decreased plasma-cholesterol levels and an increase of 7-DHC were reported, is discussed. |
| Elevation of cyclic AMP by iloprost and prostaglandin E1 increases cholesterol efflux and the binding capacity for high-density lipoproteins in human fibroblasts Middleton, A. and B. Middleton (1998), Biochim Biophys Acta 1391(2): 117-32. Abstract: Elevation of cAMP concurrently enhances cholesterol efflux and binding of HDL3 in human skin fibroblasts. These effects were observed regardless of the route by which cAMP levels were increased. Cholesterol efflux and HDL3 binding were stimulated by the cAMP analogue CPT-cAMP, the adenylate cyclase activator forskolin, and by iloprost and prostaglandin E1 (PGE1) (which elevate cAMP via receptor-mediated processes). Dideoxyforskolin and PGF2alpha, which do not elevate cAMP, altered neither cholesterol efflux nor binding of HDL3. Inhibition of protein kinase A with H89 abolished the stimulatory effects of CPT-cAMP and iloprost, suggesting protein kinase A involvement in enhancing cholesterol efflux and HDL3 binding. Enhancement of HDL3 binding by iloprost was due to increased maximal capacity of the cells to bind HDL3, i.e., a greater number of HDL3 binding sites. A positive correlation was demonstrated between changes in HDL3 binding and changes in 3Hcholesterol efflux. The data are compatible with a model in which cholesterol efflux is partially dependent upon HDL binding to the cells. A short exposure to iloprost was sufficient to stimulate cAMP synthesis, triggering a chain of events leading to increased HDL3 binding and 3Hcholesterol efflux 20-24 h later. We conclude that both cholesterol efflux and the maximal capacity for HDL3 binding are enhanced by elevation of cellular cAMP. Cyclic AMP-elevating prostanoids could initiate these responses in vivo. |
| Elevation of high-density lipoprotein cholesterol in humans during long-term therapy with amiodarone Pollak, P. T. and M. H. Tan (1999), Am J Cardiol 83(2): 296-300, A7. Abstract: The distribution of plasma lipids was studied in 18 patients receiving amiodarone for 18 months, confirming that amiodarone is associated with a 17% elevation in total cholesterol and, for the first time, documenting increases in high-density lipoprotein cholesterol. The increase in high-density lipoprotein was proportionately greater than that of low-density lipoprotein cholesterol, suggesting that the impact of changes in the predicted risk of coronary heart disease are less important than if the elevation consisted of low-density lipoprotein cholesterol alone. |
| Elevation of plasma lathosterol, as an indicator of increased cholesterol synthesis, in preterm (23-32 weeks gestation) infants given Intralipid Hamilton, J. J., M. Phang, et al. (1992), Pediatr Res 31(2): 186-92. Abstract: Hypercholesterolemia is common in preterm infants administered 10% Intralipid perhaps because of excess phospholipid in plasma causing efflux of cholesterol from tissues. The purpose of this study was to determine if cholesterol synthesis (as measured by plasma lathosterol) is increased in preterm infants (23-32 wk gestation) during infusion of up to 4 g 10% Intralipid/kg body wt/d. Two groups of infants were studied. Intralipid intake was compared to: 1) plasma cholesterol in blood sampled over the first 100 d of life (preliminary study, n = 22) and 2) plasma cholesterol, lathosterol, and apo AI and B in blood taken at birth (cord), d 3-4 of life, and at least three additional times over the next 25 d (lathosterol study, n = 22). Lathosterol was quantitated by gas liquid chromatography and apo AI and B by immunoprecipitation. In the preliminary study, plasma cholesterol levels rose (to 4.06-10.70 mM) with Intralipid administration. Infants who received less than 2 g Intralipid/kg body wt/d were not hypercholesterolemic. In the lathosterol study, plasma cholesterol increased (1.86-2.24 mM, p = 0.06) and apo AI and B did not change, but lathosterol and the cholesterol:lathosterol ratio decreased (5.24-2.88 microM, p = 0.01, and 284-124 10(2) x mmol lathosterol:mol cholesterol, p = 0.007, respectively) from birth to d 3-4 (n = 11 paired samples). Infants followed longitudinally had increased cholesterol and lathosterol (4- to 7-fold) with increasing Intralipid administration, which decreased after discontinuation of infusion. Apo AI and B decreased upon Intralipid infusion.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Elevation of serum cholesterol at high altitude and its relationship to hematocrit Temte, J. L. (1996), Wilderness Environ Med 7(3): 216-24. Abstract: The positive relationship between hematocrit and serum cholesterol may be due to dilution. Accordingly, high hematocrits would yield reduced serum pools for dilution of cholesterol, thus producing higher levels. To test this effect, the relationships between hematocrit and cholesterol were evaluated at low-altitude and high-altitude clinics. Retrospective chart reviews were conducted at Madison, WI (264 m) and Leadville, CO (3105 m) to identify family practice patients who underwent hematocrit and serum cholesterol determinations on the same day. We excluded patients with medical conditions or on medications that affect cholesterol, patients with high glucose and triglyceride levels, and patients with extreme cholesterol levels. Remaining patients (153 in each altitude group) were matched by age and sex. The mean hematocrits and cholesterol levels were compared using analysis of variance. The linear relationships between hematocrit and cholesterol were compared using analysis of covariance. The mean hematocrit was significantly higher at high altitude (47.5% versus 41.3%; p < 0.0005) as were the mean serum cholesterol (190 mg/dL versus 177 mg/dL; p < 0.002) and the low-density lipoprotein:high-density lipoprotein ratio (2.80 versus 2.27; p < 0.05). Whereas a significant, positive relationship existed between hematocrit and cholesterol at low altitude (2.15 mg/dL per %; p < 0.002), no such relationship was found at high altitude. Hematocrit and serum cholesterol were elevated for family practice patients living at high altitudes. Differences exist between altitudes in the relationship between hematocrit and cholesterol. Acclimatization to high altitude and its resultant erythropoiesis may increase serum cholesterol levels. Consequently, relocation to a high altitude may increase the risk of arteriosclerotic cardiovascular disease. |
| Elevation of serum cholesterol levels in mice by the antioxidant butylated hydroxyanisole LeBlanc, G. A. and J. S. Gillette (1993), Biochem Pharmacol 45(2): 513-5. Abstract: The food antioxidants butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) are structurally related to the hypocholesterolemic drug probucol. The purpose of this study was to determine if BHA can lower serum cholesterol levels as is observed with probucol. Treatment of mice with 0.75% BHA in their feed for 10 days resulted in a significant (P < or = 0.01) elevation of serum cholesterol levels. This effect contrasts with the cholesterol-lowering effect of probucol. Further, the degree of cholesterol elevation was comparable to that observed in mice administered 3% cholesterol in their feed for 7 days. The enzyme acyl CoA:cholesterol acyltransferase (ACAT) was decreased significantly (P < or = 0.01) in liver microsomes from BHA-treated mice. In contrast, hepatic microsomal ACAT activity was increased significantly (P < or = 0.01) in cholesterol-fed mice. These results suggested that the increased serum cholesterol observed in BHA-treated mice was not accompanied by an increase in hepatic cholesterol levels. Indeed, hepatic microsomal cholesterol levels were reduced in BHA-treated mice, but were increased significantly (P < or = 0.01) in cholesterol-fed mice. These results demonstrate that the common food additive BHA elevates serum cholesterol levels by a mechanism that apparently involves the decreased uptake of cholesterol by the liver. |
| Eligibility for cholesterol referral in community-dwelling older adults. The Cardiovascular Health Study Manolio, T. A., C. D. Furberg, et al. (1992), Ann Intern Med 116(8): 641-9. Abstract: OBJECTIVES: To assess the proportion of community-dwelling adults aged 65 years or older who are eligible for referral for lipoprotein analysis and intervention according to the National Cholesterol Education Program (NCEP) guidelines. DESIGN: Cross-sectional study based on examinations and questionnaires collected in 1989 and 1990. SETTING: Four communities in the U.S. in the Cardiovascular Health Study (CHS), a study of risk factors for heart disease and stroke in older adults. PARTICIPANTS: A sample of 4810 men and women ages 65 to 100 randomly selected and recruited from Health Care Financing Administration Medicare eligibility lists for the four communities; not institutionalized, not wheelchair-bound, not currently receiving therapy for cancer, not currently taking lipid-lowering medications, and not having eaten in the preceding 9 hours. MEASUREMENTS: Total cholesterol and lipoprotein analysis measured in all participants. RESULTS: Total cholesterol levels were less than 5.17 mmol/L (200 mg/dL) in 37% of participants, 5.17 to 6.19 mmol/L (200 to 239 mg/dL) in 39%, and 6.20 mmol/L (240 mg/dL) or greater in 24%. Compared with their counterparts, older participants, especially those over 80 years of age, were more likely to have levels below 5.17 mmol/L, as were men, nonwhites, and those with coronary heart disease or two or more coronary heart disease risk factors (P less than 0.008 for all values). Based on this screening measurement, 2174 participants were eligible for lipoprotein analysis, 80% were eligible for dietary or drug therapy using NCEP guidelines. Overall, 46% of CHS participants were eligible for lipoprotein analysis and 36% for intervention by NCEP guidelines, based on a single cholesterol measurement. CONCLUSION: A substantial proportion of older adults in this community sample were eligible for lipoprotein analysis and intervention. Prospective studies of elderly persons are needed to determine the risk for incident coronary heart disease according to NCEP classifications and the benefits of lipid-lowering treatments in persons in this age group so that intervention strategies may best be targeted to an appropriately high-risk group. |