| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Infant diet affects serum lipoprotein concentrations and cholesterol esterifying enzymes in baboons Mott, G. E., D. S. Lewis, et al. (1993), J Nutr 123(2): 155-63. Abstract: We characterized the preweaning differences in cholesterol metabolism between breast-fed and formula-fed baboons and determined if formulas with low and high polyunsaturated:saturated fatty acid (P:S) ratios simulated the effects of breast feeding. At birth, 45 infant baboons from three sires and 44 dams were assigned to breast-fed, low P:S formula or high P:S formula diet groups until weaning at 14 wk. From 4 to 14 wk breast-fed infants had higher serum cholesterol because of much higher HDL1- and HDL2-cholesterol concentrations but had lower HDL3-cholesterol than both formula-fed groups. LDL-cholesterol was higher in infants fed the low P:S fomula. Breast-fed infants had higher serum apolipoprotein E than the formula-fed groups, but diet did not affect apolipoprotein A-I or B concentrations. Breast-fed infants had higher hepatic acyl CoA cholesterol acyltransferase activity and lower plasma lecithin cholesterol acyltransferase activity. These enzyme activities were not different between infants fed low or high P:S formulas. Post-heparinized plasma lipoprotein lipase activity was greater in breast-fed infants than in those fed formula. These findings demonstrate that the P:S ratio of formulas has little effect on cholesterol metabolism during the preweaning period and suggest that factors other than fat composition account for the metabolic differences between breast feeding and commercial infant formula. |
| Infant feeding and blood cholesterol: a study in adolescents and a systematic review Owen, C. G., P. H. Whincup, et al. (2002), Pediatrics 110(3): 597-608. Abstract: OBJECTIVE: To examine the influence of infant feeding method on serum total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol. METHODS: A cross-sectional study of 13- to 16-year-olds and a systematic review of studies (all observational) on the effects of infant feeding on cholesterol in infancy (<1 year), childhood or adolescence (1-16 years), and adulthood (> or =17 years) were conducted using random effects models. Differences are presented as breastfed-bottle-fed. A total of 1532 individuals (92% white; 55% male; mean age: 15.1 years) in 10 British towns were studied, and 37 studies with 52 observations on TC (26 in infancy, 17 in childhood or adolescence, and 9 in adulthood; corresponding figures for LDL were 7, 4, and 6) were reviewed. RESULTS: Mean TC in childhood or adolescence (including the new study) was not related to infant feeding pattern (mean TC difference = 0.00; 95% confidence interval CI: -0.07 to 0.07 mmol/L). However, in infancy, mean TC was higher among those breastfed (mean TC difference = 0.64; 95% CI: 0.50-0.79 mmol/L), whereas in adults, mean TC was lower among those breastfed (mean TC difference = -0.18; 95% CI: -0.30 to -0.06 mmol/L). Patterns for LDL were similar to those for TC throughout. CONCLUSIONS: Breastfeeding is associated with increased mean TC and LDL levels in infancy but lower levels in adulthood/adult life. These results suggest that breastfeeding may have long-term benefits for cardiovascular health and may have implications for the content of formula feed milks. |
| Infant-feeding patterns are related to blood cholesterol concentration in prepubertal children aged 5-11 y: the Fleurbaix-Laventie Ville Sante study Plancoulaine, S., M. A. Charles, et al. (2000), Eur J Clin Nutr 54(2): 114-9. Abstract: OBJECTIVE: Several studies, mainly in animals, but also in humans, have shown that diet in infancy is associated with differences in blood cholesterol concentrations later in life. The objective was to examine this relationship in children aged 5-11 y after taking into account their current diet and parental hypercholesterolemia. SETTING AND SUBJECTS: 251 prepubertal boys and 223 prepubertal girls enrolled in the schools in two little towns in northern France. DESIGN AND METHODS: Cross-sectional evaluation including measurements of cholesterol concentrations on capillary blood and a single weekday food intake record. Infant feeding patterns were obtained by questionnaire given to the mothers. RESULTS: 50% of the children had been breast-fed for a median duration of less than 2 months. Cow's milk was introduced in the diet as whole milk for 33% of the children. After adjustment for age, height, and sibship, capillary cholesterol concentration was lower in boys who had been breast fed (geometric mean: 4.4, 95% confidence interval of the mean: 4.2-4.6 mmol/L) than in those fed with formula (4.7, 4.5-4.8 mmol/L, P<0.03). In girls, breastfeeding had no significant effect on blood cholesterol concentration, which was associated with the type of cow's milk given in infancy: whole milk: 4.9 mmol/L (4.7-5. 2); totally or partially skimmed milk: 4.5 mmol/L (4.2-4.6), P<0.008. The current saturated fat and cholesterol intakes and parental hypercyholesterolemia were associated with current blood cholesterol concentration in children, but did not modify its relationship with infant feeding patterns. CONCLUSION: Results of the present study suggest that diet in infancy may have longstanding effect on lipid metabolism. Sponsorship: The study was supported by funds from Eridania Beghin-Say, Groupe Fournier, Lesieur and Nestle France, Roche Diagnostic and of the MGEN (Mutuelle Generale de l'Education Nationale, contract INSERM-MGEN #9158) and a grant from the Association de Langue Francaise pour l'Etude du Diabete et du Metabolisme (ALFEDIAM). European Journal of Clinical Nutrition (2000) 54, 114-119 |
| Inflammation and a thickened mucus layer in mice with cholesterol gallstones Rege, R. V. and J. B. Prystowsky (1998), J Surg Res 74(1): 81-5. Abstract: BACKGROUND: Based on previous work which suggested that biliary crystals may induce inflammation in the gallbladder wall and that inflammation is an early event during the formation of pigment gallstones in the dog, studies were performed examining mucus layer thickness, myeloperoxidase activity, and interleukin-1 (IL-1) activity in the wall of mouse gallbladder during formation and growth of cholesterol gallstones. METHODS AND MATERIALS: The inflammatory effects of cholesterol gallstones at 2 and 4 weeks were studied in BalB/C mice fed a crushed standard mouse chow with added cholesterol (1.0%) and cholic acid (0.5%). Results were compared to those of normal mice fed standard mouse chow. The presence or absence of crystals and stones was determined by gross and microscopic examination of bile. Myeloperoxidase and IL-1 activity in the gallbladder wall was measured using well-established bioassays. Mucus layer thickness was measured by darkfield microscopy. RESULTS: All mice fed a lithogenic, 1.0% cholesterol/0.5% cholic acid diet developed cholesterol crystals and gallstones at 2 and 6 weeks. No control mice developed either crystals or gallstones. Myeloperoxidase and IL-1 activities, markers of an inflammatory response, increased significantly in the gallbladder of mice with crystals at 2 weeks. Myeloperoxidase activity increased two- to three-fold, and IL-1 activity sevenfold, by 6 weeks. Mucus layer thickness also progressively increased during the 6-week period. CONCLUSIONS: It is concluded that inflammation is an early event associated with the appearance of crystals and gallstones in bile. |
| Inflammation modifies the effects of a reduced-fat low-cholesterol diet on lipids: results from the DASH-sodium trial Erlinger, T. P., E. R. Miller, 3rd, et al. (2003), Circulation 108(2): 150-4. Abstract: BACKGROUND: Inflammatory mediators regulate key aspects of lipid metabolism. We hypothesized that inflammation could diminish the cholesterol-lowering effect of a reduced-fat/low-cholesterol diet. METHODS AND RESULTS: After a 2-week run-in period on a control diet (37% total fat, 16% saturated fat), 100 participants were randomized to the control or DASH diet (27% total fat, 6% saturated fat) for 12 weeks. Median C-reactive protein (CRP) at baseline was 2.37 mg/L (interquartile range, 1.20, 3.79). The DASH diet, net of control, had no effect on CRP. Overall, there were significant net reductions in total (-0.34 mmol/L), LDL (-0.29 mmol/L), and HDL (-0.12 mmol/L) cholesterol from the DASH diet (each, P<0.001) and little change in triglycerides (+0.05 mmol/L, P=0.21). Baseline CRP was strongly associated with lipid responsiveness to the DASH diet. Total and LDL cholesterol were reduced to a greater degree in those with a "low" (below median) compared with a "high" (above median) baseline CRP (total, -9.8% versus -3%; P for interaction=0.006; LDL cholesterol, -11.8% versus -3%; P for interaction=0.009). Reductions in HDL cholesterol (-8.8%) were similar in persons with low versus high CRP. Triglycerides were increased in those with a high CRP but not in those with a low CRP (19.8% versus +0%; P for interaction=0.019). CONCLUSIONS: In this study, the presence of increased CRP was associated with less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet. These findings document an additional mechanism by which inflammation might increase cardiovascular disease risk. |
| Inflammation, cholesterol levels, and risk of mortality among patients receiving dialysis Kalantar-Zadeh, K. and S. D. Anker (2004), Jama 291(15): 1834; author reply 1834-5. |
| Inflammation, cholesterol levels, and risk of mortality among patients receiving dialysis Ravnskov, U. (2004), Jama 291(15): 1833-4; author reply 1834-5. |
| Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators Ridker, P. M., N. Rifai, et al. (1998), Circulation 98(9): 839-44. Abstract: BACKGROUND: We studied whether inflammation after myocardial infarction (MI) is a risk factor for recurrent coronary events and whether randomized treatment with pravastatin reduces that risk. METHODS AND RESULTS: A nested case-control design was used to compare C-reactive protein (CRP) and serum amyloid A (SAA) levels in prerandomization blood samples from 391 participants in the Cholesterol and Recurrent Events (CARE) trial who subsequently developed recurrent nonfatal MI or a fatal coronary event (cases) and from an equal number of age- and sex-matched participants who remained free of these events during follow-up (control subjects). Overall, CRP and SAA were higher among cases than control subjects (for CRP P=0.05; for SAA P=0.006) such that those with levels in the highest quintile had a relative risk (RR) of recurrent events 75% higher than those with levels in the lowest quintile (for CRP RR= 1.77, P=0.02; for SAA RR= 1.74, P=0.02). The study group with the highest risk was that with consistent evidence of inflammation (elevation of both CRP and SAA) who were randomly assigned to placebo (RR=2.81, P=0.007); this risk estimate was greater than the product of the individual risks associated with inflammation or placebo assignment alone. In stratified analyses, the association between inflammation and risk was significant among those randomized to placebo (RR=2.11, P=0.048) but was attenuated and nonsignificant among those randomized to pravastatin (RR=1.29, P=0.5). CONCLUSIONS: Evidence of inflammation after MI is associated with increased risk of recurrent coronary events. Therapy with pravastatin may decrease this risk, an observation consistent with a nonlipid effect of this agent. |
| Inflammatory changes in gallbladder mucosa. Their role in the pathogenesis of cholesterol gallstones von Ritter, C. (1996), Fortschr Med 114(22-23): 277-8. |
| Inflammatory response, cholesterol metabolism, and arteriosclerosis Salazar Soler, A., X. Pinto Sala, et al. (2001), An Med Interna 18(2): 100-4. Abstract: The goal of the present review consists on the relationship between inflammatory disorders, such as that represented by systemic granulomatous diseases like sarcoidosis, and the cholesterol metabolism and its implication in the atherosclerosis process. Serum amyloid A is an acute phase reactant that transiently binds to the high density lipoproteins during an inflammatory response. Serum amyloid A may act either displacing apo A-I, which in turn result in increased catabolism of high density lipoproteins, or inhibiting lecithin-cholesterol acyltransferase activity which leads to low levels of esterified serum cholesterol. This lipoprotein alteration together with a direct effect of the serum amyloid A on the endothelium of the atheromatous plaque suggest a potential pathophysiological link between the inflammatory responses expressed by the serum concentrations of amyloid A and the development of the atherosclerotic process. |
| Inflammatory/antiinflammatory properties of high-density lipoprotein distinguish patients from control subjects better than high-density lipoprotein cholesterol levels and are favorably affected by simvastatin treatment Ansell, B. J., M. Navab, et al. (2003), Circulation 108(22): 2751-6. Abstract: BACKGROUND: The inflammatory/antiinflammatory properties of HDL were compared with HDL cholesterol in 2 groups of patients and in age- and sex-matched control subjects. METHODS AND RESULTS: Group 1 consisted of 26 patients not yet taking a statin who presented with coronary heart disease (CHD) or CHD equivalents by National Cholesterol Education Program Adult Treatment Panel III criteria studied before and 6 weeks after 40 mg/d of simvastatin. Group 2 consisted of 20 patients with documented CHD and HDL cholesterol > or =84 mg/dL. The inflammatory/antiinflammatory properties of HDL were determined by the ability of the subject's HDL to alter LDL-induced monocyte chemotactic activity (MCA) in a human artery wall coculture. Induction of MCA by a control LDL was determined in the absence or presence of the subject's HDL. Values in the absence of HDL were normalized to 1.0. Values >1.0 after the addition of HDL indicated proinflammatory HDL; values <1.0 indicated antiinflammatory HDL. Group 1 values before simvastatin were LDL cholesterol, 118+/-24 mg/dL; HDL cholesterol, 57+/-13 mg/dL; triglycerides, 125+/-64 mg/dL; and high-sensitivity C-reactive protein (hs-CRP), 1.7+/-1.9 mg/L; and MCA values were 1.38+/-0.91, compared with 0.38+/-0.14 for control subjects (P=1.5x10(-5)). After simvastatin, values were LDL cholesterol, 73+/-24 mg/dL; HDL cholesterol, 61+/-14 mg/dL; triglycerides, 99+/-52 mg/dL; and hs-CRP, 1.3+/-1.3 mg/L; and MCA values were 1.08+/-0.71. In group 2, values were LDL cholesterol, 108+/-34 mg/dL; HDL cholesterol, 95+/-14 mg/dL; triglycerides, 89+/-44 mg/dL; and hs-CRP, 0.8+/-0.7 mg/L; and MCA values were 1.28+/-0.29, compared with 0.35+/-0.11 for control subjects (P=1.7x10(-14)). Similar results were obtained with the cell-free assay. CONCLUSIONS: The inflammatory/antiinflammatory properties of HDL distinguished patients from control subjects better than HDL cholesterol and were improved with simvastatin. |
| Influence of 0.1 or 0.2% cholesterol-enriched diets on the induction of atherosclerosis and aorta reactivity in vitro Fontes Ribeiro, C. A., L. Almeida, et al. (1998), J Cardiovasc Pharmacol 31(5): 690-9. Abstract: Current knowledge of atherogenesis is largely based on animal models of hypercholesterolemia, which rarely show changes similar to the lesions described in humans. We studied the influence of two low cholesterol-enriched diets on the development of anatomopathologic lesions and on the reactivity of the isolated aorta in rabbits. Compared with controls (rabbits fed a normal diet), a 0.1% cholesterol-enriched diet over a 6- or 9-month period produced increases of the 5-hydroxytryptamine (5-HT)-induced contractile responses, as well as a decreases in acetylcholine (ACh)-induced relaxing response (endothelium-dependent, through the production of NO). Noradrenaline (NA)-induced contractions and relaxations elicited by sodium nitroprusside (SNP; endothelium independent) were not significantly modified. Because at 6 months, significant anatomopathologic intimal early lesions were not found, functional endothelial changes can explain such findings. There was a defect in NO synthesis, release, or diffusion; 5 HT, but not NA, may be responsible for inducing NO production. In 0.2% cholesterol-fed rabbits at 4 and 12 weeks, increases of 5-HT- and NA-induced contractile responses were found. In both cases, there was a decrease of ACh-induced relaxing effect, whereas responses to SNP remained unchanged. Intimal early and advanced lesions were present at both the 4- and 12-week periods. These data suggest abnormalities of the NO system. The effects obtained with NA may be explained by a possible decrease of catechol-O-methyltransferase (COMT) or monoamine oxidase (MAO) activities or both or by decreased amine uptake. The extent to which NA may induce NO production is small, because changes in NA-induced contractions are verified only in the presence of significant alterations in the endothelium. The use of a 0.2% cholesterol diet for a short time may induce atherosclerotic lesions, whereas the 0.1% cholesterol diet for a 9-month period, besides being closer to the human diet, allows the detection of functional abnormalities before the evidence of structural lesions. |
| Influence of a cholesterol rich diet in rabbits on the formation of PGI2 and TXA2 Beitz, J., A. Beitz, et al. (1992), Agents Actions Suppl 37: 235-41. Abstract: In the study was investigated whether the formation of prostanoids is changed in the different regions of aorta or in clotting whole blood in dependence on development of atherosclerosis. For this question New Zealand rabbits were fed for different periods with a cholesterol rich diet (0.5%). At the end of the different dietary periods the animals were killed and the following parameters estimated: blood: levels of total cholesterol, HDLcholesterol, VLDLcholesterol, cholesterol in the beta-migrating lipoprotein fraction, serum lipid peroxides, TXB2 formation capacity of clotting whole blood; aorta: surface of intima covered with fatty streaks, free and esterified cholesterol, triglycerides, collagen, formation of 6-keto-PGF1a and TXB2 by abdominal and thoracic aortas. The lipid parameter demonstrated a relatively strong correlation with the duration of cholesterol rich diet or the macroscopically detectable atherosclerosis, but the prostanoid formation remained unchanged. |
| Influence of a long-term load of dietary cholesterol on the rat kidney Ogawa, T., J. Yoshida, et al. (2003), Nippon Jinzo Gakkai Shi 45(4): 361-6. Abstract: The involvement of hyperlipidemia in aggravation of nephrosis has remained controversial. In this study, to examine the influence of cholesterol on the kidney, normal SD rats were loaded with a normal diet(4.4% fat, 0.09% cholesterol) plus 0.25% cholesterol for 10 months, and the urinary excretion of protein, blood cholesterol level and histological renal changes were compared with those in the control group given the normal diet alone. The urinary protein excretion was increased after 4 months of cholesterol loading and was about 6 times the control value at the end of the study(10 months). At 10 months, the blood levels of total, HDL- and LDL + VLDL-cholesterols were also increased, and the arteriosclerosis index(HDL/LDL + VLDL ratio) was about 1.3 times the control value. Histologically, segmental lesions of glomeruli containing sclerosis/PAS positive material were stronger than in the control animals. Thus, this study revealed increased blood cholesterol and urinary protein excretion and aggravated histological changes of the kidney in rats given a long-term cholesterol load, suggesting that cholesterol may be a risk factor affecting the kidney. |
| Influence of a maternal cholesterol-enriched diet on 1-14C-linoleic acid and L-4, 5-3H-leucine entry in plasma of rabbit offspring Montoudis, A., L. Simoneau, et al. (2004), Life Sci 74(14): 1751-62. Abstract: Fetal development requires an important entry of essential free fatty acids (EFFA) and essential amino acids (EAA) into the fetal circulation. We have reported that a 0.2% enriched-cholesterol diet (ECD) during rabbit gestation significantly reduces fetus weight compared to control diet. It is known that dietary linoleic acid deficiency, an EFFA, during the fetal development induces an important impair to the somatic development. Moreover, intrauterine growth retardation induced a reduction of the flux of leucine, an EAA, from maternal to fetal circulation. Therefore, we hypothesized that the administration of an ECD induces modifications of placental lipid composition concomitant alterations of the transfer of linoleic acid and leucine in fetal circulation. Quantification of placental lipids revealed that in the ECD group a reduction of total-cholesterol (TC) and free-cholesterol (FC) is observed, however an increased in FFA and phospholipids is noticed when compared to the control group. In placenta from the ECD group, the FC/ TC ratio is significantly reduced compared to the control group. In the ECD group, the liver shows an increase of TC, FC and FFA compared to the control group. However, the quantity of triacylglycerol present in the liver from the ECD is significantly reduced compared to the control group. To evaluate the placental transfer of some essential nutrients, intravenous injection of 1-14C-linoleic acid or L-4, 5-3H-leucine to term rabbit (control and ECD group) were done. Two hours later, rabbits were euthanized and we collected placenta, livers and blood from dams and offspring. The concentrations of both radiolabeled molecules (linoleic acid and its esterified form or leucine) were higher in the plasma of ECD offspring than those found in offspring from control diet. Despite such alteration of placental lipid composition, linoleic acid and leucine transfer by the placenta was not compromised but rather increased. |
| Influence of a perpetual-daylight Arctic environment on periodicity in human cholesterol synthesis Biali, S., P. J. Jones, et al. (1995), Arctic Med Res 54(3): 134-44. Abstract: To identify factors associated with control of human cholesterol synthesis, periodicity in cholesterogenesis, hormonal levels and food consumption behavior were examined in 5 healthy individuals at the beginning and end of 18 d in a perpetual daylight Arctic environment devoid of time cues. At d 2 (phase I) and d 16 (phase II), cholesterol fractional synthesis rate was determined at 6 h intervals over 30 h as deuterium incorporation into plasma free cholesterol. Total plasma cholesterol, insulin and glucose-dependent insulinotropic polypeptide were also measured at each timepoint. Food intake and sleeping patterns were recorded prior to and during each phase. Cholesterol fractional synthesis rate (FSR) exhibited periodicity in all subjects on each phase, but did not differ between phase I (FSR rate = 0.038 +/- 0.038 pools.d-1) and phase II (FSR rate = 0.037 +/- 0.072 pools.d-1) phases. Phase II FSR period length was associated with both the duration between first and last meals (r2 = 0.81, p = 0.037) and total hours spent awake (r2 = 0.99, p = 0.001). Insulin and glucose-dependent insulinotropic polypeptide levels were not associated with FSR periodicity. These results suggest that meal timing and sleep/wake cycles are more important factors than insulin and glucose-dependent insulinotropic polypeptide in controlling the rhythms of whole body cholesterol synthesis. |
| Influence of age on hepatic uptake of HDL1-cholesterol in male Wistar rats with bile duct cannulation Bravo, E., E. Pignatelli, et al. (1994), J Biochem (Tokyo) 115(5): 833-6. Abstract: We have shown previously that the age-dependent increase in plasma cholesterol levels observed in male Wistar rats is associated with relevant changes in the lipoprotein pattern (in particular, with a much higher proportion of the HDL1 class) that are evident in animals from the age of 9 months. In this study, the possibility that a decreased catabolism of HDL1 cholesterol may cause this is evaluated by infusing this lipoprotein fraction labeled with 14Ccholesterol into both young (3.5 +/- 0.5 months) and adult (13.0 +/- 1.0 months) male Wistar rats with a permanent biliary drainage. The clearance of radioactivity from the blood compartment was slower in the older animals than in the younger ones. Conversely, the incorporation of radioactivity into plasma cholesteryl esters and the secretion of radioactivity into bile was higher in the younger animals. These results support the hypothesis that the age-related increase in HDL1 proportion is due, at least in part, to a slower liver catabolism of HDL1-cholesterol. |
| Influence of alcohol intake on high density lipoprotein cholesterol levels in middle-aged men Gupta, R., B. K. Jain, et al. (1994), Indian Heart J 46(3): 145-9. Abstract: To study the influence of alcohol (ethanol) intake on high density lipoprotein cholesterol (HDLC) levels, we studied 210 healthy middle-aged men (age 45 +/- 8 years). Other factors influencing HDLC (physical exercise, diet, smoking and body mass index) were also studied. Individuals were classified according to daily ethanol consumption. There were 39 teetotallers, 29 took drink, 30 took 1-1.9, 25 took 2-2.9, 26 took 3-3.9, 28 took 4-4.9 and 33 took 5 or more drinks per day (1 drink = 14 gm ethanol). The overall mean serum total cholesterol was 191.4 +/- 53 mg/dl and HDLC was 46.4 +/- 9 mg/dl. Total cholesterol in teetotallers was not different from those consuming different amounts of alcohol. HDLC in teetotallers (44.5 +/- 8 mg/dl) was significantly lower than in those taking 1-1.9 drinks (46.7 +/- 11 mg/dl, p < 0.05) and 2-2.9 drinks/day (51.4 +/- 9 mg/dl, p < 0.01) but was not different from those consuming > or = 3.0 drinks. There was a weak positive linear correlation between ethanol and HDLC (r = 0.016). HDLC levels were significantly lower in smokers (43.5 +/- 9 vs 47.2 +/- 11 mg/dl in non-smokers), in non-vegetarians (43.5 +/- 10 vs 46.2 +/- 9 mg/dl in vegetarians) and in those with sedentary habits (42.4 +/- 7 vs 46.1 +/- 10 mg/dl in physically active). Low level ethanol consumption (< 3 drinks or 42 gm per day) is associated with increased HDLC levels. |
| Influence of alcohol intake on risk for increased low-density lipoprotein cholesterol in middle-aged Japanese men Nakanishi, N., H. Yoshida, et al. (2001), Alcohol Clin Exp Res 25(7): 1046-50. Abstract: BACKGROUND: Decreased low-density lipoprotein (LDL) cholesterol in chronic alcoholics is well known. However, the importance of light to moderate alcohol consumption is less certain. METHODS: We investigated the association of alcohol intake with risk for increased LDL cholesterol over 5 years in a cohort of 933 Japanese male office workers aged 35 to 54 years who had LDL cholesterol levels less than 140 mg/dl and were not taking medication for dyslipidemia, hypertension, diabetes, liver disease, or hyperuricemia at study entry. Incident-increased LDL cholesterol was defined by an LDL cholesterol level of 140 mg/dl or more or use of medication for dyslipidemia. Each individual's slope for LDL cholesterol was also calculated with a simple linear regression model. RESULTS: Three hundred twenty-one men developed increased LDL cholesterol during 3785 person-years of follow-up. After controlling for potential predictors of increased LDL cholesterol, the relative risk for increased LDL cholesterol compared with nondrinkers was 0.89 for those who drank 0.1 to 22.9 g/day of ethanol, 0.74 for those who drank 23.0 to 45.9 g/day of ethanol, 0.64 for those who drank 46.0 to 59.9 g/day of ethanol, and 0.54 for those who drank 69.0 g/day or more of ethanol (p < 0.001). Slopes of LDL cholesterol level decreased significantly as alcohol intake increased. From multiple linear regression analyses, alcohol intake remained as an independent negative factor for slopes of LDL cholesterol level. CONCLUSIONS: Alcohol intake is negatively associated with development of increased LDL cholesterol in middle-aged Japanese men. |
| Influence of altered serum cholesterol levels and fasting on cutaneous cholesterol synthesis Wu-Pong, S., P. M. Elias, et al. (1994), J Invest Dermatol 102(5): 799-802. Abstract: Barrier perturbation stimulates epidermal cholesterol synthesis, which plays an important role in restoring barrier function. In the present study, we examined whether changes in serum cholesterol levels or nutrition regulate epidermal cholesterol synthesis in hairless mice. Serum cholesterol levels were lowered by 50% after injection with 4-aminopyrazolo (3,4-d) pyrimidine and were increased by 51% by feeding an atherogenic diet. In contrast to most other tissues, cholesterol synthesis in the epidermis and dermis was not inhibited by elevations or stimulated by decreases in serum cholesterol levels. Additionally, feeding a high-cholesterol diet did not decrease epidermal or dermal cholesterol synthesis. However, fasting significantly decreased both epidermal (38%) and dermal (34%) cholesterologenesis. Furthermore, barrier recovery after acetone disruption of the barrier was impaired in fasted animals. However, treatment with topical lipids did not restore barrier repair rate to normal, indicating that factors in addition to lipids are necessary to overcome the effects of fasting. These results demonstrate that cholesterol synthesis in the epidermis and dermis is regulated independently of changes in serum cholesterol levels. |