| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
| First Page | Previous Page | Next Page | Last Page |
| Low density lipoprotein cholesterol and whole blood viscosity Crowley, J. P., J. Metzger, et al. (1994), Ann Clin Lab Sci 24(6): 533-41. Abstract: Whole blood viscosity (WBV) was measured in a normal population and was analyzed in relation to packed cell volume, (hematocrit, PCV), fibrinogen, white blood cell count (WBC), platelet count, and plasma lipids, including total cholesterol, triglycerides, high density lipoprotein cholesterol (HDLc) and low density lipoprotein cholesterol (LDLc). Conventional assays were used for all blood and lipid measurements. Whole blood viscosity was measured under disaggregating conditions with a disposable, porous bed viscometer. As expected, the strongest correlation was seen between WBV and PCV (r = 0.78, p < 0.001). Significant positive correlations also were demonstrated between WBV and cholesterol (r = 0.22, p < 0.001), triglycerides (r = 0.14, p < 0.001) and LDLc (r = 0.21, p < 0.001). A significant negative correlation was found between HDLc and WBV (r = -0.20, p < 0.001). Correlation analysis by sex showed only the correlation of LDLc was significant for both men and women. A stepwise multiple regression analysis of WBV indicated that LDLc, fibrinogen (Fbg) and platelet (Plt) counts correlated independently of PCV to WBV. The equation derived from multiple regression and partial correlation analysis was: WBV (mPa.sec) = -9.317 + 0.0047 (LDLc) + 0.381 (PCV) + 0.00152 (Plt) + 0.0021 (Fbg). The calculated mean specific contribution of PCV was 90.8 percent, LDLc 3.5 percent, and fibrinogen 3.3 percent to observed mean WBV. This study shows that LDLc is the principal lipoprotein independently influencing whole blood viscosity and its effect is similar in magnitude to fibrinogen. Further studies to elucidate the mechanism and clinical significance of the effects of LDLc on WBV are indicated. |
| Low density lipoprotein cholesterol lowering: are the treatment guidelines still appropriate? Deslypere, J. P. (2000), Int J Clin Pract 54(5): 307-13. Abstract: The availability of treatment guidelines has revolutionised our approach to detection, evaluation and treatment of dyslipidaemias in adults. Such guidelines focus on lowering low-density lipoprotein-cholesterol (LDL-C), the primary risk factor for coronary heart disease, and provide physicians with specific goals to be attained by dietary and, if necessary, pharmacological therapy. However, the guidelines were published in 1993, which means that the pivotal findings from large intervention trials with statins were not included. This has led to calls for the guidelines to be amended to take into account the findings of these studies and other evolving issues such as the pathogenesis of the acute coronary event and the contribution of low HDL-C and other lipid parameters. More importantly, the mostly epidemiological basis of the guidelines has instilled the concept that the lower the LDL-C level after lipid-lowering intervention the better the result in terms of prevention of coronary events. Available data now refute this assumption. Indeed, maximal therapeutic benefit is already obtained with a decrease in LDL-C level of 20-30%, irrespective of baseline levels or LDL-C levels on treatment and, until now, there have been no data to suggest that decreases in LDL-C of > 30% give any additional benefit to patients in terms of improving their long-term outcome. The concept of absolute LDL-C treatment goals therefore needs to be revisited. A more appropriate goal of lipid-lowering therapy with statins is to ensure LDL-C levels are reduced by 20-30%, with statin dosages as used in the intervention trials. Furthermore, there are insufficient data to advise that LDL-C levels should be lowered to 2.6 mmol/l. This issue will be resolved only when the results of the appropriate intervention trials are published. |
| Low density lipoprotein cholesterol, lipoprotein(a), and apo(a) isoforms in the elderly: relationship to fasting insulin. Associazione Medica Sabin Carantoni, M., G. Zuliani, et al. (1999), Nutr Metab Cardiovasc Dis 9(5): 228-33. Abstract: BACKGROUND AND AIM: Insulin resistance/hyperinsulinemia are often associated with aging and could play an important role in the development of glucose intolerance and dyslipidemia in the elderly. We investigated the relationship between plasma fasting insulin with total cholesterol (TC) and low density lipoprotein LDL cholesterol (LDL-C), triglycerides (TG), lipoprotein(a) Lp(a) levels apolipoprotein (a) apo (a) isoforms in 100 free-living "healthy" octo-nonagenarians. METHODS AND RESULTS: Fasting insulin was positively correlated with TG, whereas a negative relation was found with TC and LDL-C (r = -0.29 and r = -0.28 respectively; p < 0.01), LDL-C/apo B, HDL-C and apo A-I levels. Fasting insulin was also inversely correlated with Lp(a) levels (r = -0.22; p < 0.03), whereas the latter were significantly related with TC and LDL-C (r = 0.30 and r = 0.31; p < 0.005), TG (r = 0.21; p < 0.05) and apo B (r = 0.26; p < 0.02). There was a negative relation between Lp(a) levels and apo(a) isoforms: the greater the apo(a) molecular weight, the lower the Lp(a) level (p < 0.0001). Fasting insulin increased with apo(a) size, though the difference in insulin levels among apo(a) isoforms was not significant (p = 0.4). Multiple regression analysis showed that fasting insulin was the best predictor of LDL-C (R2 = 0.14; p = 0.002) irrespective of age, gender, BMI, waist circumference and TG, while apo(a) isoform size, BMI and waist circumference were related with Lp(a) irrespective of TC and LDL-C, TG and apo B (R2 = 0.35 to 0.37; p < 0.0001). CONCLUSIONS: These results suggest that fasting insulin levels significantly influence LDL-C metabolism in old age. Lp(a) levels seem to be very strongly related to genetic background, although an indirect relation with insulin through adiposity and/or other associated lipid abnormalities cannot be ruled out. |
| Low density lipoprotein cholesterol/apolipoprotein B-100 ratio: interaction of family history of premature atherosclerotic coronary artery disease with race and gender in 7 to 11 year olds Islam, S., B. Gutin, et al. (1994), Pediatrics 94(4 Pt 1): 494-9. Abstract: BACKGROUND. In adults, a low density lipoprotein cholesterol (LDL-C)/apolipoprotein B-100 (ApoB) ratio is an indicator of ApoB-enriched small dense LDL, which is associated with premature coronary artery disease (CAD). Since this LDL subclass may be inherited, we investigated whether a low LDL-C/ApoB ratio was associated with a positive family history of premature CAD in young children. METHODS. Subjects were 66 children aged 7 to 11 years who were recruited through a school-based family history survey, flyers, and hospital newspaper advertisements. They were divided according to family history and assessed for fatness, blood pressure, lipids, lipoproteins, and apoproteins. RESULTS. Family history interacted with gender such that girls with a positive family history had a lower LDL-C/ApoB ratio than girls with a negative family history, while the opposite was true in boys; ie, family history-positive boys had a higher ratio than family history-negative boys. The association of a low ratio with a positive family history was seen most clearly in white girls. Family history-positive whites had higher ApoB than family history-negative whites, whereas the pattern was reversed in the blacks. The LDL-C/ApoB ratio and ApoB were not related to other CAD risk factors such as fatness, blood pressure, or other lipids and lipoproteins. CONCLUSION. In young children, a low LDL-C/ApoB ratio and high ApoB levels were associated with a positive family history of CAD only in the white girls, suggesting that this group is at increased risk of genetically mediated CAD. |
| Low density lipoprotein cholesterol: is lower better? Leiter, L. A. (2000), Can J Cardiol 16 Suppl A: 20A-2A. Abstract: Low density lipoprotein cholesterol (LDL-C) reduction leads to significant decreases in coronary events, as well as in most large trials performed recently, cardiovascular and total mortality. The lowest risk of coronary events occurs among people with the lowest LDL-C levels. Achieving a target LDL-C level less than 2.5 mM in individuals at high risk of a coronary event often necessitates the use of lipid-lowering drugs, primarily statins. Review of the major clinical trials involving statins reveals that LDL-C reduction is associated with a significant reduction in coronary events in men and women, older individuals, those with various other risk factors and those with either coronary artery disease or a high risk of developing it. The greatest clinical benefits have been associated with the greatest LDL-C reductions, although the incremental benefit is less at lower levels. Ongoing studies will help determine optimal new treatment targets for LDL-C. |
| Low density lipoprotein in neonates with high cord serum cholesterol levels Sanchez-Muniz, F. J., S. Bastida, et al. (1997), Acta Paediatr 86(4): 414-8. Abstract: Differences in cord serum low density lipoprotein (LDL) composition between male and female neonates with normal or high (> or = 100 mg/dl or > or = 2.59 mmol/l) serum cholesterol levels were studied in 548 full-term newborn infants of the Toledo Study (Spain), where the absence of known perinatal factors that would alter lipid levels in cord blood was confirmed. The percentage of females with a high serum total cholesterol (TC) level was higher (p < 0.02) than that of males. ANOVA two-way analysis shows significant interaction of gender and cholesterol level upon LDL-cholesterol, triglycerides and LDL-cholesterol/Apoprotein (Apo) B ratio. However, Apo B was higher in those neonates, both male and female, with high cholesterol levels. The LDL fraction carried about 55% of TC in females with high TC levels (HF), whereas it transported just 40% in males with high TC levels (HM). LDL appeared more enriched in cholesterol than in Apo B in HF than in HM (p < 0.01). An increased level of small LDL particles should be associated with the higher triglyceride level found amongst HM. Results in LDL composition suggest that metabolic gender-related differences in infants with normal or high TC are presented at birth. |
| Low density lipoprotein is protected from oxidation and the progression of atherosclerosis is slowed in cholesterol-fed rabbits by the antioxidant N,N'-diphenyl-phenylenediamine Sparrow, C. P., T. W. Doebber, et al. (1992), J Clin Invest 89(6): 1885-91. Abstract: The oxidative modification of low density lipoprotein (LDL) may play an important role in atherosclerosis. We found that the antioxidant N,N'-diphenyl-1,4-phenylenediamine (DPPD) inhibits in vitro LDL oxidation at concentrations much lower than other reported antioxidants. To test whether DPPD could prevent atherosclerosis, New Zealand White rabbits were fed either a diet containing 0.5% cholesterol and 10% corn oil (control group) or the same diet also containing 1% DPPD (DPPD-fed group) for 10 wk. Plasma total cholesterol levels were not different between the two groups, but DPPD feeding increased the levels of triglyceride (73%, P = 0.007) and HDL cholesterol (26%, P = 0.045). Lipoproteins from DPPD-fed rabbits contained DPPD and were much more resistant to oxidation than control lipoproteins. After 10 wk, the DPPD-fed animals had less severe atherosclerosis than did the control animals: thoracic aorta lesion area was decreased by 71% (P = 0.0007), and aortic cholesterol content was decreased by 51% (P = 0.007). Although DPPD cannot be given to humans because it is a mutagen, our results indicate that orally active antioxidants can have antiatherosclerotic activity. This strongly supports the theory that oxidized LDL plays an important role in the pathogenesis of atherosclerosis. |
| Low density lipoprotein modification by cholesterol oxidase induces enhanced uptake and cholesterol accumulation in cells Aviram, M. (1992), J Biol Chem 267(1): 218-25. Abstract: Oxidation of low density lipoprotein (LDL) by cells of the arterial wall or in the presence of copper ions was shown to result in the peroxidation of its fatty acids as well as its cholesterol moiety. LDL incubation with cholesterol oxidase (CO) resulted in the conversion of up to 85% of the lipoprotein unesterified cholesterol (cholest-5-en-3-ol) to cholestenone (cholest-4-en-3-one) in a dose- and time-dependent pattern. Plasma very low density lipoprotein (VLDL) and high density lipoprotein (HDL) could be similarly modified by CO. In cholesterol oxidase-modified LDL (CO-LDL), unlike copper ion-induced oxidized LDL (Cu-Ox-LDL), there was no fatty acids peroxidation, and lipoprotein size or charge as well as LDL cholesteryl ester, phospholipids, and triglycerides content were not affected. CO-LDL, however, demonstrated enhanced susceptibility to oxidation by copper ions in comparison to native LDL. Upon incubation of CO-LDL with J-774 A.1 macrophage-like cell line, cellular uptake and degradation of the lipoprotein was increased by up to 62% in comparison to native LDL but was 15% lower than that of Cu-Ox-LDL. Similarly, the binding of CO-LDL to macrophages increased by up to 80%, and cellular cholesterol mass was increased 51% more than the mass obtained with native LDL. Several lines of evidence indicate that CO-LDL was taken up via the LDL receptor: 1) Excess amounts of unlabeled LDL, but not acetyl-LDL (Ac-LDL), effectively competed with 125I-CO-LDL for the uptake by cells. 2) The degradation of CO-LDL by various types of macrophages and by fibroblasts could be dissociated from that of Ac-LDL and was always higher than that of native LDL. 3) A monoclonal antibody to the LDL receptor (IgG-C7) and a monoclonal antibody to the LDL receptor binding domains on apoB-100 (B1B6) inhibited macrophage degradation of CO-LDL. The receptor for Cu-Ox-LDL, which is not shared with Ac-LDL, was also partially involved in macrophage uptake of CO-LDL, since Cu-Ox-LDL demonstrated some competition capability with CO-125I-LDL for its cellular degradation. CO-LDL cellular degradation was inhibited by chloroquine, thus implying lysosomal involvement in the cellular processing of the lipoprotein. Incubation of macrophages with LDL in the presence of increasing concentrations of cholestenone resulted in up to 52% enhanced lipoprotein cellular degradation suggesting that the cholestenone in CO-LDL might be involved in the enhanced cellular uptake of the modified lipoprotein.(ABSTRACT TRUNCATED AT 400 WORDS) |
| Low density lipoprotein receptor activity in human intracranial tumors and its relation to the cholesterol requirement Rudling, M. J., B. Angelin, et al. (1990), Cancer Res 50(3): 483-7. Abstract: The receptor binding of low density lipoprotein (LDL) was determined in homogenates of surgically removed specimens from primary and metastatic intracranial tumors and in some cases also from surrounding brain. Seventy-one specimens from 63 patients were analyzed. In a subsample of 16 specimens from 13 patients, the activity of 3-hydroxy-3-methylglutaryl-CoA reductase was assayed in parallel. The LDL binding in the tumors varied over a wide range. A significantly higher LDL binding activity was found when all tumor samples were compared to brain (P less than 0.05). In the three patients where LDL receptor and 3-hydroxy-3-methylglutaryl-CoA reductase activities were assayed in both tumor tissue and surrounding brain, it was found that the receptor or the enzyme activity was increased in the tumors. It is suggested that certain intracranial tumors have an increased cholesterol requirement and that this may be fulfilled by an enhanced LDL receptor activity or an increased 3-hydroxy-3-methylglutaryl-CoA reductase activity. The data indicate that the LDL receptor activity may be regulated independently of the reductase in intracranial tumors. |
| Low dose chlordecone pretreatment altered cholesterol disposition without induction of cytochrome P-450 Carpenter, H. M. and L. R. Curtis (1991), Drug Metab Dispos 19(3): 673-8. Abstract: Pretreatment of mice with low doses of chlordecone (CD) alters the pattern of distribution of a subsequent tracer dose of 14CCD. We call this preexposure effect a pretreatment disposition response (PDR) and suggest that it reflects important cellular responses to lipophilic compounds. The present study examined three possible mechanisms for CD-induced PDR (CD-PDR). The first was that CD-PDR occurred with induction of the cytochrome P-450 system. A cumulative dose of 45 mg/kg CD caused a PDR, increased the content of cytochrome P-450, and elevated the activities of ethoxyresorufin- and ethoxycoumarin-O-deethylases (EROD and ECOD). A cumulative dose of 10 mg/kg caused a PDR, but did not affect cytochrome P-450, EROD, or ECOD, indicating that an induction of the cytochrome P-450 system in not necessary for PDR. A second possibility examined was that CD-PDR resulted because of an altered affinity of a subcellular fraction. Following a pretreatment regimen designed to produce PDR, amounts of 14CCD in each fraction paralleled homogenate values in the liver and the kidney. However, when values were calculated as percentages of total label recovered, it was apparent that 14CCD levels were higher in the microsomal fraction of the liver. Finally, the possibility that CD-PDR occurred because of an interaction of CD with proteins involved in cholesterol synthesis and transport was addressed. CD pretreatment increased disposition of a dose of 14Ccholesterol to the fat at the expense of 14Ccholesterol in the liver and kidney. |
| Low dose continuously infused growth hormone results in increased lipoprotein(a) and decreased low density lipoprotein cholesterol concentrations in middle-aged men Oscarsson, J., M. Ottosson, et al. (1994), Clin Endocrinol (Oxf) 41(1): 109-16. Abstract: OBJECTIVE: Animal studies have shown that slight increases in basal GH concentrations may result in changes in lipoprotein metabolism. Such changes in GH secretion have been observed in physiological and pathophysiological states such as fasting, uncontrolled diabetes and during oestrogen treatment. The aim of this study was to investigate the possible effects of increases in basal plasma GH concentrations on lipoprotein concentrations. DESIGNS: Recombinant human growth hormone (rhGH) was given as a continuous subcutaneous infusion in a low dose (0.02 U/kg/day) in an open study. PATIENTS: Eight middle-aged (42-59 years) overweight (body mass index: 26.1-33.8 kg/m2) but otherwise healthy men were studied over a period of 14 days. MEASUREMENTS: Blood samples were obtained after an over-night fast before and after 2, 7 and 14 days of treatment. Plasma and serum were separated and used for subsequent measurements of hormone and lipoprotein concentrations. On days 0, 7 and 14 of treatment, post-heparin plasma was also obtained for determinations of plasma lipoprotein lipase and hepatic lipase activities. In addition, a hyperinsulinaemic euglycaemic glucose clamp was performed on days 0 and 13 of the study. Fat biopsies from abdominal and gluteal fat depots were obtained for measurement of lipoprotein lipase activities on days 0 and 14 of the study. RESULTS: Serum GH concentrations increased to a steady level of 2-4 mU/l during treatment. Serum insulin-like growth factor-I (IGF-I) concentrations increased throughout the treatment period to twice the pretreatment levels. Plasma insulin and blood glucose concentrations increased on day 2 of treatment. After 7 and 14 days of treatment blood glucose concentrations were not different from pretreatment levels, but plasma insulin concentrations were still elevated. Serum cholesterol and low density lipoprotein (LDL) cholesterol concentrations had decreased after 7 and 14 days of treatment. High density lipoprotein (HDL) cholesterol concentrations were not affected, but very low density lipoprotein (VLDL) cholesterol and triglyceride concentrations increased transiently at day 2 of treatment. Serum apolipoprotein (apo) A-I, apoB and apoE concentrations were not significantly affected. Serum lipoprotein(a) concentrations had increased by days 7 and 14 to 147 and 142% of pretreatment concentrations, respectively. Lipoprotein lipase and hepatic lipase activities in post-heparin plasma, as well as abdominal and gluteal adipose tissue lipoprotein lipase activities, were not affected. There was no significant change in glucose disposal rate estimated from the glucose clamp studies. CONCLUSIONS: A low dose infusion of GH results in marked changes in lipoprotein concentrations with a transient increase in VLDL cholesterol and thereafter in a decrease in LDL cholesterol. In addition, this low dose of GH resulted in marked increases in lipoprotein(a) concentrations. The observed effects of GH may partly involve changes in IGF-I and insulin secretion. |
| Low frequency electrical impulses reduce atherosclerosis in cholesterol fed rabbits Chekanov, V. S. (2003), Med Sci Monit 9(8): BR302-9. Abstract: BACKGROUND: This investigation studied whether low frequency electrical impulses (EI) induce or prevent development of new atherosclerotic plaque in previously diseased vessels. MATERIAL/METHODS: In all rabbits, an electrode was sutured to the left psoas major muscle close to the upper part of the abdominal aorta (AA), and a pacemaker was implanted on the opposite side of the AA just below diaphragm. Group 1 received a high cholesterol diet (HCD) to induce atherosclerosis but no EI (control). Euthanasia followed after 3 weeks (series I), 8 weeks (series II) and 11 weeks (series III) of HCD. In series IV animals received HCD alone for 3 weeks then EI was added to the HCD for another 8 weeks (weeks 4-11) at a rate of 30 impulses per minute (IPM) at 3V. Euthanasia followed after 11 weeks. Atherosclerotic thickness grades were assigned using a 0 (low) to 4 (high) grading system, and the surface area involved in disease was calculated. RESULTS: In control rabbits, after 11 weeks of HCD atherosclerotic thickness grade in lower abdominal aorta was 1.68 +/-0.25. In rabbits exposed to EI (30 IPM at 3V) this grade was 0.5+/-0.37 (p<0.05). The involved surface area was only 8.5+/-4.69% (series IV) vs. 32.5+/-4.0 % in control CONCLUSIONS: When applied near the AA, electrical impulses (30 IPM at 3V) decrease atherosclerotic deposits despite continuation of a high cholesterol diet. |
| Low HDL cholesterol concentration is associated with increased intima-media thickness independent of arterial stiffness in healthy subjects from families with low HDL cholesterol Alagona, C., A. Soro, et al. (2003), Eur J Clin Invest 33(6): 457-63. Abstract: BACKGROUND: Low high-density lipoprotein cholesterol (HDL-C) is associated with increased risk for developing coronary artery disease. Cardiovascular disease is characterized by increased intima-media thickness (IMT) and arterial stiffness, but the effect of low HDL on these measurements has not been reported. MATERIALS AND METHODS: We studied 18 apparently healthy subjects from families with low HDL-C and 18 control subjects, which were pair-matched to maximize statistical power. Intima-media thickness was assessed using ultrasound examination of the carotid arteries. Arterial stiffness was measured using applanation tonometry on the radial artery and pulse-wave analysis to obtain central aortic pulse-pressure waveform, from which the augmentation index, a measure of global large artery stiffness, was calculated. RESULTS: Low HDL subjects (age 41 +/- 3 years, BMI 26.6 +/- 1.0 kg m(-2) had significantly lower HDL-C than the control subjects (age 41 +/- 3 years, BMI 26.5 +/- 1.0 kg m-2; 1.00 +/- 0.05 vs. 1.49 +/- 0.09 mmol L-1, low HDL vs. control subjects, P < 0.0001). Subjects with low HDL-C had significantly thicker mean IMTs than the control subjects (0.77 +/- 0.03 vs. 0.70 +/- 0.02 mm, low HDL vs. control subjects, P < 0.01). The maximal (0.99 +/- 0.04 vs. 0.89 +/- 0.03 mm, P < 0.01), far wall (0.76 +/- 0.04 vs. 0.69 +/- 0.02 mm, P < 0.05) and carotid bulb (1.11 +/- 0.06 vs. 0.97 +/- 0.04 mm) IMTs were also significantly increased, whereas the mean common carotid and the internal artery IMT were not. The age-related increase in mean IMT was more pronounced in the low HDL subjects than the control subjects (P < 0.01 for difference between elevations of age vs. IMT slopes). There were no differences in central pressure augmentation, the augmentation index, peripheral or central blood pressures between the groups. CONCLUSIONS: A low HDL-C concentration is associated with thickening of carotid IMT independent of other risk factors in healthy affected members of low HDL families. |
| Low HDL cholesterol, aggression and altered central serotonergic activity Buydens-Branchey, L., M. Branchey, et al. (2000), Psychiatry Res 93(2): 93-102. Abstract: Many studies support a significant relation between low cholesterol levels and poor impulse, aggression and mood control. Evidence exists also for a causal link between low brain serotonin (5-HT) activity and these behaviors. Mechanisms linking cholesterol and hostile or self-destructive behavior are unknown, but it has been suggested that low cholesterol influences 5-HT function. This study was designed to explore the relationship between plasma cholesterol, measures of impulsivity and aggression, and indices of 5-HT function in personality disordered cocaine addicts. Thirty-eight hospitalized male patients (age 36.8+/-7.1) were assessed with the DSM-III-R, the Buss-Durkee Hostility Inventory (BDHI), the Barratt Impulsiveness Scale (BIS) and the Brown-Goodwin Assessment for Life History of Aggression. Fasting basal cholesterol (total, LDL and HDL) was determined 2 weeks after cocaine discontinuation. On the same day 5-HT function was assessed by neuroendocrine (cortisol and prolactin) and psychological (NIMH and 'high' self-rating scales) responses following meta-chlorophenylpiperazine (m-CPP) challenges. Reduced neuroendocrine responses, 'high' feelings and increased 'activation-euphoria' following m-CPP have been interpreted as indicating 5-HT alterations in a variety of psychiatric conditions. Significantly lower levels of HDL cholesterol were found in patients who had a history of aggression (P=0.005). Lower levels of HDL cholesterol were also found to be significantly associated with more intense 'high' and 'activation-euphoria' responses as well as with blunted cortisol responses to m-CPP (P=0.033, P=0.025 and P=0.018, respectively). This study gives further support to existing evidence indicating that in some individuals, the probability of exhibiting impulsive and violent behaviors may be increased when cholesterol is low. It also suggests that low cholesterol and alterations in 5-HT activity may be causally related. |
| Low HDL cholesterol: what are the prospects of increasing it? Ginsberg, H. N. (1995), Ann Med 27(3): 283-4. |
| Low HDL-cholesterol Schmitz, G. and K. J. Lackner (2000), Internist (Berl) 41(7): 675. |
| Low HDL-cholesterol, high triglycerides--well known but often ignored Benz, R. and P. M. Suter (2004), Schweiz Rundsch Med Prax 93(46): 1911-6. Abstract: A reduced HDL-Cholersterol and increased triglyzerides are an often seen laboratory abnormality. They are known risk factors for arteriosclerosis. However the small influence of a pharamcologic treatment on the two reduced the interest in them. We therefore want to show the relation of the triglyzerides with the HDL-Cholesterol and the nonpharmacologic treatment of these two factors. Some clinical examples are illustrating the topic. |
| Low HDL-cholesterol: a component of the metabolic syndrome only in the presence of fasting hypertriglyceridemia in type 2 diabetic patients Bo, S., P. Cavallo-Perin, et al. (2001), Diabetes Metab 27(1): 31-5. Abstract: The relation between isolated low HDL-cholesterol and the components of the metabolic syndrome is poorly known in type 2 diabetes. We evaluated cardiovascular risk parameters in type 2 diabetic patients with low HDL-cholesterol, compared to those with low HDL-cholesterol and hypertriglyceridemia, isolated hypertriglyceridemia and normal lipid parameters. Patients with low HDL-cholesterol/high triglycerides had higher BMI (29.6 +/- 5.7 vs 27.9 +/- 4.4 or vs 28.1 +/- 5.2 kg/m(2)), prevalence of obesity (69% vs 55% or vs 54%), higher levels of uric acid (339.0 +/- 83.3 vs 303.3 +/- 95.2 or vs 303.3 +/- 89.2 micromol/l) and C-peptide (0.76 +/- 0.40 vs 0.63 +/- 0.33 or vs 0.63 +/- 0.36 nmol/l) and number of components of the metabolic syndrome (27% patients with all the components) compared to patients with isolated low HDL-cholesterol or normal subjects, respectively. A similar pattern of values was evident in patients with isolated hypertriglyceridemia. With logistic regression analysis, BMI and uric acid levels were significantly associated with the presence of hypertriglyceridemia (both isolated or associated with low HDL-cholesterol), while patients with isolated low HDL-cholesterol and those without dyslipidemia displayed a similar more favourable metabolic pattern. These results indicate that low HDL-cholesterol is a component of the metabolic syndrome only in the presence of fasting hypertriglyceridemia in type 2 diabetic patients. |
| Low high-density lipoprotein cholesterol and response to simvastatin therapy in Scandinavian Simvastatin Survival Study (4S) Robins, S. (2002), Circulation 106(2): e8; author reply e8. |
| Low high-density lipoprotein cholesterol and what to do about it Kannel, W. B. (1992), Am J Cardiol 70(7): 810-4. |