| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
| First Page | Previous Page | Next Page | Last Page |
| By the way, doctor. As a regular reader of your newsletter, I have a pretty good idea of what a healthy person's cholesterol and triglyceride levels should be. But last year, I had a couple of tests, and the results were completely different. According to the first, my triglycerides were 285, my HDL 31, and my LDL 109. Eight months later, the same measurements came in at 175, 44, and 109. What could cause such a big swing? Is it something I should be worried about? Lee, T. H. (2002), Harv Health Lett 27(5): 8. |
| By the way, doctor. Ever since the 1960s, I haven't eaten more than one egg a week because egg yolks have a lot of cholesterol. Now my wife says she heard on the news that it's okay to eat eggs every day. What do you think? Komaroff, A. L. (2005), Harv Health Lett 30(6): 8. |
| By the way, doctor. I am a 67-year-old woman. I walk three miles five or six times a week and swim for half an hour every day. I take a diuretic for high blood pressure, a calcium supplement, and vitamins C and E. My HDL level is usually over 100, but it was up to 147 in my most recent cholesterol test (my total cholesterol was 223 and my LDL was 68). Should I be celebrating or worried about an unusually high HDL? Komaroff, A. L. (2004), Harv Health Lett 29(11): 8. |
| By the way, doctor. I just got my cholesterol checked, and I'm confused. LDL is bad and HDL is good, so how can they be combined into an overall number that makes any sense? Isn't that like an accountant mixing debits with credits? Wouldn't it make more sense to have a net cholesterol number (HDL minus LDL), or perhaps a ratio? Lee, T. H. (2003), Harv Health Lett 28(11): 8. |
| By the way, doctor. I take 20 mg of Lipitor and 10 mg of Zetia. My total cholesterol has declined from 177 to 145, my LDL from 133 to 93, but my "good" HDL cholesterol also went down from 46 to 41. Would you consider my low HDL level a large risk factor? If so, is there a regimen that would increase it? Komaroff, A. L. (2005), Harv Health Lett 30(3): 8. |
| By the way, doctor. I've been taking Lipitor to control my cholesterol for four years. I don't want to have a heart attack like my mother did, but is it safe to take this medication for years on end? Robb-Nicholson, C. (2004), Harv Womens Health Watch 11(10): 8. |
| By the way, doctor. I've recently heard about a new cholesterol drug called Zetia. Does it work better than a statin? Robb-Nicholson, C. (2004), Harv Womens Health Watch 11(7): 8. |
| By the way, doctor. My husband's total cholesterol was 71 for a few months. he cut back on his statin and now it's in the low 90s. His HDL is 50 and his LDL in the 40s. Should we be worried about such low levels? Lee, T. H. (2003), Harv Health Lett 29(2): 8. |
| By the way, doctor. Should I test my cholesterol at home? I recently saw an ad for a cholesterol test kit for home use. It seems like a good way to keep track of my cholesterol. Is there any reason not to use something like this? Robb-Nicholson, C. (2002), Harv Womens Health Watch 9(12): 8. |
| By the way, doctor.I read about Baycol, the cholesterol-lowering drug being taken off the market because it caused fatal muscle damage. I don't take it, but I do take another statin. Should I be worried? Lee, T. H. (2001), Harv Health Lett 27(1): 8. |
| By the way, doctor.My doctor tells me that because I have diabetes and moderately high "bad" LDL cholesterol, I should be taking a statin. Is there any statin that's better than the rest? And what side effects should I be concerned about? Lee, T. H. (2001), Harv Health Lett 26(10): 8. |
| C(27)-steroid hormones calcitriol and ecdysterone activates hydrolysis of neutral lipids--cholesterol esters and triacylglycerols--in its early pregenomic phase of action Kotsiuruba, A. V., O. M. Bukhanevich, et al. (1998), Ukr Biokhim Zh 70(5): 30-7. Abstract: We have examined in vivo capacities of two C27-steroid hormones-phytoecdysteroid ecdysterone (20-hydroxyecdysone, 10(-8)M) and calcitriol (1 alpha, 25-dihydroxyvitamin D3, 10(-12)M), as a modulators of neutral lipids hydrolysis in the brain and heart cells. Severe lines of evidence indicate that both hormones may acts as positive regulators of cholesterol esters and triacylglycerol hydrolysis in early (0.5-30 min) pregenomic phase of its actions, yielding known (DAG, free polyunsaturated fatty acids) and possible (free cholesterol) lipid second messengers. |
| CA 19.9 and HDL-cholesterol behaviour in a sporadic colorectal carcinoma sample Mendez Mora, J. L., M. Ortega Calvo, et al. (2004), An Med Interna 21(5): 227-30. Abstract: BACKGROUND AND OBJECTIVE: We have carried out a comparative prediction analysis in sporadic colorectal carcinoma of plasmatic lipids and currently tumor markers used in this neoplasia (carcinoembrionary antigen - CEA, CA 19.9 and sialic acid -SA). PATIENTS AND METHODS: Transversal hospital-based case-control study. Sample was composed by 53 sporadic colorectal neoplasia patients just before surgery and 40 non matched controls. A 90 per cent of cases were at Dukes A and B stages. A multivariable model was fitted with non-conditional logistic regression. Confidence intervals were calculated at 95 per cent of confidence. Model sensibility and specificity were performed at 50 per cent cutting point. We also explored possible interactions. RESULTS: All three tumor markers (CEA, CA 19.9 and SA) were elevated in cases (p<0.01). Multivariable model included: Total cholesterol (TC) (OR= 0.69; CI: 0.50-0.96) high density lipoprotein fraction (HDL) (OR = 0.30; CI: 0.11-0.83) very low density lipoprotein fraction (VLDL) (OR = 2.21; CI = 1.07-4.55) years of age (OR = 1.11; CI = 0.98-1.26) CA 19.9 (OR = 1.20; CI = 1.02-1.42) and alkaline phosphatase (OR = 1.09; CI = 1.01 - 1.19). No interactions were found out. Model sensibility reached 96.23% and a specificity of 92.50%. CONCLUSIONS: HDL showed a similar diagnostic strength than CA 19.9 in this sporadic colorectal carcinoma sample but with an inverse OR. This multivariable model is going to be validated. |
| Ca2+ mobilization in the aortic endothelium in streptozotocin-induced diabetic and cholesterol-fed mice Kamata, K. and M. Nakajima (1998), Br J Pharmacol 123(8): 1509-16. Abstract: 1. Experiments were performed to compare Ca2+ mobilization in the aortic endothelium in streptozotocin (STZ)-induced diabetic and cholesterol-fed mice with that in age-matched controls. 2. The intracellular free Ca2+ (Ca2+i) in the fura PE-3 loaded endothelium of aortic rings was dose-dependently increased by cumulative administration of acetylcholine (ACh). ACh caused a transient rise in Ca2+i in Ca2+-free medium. The ACh-induced increase in Ca2+i in normal or Ca2+-free medium was significantly weaker in both STZ-induced diabetic and cholesterol-fed mice. 3. The weaker Ca2+i response in Ca2+-containing medium in STZ-induced diabetic and cholesterol-fed mice was normalized by chronic administration of cholestyramine. 4. The increased low density lipoprotein (LDL) levels seen in both STZ-induced diabetic and cholesterol-fed mice were normalized by the same chronic administration of cholestyramine (300 mg kg(-1), p.o. daily for 10 weeks). Chronic administration of cholestyramine had no effect on the plasma glucose level. 5. Lysophosphatidylcholine (LPC) decreased the Ca2+i responses to ACh in the aortic endothelium from normal mice. 6. These results suggest that ACh increases both Ca2+ influx and Ca2+ release from storage in the aortic endothelium. The weaker Ca2+i influx seen in the endothelium of aortae from both STZ-induced diabetic and cholesterol-fed mice was improved by the chronic administration of cholestyramine, and we suggest that this improvement is due, at least in part, to a lowering of the plasma LDL level. It is further suggested that LPC may have an important influence over Ca2+ mobilization in the endothelium. |
| Caecal and colonic uptake of both linoleic acid and cholesterol in rats following intestinal resection Molina, M. T., V. Ruiz-Gutierrez, et al. (1990), Lipids 25(10): 594-7. Abstract: Caecal and colonic uptake of both linoleic acid and cholesterol were studied in rats after distal small bowel resection (DSBR). The results showed that the surgical operation increased the caecal and colonic uptake of linoleic acid. Supplementation with linolenic acid inhibited caecal and colonic uptake of linoleic acid. Experiments carried out in the presence of rotenone and ouabain suggest that facilitated diffusion is the predominant mechanism of caecal and colonic linoleic acid absorption, at least at low concentrations. An increase in caecal and colonic uptake of cholesterol was observed after the surgical operation. The study showed that facilitated diffusion seems to be the mechanism of linoleic acid absorption in the caecum and colon, and that both organ growth and changes in transport function of the epithelial cells of caecum and colon appear to be involved in the adaptive response of the bowel to intestinal resection. |
| Cafestol increases serum cholesterol levels in apolipoprotein E*3-Leiden transgenic mice by suppression of bile acid synthesis Post, S. M., B. de Roos, et al. (2000), Arterioscler Thromb Vasc Biol 20(6): 1551-6. Abstract: Cafestol, a diterpene present in unfiltered coffee, potently increases serum cholesterol levels in humans. So far, no suitable animal model has been found to study the biochemical background of this effect. We determined the effect of cafestol on serum cholesterol and triglycerides in different mouse strains and subsequently studied its mechanism of action in apolipoprotein (apo) E*3-Leiden transgenic mice. ApoE*3-Leiden, heterozygous low density lipoprotein-receptor (LDLR+/-) knockout, or wild-type (WT) C57BL/6 mice were fed a high- (0.05% wt/wt) or a low- (0.01% wt/wt) cafestol diet or a placebo diet for 8 weeks. Standardized to energy intake, these amounts are equal to 40, 8, or 0 cups of unfiltered coffee per 10 MJ per day in humans. In apoE*3-Leiden mice, serum cholesterol was statistically significantly increased by 33% on the low- and by 61% on the high-cafestol diet. In LDLR+/- and WT mice, the increases were 20% and 24%, respectively, on the low-cafestol diet and 55% and 46%, respectively, on the high-cafestol diet. These increases were mainly due to a rise in very low density lipoprotein (VLDL) and intermediate density lipoprotein cholesterol in all 3 mouse strains. To investigate the mechanism of this effect, apoE*3-Leiden mice were fed a high-cafestol or a placebo diet for 3 weeks. Cafestol suppressed enzyme activity and mRNA levels of cholesterol 7alpha-hydroxylase by 57% and 58%, respectively. mRNA levels of enzymes involved in the alternate pathway of bile acid synthesis, ie, sterol 27-hydroxylase and oxysterol 7alpha-hydroxylase, were reduced by 32% and 48%, respectively. The total fecal bile acid output was decreased by 41%. Cafestol did not affect hepatic free and esterified cholesterol, but it decreased LDLR mRNA levels by 37%. The VLDL apoB and triglyceride production rates, as measured after Triton injection, were 2-fold decreased by cafestol, indicating that the number of particles secreted had declined and that there was no change in the amount of triglycerides present in the VLDL particle during cafestol treatment. However, the VLDL particles contained a 4-times higher amount of cholesteryl esters, resulting in a net 2-fold increased secretion of cholesteryl esters. The decrease in triglyceride production was the result of a reduction in hepatic triglyceride content by 52%. In conclusion, cafestol increases serum cholesterol levels in apoE*3-Leiden mice by suppression of the major regulatory enzymes in the bile acid synthesis pathways, leading to decreased LDLR mRNA levels and increased secretion of hepatic cholesterol esters. We suggest that suppression of bile acid synthesis may provide an explanation for the cholesterol-raising effect of cafestol in humans. |
| Cafestol, the cholesterol-raising factor in boiled coffee, suppresses bile acid synthesis by downregulation of cholesterol 7 alpha-hydroxylase and sterol 27-hydroxylase in rat hepatocytes Post, S. M., E. C. de Wit, et al. (1997), Arterioscler Thromb Vasc Biol 17(11): 3064-70. Abstract: Consumption of boiled coffee raises serum cholesterol levels in humans. The diterpenes cafestol and kahweol in boiled coffee have been found to be responsible for the increase. To investigate the biochemical background of this effect, we studied the effects of cafestol and a mixture of cafestol/kahweol/isokahweol (48:47:5 w/w) on bile acid synthesis and cholesterol 7 alpha-hydroxylase and sterol 27-hydroxylase in cultured rat hepatocytes. Dose-dependent decreases of bile acid mass production and cholesterol 7 alpha-hydroxylase and sterol 27-hydroxylase activity were found, showing a maximal reduction of -91%, -79%, and -49% respectively, at a concentration of 20 micrograms/mL cafestol. The decrease in 7 alpha-hydroxylase and 27-hydroxylase activity paralleled well the suppression of the respective mRNAs, being -79% and -77%, and -49% and -46%, respectively, at 20 micrograms/mL cafestol. Run-on data showed a reduction in 7 alpha-hydroxylase and 27-hydroxylase gene transcriptional activity after incubation with cafestol. The mixture of cafestol/kahweol/isokahweol was less potent in suppression of bile acid synthesis and cholesterol 7 alpha-hydroxylase. Cafestol (20 micrograms/mL) had no effect on lithocholic acid 6 beta-hydroxylase mRNA, another enzyme involved in bile acid synthesis. LDL-receptor, HMG-CoA reductase, and HMG-CoA synthase mRNAs were significantly decreased by cafestol (-18%, -20%, and -43%, respectively). We conclude that cafestol suppresses bile acid synthesis by downregulation of cholesterol 7 alpha-hydroxylase and of, to a lesser extent, sterol 27-hydroxylase in cultured rat hepatocytes, whereas kahweol and isokahweol are less active. We suggest that suppression of bile acid synthesis may provide an explanation for the cholesterol-raising effect of cafestol in humans. |
| Caffeinated and decaffeinated coffee effects on plasma lipoprotein cholesterol, apolipoproteins, and lipase activity: a controlled, randomized trial Superko, H. R., W. Bortz, Jr., et al. (1991), Am J Clin Nutr 54(3): 599-605. Abstract: Coffee consumption has been associated with elevated plasma cholesterol. One hundred eighty-one men consumed a standard caffeinated coffee for 2 mo followed by randomization to continue caffeinated coffee (control), change to decaffeinated coffee or no coffee for 2 mo. Plasma low-density-lipoprotein (LDL) cholesterol and apolipoprotein B concentrations increased significantly (0.12 +/- 0.65 mmol/L, P less than 0.025; 0.06 +/- 0.12 g/L, P less than 0.0004, respectively) in the group that changed to decaffeinated coffee. In a subgroup (n = 51), post-heparin lipoprotein lipase decreased significantly more (-270 mmol free fatty acids.L-1.h-1, P less than 0.003) in the decaffeinated-coffee group. Resting heart rate and blood pressure did not change significantly. Change from caffeinated to decaffeinated coffee increased plasma LDL cholesterol and apolipoprotein B whereas discontinuation of caffeinated coffee revealed no change. This finding suggests that a coffee component other than caffeine is responsible for the LDL cholesterol, apolipoprotein B, and lipase activity changes reported in this investigation. |
| Caffeine and cholesterol: interactions with hostility Lane, J. D., C. F. Pieper, et al. (1994), Psychosom Med 56(3): 260-6. Abstract: The consumption of caffeinated beverages has been linked to elevated serum cholesterol and an increased risk of coronary disease, although the relationships are inconsistent across studies and remain controversial. The effect of caffeine on cholesterol and coronary disease risk may be modulated by other factors. Using cohort data from a subsample of the University of North Carolina Alumni Heart Study, we investigated whether the relationships between caffeinated beverage consumption and serum lipid and lipoprotein levels in middle-aged men and women were modulated by levels of trait hostility. After adjustment for other risk factors, higher caffeinated beverage intake was associated with higher low-density lipoprotein cholesterol levels and a higher ratio of total to high-density lipoprotein cholesterol, both indicative of greater coronary disease risk. The interactive effects of hostility and caffeine intake were ambiguous, although there were trends for caffeine intake to have stronger effects on low-density lipoprotein and on total cholesterol in people with less hostility. Additional studies of personality characteristics and other factors that can modulate the cholesterol-raising effects of coffee drinking may be warranted because they might clarify the health consequences associated with coffee drinking and lead to the identification of individuals who would benefit most from changes in their coffee drinking. |
| Calcification of aortic wall in cholesterol-fed rabbits Rokita, E., T. Cichocki, et al. (1991), Atherosclerosis 87(2-3): 183-93. Abstract: Development of the mineralization process in the course of atherogenesis was studied using the cholesterol-fed rabbit model. The aorta samples were investigated by means of proton and electron microprobes, infrared spectroscopy and X-ray diffraction as well as selected histochemical staining. Blood serum was analysed every 2 weeks to determine the content of cholesterol, triglycerides, inorganic phosphorus, ionized calcium, elemental composition as well as activity of alkaline phosphatase. It was found that the administered diet did not disturb the calcium and phosphorus homeostasis. Histochemical findings confirmed the formation of lipid-rich lesions blocking the lumen of the vessel. The dystrophic calcification was observed only in the atheroma, while in the tunica media a slight mineralization similar to that found in controls was observed after 210 days of the diet. In the atheroma the only phase detected was a defective hydroxyapatite. The perfection of the crystals, as well as the diameter of the deposits, increased during the course of the diet reaching about 2 microns after 210 days. The crystals were not contaminated with carbonate groups regardless of the duration of the diet. |