| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Failure of the intracellular itinerary of beta very low density lipoproteins to augment cholesterol esterification in macrophages from Watanabe heritable hyperlipidemic rabbits Daugherty, A. and D. L. Rateri (1991), J Biol Chem 266(26): 17269-75. Abstract: beta very low density lipoproteins (beta-VLDL) interact with mouse peritoneal macrophages via specific receptors leading to pronounced stimulation of cholesterol esterification. The present study has defined an alternative pathway for the processing of beta-VLDL in alveolar macrophages from Watanabe heritable hyperlipidemic (WHHL) rabbits. Macrophages from either New Zealand (NZ) or WHHL rabbits degraded 125I-beta-VLDL to an equivalent extent. Degradation was competed to a similar extent in both cell types by either excess unlabeled beta-VLDL or low density lipoprotein, indicative of a specific receptor involvement. Accumulation of intracellular degradation products of beta-VLDL labeled with the residualizing label, dilactitol-125I-tyramine, was similar in both cell types demonstrating that degradation was not due to secreted proteolytic enzymes. beta-VLDL promoted the incorporation of 3Holeate into cholesteryl-3Holeate and increased the cellular mass of cholesterol in NZ macrophages. In contrast, beta-VLDL did not augment cholesteryl-3Holeate deposition in WHHL macrophages. This lack of cholesterol esterification occurred despite equivalent acyl-CoA:cholesterol acyltransferase activity in microsomal fractions of both cell types, and similar augmentations in cholesteryl-3Holeate during incubation with phospholipase C-treated LDL. Incubation of WHHL macrophages with beta-VLDL increased cellular cholesterol mass, although the response was attenuated compared to NZ cells. To determine whether these disparities in cholesterol esterification were related to the catabolic fate of beta-VLDL-derived cholesterol esters, 3Hcholesteryl oleate was exchanged into the core of beta-VLDL and incubated with macrophages in medium containing 14Coleate. NZ macrophages accumulated both 3Hcholesterol and 3Hcholesteryl-14Coleate after 5 h, indicating hydrolysis and re-esterification of cholesterol esters. In contrast, WHHL macrophages only accumulated 3Hcholesterol esters, suggesting uptake of cholesterol esters without subsequent hydrolysis. These data demonstrate that WHHL macrophages possess a pathway for the intracellular processing of beta-VLDL that permits internalization of the particle without stimulation of cholesterol esterification. |
| Failure to achieve recommended LDL cholesterol levels by suboptimal statin therapy relates to elevated cardiac event rates Baessler, A., M. Fischer, et al. (2005), Int J Cardiol 101(2): 293-8. Abstract: OBJECTIVES: The majority of patients with myocardial infarction (MI) and hypercholesterolaemia does not achieve guideline recommended low-density lipoprotein cholesterol (LDL) levels. Suboptimal dosages of statins explain this dilemma in most patients. DESIGN AND SETTING: We evaluated the relationship between statin treatment quality (optimal: LDL<115 mg/dl, suboptimal: LDL>/=115 mg/dl, no statin therapy despite hypercholesterolaemia) and the subsequent incidence of coronary events (coronary death, nonfatal MI, bypass surgery) over a 30 months follow-up in a large cohort of post MI patients with hypercholesterolaemia (n=2045). Analysis was performed in a nested case-control manner comparing 173 cases with a coronary event and 346 matched controls. RESULTS: Patients who developed a coronary event were treated optimally in 11.0%, suboptimally in 43.4% (p<0.05 vs. optimal treatment) and were untreated in 45.7% (p<0.001 vs. optimal treatment). Respective numbers in event-free patients were 21.4%, 47.7%, and 30.9%. After adjustment for most potential confounders, including all cardiovascular risk factors and medication, the relative risk of future non-fatal MI and coronary death associated with a suboptimal statin treatment was 2.02 (95% CI 1.04 to 4.18) compared to optimal statin treatment. Moreover, the statin equivalent dose in optimally treated individuals was significantly higher than in suboptimally treated individuals (0.85+/-0.03 vs. 0.78+/-0.02, p<0.05). CONCLUSION: In this community-based study, a lipid lowering therapy with statins into the recommended target range of LDL levels may be associated with decreased cardiovascular risk compared to a statin therapy without titrating the LDL level below 115 mg/dl. Thus, the quality of statin treatment was identified as an independent predictor of coronary events in post MI patients. |
| Failure to cleave sterol regulatory element-binding proteins (SREBPs) causes cholesterol auxotrophy in Chinese hamster ovary cells with genetic absence of SREBP cleavage-activating protein Rawson, R. B., R. DeBose-Boyd, et al. (1999), J Biol Chem 274(40): 28549-56. Abstract: We describe a line of mutant Chinese hamster ovary cells, designated SRD-13A, that cannot cleave sterol regulatory element-binding proteins (SREBPs) at site 1, due to mutations in the gene encoding SREBP cleavage-activating protein (SCAP). The SRD-13A cells were obtained by two rounds of gamma-irradiation followed first by selection for a deficiency of low density lipoprotein receptors and second for cholesterol auxotrophy. In the SRD-13A cells, the only detectable SCAP allele encodes a truncated nonfunctional protein. In the absence of SCAP, the site 1 protease fails to cleave SREBPs, and their transcriptionally active NH(2)-terminal fragments cannot enter the nucleus. As a result, the cells manifest a marked reduction in the synthesis of cholesterol and its uptake from low density lipoproteins. The SRD-13A cells grow only when cholesterol is added to the culture medium. SREBP cleavage is restored and the cholesterol requirement is abolished when SRD-13A cells are transfected with expression vectors encoding SCAP. These results provide formal proof that SCAP is essential for the cleavage of SREBPs at site 1. |
| Fall in cholesterol after changes in composition of cooking oil in Mauritius Chandrasekharan, N. and K. Sundram (1997), Bmj 314(7079): 516. |
| Fall in total cholesterol concentration over five years in association with changes in fatty acid composition of cooking oil in Mauritius: cross sectional survey Uusitalo, U., E. J. Feskens, et al. (1996), Bmj 313(7064): 1044-6. Abstract: OBJECTIVE: To determine the extent to which reducing the saturated fatty acid composition of a ubiquitously used cooking oil influenced changes in cholesterol concentration in the population during a five year intervention programme in Mauritius. DESIGN: Cross sectional surveys in 1987 and 1992 determined mean total cholesterol concentrations in the population. A random sample of respondents in the 1992 survey completed a nutrition questionnaire that included questions on diet in the previous 24 hours. SETTING: Mauritius. INTERVENTION: In 1987 the government of Mauritius changed the composition of the commonly used cooking oil from being mostly palm oil (high in saturated fatty acids) to being wholly soya bean oil (high in unsaturated fatty acids). SUBJECTS: 5080 and 5162 subjects in 1987 and 1992 cross sectional surveys. 2059 subjects aged 30-64 years were randomly selected from the respondents of the 1992 survey to take part in the nutrition survey. MAIN OUTCOME MEASURES: Fatty acid composition of phospholipids in pooled serum samples from men and women from the two surveys; measured and predicted change in serum cholesterol concentration. RESULTS: From 1987 to 1992 total cholesterol concentrations fell significantly by 0.79 mmol/l (P < 0.001) in men and 0.82 mmol/l (P < 0.001) in women. The estimated intake of saturated fatty acids decreased by 3.5% of energy intake in men and by 3.6% in women, and the intake of polyunsaturated fatty acids increased by 5.5% and 5.6% of energy intake, respectively. These changes were reflected in changes in the fatty acid composition of serum phospholipids, and according to Keys' formula these changes explained much of the decrease in serum cholesterol concentrations (predicted decrease of 0.38 mmol/l in men and by 0.40 mmol/l in women). CONCLUSION: Dietary changes that entailed a reduction in the saturated fat content of a ubiquitous cooking oil explained most of the observed decrease in serum cholesterol concentration over five years in the population of Mauritius. |
| False negative results in the Roche assay for HDL-cholesterol Bakker, A. J., A. Zijlstra, et al. (2003), Ann Clin Biochem 40(Pt 5): 572-5. Abstract: Measurement of HDL-cholesterol is important in the risk evaluation of cardiovascular disease. Recently, we encountered a 61-year-old man with a negative result for HDL-cholesterol using the Roche assay. Further analysis revealed that this patient had a monoclonal Ig type IgMkappa, with an electrophoresis-based concentration of 55.8 g/L, which apparently caused the negative result for HDL-cholesterol. Analysis of serum samples from other patients with monoclonal or polyclonal hypergammaglobulinaemia revealed that false negative results in the Roche assay for HDL-cholesterol may occur incidentally. Since negative results are detected easily in the laboratory, such patients do not pose a problem in daily practice. However, it is reasonable to suppose that false low results could also be caused by monoclonal as well as polyclonal Igs. Since such false low results remain undetected, vascular risk estimates consequently are altered and unnecessary treatment might be started. |
| Falsely low direct HDL-cholesterol results in a patient with dysbetalipoproteinemia Roberts, W. L., E. T. Leary, et al. (2000), Clin Chem 46(4): 560-2. |
| Familial aggregation of serum total cholesterol: a population-based family study in eastern Finland Fuentes, R. M., I. L. Notkola, et al. (2000), Prev Med 31(5): 603-7. Abstract: BACKGROUND: The Finnish population has a high risk of coronary heart disease, which is associated to a high population level of serum total cholesterol (CHOL) already evident at early ages. The study investigated the familial aggregation of CHOL in a sample of families with young offspring from eastern Finland. METHODS: Fifteen-year-old offspring were examined during 1996-1997 and their biological parents were examined during 1993-1994. A total of 224 children were invited and 184 families participated, of which 123 were included in the analysis with complete data. The main outcome measure was the CHOL (millimoles per liter). RESULTS: Significant positive familial correlations of CHOL were found for the pairs of mother/offspring (r = 0.35, P < 0.001, n = 111), father/offspring (r = 0.29, P = 0.007, n = 82), mother/daughter (r = 0.46, P = 0.001, n = 49), mother/son (r = 0.27, P = 0.036, n = 62), and father/daughter (r = 0.35, P = 0.035, n = 36). The adjustments for the offspring's gender and body mass index (BMI) and the parent's age, BMI, education, and family history of acute myocardial infarction did not alter these results. There was a higher proportion of the offspring in the highest quartile of CHOL when the mother had CHOL > or =5 mmol/L (OR = 3.26, 95% CI = 1.2-8.9, n = 111). CONCLUSIONS: The study confirmed the familial aggregation of CHOL. The consistent CHOL association between the mother and the offspring may indicate the key role of the mother for the primary prevention of hypercholesterolemia. |
| Familial clustering of arterial blood pressure, HDL cholesterol, and pro-insulin but not of insulin resistance and microalbuminuria in siblings of patients with type 2 diabetes Pontiroli, A. E., L. D. Monti, et al. (2000), Diabetes Care 23(9): 1359-64. Abstract: OBJECTIVE: To test the hypothesis that selected abnormalities cluster in type 2 diabetic families. Offspring of patients with type 2 diabetes have a 40-60% chance of developing type 2 diabetes and an increased frequency of impaired glucose tolerance (IGT) or unknown diabetes. These offspring also show metabolic abnormalities of type 2 diabetes, such as insulin resistance, high insulin and pro-insulin, low HDL cholesterol levels, arterial hypertension, and microalbuminuria. RESEARCH DESIGN AND METHODS: We studied 87 families including at least one type 2 diabetic patient, i.e., 87 probands and 146 siblings; 60 spouses of probands with no family history of diabetes were compared with siblings. Familial clustering was evaluated by 2 methods: concordance of siblings and probands for a given abnormality (method 1) and intraclass correlation coefficients of values within each family (method 2). RESULTS: At oral glucose tolerance testing, 24 siblings had type 2 diabetes, 31 siblings had IGT, and 14 spouses had IGT (P = 0.0012 vs. siblings). With method 1, familial clustering occurred for microalbuminuria, insulin resistance, arterial hypertension, HDL cholesterol and pro-insulin levels; with method 2, familial clustering was observed for the same variables except for microalbuminuria. With both method 1 and 2, familial clustering for insulin resistance disappeared, whereas familial clustering for arterial blood pressure, HDL cholesterol, and pro-insulin remained after correction for BMI; after further restriction of analysis to probands and to siblings with normal glucose tolerance, familial clustering for pro-insulin was observed only with method 2. CONCLUSIONS: These data indicate that siblings of diabetic patients are at high risk for selected features of type 2 diabetes. |
| Familial history of cancer and dietary pattern, serum cholesterol, serum protein and blood hemoglobin Yamaguchi, N., J. Yamamura, et al. (1990), Gan No Rinsho Spec No: 377-81. Abstract: The relationships between the history of cancer in parents and the dietary pattern, serum cholesterol, serum protein and blood hemoglobin were examined to assess the possible role of lifestyle transmission in the familial aggregation of cancer. Individuals with history of cancer in parents were selected from a population of 1,221 individuals. Five age- and sex-matched controls for each case were selected from individuals, the parents of whom were alive at the age of the case parent. Intake of miso soup, pickles and milk product showed associations with the history of cancer in parents. It was also found that serum cholesterol was significantly lower in individuals with history of cancer other than stomach in the mother. Interestingly, serum protein, especially the globulin fraction, was found to be significantly lower among individuals with the history of cancer in parents. These findings suggest that lifestyle transmission might play some role in the familial aggregation of cancer. |
| Familial hypercholesterolemia and intracavernous venous spilling of cholesterol in a child with large suprasellar dermoid cyst. Case report Lunardi, P. and P. Missori (1995), Neurosurg Rev 18(1): 49-52. Abstract: A unique case of suprasellar dermoid cyst and familial hypercholesterolemia in a child is reported. Such an association, which strengthens the congenital hypothesis of dermoid cysts, could be a manifestation of a complex dyslipidemic inherited syndrome, at least in children. Surgical removal of the dermoid cyst which spilled cholesterol into the cavernous and intercavernous sinuses, allowed reduction of cholesterol levels in the postoperative period. |
| Familial lecithin:cholesterol acyltransferase deficiency: further resolution of lipoprotein particle heterogeneity in the low density interval Guerin, M., P. J. Dolphin, et al. (1993), Atherosclerosis 104(1-2): 195-212. Abstract: Patients presenting with a familial deficiency of lecithin:cholesterol acyltransferase (LCAT) typically exhibit multiple quantitative and qualitative perturbations of apo B- and apo A-I-containing plasma lipoproteins. Marked particle heterogeneity has been detected over the low-density range (d = 1.019-1.063 g/ml), involving lipoprotein(X) (LP-X) and large molecular weight LDL (LM-LDL). We describe the chromatographic fractionation and characterization of the major particle species distributed within the low-density interval in a new French LCAT-deficient family. Detailed analyses of the plasma lipoprotein and apolipoprotein spectrum are reported. The plasma lipoproteins were enriched in unesterified cholesterol and phospholipids with markedly reduced concentrations of cholesteryl esters. By a combination of gel filtration and affinity chromatography on heparin-sepharose, the heterogeneous mixture of low-density particles was resolved into three distinct particle populations: LP-X (diameter 400 A) corresponding to LM-LDL, an apo A-I and albumin-containing particle similar to LP-X2 (diameter 300 A), and cholesteryl ester-deficient (0.9%) triglyceride-rich (58.4%) LDL containing apo B-100 (diameter 260-270 A). Use of affinity chromatography allowed separation of HDL-like particles (diameter 140-160 A) which were rich in free cholesterol (21.4%) and phospholipids (52.9%) and which were isolated in association with LP-X upon gel filtration chromatography. Ultracentrifugal density gradient analysis of plasma from the LCAT-deficient subject over a period of 3 years showed a net shift of the lipoprotein distribution in the low density range due to an increase in plasma LP-X levels. We propose that the presence of LP-X in the plasma is correlated with a progressive alteration in the renal function recently observed in this patient. |
| Familial lecithin:cholesterol acyltransferase deficiency: molecular analysis of a compound heterozygote: LCAT (Arg147 --> Trp) and LCAT (Tyr171 --> Stop) Guerin, M., C. Dachet, et al. (1997), Atherosclerosis 131(1): 85-95. Abstract: Lecithin:cholesterol acyltransferase (LCAT) is responsible for the formation of the majority of plasma cholesteryl esters. Familial LCAT deficiency is associated with corneal opacity, anemia and proteinurea and typically results in renal failure in the 4-5th decade; this syndrome is equally characterized by the quasi-absence of plasma LCAT activity with variable enzyme mass and very low levels of plasma cholesteryl esters. In this study, we report detailed analyses of plasma lipids and lipoprotein profile in two sisters (CM and ML) presenting classical homozygous LCAT-deficiency; the younger sibling (CM) had proteinurea from an early age whereas the older sister (ML) has never exhibited renal dysfunction. We investigated the molecular defect in the 45 year-old woman (proband CM) exhibiting all clinical and biochemical features of familial LCAT deficiency: a plasma cholesterol level of 105 mg/dl, of which 95% was unesterified, an HDL-cholesterol of 6.5 mg/dl and an apo A-I level of 52 mg/dl. The proband (CM) displayed a plasma cholesterol esterification rate which corresponded to 2% of normal LCAT activity; plasma LCAT protein concentration was 0.56 microg/ml and equivalent to approximately 10% of normal LCAT mass. Analysis by single strand conformation polymorphism (SSCP) of the PCR products corresponding to exons 4 and 5 of the LCAT gene revealed a visible band shift. Sequence analyses of exons 4 + 5 revealed two separate single point mutations: a C --> T transition replacing Arg147 by Trp and a T --> G transition converting Tyr171 to a stop codon. The presence of these two point mutations was confirmed by restriction enzyme analyses: the C --> T transition abolished a MwoI site whereas the T --> G transition created an AvrII site. The Arg147 mutation was associated with a non-secreted protein. The Tyr171 mutation resulted in formation of a truncated protein lacking the catalytic site. In summary, we have identified an LCAT deficient patient corresponding to a compound heterozygote for the Arg147 --> Trp mutation and a new molecular defect involving a Tyr171 --> Stop mutation in the LCAT gene. |
| Familial massive tendon xanthomatosis with decreased high-density lipoprotein-mediated cholesterol efflux Matsuura, F., K. Hirano, et al. (2005), Metabolism 54(8): 1095-101. Abstract: We experienced a family with novel massive tendon xanthomatosis which can be excluded from known disease causing xanthomatosis. The proband was a 58-year-old man who had necrosis in his massive Achilles tendon xanthoma. Three of 5 brothers including him and his nephew had the same clinical phenotype. The systemic tendon xanthomatosis became apparent around 30 years of their age. The proband and his elder brother had mild elevations of serum total cholesterol level (251 and 228 mg/dL, respectively). The low-density lipoprotein receptor activity of the proband's lymphocytes was normal. Neither plant sterol nor cholestanol level was increased in the proband's plasma. Magnetic resonance image of the proband's Achilles tendon demonstrated a massive expansion of the soft tissue with salami sausage-like appearance in his heels (50 mm in thickness). The physiological function of macrophages (MPhi) from the patients was investigated to clarify the mechanism for the formation of xanthomatosis. There was no significant difference in the uptake of oxidized low-density lipoprotein between the proband's MPhi and the control. High-density lipoprotein 3-mediated cholesterol efflux from the patients' MPhi (n = 2) was significantly reduced compared with the controls (n = 3), whereas there was no difference in apolipoprotein (apo) A-I-mediated cholesterol efflux between the patients' MPhi and the controls. Furthermore, there was no reduction of the messenger RNA levels of ATP-binding cassette transporter 1 (ABCA1), which is involved in apo A-I-mediated cholesterol efflux, in the proband's MPhi compared with the control. The present study demonstrates that the mechanism for the formation of novel familial massive tendon xanthomatosis may be, at least in part, associated with decreased high-density lipoprotein 3, but not free apo A-I-mediated cholesterol efflux from MPhi in vivo. |
| Familial type V hyperlipoproteinemia with hyper-remnant-like particle-cholesterol accompanied with apolipoprotein E3/E4 phenotype Nagai, T., T. Tomizawa, et al. (1996), Intern Med 35(5): 388-91. Abstract: A 41-year-old woman and her 2 sons had Type V hyperlipoproteinemia. Interestingly, the patient and her younger son had higher levels of remnant-like particle (RLP)-cholesterol than her elder son; the former two had apolipoprotein E phenotype E3/E4, while the latter had E3/E3. Hyper-RLP-ch levels may be associated with the apolipoprotein E4 phenotype. Moreover, after administration of bezafibrate, the patient's triglyceride, RLP-cholesterol and RLP-triglyceride levels decreased markedly and the chylomicron fraction disappeared. Further studies may be necessary to determine if hypertriglyceridemic patients with or without apolipoprotein E4 show a greater reduction in serum TG levels with lipid-lowering agents. |
| Family history of coronary artery disease and cholesterol: screening children in a disadvantaged inner-city population Wadowski, S. J., R. J. Karp, et al. (1994), Pediatrics 93(1): 109-13. Abstract: BACKGROUND AND PURPOSE. Little information relating to cholesterol levels and screening for hypercholesterolemia in inner-city children exists. For this study, given the disrupted family backgrounds of many of our patients and the unreliability of family histories, our hypothesis was that in comparison with other samples, family history of coronary heart disease would be a poor screening tool for the identification of children with elevations in total serum cholesterol (TSC). SUBJECTS AND METHODS. During 15 months, more than 400 pediatric outpatients, 2 through 14 years old, were screened for a family history of atherosclerotic disease. These children were attending a clinic serving a disadvantaged black and Hispanic population at Kings County Hospital Center. Nonfasting TSC levels were measured in 300 children. Positive risk for coronary heart disease was determined by the presence of a family history of coronary heart disease (defined as angina, stroke, or myocardial infarction in any parent or grandparent) at less than 55 years age. RESULTS. The mean TSC level was 4.27 mmol/L SD +/- 0.85) (165.0 mg/dL SD +/- 32.8). The 29.4% of this population with a history suggestive of high risk for hypercholesterolemia had a mean TSC of 4.48 mmol/L (SD +/- 0.971) (173.2 mg/dL SD +/- 37.5), and those with no risk history had a mean TSC of 4.18 mmol/L (SD +/- 0.750) (161.4 mg/dL SD +/- 29.9) (P <.005). Use of family history of coronary artery disease as a screening tool had a sensitivity of 39.3%, a specificity of 74.5%, and a positive predictive value of 39.8% for detection of moderate hypercholesterolemia (TSC > or = 4.66 mmol/L 180 mg/dL). CONCLUSIONS. This population's mean TSC level did not differ (P >.10) from those obtained in multiple large studies of average North American populations, and the predictive value and sensitivity of family history as a screening tool was comparable, although the prevalence of a positive family history was greater. The findings may be due to a greater prevalence of coronary artery disease at a young age in these families. In this population, a positive risk history is an important indicator for further evaluation of these children. |
| Family history of early cardiovascular disease in children with moderate to severe hypercholesterolemia: relationship to lipoprotein (a) and low-density lipoprotein cholesterol levels Barth, J. A., R. J. Deckelbaum, et al. (1999), J Lab Clin Med 133(3): 237-44. Abstract: Lipoprotein (a) (Lp(a)) is an established cardiovascular risk factor in adults. We sought to evaluate whether raised Lp(a) levels were predictive of a family history of early cardiovascular disease (CVD) in children already at increased risk for premature atherosclerosis because of elevated low-density lipoprotein (LDL) cholesterol levels. Lp(a) and serum lipid levels were measured in 69 children and offspring with established moderate to severe hypercholesterolemia (serum cholesterol > 170 mg/dL) who were aged 10.7 +/- 4.3 years (range 1.5 to 21 years) and had been referred to a pediatric lipid center. The children represented families with a positive (n = 27) or negative (n = 42) history for premature CVD (<55 years of age in parent or grandparent). In all children, Lp(a) levels ranged from 1 to 140 mg/dL, with a median of 29 mg/dL. Mean total cholesterol, LDL cholesterol, and high-density lipoprotein (HDL) cholesterol levels were 234 mg/dL, 166 mg/dL, and 45 mg/dL, respectively. There was no difference in median Lp(a) levels between the children with a positive family history and those with a negative family history (29.9 mg/dL vs 29.0 mg/dL, respectively). In contrast, children with a positive family history showed significantly higher LDL cholesterol levels (186 +/- 61 mg/dL vs 153 +/- 52 mg/dL, P =.02). Thus, in this group of hypercholesterolemic children, LDL cholesterol but not Lp(a) levels were associated with a family history of premature CVD. Further studies are needed to identify additional specific risk factors associated with the development of CVD in this population. |
| Family history of ischemic heart disease with respect to mean twin-pair cholesterol and subsequent ischemic heart disease in the NHLBI twin study Reed, T., R. R. Fabsitz, et al. (1990), Genet Epidemiol 7(5): 335-47. Abstract: This study examines the independent and interactive effects of family history scores (FHxS) for the prevalence of ischemic heart disease with plasma lipids and subsequent morbidity and mortality from ischemic heart disease. FHxS were calculated for 514 sets of middle aged male twins who participated in the entry examination of the NHLBI Veteran twin study in 1969-1973. Comparison of the FHxS with the level of plasma total cholesterol and HDL cholesterol (HDLc) paralleled earlier reported findings in young adults; individuals with high total cholesterol in two exams 8-12 years apart had significantly (P less than.01) higher FHxS. The same relationship was noted when using the mean twin-pair cholesterol level at the initial exam when the twins were in their 40s. Using the pair means over two exams as the cotwins aged into their 50s, the association of FHxS with total cholesterol declined and pairs with HDLc persistently in the highest quintile at both exams had significantly (P less than.01) lower FHxS. The changes in the pattern of association of lipid fractions with FHxS with age parallel the reported age decline of total cholesterol as a risk factor for heart disease. Assessment of ischemic heart disease events up to January 1988 revealed a highly significant association (P less than.0001) of later ischemic heart disease events with FHxS. At each level of lipid categorization pairs who later had events had higher FHxS than those without any subsequent heart disease; these differences were significant in all but the low risk lipid groups (low total cholesterol, high HDLc, and low total cholesterol/HDLc ratio). We conclude that FHxS is related to total cholesterol and HDLc but also is an independent predictor of subsequent ischemic heart disease after 14-18 years of follow-up. |
| Family resemblance in energy, fat, and cholesterol intake: a study among three generations of women Stafleu, A., W. A. Van Staveren, et al. (1994), Prev Med 23(4): 474-80. Abstract: BACKGROUND. Transfer of nutrition habits within the family may contribute to the establishment of a high-fat diet. Several studies show a significant correlation in nutrient intake between parents and children living in the same household. This study describes family resemblances in nutrient intake among adult women living apart. METHODS. Family resemblance in fat intake was assessed in three generations of adult women by means of a short food-frequency questionnaire. Data were collected on 291 maternally related family members (97 young adult women, their mothers, and their grandmothers). RESULTS. Weak correlations (0.13-0.27) were found between nutrient intake of the younger and middle generation. Correlations between the middle and older generation (-0.03-0.29) and between the younger and older generation (-0.03-0.33) tended to be lower. CONCLUSIONS. This study shows that family resemblance in nutrient intake is weak for adult women living apart. There seems to be more impact of middle-aged mother's eating habits on the fat intake of their adult daughters than of elderly women's eating habits on their middle-aged daughters. |
| Farm-grown mushrooms (Agaricus campestris) in the diet of rats do not affect plasma and liver cholesterol concentrations Beynen, A. C., A. M. Fielmich, et al. (1996), Nahrung 40(6): 343-5. |