To evaluate the impact on lipid and carbohydrate variables of a combined one-third ethinyl estradiol (EE)/levonorgestrel (LNG) dose reduction in oral contraceptives.
In an open-label, randomized study, a dose-reduced oral contraceptive containing 20 microg EE and 100 microg LNG (20 EE/100 LNG) was compared with a reference preparation containing 30 microg EE and 150 microg LNG (30 EE/150 LNG). One-year data from 48 volunteers were obtained.
We found a decrease of HDL2 cholesterol and increases of low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol and total triglycerides in both treatment groups from baseline to the 13th treatment cycle. Although for four of six variables, the changes in the 20 EE group were lower compared with the 30 EE group, none of the differences between the two treatments were statistically significant. The median values for the fasting levels of insulin, C-peptide and free fatty acids slightly increased or remained unchanged while the fasting glucose levels slightly decreased after 13 treatment cycles. While the glucose area under the curve (AUC) (0-3 h) was similar in both groups during the OGTT, the insulin AUC(0-3 h) was less increased in the 20 EE/100 LNG group compared with the 30 EE/150 LNG group. None of the differences between the treatment groups for any of the carbohydrate metabolism variables were statistically significant at any time point. Both study treatments were safe and well tolerated by the volunteers.
Similar effects on the lipid and carbohydrate profiles were found for both preparations. The balanced one-third EE dose reduction in this new oral contraceptive caused slightly lower, but insignificant, changes in the lipid and carbohydrate variables compared with the reference treatment.
The Cardiovascular Risk in Young Finns Study is an on-going multicentre study of atherosclerosis precursors in Finnish children and young adults. We have collected risk factor data in the 21-year follow-up performed in 2001. The aims of this analysis were to examine the levels, secular trends and east-west difference in risk factors amongst young adults.
Population based follow-up study.
A total of 2283 participants aged 24-39 years in 2001 (63.5% of the original cohort).
Levels of serum lipids, apolipoproteins, blood pressure and smoking.
The mean serum total cholesterol, low density lipoprotein cholesterol, high density lipoprotein (HDL) cholesterol and triglyceride concentrations in 24-39-year-old adults were 5.16, 3.27, 1.29 and 1.34 mmol L(-1), respectively. Total cholesterol (5.21 vs. 5.12 mmol L(-1), P = 0.046), HDL cholesterol (1.31 vs. 1.28 mmol L(-1), P = 0.027), systolic blood pressure (118 vs. 115 mmHg, P
The Special Turku Coronary Risk Factor Intervention Project (STRIP) is a prospective infancy-onset randomized dietary intervention trial targeting dietary fat quality and cholesterol intake, and favoring consumption of vegetables, fruit, and whole-grains. Diet (food records) and circulating metabolites were studied at six time points between the ages of 9-19 years (n = 549-338). Dietary targets for this study were defined as (1) the ratio of saturated fat (SAFA) to monounsaturated and polyunsaturated fatty acids (MUFA + PUFA)
Achieving cholesterol targets by individualizing starting doses of statin according to baseline low-density lipoprotein cholesterol and coronary artery disease risk category: the CANadians Achieve Cholesterol Targets Fast with Atorvastatin Stratified Titration (CanACTFAST) study.
Despite an increasing body of evidence on the benefit of lowering elevated levels of low-density lipoprotein cholesterol (LDL-C), there is still considerable concern that patients are not achieving target LDL-C levels.
The CANadians Achieve Cholesterol Targets Fast with Atorvastatin Stratified Titration (CanACTFAST) trial tested whether an algorithm-based statin dosing approach would enable patients to achieve LDL-C and total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C) ratio targets quickly.
Subjects requiring statin therapy, but with an LDL-C level of 5.7 mmol/L or lower, and triglycerides of 6.8 mmol/L or lower at screening participated in the 12-week study, which had two open-label, six-week phases: a treatment period during which patients received 10 mg, 20 mg, 40 mg or 80 mg of atorvastatin based on an algorithm incorporating baseline LDL-C value and cardiovascular risk; and patients who achieved both LDL-C and TC/HDL-C ratio targets at six weeks continued on the same atorvastatin dose. Patients who did not achieve both targets received dose uptitration using a single-step titration regimen. The primary efficacy outcome was the proportion of patients achieving target LDL-C levels after 12 weeks.
Of 2016 subjects screened at 88 Canadian sites, 1258 were assigned to a study drug (1101 were statin-free and 157 were statin-treated at baseline). The proportion of subjects who achieved LDL-C targets after 12 weeks of treatment was 86% (95% CI 84% to 88%) for statin-free patients and 54% (95% CI 46% to 61%) for statin-treated patients. Overall, 1003 subjects (80%; 95% CI 78% to 82%) achieved both lipid targets.
Algorithm-based statin dosing enables patients to achieve LDL-C and TC/HDL-C ratio targets quickly, with either no titration or a single titration.
The effects of acquired obesity on lipid profile and lipoprotein composition in rare BMI-discordant monozygotic (MZ) twin pairs were studied.
Abdominal fat distribution, liver fat (magnetic resonance imaging and spectroscopy), fasting serum lipid profile (ultracentrifugation, gradient gel-electrophoresis, and colorimetric enzymatic methods), and lifestyle factors (questionnaires and diaries) were assessed in 15 BMI-discordant (within-pair difference [?] in BMI >3 kg/m2) and nin concordant (?BMI
We present fractile data on serum lipids and apolipoproteins A-l and B for children and young adults from the cardiovascular risk in young Finns study cohort of 1986. The sample comprised 2370 fasting children and young adults (1114 males and 1256 females) aged 9, 12, 15, 18, 21 and 24 years. The determinations were performed in duplicate with standard methods. LDL-cholesterol values were calculated. The limits for clearly pathological values (exceeding the 97.5th percentile) irrespective of age and gender were 7.5 mmol/l, 5.0 mmol/l, 3.5 mmol/l and 1.4 g/l for serum total cholesterol, LDL-cholesterol, triglycerides and apolipoprotein B, respectively. Corresponding values (below the 2.5th percentile) for HDL-cholesterol, apolipoprotein A-l, HDL2- and HDL3-cholesterol were 0.80 mmol/l, 1.0 mg/l, 0.20 mmol/l and 0.70 mmol/l, respectively. Approximately 79%, 33% and 7% of males had serum total cholesterol values greater than 4.0 mmol, 5.0 mmol/l and 6.0 mmol/l, respectively. Corresponding percentages for females were 87%, 43% and 10%. However, age-related differences were marked. The prevalence of values, e.g. greater than 6 mmol/l according to age, ranged from 6 to 13% in females and from 3 to 12% in males, emphasizing the need for age-specific reference values. Additionally, postpubertal values for total and LDL-cholesterol tended to be slightly lower compared to prepubertal values, indicating that the reference values for adults do not apply to adolescents and young adults. The age-related changes in lipid levels were evident in each fractile and were especially accentuated in higher fractiles. Fluctuations with age were more pronounced in males than in females. These results are intended to be applied as reference values for diagnosing dyslipidemias.
Non-HDL-cholesterol (non-HDL-C) has been reported to be a better marker of cardiovascular risk than LDL-cholesterol (LDL-C) especially in individuals with high triglyceride values. Further, levels of remnant cholesterol have been suggested to in part explain residual risk not captured with LDL-C. The aim of the present study was to define reference values for non-HDL-C and remnant cholesterol based on data from the Nordic Reference Interval Project (NORIP).
We analyzed the test results for total cholesterol, HDL-cholesterol and triglycerides from 1392 healthy females and 1236 healthy males. Non-HDL-C was calculated as measured total cholesterol minus measured HDL-cholesterol. Remnant cholesterol was calculated using the Friedewald equation for LDL-C: measured total cholesterol minus measured HDL-cholesterol and minus calculated LDL-cholesterol. The 2.5th and 97.5th percentiles for these markers were calculated according to the International Federation of Clinical Chemistry guidelines on the statistical treatment of reference values.
The offspring of individuals with a history of premature myocardial infarction are at increased risk of premature coronary attacks. The aim of this study was to determine parent/offspring associations of coronary risk factors in families affected by premature myocardial infarction and to compare these to corresponding control families.
The cohort of cases consisted of 71 male survivors of myocardial infarction and their 128 descendants (aged 7-18 years). As control families, 85 randomly selected healthy males with their 66 descendants were investigated. Besides traditional risk factors, serum high sensitive C-reactive protein (hsCRP), apolipoprotein (apo) E phenotypes and lipoprotein(a) were analyzed.
In the offspring of the patients, fibrinogen and atherogenic lipoprotein parameters were higher than in the corresponding controls, but hsCRP, lipoprotein(a) and anthropometric data did not differ between the groups. The adult-offspring positive correlations were detected in fibrinogen and in almost all measured lipoprotein fractions in the affected families; amongst the controls, the association was observed only for triglyceride levels. Multiple logistic regression analysis demonstrated independent association of offspring apoB, apoA-I and fibrinogen levels with a family history of premature myocardial infarction.
The most informative predictors of future coronary attacks during childhood are apoB-100 and apoB/apoA-I ratio; serum hsCRP and lipoprotein(a) do not have predictive value in childhood.
BACKGROUND: The risk of myocardial infarction is lower among light-to-moderate alcohol drinkers compared with abstainers. We tested associations between alcohol intake and risk of myocardial infarction and risk factors and whether these associations are modified by variations in alcohol dehydrogenases. METHODS AND RESULTS: We used information on 9584 men and women from the Danish general population in the Copenhagen City Heart Study. During follow-up, from 1991 to 2007, 663 incident cases of myocardial infarction occurred. We observed that increasing alcohol intake was associated with decreasing risk of myocardial infarction, decreasing low-density lipoprotein cholesterol and fibrinogen, increasing diastolic and systolic blood pressure and high-density lipoprotein cholesterol, and with U-shaped nonfasting triglycerides. In contrast, ADH1B and ADH1C genotypes were not associated with risk of myocardial infarction or with any of the cardiovascular biochemical risk factors, and there was no indication that associations between alcohol intake and myocardial infarction and between alcohol intake and risk factors were modified by genotypes. CONCLUSIONS: Increasing alcohol intake is associated with decreasing risk of myocardial infarction, decreasing low-density lipoprotein cholesterol and fibrinogen, increasing diastolic and systolic blood pressure and high-density lipoprotein cholesterol, and U-shaped nonfasting triglycerides. These associations were not modified by ADH1B and ADH1C are genotypes.