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PubMed2026

Parental longevity and polygenic longevity scores in relation to ageing-related factors in a population of 70-year-olds followed over six years: The Gothenburg H70 Birth Cohort Study.

As societies age, a deeper understanding of ageing-related factors that contribute to longevity is needed. We therefore investigated possible longevity factors (social, medical, and biological) in relation to parental longevity (PL) and polygenic longevity scores (PGLSs). We examined 1126 70-year-olds from the Swedish population-based Gothenburg H70 Birth Cohort study in 2014-2016 (response rate 72%), with follow-up in 2019-2022 (response rate 77.6%). Comprehensive examinations included self-reported information on parents' ages, socioeconomic factors, mental, cardiovascular, and neurological health, anthropometry, laboratory data, and genotyping to construct two continuous PGLSs variables (with and without the APOE locus). PL groups were categorised as high if both parents survived to age 85 (17.2%); medium if one parent had survived (43.3%), and low if neither parent had survived to age 85 (39.4%). Higher PL and higher PGLSs were related to less hypertension, higher educational level, better childhood, and current socioeconomic status. In addition, higher PL was associated with higher MMSE score, total cholesterol, HDL-cholesterol (HDL-c) and LDL-cholesterol (LDL-c), lower BMI, homocysteine and inflammatory markers (IL-6, CRP) levels, and less smoking, whereas higher PGLSs was related to less myocardial infarction. At follow-up, high-PL was associated with less increase in plasma pTau217. PGLSs were mainly related to socioeconomic and cardiovascular factors, while individuals with long-lived parents, in addition, had several other characteristics of longevity, such as less inflammation, homocysteine, and markers of dementia. PL may be a proxy for biological ageing and used as a screening for ageing-related disorders in the context of prevention.

APOE↗

PubMed1976

Neonatal screening for hyperlipoproteinemia. Methods for direct estimation of cord serum VLDL + LDL.

The early detection of hyperlipoproteinemia in newborn infants has so far been based upon estimation of cord blood total lipids (cholesterol and triglyceride) and lipoprotein-lipids (VLDL-, LDL- and HDL-cholesterol). To be able to make a direct estimation of cord serum beta-lipoproteins (VLDL + LDL) two quite different methods were modified, one immunological and the other turbidimetric. Good correlations were found to VLDL- + LDL-cholesterol isolated in the ultracentrifuge (r = 0.848 and 0.831, respectively). If neonatal screening for hyperlipoproteinemia is considered, we recommend the very easy and inexpensive turbidimetric method. Furthermore, using cord serum, two conventional precipitation methods with heparin-CaCl2 and heparin-MnCl2 were compared by ultracentrifugation and high correlations were found (r = 0.923 and 0.899, respectively). A clamping study showed that following early clamping of the cord, the concentration of cord serum lipids and lipoproteins did not change markedly within the first five minutes. Storing experiments showed that serum should be separated within the first 12 h to avoid unpredictable changes in the concentration of cord serum lipids and lipoproteins.

Animals↗

PubMed1979

The effect of cholestyramine on lipoprotein lipids in patients with primary type IIA hyperlipoproteinemia.

The effect of 3 months' treatment with cholestyramine on lipoprotein lipids was investigated in 12 patients. VLDL, LDL and HDL were separated by preparative ultracentrifugation. There was a significant decrease of serum cholesterol and phospholipids and an increase of serum triglycerides. All the VLDL-lipids increased by nearly 30%. The LDL-lipids decreased with a tendency for normalisation of their atypical lipid composition. The small but significant alterations of HDL triglycerides and cholesterol are correlated with the corresponding alterations of the other lipoproteins; the HDL-phospholipids were unchanged. The LDL/HDL-lipid ratios were decreased but not normalised. The 30% decrease of LDL-cholesterol is negatively correlated with an increase in all the VLDL-lipids.

Cholesterol↗

PubMed1979

Diabetes, blood lipids, lipoproteins, and change of environment: restudy of the "new immigrant Yemenites" in Israel.

Restudy of 306 "new immigrant Yemenite" Jews, an ethnic group in which, upon their arrival in Israel, no diabetes was detected, revealed, 25 yr after their immigration, an increased incidence of diabetes and higher plasma and lipoprotein-lipid levels. The prevalence of diabetes (defined as "glucose intolerance") rose to 11.8% (13.2% males and 9.7% females). Obesity in females resulted in increased prevalence of diabetes in all age groups, while in males it affected the older age group only. The male/female diabetic ratio was affected by weight status--in the underweight, diabetes was more prevalent in males, in the overweight, the rate of diabetes in females equaled that of males. In nondiabetics (those with normal glucose tolerance), neither the glucose tolerance nor the insulin response deteriorated with aging. Most diabetics had a delayed insulin response. However, about 50% of nondiabetics and diabetics had insulin response peak at 60 min and similar insulin levels. It appears that in newly discovered adult-onset diabetics in this population there is no shortage of insulin, but rather shortage of insulin action. In nondiabetics, the levels of plasma cholesterol and triglycerides (TG) were higher than levels upon their arrival. In diabetics, the plasma TG, cholesterol, and LDL-cholesterol levels were higher when compared to those of nondiabetics, especially in the group of overweight males. Hyperlipoproteinemia was diagnosed in 27.7% of diabetics and 11.0% of nondiabetics. In diabetics, the HDL/LDL cholesterol ratio was found to be reduced, significantly so in overweight diabetics.

Adult↗

PubMed2025

GWAS of CRP response to statins further supports the role of APOE in statin response: A GIST consortium study.

Statins are first-line treatments in the primary and secondary prevention of cardiovascular disease. Clinical studies show statins act independently of lipid-lowering mechanisms to decrease C-reactive protein (CRP), an inflammation marker. We aim to elucidate genetic loci associated with CRP statin response. CRP statin response is the change in log-CRP between off-treatment and on-treatment measurements. Cohort-level Genome-Wide Association Studies (GWAS) of CRP response were performed using 1000 Genomes imputed data, testing ∼10 million common genetic variants. GWAS meta-analysis combined results from seven cohorts and clinical trials totalling 14,070 statin-treated individuals of European ancestry within the GIST consortium. Secondary analyses included statin-by-placebo interaction analyses, and lookups in African ancestry cohorts. Our GWAS identified two genome-wide significant (P < 5e-8) loci: APOE and HNF1A for CRP statin response corrected for baseline CRP. The missense lead variant rs429358 at APOE, contributing to the APOE-E4 haplotype, is a risk locus for dyslipidaemia, Alzheimer's and coronary artery disease (CAD). The HNF1A locus is associated with diabetes, cholesterol levels, and CAD. Both loci are also associated with baseline CRP levels, and neither locus achieved a significant (P < 0.05) result from the statin v. placebo interaction meta-analysis using randomized clinical trial data. However, the interaction result (P-int=0.09) for APOE was suggestive and possibly underpowered. The APOE-E4 signal may therefore be associated with both CRP and LDL-cholesterol statin response. Combined with suggestions in the literature that APOE also leads to differential statin benefit in Alzheimer's, the APOE locus warrants further investigation for potential genetic effects on healthcare with statin treatment.

Humans↗

PubMed1979

Long-term effect of sotalol on plasma lipids.

1. We studied the effect on plasma lipids of sotalol given orally over a 12 month period to patients with essentially hypertension. 2. Plasma free fatty acid concentration was lower than initially at 1, 3, 6 and 12 months. The difference was significant (P less than 0.01) at 1 and 3 months. 3. Plasma cholesterol (VLDL + LDL-cholesterol) increased during treatment. Plasma total cholesterol increased from 5.49 +/- SD 0.94 mmol/l at the beginning to 6.37 +/- 1.10 mmol/l at 12 months (P less than 0.01). 4. HDL-cholesterol concentration and the ratio of HDL-cholesterol to total cholesterol decreased significantly. The ratios were 0.28 and 0.18 at the beginning and at 12 months respectively (P less than 0.001). 5. Plasma triglycerides increased simultaneously from 1.14 +/- 0.31 to 1.89 +/- 0.99 mmol/l (P less than 0.01).

Adult↗

PubMed1976

[Sitosterol in familial hyperlipoproteinemia type II. A randomized double-blind cross-over study].

The effect of beta-sitosterol on the lipid and lipoprotein level was evaluated in a randomised double-blind cross-over trial in 24 patients with primary familial type II hyperlipoproteinaemia over a period of 16 weeks. All patients completed the trial, however 10 of them had to be excluded from the evaluation due to fluctuations of their body weight or unreliable drug intake. Sitosterol lowered the total cholesterol level by 12.5% (P less than 0.01) from 9.96 mmol/l (3.69 g/l) to 8.37 mmol/l (3.23 g/l). The LDL-cholesterol level was lowered by 19.5% (P less than 0.05). The sitosterol concentration in plasma was consistently lower than 0.3% of total cholesterol. No side effects or tachyphylaxis was observed in the course of the trial. A return to normal of an increased serum cholesterol level by a combination of a lipid lowering diet and sitosterol monotherapy was only achieved in one patient.

Adolescent↗

PubMed1977

[Familial hypobetalipoproteinaemia and diabetes mellitus (author's transl)].

In a 60-year-old patient with manifest diabetes mellitus and in his 63-year-old brother with latent diabetes mellitus hypobeta-lipoproteinaemia was diagnosed. Cholesterol values were around 1,8 mmol/1 in whole serum samples. The LDL-cholesterol fraction was 1,04 mmol/1. The beta-lipoprotein band in the lipoprotein electrophoresis was markedly reduced. Apolipoprotein B measured by radial immuno-diffusion was about 30% of the normal for age. The components of LDL were normal. Values of hepatic triglyceride lipase and lipoprotein lipase in heparinised plasma were within the normal range. The simultaneous occurrence of hypobetalipoproteinaemia and diabetes mellitus is described here for the first time.

Adult↗

PubMed1976

Degradation of cationized low density lipoprotein and regulation of cholesterol metabolism in homozygous familial hypercholesterolemia fibroblasts.

Cultured fibroblasts derived from patients with homozygous familial hypercholesterolemia, which lack functional low density lipoprotein (LDL) receptors, fail to bind, take up, or degrade the lipoprotein with high affinity; therefore LDL-cholesterol is not made available for suppression of cholesterol synthesis or activation of cholesteryl ester formation. When LDL was given a positive charge by reaction with N,N-dimethyl-1,3-propanediamine (cationized LDL), the rate of degradation of the lipoprotein was increased by more than 100-fold in the homozygous familial hypercholesterolemia fibroblasts. Degradation of cationized LDL was inhibited by chloroquine, suggesting that it occurred in cellular lysosomes. Although the cationized LDL entered the cell through a mechanism independent of the LDL receptor, the cholesterol liberated from the degradation of the lipoprotein became available for suppression of cholesterol synthesis and stimulation of cholesteryl ester formation in the homozygous familial hypercholesterolemia fibroblasts. The rate of degradation of albumin by fibroblasts was also increased by more than 100-fold when this protein was coupled to N,N-dimethyl-1,3-propanediamine. The ability to deliver a protein to lysosomes by giving it a strong positive charge may have potential relevance not only to familial hypercholesterolemia, but also to inborn errors of metabolism that involve deficiencies in lysosomal enzymes.

Biological Transport↗

PubMed1976

Combined para-aminosalicylic acid and dietary therapy in long-term control of hypercholesterolemia and hypertriglyceridemia (Types IIa and IIb hyperlipoproteinemia).

The hypolipidemic effect of PAS-C-diet treatment was studied in 63 patients with Types IIa and IIb hyperlipoproteinemia for 6-36 months. Serum lipids and body weights of all patients were stabilized by a low cholesterol-saturated fat-refined carbohydrate diet before the initiation of an eight-week placebo-drug single-blind crossover study. During the placebo period the plasma lipids levels, mean +/- SD: cholesterol 355 +/- 63.5 mg%, triglyceride 141 +/- 68.7 mg%, and LDL-cholesterol 279 +/- 56.8 mg% were lowered to 274 +/- 53.1 mg+, 98 +/- 40.6 mg%, and 209 +/- 52.9 mg%, respectively (P less than 0.001 in each instance), with 7.5-11.0 grams of PAS-C/day given in one to three divided doses. In ten patients who have completed three years of treatment similar results were obtained. They showed no tendency to develop drug tolerance. Eight had watery diarrhea during the initial period which promptly subsided with interruption of drug therapy. Reintroduction of PAS-C in smaller dose (4.5 g/day) with gradual increment to effective dosage level was tolerated by all. No hematologic, hepatic, and ophthalmologic abnormalities were demonstrated by periodic monitoring. The hypoplipidemic effect of the drug was found to be diminished by alcohol and caloric excess.

Adolescent↗

PubMed1975

Role of the low density lipoprotein receptor in regulating the content of free and esterified cholesterol in human fibroblasts.

The transfer of normal human fibroblasts from medium containing whole serum to medium devoid of lipoproteins produced a 90 percent decrease in the cellular content of cholesteryl esters and a 30 percent decrease in the free cholesterol content. When these lipoprotein-deprived cells were subsequently incubated with human low density lipoprotein (LDL), there was a 7-fold increase in the cellular content of esterified cholesterol and a 1.6-fold increase in the cellular content of free cholesterol. The concentration at which LDL produced its half-maximal effect in elevating cellular sterol content (30 mug/ml of LDL-cholesterol) was similar to the half-maximal concentration previously reported for high affinity binding of LDL to its cell surface receptor. High density lipoprotein (HDL) and whole serum from a patient with abetalipoproteinemia (neither of which contains a component that binds to the LDL receptor) did not produce a significant increase in the content of either cholesterol or cholesteryl esters in normal cells. Furthermore, in fibroblasts from patients with the homozygous form of familial hypercholesterolemia, which lack functional LDL receptors, LDL had no effect in raising the cellular content of either free or esterified cholesterol even when present in the medium at concentrations as high as 450 mug sterol/ml. It is concluded that LDL-receptor interactions constitute an important biochemical mechanism for the regulation of the cholesterol content of normal human fibroblasts. Moreover, when considered in light of current concepts of LDL metabolism in intact mammals, the present data suggest that a major function of plasma LDL may be to transport cholesterol from its site of synthesis in liver and intestine to its site of uptake in peripheral tissues.

Abetalipoproteinemia↗

PubMed2025

Robust pleiotropy-decomposed polygenic scores identify distinct contributions to elevated coronary artery disease polygenic risk.

BACKGROUND: Polygenic risk score (PRS) have proved to offer robust risk prediction for coronary artery disease (CAD). However, the global CAD PRS summarizes the joint effects of all the markers in the genome, masking potential genetic heterogeneity that may be important for disease interpretation and targeted interventions. METHODS: Using summary-level data, we identified 43 significant CAD-related traits based on genetic correlations, and further classified them into eight pleiotropy clusters based on their biological functions. We then partitioned the genome into 2,353 near-independent regions. Variants in each region were assigned to the trait most genetically similar to CAD, and then were labeled with the corresponding pleiotropy cluster. We grouped variants without labels into a ninth, non-specific cluster. The Pleiotropy Decomposed (PD) PRSs for each of the nine clusters were calculated using variants assigned to each cluster for 407,903 samples of European ancestry from the UK Biobank (UKBB). RESULTS: We decomposed the CAD PRS into nine PD-PRSs and further stratified individuals with high CAD-PRS into nine subgroups. Each PD-PRS accounted for a higher proportion of the global CAD-PRS within its corresponding subgroup than in the remaining subjects with high CAD-PRS (e.g., 25.2% (0.07) vs. 10.06% (0.07) for lipids-PD-PRS). Additionally, these subgroups showed distinct clinical features. For example, in the lipids-related subgroup, lipoprotein(a) and LDL-cholesterol levels were 67.5% and 18.3% higher, respectively, compared to the remaining high-risk individuals. Furthermore, significant interactions were observed between blood pressure and BP PD-PRS, and between current smoking and respiratory system PD-PRS. CONCLUSION: Our findings suggest that PD-PRSs may reveal substantial genetic and phenotypic heterogeneity among individuals with high CAD-PRS. The unique PD-PRS compositions of each individual can highlight the relative importance of different pleiotropic regions.

Humans↗

PubMed1979

Treatment of post-menopausal hypercholesterolaemia with estradiol.

Replacement therapy with estradiol valerate in 29 post-menopausal women reduced low-density lipoprotein (LDL) cholesterol concentrations by 22% and increased high-density lipoprotein (HDL) cholesterol by 21% after 12 months. Apart from a 67% increase of HDL-triglyceride estradiol had only a slight effect on the levels of lipoprotein triglycerides. Post-heparin plasma lipoprotein lipase (LPL) activity was significantly decreased in subjects with normal pre-treatment very-low-density lipoprotein (VLDL) triglyceride levels, and hepatic lipase (HL) activity was significantly decreased in the group as a whole. It is suggested that estradiol replacement therapy should be considered in climacteric women with high LDL-cholesterol or low HDL-cholesterol levels, or both.

Adult↗

PubMed2026

Lipoprotein(a): Actionable today, treatable tomorrow?

BACKGROUND: Lipoprotein(a) (Lp(a)) is an atherogenic, low-density lipoprotein (LDL)-like particle whose concentrations, mostly genetically determined, are elevated in about 20% of individuals. It is a major and under-recognised independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis. OBJECTIVE: To review current evidence, international recommendations and future directions around testing and management of elevated Lp(a). DISCUSSION: Among other high-risk groups, measuring Lp(a) is recommended in people with ASCVD or aortic valve stenosis, especially if they are of young-onset, familial, unusually severe or progressive. Indeed, some international guidelines advocate measuring Lp(a) in all adults as part of cardiovascular risk assessment. While specific Lp(a)-lowering therapies are not yet available, risk-reducing measures for people with raised Lp(a) include addressing absolute ASCVD risk by diet and lifestyle measures, along with pharmacological LDL-cholesterol reduction. Aspirin might also have a role in primary prevention. Lp(a)-lowering therapies that act by preventing its formation are the subjects of ongoing clinical trials focused on cardiovascular outcomes, the first of which is expected to report in late 2026.

Humans↗

PubMed1977

Plasma high-density lipoprotein cholesterol level. Influence of risk factor intervention.

Determinants of circulating high density lipoproteins (HDL) were sought in 301 men studied during a year of participation in a coronary prevention program. Mean plasma HDL-cholesterol concentration rose by 2.8 mg/dl (6%) in the group receiving multifactor intervention, but the change did not differ significantly from that in the comparison group. Larger changes in both directions were seen in many individuals. Multiple regression analysis of these changes indicates that increased plasma HDL levels occur when plasma triglyceride level is decreased, cigarette smoking is reduced, and habitual alcohol intake is increased. Increases in the concentration of HDL-cholesterol also tended to accompany adherence to the fat-controlled diet, reduction in LDL-cholesterol level, and loss of body weight. Conventional coronary prevention programs are unlikely to have an adverse influence on this new, risk-lowering factor.

Adult↗

PubMed1978

[Clofibrate in type IIa hyperlipoproteinemia. Reduction of apolipoprotein B (author's transl)].

After changing over from the usual eating habits to a "reasonable" restricted diet rich in polyene saturated fats and saturated fatty acids, additional treatment with 1 g clofibrate twice daily produces a significant reduction of concentration of total cholesterol and Apo B by about 24% in the serum of patients with Type IIa hyperlipoproteinemia after 2 weeks. In contrast to this the serum concentration of triglycerides and phospholipids shows an insignificant tendency to fall during the whole duration of the trial. The results suggest that the additional cholesterol reducing action of clofibrate in patients with hyperlipoproteinemia Type IIa who have already been treated by diet is mainly achieved by the reduction of LDL-cholesterol, the atherogenic properties of which are well known.

Adult↗

PubMed1979

[Influence of "prudent" diet and clofibrate upon apolipoprotein B in hyperlipoproteinemia type IIa (author's transl)].

If patients with hyperlipoproteinemia type IIa are treated with diet and additionally over a period of two weeks with 2 grams of Clofibrate daily, the cholesterol-level in the serum decreases. This decrease is caused mainly by a reduction of the apolipoprotein B and the LDL-cholesterol in serum. If elevated cholesterol-levels in the serum are reduced through a "prudent" diet, the concentration of apolipoprotein B in serum remains the same. It is not fully understood which influence a diet, which is rich in poly-unsaturated fatty acids and has a low content of saturated fatty acids and carbohydrates, has upon the lipoproteins in the serum. The mode of action of this diet and its significance for the concentration of HDL need further investigation.

Aged↗

PubMed1979

[The effect of lipid level lowering diets on bile lipids and plasma lipoproteins in normal persons].

The effects of two fat-modified diets, one rich in polyunsaturated and the other in oleic acids, were studied in 10 healthy young males with regard to bile lipid composition, plasma lipids and lipoproteins. The two experimental diets were given for 2 weeks each and findings compared with those from the subject's normal diet. The fat-modified diets had marked but comparable effects on plasma total cholesterol (decreases by 23% and 16% respectively), on LDL-cholesterol (decreases by 27% and 17% respectively) and on HDL-cholesterol (decreases by 26% and 27% respectively). HDL apolipoproteins A-I and A-II were unaffected. Therefore, the apo A-I/HDL-cholesterol and apo A-II/HDL-cholesterol ratios significantly increased. The "lithogenic index" as a measure for the relationship of cholesterol to bile acids and phospholipids, and thus for the solubility of cholesterol in gallbladder bile, was not affected by the lipid lowering diets, which therefore should not increase the risk of cholelithiasis.

Adult↗