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Cardiovascular disease
Published in Sally Robinson, Priorities for Health Promotion and Public Health, 2021
An individual is at higher risk of developing cardiovascular disease if it is present in the family. This may be due to several genes which in combination encourage high blood pressure or high blood cholesterol. Familial hypercholesterolaemia, which means very high LDL blood cholesterol, is an example of an inherited condition caused by at least one parent passing on a mutated gene Sex
Xanthelasma
Published in K. Gupta, P. Carmichael, A. Zumla, 100 Short Cases for the MRCP, 2020
K. Gupta, P. Carmichael, A. Zumla
These are: Eruptive xanthomas: these occur as firm, raised papules with pale yellow centres over the buttocks, elbows, knees and extensor aspect of the forearms. Associations include familial lipoprotein lipase deficiency, familial combined hyperlipidaemia and uncontrolled diabetes mellitus.Planar or palmar xanthomas: often yellow to orange in colour, being most commonly found in the palmar and digital creases. They occur in type III hyperlipidaemia.Tendon xanthomas: these occur in the extensor tendons on the hands, elbows, knees and ankles. Most are characteristic of familial hypercholesterolaemia.• Go over Fredrickson's or the WHO classification of hyperlipidaemias.
Dietary Fiber and Coronary Heart Disease
Published in Robert E.C. Wildman, Richard S. Bruno, Handbook of Nutraceuticals and Functional Foods, 2019
Thunder Jalili, Eunice Mah, Denis M. Medeiros, Robert E.C. Wildman
Elevated serum cholesterol levels can result from a variety of influences. Severely high serum cholesterol is usually due to familial hypercholesterolemia, a condition characterized by genetic defects in LDL receptor activity that result in accumulation of LDL cholesterol in the blood. Elevated serum cholesterol may also occur as a secondary effect of disorders such as diabetes or hypothyroidism, and in alcoholics. More commonly, cholesterol disorders are characterized by mild or moderate hypercholesterolemia and are generally dietary in origin, and recent evidence has shifted the dietary culprits away from simple intake of saturated fats and more toward eating patterns that include increased intake of processed carbohydrates and sugars, both of which are more common in a Western diet.
Red wine consumption mitigates the cognitive impairments in low-density lipoprotein receptor knockout (LDLr−/−) mice
Published in Nutritional Neuroscience, 2021
Gabriela Cristina De Paula, Jade de Oliveira, Daiane Fátima Engel, Samantha Cristiane Lopes, Eduardo Luiz Gasnhar Moreira, Claudia Pinto Figueiredo, Rui Daniel Prediger, Andreza Fabro de Bem
Familial hypercholesterolemia is linked to genetic abnormalities that affect low-density lipoprotein receptor (LDLr) function and implies a hypocatabolism of lipoproteins, mainly LDL particles, and leading to high levels of plasma cholesterol since childhood [11]. LDL particles are not able to cross the intact blood–brain barrier (BBB), however some evidence have linked BBB disruption with hypercholesterolemia [12] and other metabolic disorders [13,14]. Thus, one plausible hypothesis to explain the effect of hypercholesterolemia in cognition is the endothelial dysfunction in the neurovascular unit (NVU). NVU is comprised of different cell types, including specialized vascular cells (endothelial cells and pericytes), glia (astrocytes, oligodendrocytes and microglia) and neurons that contribute to neurovascular coupling [15]. Through NVU, the endothelial cells together with the cellular junctions make up the BBB, working as a key homeostatic site of the central nervous system (CNS) [16]. Molecular changes in these cells, such as that caused by hypercholesterolemia, can lead to BBB disruption and to CNS impairment [16]. The neurovascular abnormalities contribute to neurodegeneration and cognitive decline, raising the vascular hypothesis for Alzheimer's disease [17]. According to this hypothesis, loss of BBB integrity leads to an oxidative-inflammatory cycle in the brain vasculature, initiating a neuroinflammation environment that results in disruption of Aβ peptide metabolism and neuronal dysfunction, supporting the onset of Alzheimer's disease [18].
An update on emerging drugs for the treatment of hypercholesterolemia
Published in Expert Opinion on Emerging Drugs, 2021
Adam J Nelson, Kristen Bubb, Stephen J Nicholls
Angiopoietin-like 3 (ANGPTL3) plays an important role primarily in the regulation of metabolism of triglyceride rich lipoproteins (TRLs). This family of ANGPTL proteins are endogenous inhibitors of lipoprotein lipase, the major factor within the circulation responsible for hydrolysis of TRLs [59]. Loss of function ANGPTL3 variants are associated with lower levels of both triglyceride and LDL cholesterol and a 41% lower risk of coronary heart disease [60]. In patients with homozygous familial hypercholesterolemia, administration of intravenous evinacumab, an ANGPTL3 monoclonal antibody, every 4 weeks produced a 49% reduction in LDL cholesterol levels compared with placebo after 24 weeks. Evinacumab was well tolerated by the patients [61]. This provides an additional therapeutic strategy for the management of patients with homozygous familial hypercholesterolemia
Treatment of heterozygous familial hypercholesterolemia: what does the future hold?
Published in Expert Review of Clinical Pharmacology, 2020
Georgios Polychronopoulos, Konstantinos Tziomalos
Familial hypercholesterolemia (FH) is caused by mutations in one of the genes involved in low-density lipoprotein (LDL) receptor-mediated catabolism of LDL [1]. Approximately 50% of patients with FH have an identifiable mutation and among them, 85–90% have loss-of-function mutations in the LDL receptor gene, 1–12% has loss-of-function mutations in the apolipoprotein B gene and 2–4% has gain-of function mutations in the proprotein convertase subtilisin kexin 9 (PCSK9) gene [2]. Heterozygous FH (heFH) affects approximately 1:311 individuals in the general population [3]. Patients with heFH have markedly increased risk for early-onset atherosclerotic cardiovascular disease (CVD) [4–6]. Diagnosis of heFH is based on a history of premature CVD, identification of deposits of cholesterol in the skin and eyes (tendon xanthomata and arcus cornealis), LDL cholesterol (LDL-C) levels and genetic testing [5,7].