Is Cholesterol Genetic Or Environmental

Study Shows Possible Link Between Air Pollution And Higher Cholesterol Levels

Cholesterol, Genetics, and Metabolism

High cholesterol, especially the bad type, or low-density lipoprotein , is a known risk factor for the development of cardiovascular disease which can lead to heart attacks. After entering the bloodstream, the fatty substance can build up along the walls of arteries and cause clots that slow or stop the flow of blood to the heart.

There are many causes of high cholesterol, including genetics, a high-fat diet, and lack of exercise. One other factor researchers are investigating is whether air pollutants like fine particle pollution, also called PM2.5, contribute to high cholesterol levels, especially LDL. Particle pollution is regulated because, at excessive exposures, it can be hazardous to health. Particles can form as the result of emissions from motor vehicles, industry, smoke from wildfires, and other sources of fossil fuel combustion.

Extensive studies over the past two decades have shown that air pollution can impact the heart and can cause heart attacks in people with cardiovascular disease. One funded by EPA revealed PM2.5 can accelerate narrowing of the arteries, known as atherosclerosis, which sets up conditions for more clotting and a heart attack. More recently, attention has been given to the potential impact on cholesterol levels in those with heart disease. Researchers at EPA are using new diagnostic technology and air quality modeling to better understand the potential links between air quality and high cholesterol.

Genetic And Environmental Determinants Of Plasma High Density Lipoprotein Cholesterol And Apolipoprotein Ai Concentrations In Healthy Middle

Published online by Cambridge University Press:;31 July 2002

P.;J. TALMUD: Affiliation:Division of Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Rayne Building, Royal Free and University College Medical School, 5 University St, London WC1E 6JJ, UK
E. HAWE: Affiliation:Division of Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Rayne Building, Royal Free and University College Medical School, 5 University St, London WC1E 6JJ, UK
K. ROBERTSON: Affiliation:Division of Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Rayne Building, Royal Free and University College Medical School, 5 University St, London WC1E 6JJ, UK
G.;J. MILLER: Affiliation:MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, The Medical College of St Bartholomew’s Hospital, Charterhouse Square, London EC1M 6BQ, UK
N.;E. MILLER: Affiliation:Department of Cardiovascular Biochemistry, St Bartholomew’s and the Royal London School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK
S.;E. HUMPHRIES: Affiliation:Division of Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Rayne Building, Royal Free and University College Medical School, 5 University St, London WC1E 6JJ, UK

Both Genetics And Diet Influence Cholesterol Levels

Date:: Center For The Advancement Of Health
Summary:: New research on twins shows that genetics plays a predominate role in differences in cholesterol levels between people. However, a persons diet also is significantly associated with cholesterol level independent of inherited factors.

New research on twins shows that genetics plays a predominate role in differences in cholesterol levels between people. However, a persons diet also is significantly associated with cholesterol level independent of inherited factors.

Identical twins who differed the most in their dietary intake had corresponding differences in blood cholesterol measures, showing that the association between diet and cholesterol levels was independent of genetic factors, say Jeanne M. McCaffery and Michael F. Pogue-Geile, who conducted the research in the Department of Psychology at the University of Pittsburgh.

This is the first research in twins to demonstrate an environmental association between diet and cholesterol, according to the study published in the September issue of Health Psychology.

Because twins share all their genes, differences between co-twins, and the correlations of these differences seen here must be attributable to environmental effects of some nature, they say.

Jeanne M. McCaffery currently works at Centers for Behavioral and Preventive Medicine at Brown Medical School.

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Confirmatory Cgas In Eurospan

A food- and activity-adjusted candidate gene association study of the final 39 candidate SNPs in the Scottish sample was applied using similar lifestyle covariates . We replicated the effect of rs2000999 in the HP gene on TC level and the effect of rs1532624 in CETP on HDL-C. In the Swedish cohort , the unadjusted genetic effect of rs2000999 in the HP gene is equivalent to a moderately large difference in average TC level of 20.21 mg/dl between the homozyguous genotypes MeanSE,unadj=243.16222.95, Effect SizeSE,unadj=0.41, Effect SizeSE,adj=0.44)=/SDpooled). Equivalent effects were observed in the Scottish replication sample MSC,unadj=235.36 mg/dl222.54 mg/dl=12.82 mg/dl, ESSC,unadj=0.29, ESSC,adj=0.52). SNP rs1532624 in the CETP gene is associated with a large, unadjusted difference in HDL-C level of 9.99 mg/dl MSE,unadj=68.14 mg/dl58.15 mg/dl, ESSE,unadj=0.73, ESSE,adj=0.48) in the discovery cohort and similar effects regarding direction and size in the replication cohort MSC,unadj=69.79 mg/dl60.75 mg/dl=9.04 mg/dl; ESSC, unadj=0.59, ESSC, adj=0.57).

No other associations, including LDL cholesterol or triglycerides levels, were replicated . The genome-wide significant SNP rs2292883 in the Melanophilin gene found in the Swedish cohort was not confirmed.

Genotyping Imputation And Quality Control

Genome-wide SNPs were genotyped using the Illumina’s InfiniumOmni2.5Exome-8v1.2 Bead-Chip platform. We performed stringent genotype quality control procedures: locus missing , minor allele frequency , call rate , and Hardy-Weinberg Equilibrium . The final number of SNPs included in the subsequent GWAS analysis was 1,365,181.

We used the IMPUTE2 software to impute un-typed SNPs using the LD information from 1,000 Genomes Project Phase 3 reference panel . We used R2> 0.6, MAF > 0.05 and HWE > 1 × 104 to filter the imputed data, and the 7,405,822 SNPs were used to explore the association with plasma cholesterol level.

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Treatment For Familial Hypercholesterolaemia

There is no cure for familial hypercholesterolaemia. Treatment aims to reduce the persons risk of coronary artery disease and heart attack, and may include:

Dietary changes recommended dietary changes include reduced intake of saturated fats and cholesterol-rich foods, and increased intake of fibre. Modifying the diet is usually the first line of treatment. After three months, test results will show whether more aggressive treatment is needed.
Plant sterols and stanols these substances are structurally similar to cholesterol, but arent absorbed by the cells. Studies show that increasing the intake of plant sterols and stanols can substantially reduce blood cholesterol. Sources include corn, rice, vegetable oils and nuts.
Exercise regular exercise has been shown to reduce blood cholesterol levels. Any exercise program should be supervised by your doctor.
Weight loss obesity is a risk factor. Maintaining a healthy weight for your height can reduce your risk of coronary artery disease and heart attack.
Avoid smoking cigarette smoke encourages cholesterol to stick to artery walls. Quitting can significantly reduce your risk of heart attack.
Medication very few people with familial hypercholesterolaemia will be able to reduce their cholesterol levels by diet and lifestyle changes alone. Most will need special cholesterol-lowering drugs.

Obesity Or Large Waist Circumference

Some people are genetically predisposed toward obesity or a large waist circumference. Both can increase your risk for high cholesterol. Lifestyle factors also play a role in these two risk factors.

Obesity is defined as a body mass index of 30 or higher.

A large waist circumference is 40 or more inches for men and 35 or more inches for women. Fat that accumulates in your waist increases your risk of elevated cholesterol and other cardiovascular complications.

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Symptoms Of Familial Hypercholesterolaemia

High blood cholesterol can be asymptomatic, which means the person may not even realise they have it. Some of the signs and symptoms of familial hypercholesterolaemia can include:

family history of the disorder
family history of heart attacks at an early age
high LDL cholesterol levels that resist treatment in one or both parents
cholesterol deposits on the knees, elbows and buttocks
high blood cholesterol levels
chest pain caused by narrowed coronary arteries
heart attack early in life.

Exploratory Gwas In Nsphs

Genes and Environment

We performed a GWAS with a lifestyle-adjusted model which included not only sex and age, but also daily intake of game meat, non-game meat, fish, milk products, physical activity at work and at leisure as covariates. We focused on the 0.05% of all SNPs with the lowest p-values in the diet- and activity-adjusted model . For total cholesterol, 88 of these were located in a gene and 14 in genes that have been associated with energy metabolism . For LDL-C, 65 SNPs were located in a gene, of which 8 were functionally relevant. Several of the SNPs for LDL-C were identical with those affecting total cholesterol, as expected from the high correlation between both phenotypes. For HDL-C, SNP rs2292883, located in the MLPH gene , showed a genome-wide significant p-value . 69 SNPs for HDL-C were located in a gene and 14 of those genes were reported as having a metabolic effect. Finally, for triglycerides, 63 SNPs were located in a gene, but only 4 SNPs in genes with a functional annotation of interest .

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Familial Hypercholesterolemia Vs High Cholesterol

If you have a close relative, such as a parent, sibling, or grandparent, who has high levels of cholesterol, youre more likely to have it yourself. This is largely due to the passing on of genes from parents to children that increase levels of cholesterol in the blood, such as a gene that codes for a defective receptor. This is known as familial hypercholesterolemia.

Familial hypercholesterolemia is a form of inherited high cholesterol. People with this condition generally have higher cholesterol levels than people without this condition, despite lifestyle choices. Thats because people with this condition arent able to regulate cholesterol levels as efficiently as other people. People with familial hypercholesterolemia cant control their cholesterol through diet and exercise alone, and may instead need to also use medication.

Having a genetic risk for high cholesterol doesnt guarantee that youll have high cholesterol. It just means that you have an increased risk. Let your doctor know about your concerns. They can help you manage your cholesterol and monitor your levels so that if you do develop high cholesterol, you can begin treatment right away.

Interactions Among Genes Involved In Reverse Cholesterol Transport And In The Response To Environmental Factors In Dyslipidemia In Subjects From The Xinjiang Rural Area

Contributed equally to this work with: Xinping Wang, Heng Guo

Roles Formal analysis, Writing original draft

Affiliation Department of Public Health, Shihezi University School of Medicine, Shihezi, China
Contributed equally to this work with: Xinping Wang, Heng Guo

Roles Data curation

Affiliation Department of Public Health, Shihezi University School of Medicine, Shihezi, China

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When High Cholesterol Is A Family Affair

An inherited form of high cholesterol familial hypercholesterolemia demands serious action.

Most of us with high cholesterol have the garden-variety type brought on by eating too much cholesterol and saturated fat and too few fruits, vegetables, and whole grains. More than half a million Americans, though, have a more dangerous type. It stems from an inherited error that can send harmful low-density lipoprotein cholesterol into the stratosphere. This often undetected condition, called familial hypercholesterolemia, can cause an early heart attack, stroke, or premature death. Since the name of the disease is a mouthful, we’ll refer to it as FH.

Twin Samples Collection And Phenotypic Measurement

How a small molecule promotes removal of excess ...

The twin samples were collected from Qingdao Twin Registry and the details can be found in the literatures . Twins who were pregnancy and lactation, as well as incomplete co-twin pairs were excluded. Twin pairs that taking cholesterol-lowering drugs also were excluded. The study included 382 twin pairs for heritability analysis and 139 dizygotic twin pairs for GWAS with a mean age of 51.6 ± 7.7. All twin samples undertook the blood sampling and a physical examination after a 1012 h overnight fast and completed a questionnaire. The zygosity of same sex and blood type was identified by using 16 multiple short tandem sequence repeat DNA markers . According to the standard procedure using an automatic biochemical analyzer , we tested participants’ fasting blood cholesterol sample in the Qingdao Diabetes Hospital. Friedewald equation was used to calculate the LDL-C level: LDL-C = TCHDL-C .

The Regional Ethics Committee of the Qingdao CDC Institutional Review Boards approved this study and the ethical principles followed the Helsinki Declaration. All subjects signed the written informed consent.

Current Views On Genetics And Epigenetics Of Cholesterol Gallstone Disease

Piero Portincasa

1Division of Internal Medicine Hospital of Bisceglie, 76011 Bisceglie, Italy

2Saint Louis University School of Medicine, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Edward Doisy Research Center, St. Louis, MO 63104, USA

3Clinica Medica A. Murri, Department of Biomedical Sciences & Human Oncology, University Aldo Moro of Bari Medical School, 70124 Bari, Italy

4European Society for Clinical Investigation , 3584 CJ Utrecht, The Netherlands

Academic Editor:

Abstract

1. Introduction

Independent

Low grade physical activity

Prolonged fasting

Nonalcoholic fatty liver disease

Gallbladder and/or intestinal stasis

A comprehensive analysis of these latter aspects as key factors in linking cholesterol homeostasis to gene expression and to the environment might provide a clue for both the prevention of gallstone formation in subjects at risk and future therapeutic approaches via manipulation of cholesterol homeostasis.

2. Cholesterol Homeostasis and the Formation of Cholesterol Gallstones

2.1. Multifactorial Contributions to the Pathogenesis of Gallstones

LITHLITHLITH

2.2. Liver, Bile, Intestine, Gene Expression, and Cholesterol Homeostasis

The liver plays a central role in cholesterol homeostasis and lipoprotein metabolism since it is mainly involved in synthesis and catabolism of cholesterol and lipoproteins and is the exclusive excretory route for cholesterol from the body .

Genetics Of Familial Hypercholesterolaemia

Cholesterol is delivered to cells via the bloodstream. Normally, the tiny particles of LDL cholesterol attach to receptor sites on the targeted cells and are then absorbed. A gene on chromosome 19, called the LDLR gene, controls the production of these receptors. Most familial hypercholesterolaemia is due to a mutation of the LDLR gene that changes the way the receptors develop, either in number or structure. This means that LDL cholesterol is not well absorbed into cells, and remains circulating in the blood.High blood cholesterol is a risk factor in coronary artery disease, because it sticks to the artery walls, produces fatty plaques and narrows the diameter of the arteries . Less commonly, familial hypercholesterolemia is caused by a mutation on other genes, such as APOB or PCSK9.

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Factors Known To Influence Plasma Hdl

Smoking was defined as ever having smoked . Body mass index was calculated from height and length . Alcohol use was determined at the time of the first visit to the lipid clinic . Hypertension was defined when the diagnosis had been made and when antihypertensive medication was prescribed, or if three consecutive measurements of blood pressure were >140âmmHg systolic or >90âmmHg diastolic. Concomitant beta-blocker and/or diuretic use were assessed at the time of determination of plasma HDL-C concentration . Diabetes mellitus was defined when the diagnosis had been made and medication was prescribed, or by a fasting plasma glucose of >6.9âmmol/l.

How To Face Your Family History

Cholesterol Education

Lifestyle choices and medications can help undo the damage of faulty genes and deep-seated family traditions.

âI grew up eating lots of cheese, and I love cheese, but now I avoid high-fat dairy products,â Addis says. âAnd I choose not to eat red meat and whole eggs.â She wears an activity tracker to keep her motivated to stay active. Her medications help with what diet and exercise canât do.

Today, her cholesterol holds steady between 220 and 240 on her current medications.

What keeps her going, Addis says, is thinking in positives, rather than negatives. âWhen your doctor says you have high cholesterol and you need to do something about it, you think youâre not supposed to have this, youâre not supposed to have that. But I thought of the new things I could try,â she says.

âIt really helped me to start exploring cooking more, to think more about using spices, interesting ingredients, and trying new recipes. Thereâs a lot of really good stuff out there that doesnât have to be high in fat. You can eat healthier food and still have really tasty food.â

Thatâs a legacy anyone would love to pass on.

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What Causes Unhealthy Levels Of Cholesterol To Occur In Your Body

There are two main forms of cholesterol. The first, LDL cholesterol, is often called bad cholesterol. Its considered unhealthy to have high levels of LDL cholesterol in your body. The other, HDL cholesterol, is sometimes referred to as good cholesterol. Higher levels of HDL cholesterol can be a sign of good health.

If your doctor tells you that you have high cholesterol, theyre usually referring to either high levels of LDL cholesterol or a high level of total cholesterol. Total cholesterol is also sometimes called serum cholesterol. Its the sum of LDL and HDL cholesterol and 20 percent of your triglycerides. LDL cholesterol and total cholesterol can be used as indicators of your risk of developing cardiovascular disease and other complications.

A variety of risk factors contribute to unhealthy levels of cholesterol, including genetics, lifestyle choices, or a combination of the two.

Commingling Analysis Familial Correlation Coefficients And Heritability Analyses

Commingling analysis of various lipid profiles was performed using the ADMIX program to test whether the data were best described by one, two, or more component distributions. The parameters for each component’s mean, variance, and proportion were estimated by the maximum likelihood method. Hypothesis testing for nested models was carried out with the likelihood ratio test. The correlations of various lipid profiles between spouse, parent-offspring, and siblings were estimated by using the FCOR program in SAGE . We tested if the correlation coefficients were different from zero and tested if the two family coefficients between two samples by the methods of Snedecor and Cochran . To estimating the shared environmental effects by inclusion of household effects, we used the variance component models to evaluate the heritability and common shared environmental factors, implemented in SOLAR software .