ATP Binding Cassette Transporter 1
Hydroxymethylglutaryl CoA Reductases
Bile Acids and Salts
Cholesterol Ester Transfer Proteins
ATP-Binding Cassette Transporters
Scavenger Receptors, Class B
Hydroxymethylglutaryl-CoA Reductase Inhibitors
High-Density Lipoproteins, Pre-beta
Orphan Nuclear Receptors
Cholesterol Side-Chain Cleavage Enzyme
Hyperlipoproteinemia Type II
Sterol Regulatory Element Binding Protein 2
Lecithin Acyltransferase Deficiency
Phospholipid Transfer Proteins
Body Mass Index
Metabolic Syndrome X
Fatty Acids, Unsaturated
Chromatography, Thin Layer
Receptors, Cytoplasmic and Nuclear
Rats, Inbred Strains
Dose-Response Relationship, Drug
Diabetes Mellitus, Type 2
Niemann-Pick Disease, Type C
Sterol Regulatory Element Binding Protein 1
Serum triglyceride: a possible risk factor for ruptured abdominal aortic aneurysm. (1/5144)BACKGROUND: We aimed to determine the relationship between ruptured abdominal aortic aneurysm (AAA) and serum concentrations of lipids and apolipoproteins. METHODS: A cohort of 21 520 men, aged 35-64 years, was recruited from men attending the British United Provident Association (BUPA) clinic in London for a routine medical examination in 1975-1982. Smoking habits, weight, height and blood pressure were recorded at entry. Lipids and apolipoproteins were measured in stored serum samples from the 30 men who subsequently died of ruptured AAA and 150 matched controls. RESULTS: Triglyceride was strongly related to risk of ruptured AAA. In univariate analyses the risk in men on the 90th centile of the distribution relative to the risk in men on the 10th (RO10-90) was 12 (95% confidence interval [CI] : 3.8-37) for triglyceride, 5.5 (95% CI: 1.8-17) for apolipoprotein B (apoB) (the protein component of low density lipoprotein [LDL]), 0.15 (95% CI : 0.04-0.56) for apo A1 (the protein component of high density lipoprotein [HDL]), 3.7 (95% CI: 1.4-9.4) for body mass index and 3.0 (95% CI: 1.1-8.5) for systolic blood pressure. Lipoprotein (a) (Lp(a)) was not a significant risk factor (RO10-90 = 1.6, 95% CI: 0.6-3.0). In multivariate analysis triglyceride retained its strong association. CONCLUSION: Triglyceride appears to be a strong risk factor for ruptured AAA, although further studies are required to clarify this. If this and other associations are cause and effect, then changing the distribution of risk factors in the population (by many people stopping smoking and adopting a lower saturated fat diet and by lowering blood pressure) could achieve an important reduction in mortality from ruptured AAA. (+info)
Association of the inflammatory state in active juvenile rheumatoid arthritis with hypo-high-density lipoproteinemia and reduced lipoprotein-associated platelet-activating factor acetylhydrolase activity. (2/5144)OBJECTIVE: To investigate the relationship between the quantitative and qualitative abnormalities of apolipoprotein B (Apo B)- and Apo A-I-containing lipoproteins and between lipoprotein-associated platelet-activating factor acetylhydrolase (PAF-AH) activity in patients with juvenile rheumatoid arthritis (JRA) as a function of the inflammatory state. METHODS: Twenty-six JRA patients and 22 age- and sex-matched control subjects with normal lipid levels participated in the study. Fourteen patients had active disease, and 12 had inactive disease. Plasma lipoproteins were fractionated by gradient ultracentrifugation into 9 subfractions, and their chemical composition and mass were determined. The PAF-AH activity associated with lipoprotein subfractions and the activity in plasma were also measured. RESULTS: Patients with active JRA had significantly lower plasma total cholesterol and high-density lipoprotein (HDL) cholesterol levels as compared with controls, due to the decrease in the mass of both the HDL2 and HDL3 subfractions. Patients with active JRA also had higher plasma triglyceride levels, mainly due to the higher triglyceride content of the very low-density lipoprotein plus the intermediate-density lipoprotein subfraction. The plasma PAF-AH activity in patients with active JRA was lower than that in controls, mainly due to the decrease in PAF-AH activity associated with the intermediate and dense low-density lipoprotein subclasses. The lipid abnormalities and the reduction in plasma PAF-AH activity were significantly correlated with plasma C-reactive protein levels and were not observed in patients with inactive JRA. CONCLUSION: This is the first study to show that patients with active JRA exhibit low levels of HDL2 and HDL3 and are deficient in plasma PAF-AH activity. These alterations suggest that active JRA is associated with partial loss of the antiinflammatory activity of plasma Apo B- and Apo A-I-containing lipoproteins. (+info)
Chlamydia pneumoniae antibodies are associated with an atherogenic lipid profile. (3/5144)OBJECTIVE: To determine, within a representative population group of men and women, whether alteration of the lipid profile might underlie the reported association between Chlamydia pneumoniae and ischaemic heart disease. DESIGN AND SETTING: Cross sectional survey in an area with a high incidence of ischaemic heart disease. SUBJECTS: 400 randomly selected participants in the World Health Organisation MONICA project's third population survey in Northern Ireland. MAIN OUTCOME MEASURES: Stored sera were examined by microimmunofluorescence for IgG antibodies to C pneumoniae at a dilution of 1 in 64. Mean total and high density lipoprotein (HDL) cholesterol were compared between seropositive and seronegative individuals with adjustment for age, measures of socioeconomic status, smoking habit, alcohol consumption, body mass index, and the season during which blood had been taken. RESULTS: In seropositive men, adjusted mean serum total cholesterol and HDL cholesterol were 0.5 mmol/l (9.2%) higher and 0.11 mmol/l (9.3%) lower, respectively, than in seronegative men. Differences in women did not achieve statistical significance, but both total cholesterol and HDL cholesterol were higher (3.6% and 5.8%, respectively) in seropositive than in seronegative individuals. CONCLUSIONS: There is serological evidence that C pneumoniae infection is associated with an atherogenic lipid profile in men. Altered lipid levels may underlie the association between C pneumoniae and ischaemic heart disease. (+info)
Effect of fasting on temporal variation in the nephrotoxicity of amphotericin B in rats. (4/5144)Evidence for temporal variation in the nephrotoxicity of amphotericin B was recently reported in experimental animals. The role of food in these variations was determined by studying the effect of a short fasting period on the temporal variation in the renal toxicity of amphotericin B. Twenty-eight normally fed and 28 fasted female Sprague-Dawley rats were used. Food was available ad libitum to the fed rats, while the fasted animals were fasted 12 h before and 24 h after amphotericin B injection to minimize stress for the animals. Water was available ad libitum to both groups of rats, which were maintained on a 14-h light, 10-h dark regimen (light on at 0600 h). Renal toxicity was determined by comparing the levels of excretion of renal enzyme and the serum creatinine and blood urea nitrogen (BUN) levels at the time of the maximal (0700 h) or the minimal (1900 h) nephrotoxicity after the intraperitoneal administration of a single dose of dextrose (5%; control group) or amphotericin B (50 mg/kg of body weight; treated group) to the rats. The nephrotoxicities obtained after amphotericin B administration at both times of day were compared to the nephrotoxicities observed for time-matched controls. In fed animals, the 24-h urinary excretion of N-acetyl-beta-D-glucosaminidase and beta-galactosidase was significantly higher when amphotericin B was injected at 0700 and 1900 h. The excretion of these two enzymes was reduced significantly (P < 0.05) in fasting rats, and this effect was larger at 0700 h (P < 0.05) than at 1900 h. The serum creatinine level was also significantly higher (P < 0.05) in fed animals treated at 0700 h than in fed animals treated at 1900 h. Fasting reduced significantly (P < 0.05) the increase in the serum creatinine level, and this effect was larger in the animals treated at 0700 h. Similar data were obtained for BUN levels. Amphotericin B accumulation was significantly higher (P < 0.05) in the renal cortexes of fed rats than in those of fasted animals, but there was no difference according to the time of injection. These results demonstrated that fasting reduces the nephrotoxicity of amphotericin B and that food availability is of crucial importance in the temporal variation in the renal toxicity of amphotericin B in rats. (+info)
The impact of an amino acid-based peritoneal dialysis fluid on plasma total homocysteine levels, lipid profile and body fat mass. (5/5144)BACKGROUND: The caloric load from glucose-based peritoneal dialysis (PD) fluids contributes to hypertriglyceridaemia, adiposity and, as result of anorexia, protein malnutrition in PD patients. It has been suggested that replacement of a glucose-based by an amino acids-based PD fluid (AA-PDF) for one exchange per day might improve the nutritional status and lipid profile. Due to the uptake of methionine from the dialysate, however, exposure to AA-PDF might aggravate hyperhomocysteinaemia, a frequently occurring risk factor for atherosclerosis in uraemic patients. METHODS: We studied the impact of a once daily exchange with 1.1% AA-PDF instead of glucose-based PD fluid for 2 months on plasma methionine and total homocysteine (tHcy) levels, lipid profile, butyrylcholinesterase (BChE) and body fat mass of seven stable PD patients. Results are expressed as mean+/-SEM. RESULTS: Methionine levels did not increase significantly during therapy, but tHcy levels increased substantially from 60+/-12 to 84+/-19 micromol/l after 1 month (P=0.039), and to 85+/-22 micromol/l after 2 months of AA-PDF treatment. Serum triglyceride concentration decreased from 3.0+/-0.4 mmol/l at entry to 2.6+/-0.5 mmol/l (at 1 month, P=0.041 vs baseline). Serum BChE also decreased from 6.9+/-0.4 U/ml at entry to 6.3+/-0.4 U/ml after 2 months (P=0.014). Total cholesterol concentration and cholesterol fractions did not change. The reduced exposure to glucose-based PD fluid for 2 months resulted in a 0.5 kg reduction in fat mass which was due mainly to a reduction in fat mass of the trunk region (0.3 kg, P=0.031). CONCLUSIONS: It is concluded that methionine-containing AA-PDF induces an increase in the plasma tHcy level. This might, potentially, offset the beneficial effects of an improved serum lipid profile and reduced fat mass on the risk of cardiovascular disease in PD patients. Lowering the methionine content of the fluid, therefore, may be required to overcome this adverse effect. (+info)
Survey of total error of precipitation and homogeneous HDL-cholesterol methods and simultaneous evaluation of lyophilized saccharose-containing candidate reference materials for HDL-cholesterol. (6/5144)BACKGROUND: Standardization of HDL-cholesterol is needed for risk assessment. We assessed for the first time the accuracy of HDL-cholesterol testing in The Netherlands and evaluated 11 candidate reference materials (CRMs). METHODS: The total error (TE) of HDL-cholesterol measurements was assessed in native human sera by 25 Dutch clinical chemistry laboratories. Concomitantly, the suitability of lyophilized, saccharose-containing CRMs (n = 11) for HDL-cholesterol was evaluated. RESULTS: In the precipitation method group, which included 25 laboratories and four methods, the mean (minimum-maximum) TE was 11.5% (2.7-25.2%), signifying that 18 of 25 laboratories satisfied the TE goal of +info)
Elevated hepatic lipase activity and low levels of high density lipoprotein in a normotriglyceridemic, nonobese Turkish population. (7/5144)Low levels of high density lipoprotein cholesterol (HDL-C) are associated with increased risk of coronary heart disease and, in the United States, are often associated with hypertriglyceridemia and obesity. In Turkey, low HDL-C levels are highly prevalent, 53% of men and 26% of women having HDL-C levels <35 mg/dl, in the absence of hypertriglyceridemia and obesity. In this study to investigate the cause of low HDL-C levels in Turks, various factors affecting HDL metabolism were assessed in normotriglyceridemic Turkish men and women living in Istanbul and in non-Turkish men and women living in San Francisco. Turkish men and women had significantly lower HDL-C levels than the San Francisco men and women, as well as markedly lower apolipoprotein A-I levels (25 and 39 mg/dl lower, respectively). In both Turkish and non-Turkish subjects, the mean body mass index was <27 kg/m2, the mean triglyceride level was <120 mg/dl, and the mean total cholesterol was 170-180 mg/dl. The mean hepatic triglyceride lipase activity was 21% and 31% higher in Turkish men and women, respectively, than in non-Turkish men and women, and remained higher even after subjects with a body mass index >50th percentile for men and women in the United States were excluded from the analysis. As no dietary or behavioral factors have been identified in the Turkish population that account for increased hepatic triglyceride lipase activity, the elevation most likely has a genetic basis. high density lipoprotein in a normotriglyceridemic, nonobese Turkish population. (+info)
Comparison of synthetic saponin cholesterol absorption inhibitors in rabbits: evidence for a non-stoichiometric, intestinal mechanism of action. (8/5144)The hypocholesterolemic activities of pamaqueside and tiqueside, two structurally similar saponins, were evaluated in cholesterol-fed rabbits. The pharmacological profiles of the saponins were virtually identical: both dose-dependently decreased the intestinal absorption of labeled cholesterol 25-75%, increased fecal neutral sterol excretion up to 2.5-fold, and decreased hepatic cholesterol content 10-55%. High doses of pamaqueside (>5 mg/kg) or tiqueside (>125 mg/kg) completely prevented hypercholesterolemia. Decreases in plasma and hepatic cholesterol levels were strongly correlated with increased neutral sterol excretion. Ratios of neutral sterol excreted to pamaqueside administered were greater than 1:1 at all doses, in opposition to the formation of a stoichiometric complex previously suggested for tiqueside and other saponins. Ratios in tiqueside-treated rabbits were less than unity, a reflection of its lower potency. Pamaqueside-treated rabbits exhibited a more rapid decline in plasma cholesterol concentrations than control animals fed a cholesterol-free diet, indicating that the compound also inhibited the absorption of biliary cholesterol. Intravenous administration of pamaqueside had no effect on plasma cholesterol levels despite plasma levels twice those observed in rabbits given pamaqueside orally. These data indicate that pamaqueside and tiqueside induce hypocholesterolemia by blocking lumenal cholesterol absorption via a mechanism that apparently differs from the stoichiometric complexation of cholesterol hypothesized for other saponins. (+info)
There are several types of hypercholesterolemia, including:
1. Familial hypercholesterolemia: This is an inherited condition that causes high levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood.
2. Non-familial hypercholesterolemia: This type of hypercholesterolemia is not inherited and can be caused by a variety of factors, such as a high-fat diet, lack of exercise, obesity, and certain medical conditions, such as hypothyroidism or polycystic ovary syndrome (PCOS).
3. Mixed hypercholesterolemia: This type of hypercholesterolemia is characterized by high levels of both LDL and high-density lipoprotein (HDL) cholesterol in the blood.
The diagnosis of hypercholesterolemia is typically made based on a physical examination, medical history, and laboratory tests, such as a lipid profile, which measures the levels of different types of cholesterol and triglycerides in the blood. Treatment for hypercholesterolemia usually involves lifestyle changes, such as a healthy diet and regular exercise, and may also include medication, such as statins, to lower cholesterol levels.
There are several types of hyperlipidemia, including:
1. High cholesterol: This is the most common type of hyperlipidemia and is characterized by elevated levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol.
2. High triglycerides: This type of hyperlipidemia is characterized by elevated levels of triglycerides in the blood. Triglycerides are a type of fat found in the blood that is used for energy.
3. Low high-density lipoprotein (HDL) cholesterol: HDL cholesterol is known as "good" cholesterol because it helps remove excess cholesterol from the bloodstream and transport it to the liver for excretion. Low levels of HDL cholesterol can contribute to hyperlipidemia.
Symptoms of hyperlipidemia may include xanthomas (fatty deposits on the skin), corneal arcus (a cloudy ring around the iris of the eye), and tendon xanthomas (tender lumps under the skin). However, many people with hyperlipidemia have no symptoms at all.
Hyperlipidemia can be diagnosed through a series of blood tests that measure the levels of different types of cholesterol and triglycerides in the blood. Treatment for hyperlipidemia typically involves dietary changes, such as reducing intake of saturated fats and cholesterol, and increasing physical activity. Medications such as statins, fibric acid derivatives, and bile acid sequestrants may also be prescribed to lower cholesterol levels.
In severe cases of hyperlipidemia, atherosclerosis (hardening of the arteries) can occur, which can lead to cardiovascular disease, including heart attacks and strokes. Therefore, it is important to diagnose and treat hyperlipidemia early on to prevent these complications.
Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.
There are several types of arteriosclerosis, including:
1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.
Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.
The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.
The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.
Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.
Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.
In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.
Cholelithiasis is a common condition that affects millions of people worldwide. It can occur at any age but is more common in adults over 40 years old. Women are more likely to develop cholelithiasis than men, especially during pregnancy or after childbirth.
The symptoms of cholelithiasis can vary depending on the size and location of the gallstones. Some people may not experience any symptoms at all, while others may have:
* Abdominal pain, especially in the upper right side of the abdomen
* Nausea and vomiting
* Shaking or chills
* Loss of appetite
* Yellowing of the skin and eyes (jaundice)
If left untreated, cholelithiasis can lead to complications such as inflammation of the gallbladder (cholangitis), infection of the bile ducts (biliary sepsis), or blockage of the common bile duct. These complications can be life-threatening and require immediate medical attention.
The diagnosis of cholelithiasis is usually made through a combination of imaging tests such as ultrasound, CT scan, or MRI, and blood tests to check for signs of inflammation and liver function. Treatment options for cholelithiasis include:
* Watchful waiting: If the gallstones are small and not causing any symptoms, doctors may recommend monitoring the condition without immediate treatment.
* Medications: Oral medications such as bile salts or ursodiol can dissolve small gallstones and relieve symptoms.
* Laparoscopic cholecystectomy: A minimally invasive surgical procedure to remove the gallbladder through small incisions.
* Open cholecystectomy: An open surgery to remove the gallbladder, usually performed when the gallstones are large or there are other complications.
It is important to seek medical attention if you experience any symptoms of cholelithiasis, as early diagnosis and treatment can help prevent complications and improve outcomes.
People with Tangier disease often have extremely high levels of low-density lipoprotein (LDL) cholesterol, which can lead to the development of cardiovascular disease at an early age. The disorder is caused by mutations in the gene that codes for a protein called ATP-binding cassette transporter 1 (ABC1), which plays a critical role in the transport of cholesterol and other lipids in the body.
The symptoms of Tangier disease can vary depending on the severity of the disorder, but may include:
* High levels of LDL cholesterol
* Low levels of HDL cholesterol
* Abnormal liver function tests
* Yellowing of the skin and eyes (jaundice)
* Muscle cramps
* Heart disease
Tangier disease is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the disorder typically involves a combination of dietary modifications, medications, and lipid-lowering therapy to reduce the levels of LDL cholesterol and increase the levels of HDL cholesterol. In some cases, a liver transplant may be necessary to treat the liver damage that can occur as a result of the disorder.
There are several types of dyslipidemias, including:
1. Hyperlipidemia: Elevated levels of lipids and lipoproteins in the blood, which can increase the risk of CVD.
2. Hypolipidemia: Low levels of lipids and lipoproteins in the blood, which can also increase the risk of CVD.
3. Mixed dyslipidemia: A combination of hyperlipidemia and hypolipidemia.
4. Familial dyslipidemia: An inherited condition that affects the levels of lipids and lipoproteins in the blood.
5. Acquired dyslipidemia: A condition caused by other factors, such as poor diet or medication side effects.
Dyslipidemias can be diagnosed through a variety of tests, including fasting blood sugar (FBS), lipid profile, and apolipoprotein testing. Treatment for dyslipidemias often involves lifestyle changes, such as dietary modifications and increased physical activity, as well as medications to lower cholesterol and triglycerides.
In conclusion, dyslipidemias are abnormalities in the levels or composition of lipids and lipoproteins in the blood that can increase the risk of CVD. They can be caused by a variety of factors and diagnosed through several tests. Treatment often involves lifestyle changes and medications to lower cholesterol and triglycerides.
Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.
The symptoms of coronary disease can vary depending on the severity of the condition, but may include:
* Chest pain or discomfort (angina)
* Shortness of breath
* Swelling of the legs and feet
* Pain in the arms and back
Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.
Preventative measures for coronary disease include:
* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.
There are three main types of Niemann-Pick diseases:
1. Type A: This is the most common and severe form of the disease, and it typically affects infants before the age of one. It is characterized by progressive loss of motor skills, seizures, and death before the age of two.
2. Type B: This form of the disease usually presents in adulthood and is characterized by gradually worsening neurological symptoms, including muscle weakness, ataxia (loss of coordination), and dementia. Life expectancy for individuals with type B Niemann-Pick disease is typically between 20 and 40 years.
3. Type C: This form of the disease is less severe than types A and B and is often diagnosed in childhood or adolescence. It is characterized by a range of symptoms, including developmental delays, learning disabilities, and mild neurological problems.
Niemann-Pick diseases are caused by mutations in the genes that code for proteins involved in lipid metabolism. These proteins play a crucial role in the transport of lipids within cells, particularly in the brain and other organs. Without these proteins, lipids accumulate in cells and cause damage to their membranes and organelles.
There is currently no cure for Niemann-Pick diseases, but researchers are working on developing new treatments that may help alleviate some of the symptoms and slow the progression of the disease. These treatments include enzyme replacement therapy, gene therapy, and small molecule therapies. In addition, clinical trials are underway to evaluate the safety and effectiveness of these new treatments in humans.
In summary, Niemann-Pick diseases are a group of rare and severe genetic disorders that affect the transport of lipids within cells. There is currently no cure for these diseases, but researchers are working on developing new treatments that may help alleviate some of the symptoms and slow the progression of the disease.
Answer: Type A, B, and C Niemann-Pick disease are three forms of a group of rare genetic disorders that affect lipid metabolism, with types A and B being more severe and type C being less severe.
1. Coronary artery disease: The narrowing or blockage of the coronary arteries, which supply blood to the heart.
2. Heart failure: A condition in which the heart is unable to pump enough blood to meet the body's needs.
3. Arrhythmias: Abnormal heart rhythms that can be too fast, too slow, or irregular.
4. Heart valve disease: Problems with the heart valves that control blood flow through the heart.
5. Heart muscle disease (cardiomyopathy): Disease of the heart muscle that can lead to heart failure.
6. Congenital heart disease: Defects in the heart's structure and function that are present at birth.
7. Peripheral artery disease: The narrowing or blockage of blood vessels that supply oxygen and nutrients to the arms, legs, and other organs.
8. Deep vein thrombosis (DVT): A blood clot that forms in a deep vein, usually in the leg.
9. Pulmonary embolism: A blockage in one of the arteries in the lungs, which can be caused by a blood clot or other debris.
10. Stroke: A condition in which there is a lack of oxygen to the brain due to a blockage or rupture of blood vessels.
The condition is caused by mutations in the genes that code for proteins involved in cholesterol transport and metabolism, such as the low-density lipoprotein receptor gene (LDLR) or the PCSK9 gene. These mutations lead to a decrease in the ability of the liver to remove excess cholesterol from the bloodstream, resulting in high levels of LDL cholesterol and low levels of HDL cholesterol.
Hyperlipoproteinemia type II is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases can be caused by spontaneous mutations or incomplete penetrance, where not all individuals with the mutated gene develop the condition.
Symptoms of hyperlipoproteinemia type II can include xanthomas (yellowish deposits of cholesterol in the skin), corneal arcus (a white, waxy deposit on the iris of the eye), and tendon xanthomas (small, soft deposits of cholesterol under the skin). Treatment typically involves a combination of dietary changes and medication to lower LDL cholesterol levels and increase HDL cholesterol levels. In severe cases, liver transplantation may be necessary.
Hyperlipoproteinemia type II is a serious condition that can lead to cardiovascular disease, including heart attacks, strokes, and peripheral artery disease. Early diagnosis and treatment are important to prevent or delay the progression of the disease and reduce the risk of complications.
The primary symptom of LCAT deficiency is a high level of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood. This can lead to the development of cholesterol deposits in the skin, eyes, and other tissues, which can cause a range of health problems including xanthomas (yellowish patches on the skin), corneal arcus (a cloudy ring around the cornea of the eye), and xanthelasma (yellowish patches on the eyelids).
Treatment for LCAT deficiency typically involves a combination of dietary changes, such as reducing intake of saturated fats and cholesterol, and medication to lower cholesterol levels. In some cases, liver transplantation may be necessary.
Prevention of LCAT deficiency is not possible, as it is a genetic disorder that is inherited in an autosomal recessive pattern. This means that a child must inherit two copies of the mutated LCAT gene, one from each parent, to develop the condition. However, early detection and treatment can help manage the symptoms and prevent complications.
The diagnosis of LCAT deficiency is based on a combination of clinical features, laboratory tests, and genetic analysis. Laboratory tests may include measurements of lipid levels in the blood, as well as assays for LCAT enzyme activity. Genetic testing can identify the presence of mutations in the LCAT gene that cause the condition.
Overall, LCAT deficiency is a rare and potentially serious genetic disorder that affects the body's ability to metabolize cholesterol and other fats. Early diagnosis and treatment can help manage the symptoms and prevent complications, but there is currently no cure for the condition.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
There are several causes of hypertriglyceridemia, including:
* Genetics: Some people may inherit a tendency to have high triglyceride levels due to genetic mutations that affect the genes involved in triglyceride metabolism.
* Obesity: Excess body weight is associated with higher triglyceride levels, as there is more fat available for energy.
* Diabetes: Both type 1 and type 2 diabetes can lead to high triglyceride levels due to insulin resistance and altered glucose metabolism.
* High-carbohydrate diet: Consuming high amounts of carbohydrates, particularly refined or simple carbohydrates, can cause a spike in blood triglycerides.
* Alcohol consumption: Drinking too much alcohol can increase triglyceride levels in the blood.
* Certain medications: Some drugs, such as anabolic steroids and some antidepressants, can raise triglyceride levels.
* Underlying medical conditions: Certain medical conditions, such as hypothyroidism, kidney disease, and polycystic ovary syndrome (PCOS), can also contribute to high triglyceride levels.
Hypertriglyceridemia is typically diagnosed with a blood test that measures the level of triglycerides in the blood. Treatment options for hypertriglyceridemia depend on the underlying cause of the condition, but may include lifestyle modifications such as weight loss, dietary changes, and medications to lower triglyceride levels.
The most common form of hypolipoproteinemia is familial hypobetalipoproteinemia (FHBL), which is caused by mutations in the gene encoding apoB, a protein component of low-density lipoproteins (LDL). People with FHBL have extremely low levels of LDL cholesterol and often develop symptoms such as fatty liver disease, liver cirrhosis, and cardiovascular disease.
Another form of hypolipoproteinemia is familial hypoalphalipoproteinemia (FHAL), which is caused by mutations in the gene encoding apoA-I, a protein component of high-density lipoproteins (HDL). People with FHAL have low levels of HDL cholesterol and often develop symptoms such as cardiovascular disease and premature coronary artery disease.
Hypolipoproteinemia can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the disorder typically involves managing associated symptoms and reducing lipid levels through diet, exercise, and medication. In some cases, liver transplantation may be necessary.
Prevention of hypolipoproteinemia is challenging, as it is often inherited in an autosomal recessive pattern, meaning that both parents must be carriers of the mutated gene to pass it on to their children. However, genetic counseling and testing can help identify carriers and allow for informed family planning.
Overall, hypolipoproteinemia is a rare and complex group of disorders that affect lipid metabolism and transport. While treatment and management options are available, prevention and early diagnosis are key to reducing the risk of complications associated with these disorders.
The symptoms of SLOS can vary in severity and may include:
1. Developmental delays and intellectual disability
2. Distinctive facial features, such as a prominent forehead, narrow eyes, and a short nose
3. Skeletal abnormalities, including short stature, joint deformities, and scoliosis
4. Heart defects, such as atrial septal defects or ventricular septal defects
5. Kidney problems, such as kidney stones or chronic kidney disease
6. Vision problems, such as cataracts or glaucoma
7. Hearing loss or deafness
8. Increased risk of infections
9. Poor muscle tone and coordination
10. Delayed motor milestones
SLOS is usually diagnosed by a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment is focused on managing the symptoms and preventing complications. This may include medications to control seizures, physical therapy to improve muscle tone and coordination, and speech and language therapy to address communication difficulties.
The prognosis for individuals with SLOS varies depending on the severity of the mutation and the presence of other health problems. Some individuals with mild forms of the disorder may have a relatively normal life expectancy, while others with more severe forms may have a shorter life span. Early diagnosis and intervention are critical to improving outcomes for individuals with SLOS.
There are several types of hyperlipoproteinemias, each with distinct clinical features and laboratory findings. The most common forms include:
1. Familial hypercholesterolemia (FH): This is the most common type of hyperlipoproteinemia, caused by mutations in the LDLR gene that codes for the low-density lipoprotein receptor. FH is characterized by extremely high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to premature cardiovascular disease, including heart attacks and strokes.
2. Familial hypobetalipoproteinemia (FHBL): This rare disorder is caused by mutations in the APOB100 gene that codes for a protein involved in lipid metabolism. FHBL is characterized by very low levels of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, as well as a deficiency of Apolipoprotein B-100, a protein that helps transport lipids in the blood.
3. Hypertriglyceridemia: This condition is caused by mutations in genes that regulate triglyceride metabolism, leading to extremely high levels of triglycerides in the blood. Hypertriglyceridemia can increase the risk of pancreatitis and other health problems.
4. Lipoprotein lipase deficiency: This rare disorder is caused by mutations in the LPL gene that codes for the enzyme lipoprotein lipase, which helps break down triglycerides in the blood. Lipoprotein lipase deficiency can lead to very high levels of triglycerides and cholesterol in the blood, increasing the risk of pancreatitis and other health problems.
5. Familial dyslipidemia: This is a group of rare inherited disorders that affect lipid metabolism and can cause extremely high or low levels of various types of cholesterol and triglycerides in the blood. Some forms of familial dyslipidemia are caused by mutations in genes that code for enzymes involved in lipid metabolism, while others may be caused by unknown factors.
6. Chylomicronemia: This rare disorder is characterized by extremely high levels of chylomicrons (type of triglyceride-rich lipoprotein) in the blood, which can increase the risk of pancreatitis and other health problems. The exact cause of chylomicronemia is not fully understood, but it may be related to genetic mutations or other factors that affect lipid metabolism.
7. Hyperchylomicronemia: This rare disorder is similar to chylomicronemia, but it is characterized by extremely high levels of chylomicrons in the blood, as well as very low levels of HDL (good) cholesterol. Hyperchylomicronemia can increase the risk of pancreatitis and other health problems.
8. Hypoalphalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein A-I (ApoA-I), a protein that plays a key role in lipid metabolism and helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypoalphalipoproteinemia can increase the risk of pancreatitis and other health problems.
9. Hypobetalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein B (ApoB), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypobetalipoproteinemia can increase the risk of pancreatitis and other health problems.
10. Sitosterolemia: This rare genetic disorder is caused by mutations in the gene that codes for sterol-CoA-desmethylase (SCD), an enzyme involved in the metabolism of plant sterols. Sitosterolemia can cause elevated levels of plant sterols and sitosterol in the blood, which can increase the risk of pancreatitis and other health problems.
11. Familial hyperchylomicronemia type 1 (FHMC1): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC1 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
12. Familial hyperchylomicronemia type 2 (FHMC2): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein A-IV (APOA4), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC2 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
13. Lipoprotein (a) deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein (a), a protein that helps to regulate the levels of lipoproteins in the blood. Lipoprotein (a) deficiency can cause low levels of lipoprotein (a) and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
14. Chylomicron retention disease: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of chylomicrons in the blood. Chylomicron retention disease can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
15. Hypertriglyceridemia-apolipoprotein C-II deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of triglycerides in the blood. Hypertriglyceridemia-apolipoprotein C-II deficiency can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
16. Familial partial lipodystrophy (FPLD): This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the arms, legs, and buttocks. FPLD can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
17. Lipodystrophy: This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the face, arms, and legs. Lipodystrophy can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
18. Abetalipoproteinemia: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein B, a protein that helps to regulate the levels of lipids in the blood. Abetalipoproteinemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
19. Chylomicronemia: This rare genetic disorder is characterized by the presence of excessively large amounts of chylomicrons (type of lipid particles) in the blood. Chylomicronemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
20. Hyperlipidemia due to medications: Certain medications, such as corticosteroids and some anticonvulsants, can cause elevated levels of lipids in the blood.
It's important to note that many of these disorders are rare and may not be common causes of high triglycerides. Additionally, there may be other causes of high triglycerides that are not listed here. It's important to talk to a healthcare provider for proper evaluation and diagnosis if you have concerns about your triglyceride levels.
The most common form of xanthomatosis is called familial hypercholesterolemia, which is caused by a deficiency of low-density lipoprotein (LDL) receptors in the body. This results in high levels of LDL cholesterol in the blood, which can lead to the accumulation of cholesterol and other lipids in the skin, eyes, and other tissues.
Other forms of xanthomatosis include:
* Familial apo A-1 deficiency: This is a rare disorder caused by a deficiency of apolipoprotein A-1 (apoA-1), a protein that plays a critical role in the transportation of triglycerides and cholesterol in the blood.
* familial hyperlipidemia: This is a group of rare genetic disorders that are characterized by high levels of lipids in the blood, including cholesterol and triglycerides.
* Chylomicronemia: This is a rare disorder caused by a deficiency of lipoprotein lipase, an enzyme that breaks down triglycerides in the blood.
The symptoms of xanthomatosis vary depending on the specific form of the condition and the organs affected. They may include:
* Yellowish deposits (xanthomas) on the skin, particularly on the elbows, knees, and buttocks
* Deposits in the eyes (corneal arcus)
* Fatty liver disease
* High levels of cholesterol and triglycerides in the blood
* Abdominal pain
* Weight loss
Treatment for xanthomatosis typically involves managing the underlying genetic disorder, which may involve dietary changes, medication, or other therapies. In some cases, surgery may be necessary to remove affected tissue.
In summary, xanthomatosis is a group of rare genetic disorders that are characterized by deposits of lipids in the skin and other organs. The symptoms and treatment vary depending on the specific form of the condition.
1. Abdominal obesity (excess fat around the waistline)
2. High blood pressure (hypertension)
3. Elevated fasting glucose (high blood sugar)
4. High serum triglycerides (elevated levels of triglycerides in the blood)
5. Low HDL cholesterol (low levels of "good" cholesterol)
Having three or more of these conditions is considered a diagnosis of metabolic syndrome X. It is estimated that approximately 34% of adults in the United States have this syndrome, and it is more common in women than men. Risk factors for developing metabolic syndrome include obesity, lack of physical activity, poor diet, and a family history of type 2 diabetes or CVD.
The term "metabolic syndrome" was first introduced in the medical literature in the late 1980s, and since then, it has been the subject of extensive research. The exact causes of metabolic syndrome are not yet fully understood, but it is believed to be related to insulin resistance, inflammation, and changes in body fat distribution.
Treatment for metabolic syndrome typically involves lifestyle modifications such as weight loss, regular physical activity, and a healthy diet. Medications such as blood pressure-lowering drugs, cholesterol-lowering drugs, and anti-diabetic medications may also be prescribed if necessary. It is important to note that not everyone with metabolic syndrome will develop type 2 diabetes or CVD, but the risk is increased. Therefore, early detection and treatment are crucial in preventing these complications.
There are several different types of obesity, including:
1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.
Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.
Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:
1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.
Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.
Common symptoms of type 2 diabetes include:
* Increased thirst and urination
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections
If left untreated, type 2 diabetes can lead to a range of complications, including:
* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation
The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:
* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.
There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.
Symptoms of NPC typically appear in infancy or childhood and can include:
* Delayed development and intellectual disability
* Loss of motor skills
* Vision loss and blindness
* Hearing loss and deafness
* Increased risk of infections
* Enlargement of the liver and spleen
There is currently no cure for NPC, but various treatments can help manage the symptoms. These may include:
* Medications to control seizures and muscle stiffness
* Physical therapy to maintain muscle strength and mobility
* Occupational therapy to improve daily functioning
* Speech therapy to address communication difficulties
* Liver transplantation in some cases
NPC is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. It can be challenging to diagnose NPC because the symptoms are similar to those of other disorders, and the genetic mutations responsible for the disease can be difficult to identify.
There is ongoing research into the causes and treatment of NPC, including gene therapy and small molecule therapies. However, more work needs to be done to understand the underlying mechanisms of the disease and to develop effective treatments.
The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.
CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:
* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Lack of exercise
Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:
* Electrocardiogram (ECG or EKG)
* Stress test
* Coronary angiography
Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.
Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.
There are several factors that can contribute to the development of insulin resistance, including:
1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.
There are several ways to diagnose insulin resistance, including:
1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.
There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:
1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.
Medications that may be used to treat insulin resistance include:
1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.
It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.
The condition is caused by mutations in genes that code for proteins involved in lipid metabolism, such as the low-density lipoprotein receptor gene (LDLR), apolipoprotein A-1 gene (APOA1), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. These mutations can lead to the overproduction or underexpression of certain lipids, leading to the characteristic lipid abnormalities seen in HeFH.
HeFH is usually inherited in an autosomal dominant manner, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by recessive inheritance or de novo mutations. The condition can affect both children and adults, and it is important for individuals with HeFH to be monitored closely by a healthcare provider to manage their lipid levels and reduce the risk of cardiovascular disease.
Treatment for HeFH typically involves a combination of dietary modifications, such as reducing saturated fat intake and increasing fiber and omega-3 fatty acid intake, and medications, such as statins, to lower cholesterol levels. In some cases, apheresis or liver transplantation may be necessary to reduce lipid levels. Early detection and management of HeFH can help prevent or delay the development of cardiovascular disease, which is the leading cause of death worldwide.
The most common types of biliary fistulas are:
1. Bile duct-enteric fistula: This type of fistula connects the bile ducts to the small intestine.
2. Bile duct-skin fistula: This type of fistula connects the bile ducts to the skin, which can lead to a bile leak and infection.
3. Bile duct-liver fistula: This type of fistula connects the bile ducts to the liver, which can cause bleeding and infection.
Symptoms of biliary fistula may include:
* Jaundice (yellowing of the skin and whites of the eyes)
* Pale or clay-colored stools
* Dark urine
* Loss of appetite
* Weight loss
Diagnosis of biliary fistula is typically made through a combination of imaging tests such as endoscopy, CT scan, and MRI. Treatment options for biliary fistula include:
1. Endoscopic therapy: This may involve the use of an endoscope to repair or close off the fistula.
2. Surgery: In some cases, surgery may be necessary to repair or remove the damaged bile ducts.
3. Stent placement: A stent may be placed in the bile ducts to help keep them open and allow for proper drainage.
It is important to seek medical attention if you experience any symptoms of biliary fistula, as it can lead to serious complications such as infection or bleeding.
The main clinical features of hypoalphalipoproteinemias include:
1. Low levels of HDL-C (high-density lipoprotein cholesterol) and/or LDL-C (low-density lipoprotein cholesterol) in the blood, leading to a increased risk of cardiovascular disease.
2. Elevated levels of triglycerides in the blood.
3. Elevated levels of very low-density lipoproteins (VLDL) and intermediate-density lipoproteins (IDL) in the blood.
4. Decreased levels of apolipoprotein A-I and/or apolipoprotein E in the blood.
5. Abnormal fatty acid metabolism.
6. Increased risk of pancreatitis.
7. Increased risk of hemorrhagic stroke.
8. Cognitive impairment.
9. Neurological manifestations such as ataxia, seizures, and peripheral neuropathy.
10. Eye disorders such as retinal degeneration and cataracts.
The diagnosis of hypoalphalipoproteinemia is based on a combination of clinical features, laboratory tests, and genetic analysis. Treatment for these disorders is primarily focused on managing the symptoms and preventing complications, such as cardiovascular disease and pancreatitis. This may include dietary modifications, medications to lower triglycerides and raise HDL-C, and in some cases, liver transplantation.
Hypoalphalipoproteinemias are rare genetic disorders that affect the metabolism of lipids and can lead to a range of clinical manifestations including cardiovascular disease, pancreatitis, and cognitive impairment. Early diagnosis and management are critical to preventing complications and improving outcomes for individuals with these disorders.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Gallstones can be made of cholesterol, bilirubin, or other substances found in bile. They can cause a variety of symptoms, including:
* Abdominal pain (often in the upper right abdomen)
* Nausea and vomiting
* Yellowing of the skin and eyes (jaundice)
* Tea-colored urine
* Pale or clay-colored stools
Gallstones can be classified into several types based on their composition, size, and location. The most common types are:
* Cholesterol gallstones: These are the most common type of gallstone and are usually yellow or green in color. They are made of cholesterol and other substances found in bile.
* Pigment gallstones: These stones are made of bilirubin, a yellow pigment found in bile. They are often smaller than cholesterol gallstones and may be more difficult to detect.
* Mixed gallstones: These stones are a combination of cholesterol and pigment gallstones.
Gallstones can cause a variety of complications, including:
* Gallbladder inflammation (cholecystitis)
* Infection of the bile ducts (choledochalitis)
* Pancreatitis (inflammation of the pancreas)
* Blockage of the common bile duct, which can cause jaundice and infection.
Treatment for gallstones usually involves surgery to remove the gallbladder, although in some cases, medications may be used to dissolve small stones. In severe cases, emergency surgery may be necessary to treat complications such as inflammation or infection.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Lack of exercise
* High sodium intake
* Low potassium intake
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
There are several types of diabetes mellitus, including:
1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.
The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:
1. Increased thirst and urination
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds
If left untreated, diabetes mellitus can lead to a range of complications, including:
1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.
It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.
The condition is caused by mutations in genes that code for enzymes involved in lipid metabolism, such as ACY1 and APOB100. These mutations lead to a deficiency in the breakdown and transport of lipids in the body, resulting in the accumulation of chylomicrons and other lipoproteins in the blood.
Symptoms of hyperlipoproteinemia Type IV can include abdominal pain, fatigue, and joint pain, as well as an increased risk of pancreatitis and cardiovascular disease. Treatment typically involves a combination of dietary modifications, such as reducing intake of saturated fats and cholesterol, and medications to lower lipid levels. In severe cases, liver transplantation may be necessary.
Hyperlipoproteinemia Type IV is a rare disorder, and the prevalence is not well-defined. However, it is estimated to affect approximately 1 in 100,000 individuals worldwide. The condition can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.
In summary, hyperlipoproteinemia Type IV is a rare genetic disorder that affects the metabolism of lipids and lipoproteins in the body, leading to elevated levels of chylomicrons and other lipoproteins in the blood, as well as low levels of HDL. The condition can cause a range of symptoms and is typically treated with dietary modifications and medications.
There are several types of inborn errors of lipid metabolism, each with its own unique set of symptoms and characteristics. Some of the most common include:
* Familial hypercholesterolemia: A condition that causes high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to heart disease and other health problems.
* Fabry disease: A rare genetic disorder that affects the body's ability to break down certain fats, leading to a buildup of toxic substances in the body.
* Gaucher disease: Another rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.
* Lipoid cerebral degeneration: A condition that causes fatty deposits to accumulate in the brain, leading to cognitive decline and other neurological problems.
* Tangier disease: A rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.
Inborn errors of lipid metabolism can be diagnosed through a variety of tests, including blood tests and genetic analysis. Treatment options vary depending on the specific disorder and its severity, but may include dietary changes, medication, and other therapies. With proper treatment and management, many individuals with inborn errors of lipid metabolism can lead active and fulfilling lives.
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- However, there was a change to the total cholesterol, HDL-cholesterol, and triglycerides lab equipment. (cdc.gov)
- 200mg/dl triglycerides involved 50-kDa dextran sulfate-MgCl 2 precipitation and cholesterol determination. (elsevier.com)
- Furthermore, missense variants at two novel loci-PNPLA3 p.Ile148Met and PKD1L3 p.Thr429Ser-also influence levels of triglycerides and low-density lipoprotein cholesterol, respectively. (nih.gov)
- Over time, this may cause your liver to pump out more cholesterol and blood fats called triglycerides. (medicinenet.com)
- But having too much cholesterol in your blood raises your risk of coronary artery disease . (medlineplus.gov)
- With HDL cholesterol, higher numbers are better, because a high HDL level can lower your risk for coronary artery disease and stroke . (medlineplus.gov)
- Despite this association, a small proportion of subjects with elevated HDL-C develop coronary artery disease (CAD). (atherosclerosis-journal.com)
- Plasma LDL-IIIb cholesterol concentrations were related to changes in coronary artery stenosis and cardiovascular events in patients with coronary artery disease and low HDL-cholesterol. (plos.org)
- Red wine is thought to be particularly beneficial as it can boost HDL while its polyphenols have been linked in some studies to help lower harmful, small dense LDL ("bad") particles that are known to be drivers of coronary artery disease. (eatthis.com)
- HDL and LDL are two types of lipoproteins.They are a combination of fat (lipid) and protein. (medlineplus.gov)
- HDL stands for high-density lipoproteins. (medlineplus.gov)
- Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol. (nih.gov)
- In order for cholesterol to travel through blood, it must attach itself to small fat-carrying proteins called lipoproteins. (projectswole.com)
- The least dense lipoproteins are the chylomicrons, which carry very little cholesterol. (projectswole.com)
- Next, come the very low-density lipoproteins (VLDL), which roughly carry 15% of the circulating cholesterol. (projectswole.com)
- Lastly comes the "good" cholesterol, high-density lipoproteins (HDL), which are the smallest and densest of the lipid-carriers. (projectswole.com)
- Total and high-density lipoprotein cholesterol in adults: National Health and Nutrition Examination Survey, 2011-2012. (cdc.gov)
- High density lipoprotein cholesterol (HDL-C) levels are negatively associated with cardiovascular disease in large epidemiological studies. (atherosclerosis-journal.com)
- Background: Accurate high-density lipoprotein cholesterol (HDL-C) measurements are important for management of cardiovascular diseases. (elsevier.com)
- Conclusions: Osaka UC and DCM were highly accurate, precise, and stable for many years, assisting manufacturers to calibrate products for clinical laboratories to accurately measure HDL-C for patients, calculate non-HDL-C, and estimate low-density lipoprotein cholesterol with the Friedewald equation. (elsevier.com)
- High levels of high-density lipoprotein cholesterol can actually be a result of certain medications. (healthreporter.com)
- RESULTS: Serum high density lipoprotein cholesterol (HDL-c), glucose and glycated hemoglobin were higher (P=0.028, P lt 0.001 and P=0.002, respectively), whereas serum transaminases and gamma glutamil transferase levels were lower in patients with advanced fibrosis than in those with no/ mild fibrosis (P=0.010, P lt 0.001 and P=0.005, respectively). (ac.rs)
- Another novel gene, TEAD2, is found to be associated with high-density lipoprotein cholesterol through gene-based association analysis. (nih.gov)
- In this group, however, there was an inverse linear trend between serum cotinine and high density lipoprotein cholesterol (p (cdc.gov)
- According to "the experience and wisdom of 200 of the country's leading experts in cardiovascular diseases," in a report representing 29 nationwide medical organizations, together with the American Heart Association and the American College of Cardiology, we've recognized for practically half a century that "coconut oil is one of the most potent agents for elevating [blood] serum cholesterol level. (healthyfountain.com)
- CONCLUSIONS: Among patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of less than 70 mg per deciliter (1.81 mmol per liter), there was no incremental clinical benefit from the addition of niacin to statin therapy during a 36-month follow-up period, despite significant improvements in HDL cholesterol and triglyceride levels. (nih.gov)
- Factors you can control - such as inactivity, obesity and an unhealthy diet - contribute to harmful cholesterol and triglyceride levels. (mayoclinic.org)
- 1 Depending on the overall cardiovascular risk and LDL-cholesterol levels, Current European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) guidelines also recommend LDL-cholesterol lowering for primary prevention of cardiovascular disease. (eso-stroke.org)
- A recent risk-evaluation and risk-modelling study from the Multinational Cardiovascular Risk Consortium sheds light on this important issue: Worrying about cholesterol is in fact worth it - even at young age. (eso-stroke.org)
- Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. (eso-stroke.org)
- Targeting HDL-cholesterol to reduce residual cardiovascular risk. (ox.ac.uk)
- BACKGROUND: In patients with established cardiovascular disease, residual cardiovascular risk persists despite the achievement of target low-density lipoprotein (LDL) cholesterol levels with statin therapy. (nih.gov)
- With addition of reagent 2, HDL-cholesterol esters are converted to HDL-cholesterol by PEG-cholesterol esterase. (cdc.gov)
- Test whether angiographically-documented changes in percent stenosis and clinical endpoints (coronary-related deaths, myocardial infarctions, stroke, revascularization for worsening ischemia) in the HDL-Atherosclerosis Treatment Study (HATS) were attributable to specific LDL-subclasses. (plos.org)
- Williams PT, Zhao X-Q, Marcovina SM, Brown BG, Krauss RM (2013) Levels of Cholesterol in Small LDL Particles Predict Atherosclerosis Progression and Incident CHD in the HDL-Atherosclerosis Treatment Study (HATS). (plos.org)
- The HDL-Atherosclerosis Treatment Study (HATS) was a double-blind randomized controlled clinical trial of simvastatin plus niacin and/or a mixture of antioxidants in 160 patients selected for clinical coronary disease with at least 3 stenoses of at least 30 percent of the luminal diameter or 1 stenosis of at least 50 percent, and low high-density lipoprotein (HDL)-cholesterol  . (plos.org)
- Physical activity can lower bad cholesterol ( LDL ), raise good cholesterol (HDL), and lower the risk for heart disease in adults, according to a study published in the journal Atherosclerosis in December 2015. (everydayhealth.com)
- Gradient gel electrophoresis of on-study LDL-subclass cholesterol concentrations were measured in 32 placebo, 33 simvastatin-niacin, 38 antioxidant, and 39 simvastatin-niacin & antioxidant treated participants. (plos.org)
- That's why we used to offer individuals high-dose niacin-to lift their HDL. (healthyfountain.com)
- The "lack of benefit of raising the HDL cholesterol level with the use of niacin…seriously undermine [ s ] the hypothesis that HDL cholesterol is a causal risk factor. (healthyfountain.com)
- It is unclear whether extended-release niacin added to simvastatin to raise low levels of high-density lipoprotein (HDL) cholesterol is superior to simvastatin alone in reducing such residual risk. (nih.gov)
- It is sometimes called the "good" cholesterol because it carries cholesterol from other parts of your body back to your liver. (medlineplus.gov)
- To raise your HDL level, you need to eat good fats instead of bad fats. (medlineplus.gov)
- Also called "good" cholesterol. (nih.gov)
- The effect of "good" cholesterol on cardiovascular disease may be more complicated than previously thought, according to a new analysis. (nih.gov)
- HDL, or high-density lipoprotein, is considered good cholesterol. (healthreporter.com)
- The table below shows different HDL test results and whether they are good for your health. (healthreporter.com)
- However I've had a look at the detailed results and the one that stands out to me is my HDL ratio - high-density lipoprotein is the good cholesterol that removes excessive LDL. (liveforever.club)
- So I want to attack both low HDL and high body fat at the same time, therefore increasing good oils isn't an option - but I'll definitely be being more careful on bad oils and modify my diet to be lower in fat overall. (liveforever.club)
- Even if virgin coconut oil and different saturated fat increase LDL "bad" ldl cholesterol, isn't that countered by the enhance in HDL "good" ldl cholesterol? (healthyfountain.com)
- Saturated fat could make HDL, the so-called good ldl cholesterol, go up, so what's the drawback? (healthyfountain.com)
- Swimming, which is also aerobic exercise, can be a good choice for your cholesterol-lowering fitness program. (everydayhealth.com)
- In one study, men who strength-trained saw improvements related to high-density lipoprotein (HDL), the "good" cholesterol, compared with men who did not strength-train, regardless of their weight. (everydayhealth.com)
- HDL , the "good" cholesterol, picks up excess cholesterol and takes it back to your liver. (mayoclinic.org)
- It boosts your good HDL cholesterol levels. (eatthis.com)
- One of the ways low to moderate wine drinking heart health is by boosting HDL ("good") cholesterol levels. (eatthis.com)
- Light to moderate drinking can raise good HDL cholesterol. (eatthis.com)
- Research shows that it raises your risk for high LDL ("bad") cholesterol and lowers levels of HDL ("good") cholesterol. (medicinenet.com)
- HDL cholesterol is known as the good cholesterol because it transports or moves cholesterol from the artery walls back to the liver. (nih.gov)
- My total cholesterol level is way below the recommended 5 mmol/L (193 mg/DL) at 3.1 but total/HDL ratio is 2.95. (liveforever.club)
- Transcend's target is a ratio of less than 2.5, and as my total cholesterol is already pretty low, my only option is to try to increase my HDL. (liveforever.club)
- And looking back over my blood test results spanning 5 years my HDL ratio has increased 2.55 to 2.95 - but even when I was really fit it still wasn't in the optimal range. (liveforever.club)
- Effects of dietary cholesterol and saturated to polyunsaturated fatty-acid ratio on the hererogeneity of LDL and HDL particles in the 1.040-1.090 g/ml interval in the preruminant calf, Bos spp. (edpsciences.org)
- It is sometimes called the "bad" cholesterol because a high LDL level leads to a buildup of cholesterol in your arteries. (medlineplus.gov)
- LDL cholesterol builds up in the walls of your arteries, making them hard and narrow. (mayoclinic.org)
- This means an unusually dangerous amount of cholesterol is present in your blood, and therefore arteries, at any given time. (projectswole.com)
- Increasing LCAT should improve the body's ability to process cholesterol from arteries. (nih.gov)
- Coconut oil elevated ldl cholesterol about 14 % over the management, which was in step with seven different interventional trials published thus far in a 2016 overview. (healthyfountain.com)
Lung and Blood Institute1
- According to the National Heart, Lung, and Blood Institute (NHLBI), a person's first cholesterol screening should occur between the ages of 9 and 11, and then be repeated every five years after that. (mayoclinic.org)
- Your liver makes cholesterol, and it is also in some foods, such as meat and dairy products. (medlineplus.gov)
- Your liver then removes the cholesterol from your body. (medlineplus.gov)
- In truth, a big enhance in blood ldl cholesterol was discovered inside hours of consuming a slice of cake made out of both coconut oil (or cod liver oil for that matter), however not from the similar cake made out of flaxseed oil. (healthyfountain.com)
- CONCLUSIONS: In conclusion, we found that older age and higher HDL-c, are independent predictors for advanced liver fibrosis assessed with the BARD score. (ac.rs)
- For example, your genetic makeup might make it more difficult for your body to remove LDL cholesterol from your blood or break it down in the liver. (mayoclinic.org)
- These actually carry cholesterol from the cells to the liver so that they can be processed as bile acids, excreted in the bile as cholesterol, or returned to the plasma as a component of VLDL. (projectswole.com)
- Your liver makes, processes, and breaks down cholesterol. (medicinenet.com)
- When your liver doesn't work properly, it can affect your cholesterol levels. (medicinenet.com)
- Along with processing cholesterol, your liver also breaks down alcohol. (medicinenet.com)
- Bile acids are amphiphilic molecules synthesized from cholesterol in the liver. (diabetesjournals.org)
- The liver processes the cholesterol so it can be removed from the body. (nih.gov)
- An enzyme called LCAT helps make HDL in the blood which may enable HDL to transport it to the liver. (nih.gov)
- Improving a person's HDL levels can decrease their risk of heart disease. (nih.gov)
- The US Centers for Disease Control and Prevention (CDC) and Cholesterol Reference Method Laboratory Network (CRMLN) perform ultracentrifugation (UC) reference measurement procedure (RMP) to value assign HDL-C. Japanese CRMLN laboratory (Osaka) concurrently runs UC procedure and the designated comparison method (DCM). (elsevier.com)
Levels of Cholesterol2
High in saturated1
- Diets that are high in saturated fats, refined carbs, and alcohol can raise your LDL and HDL cholesterol. (healthreporter.com)
- You can boost your HDL level by losing weight, especially if you have lots of fat around your waist. (medlineplus.gov)
- So, identical to having a excessive variety of trainers and gymnasium shorts may predict a decrease danger of coronary heart assault, having a excessive HDL additionally predicts a decrease danger of coronary heart assault. (healthyfountain.com)
- And, should you intervene and actively decrease individuals's LDL by way of food regimen or medicine, their coronary heart illness danger drops-however not so with HDL. (healthyfountain.com)
- People who dwell their entire lives with excessive HDL ranges don't appear to have a decrease danger of coronary heart assault, and should you give individuals a drug that will increase their HDL, it doesn't assist. (healthyfountain.com)
- rhLCAT may be able to improve HDL levels and help decrease risk of worsening heart disease. (nih.gov)
- Multivariate ordinal regression analysis showed independent associations and predictions of ages (OR=1.071, 95% CI 1.004-1.097, P lt 0.001), and HDL-c levels (OR= 2.549, 95% CI 1.087-5.989, P=0.032) on BARD score categories in patients with NAFLD. (ac.rs)
- Cholesterol is a waxy substance found in your blood. (mayoclinic.org)
- When there's too much cholesterol in your blood, the cholesterol from LDL can increase your risk for developing cardiovascular diseases such as heart attack and stroke. (nih.gov)
- Only recently, the treat stroke to target trial has demonstrated the benefit of aggressive LDL-cholesterol lowering for secondary stroke prevention. (eso-stroke.org)
- A comparison of two ldl cholesterol targets after ischemic stroke. (eso-stroke.org)
- In truth, HDL ranges " are among the most consistent and robust predictors of CVD [cardiovascular disease] risk. (healthyfountain.com)
- LDL , the "bad" cholesterol, transports cholesterol particles throughout your body. (mayoclinic.org)
- However, while treatment trials have shown that lowering LDL reduces the risk of heart disease, recent clinical trials haven't found that medicines aimed at raising HDL reduce the risk of heart attack. (nih.gov)
- A team led by Dr. Sekar Kathiresan of Massachusetts General Hospital, Broad Institute and Harvard Medical School explored the relationship between HDL and heart disease using an approach called Mendelian randomization. (nih.gov)
- If HDL is directly involved in heart disease, then inherited genetic variations that affect HDL levels should affect the risk of disease. (nih.gov)
- Surprisingly, the researchers found that carriers of the HDL-boosting variant had the same risk for heart attack as non-carriers. (nih.gov)
- The increase in HDL cholesterol linked to the genetic risk score wasn't associated with a lower risk of heart attack either. (nih.gov)
- In contrast, the genetic score for LDL cholesterol accurately predicted heart attack risk. (nih.gov)
- These results show that some ways of raising HDL cholesterol might not reduce risk of myocardial infarction [heart attack] in human beings. (nih.gov)
- Future studies will be needed to understand both the role of HDL cholesterol and why its levels are associated with heart disease risk. (nih.gov)
- It's possible that HDL itself may not directly lower the risk of heart disease but that blood HDL reflects another factor that does. (nih.gov)
- An HDL cholesterol level of 119mg/dL is above optimal and can increase your risk of coronary heart disease and other cardiovascular diseases. (healthreporter.com)
- You can monitor your cholesterol test results with a heart health app . (healthreporter.com)
- It provides a space for users to monitor all aspects of their heart health, including blood pressure, LDL, and HDL levels. (healthreporter.com)
- If your doctor suspects that your medications are causing your HDL levels to be above 119mg/dL, they may discuss dosage changes and other ways to reduce your HDL levels and your risk of heart disease while also keeping you on the medications you need. (healthreporter.com)
- If you find you have high levels of HDL cholesterol and other family members have been diagnosed with heart disease before the age of 60 or died of a heart attack, your doctor may refer you to a specialist. (healthreporter.com)
- Eating a whole, healthy, and balanced diet is one of the best ways that you can go about reducing your cholesterol level and, by extension, your risk of heart disease. (healthreporter.com)
- The motive we know LDL ldl cholesterol actually is dangerous is as a result of individuals who had been simply born with genetically low LDL ldl cholesterol find yourself having a low danger of coronary heart illness. (healthyfountain.com)
- In easy phrases: "High HDL may not protect the heart. (healthyfountain.com)
- Physical activity is effective at lowering bad cholesterol levels because exercising muscles requires energy, explains Karol Watson, MD, PhD , a professor of medicine and cardiology, co-director of the UCLA Program in Preventive Cardiology, and director of the UCLA Barbra Streisand Women's Heart Health Program. (everydayhealth.com)
- Brisk walking is great for lowering cholesterol, according to the American Heart Association, and most anyone can do it. (everydayhealth.com)
- Running helps lower your cholesterol by increasing your heart rate. (everydayhealth.com)
- You don't have to run a marathon or even a 5K to benefit your cholesterol levels - you simply have to get your heart pumping. (everydayhealth.com)
- Your doctor might also suggest more-frequent tests if you have a family history of high cholesterol, heart disease or other risk factors, such as diabetes or high blood pressure. (mayoclinic.org)
- It's linked with obesity, heart disease, and high cholesterol. (medicinenet.com)
- To see if rhLCAT is a safe and effective method of improving HDL levels in people with heart disease. (nih.gov)
- How can I raise my HDL level? (medlineplus.gov)
- Getting regular exercise can raise your HDL level, as well as lower your LDL. (medlineplus.gov)
- Some cholesterol medicines , including certain statins , can raise your HDL level, in addition to lowering your LDL level. (medlineplus.gov)
- Health care providers don't usually prescribe medicines only to raise HDL. (medlineplus.gov)
- Clinical trials are now underway to examine the cardiovascular benefits and risks of drug treatments that raise HDL levels. (nih.gov)
- These oils can raise LDL cholesterol. (medicinenet.com)
- Some medicines for high blood pressure, such as diuretics and older forms of beta-blockers, can also raise your cholesterol. (medicinenet.com)
- Research shows that high cholesterol may harm kidney function and raise your risk of kidney disease. (medicinenet.com)
- While circulating blood cholesterol is important to know about, you can also gauge increased cholesterol levels my examining the molecules that transport the cholesterol to the cells. (projectswole.com)
- When there's too much sugar, it may attach to proteins, such as cholesterol molecules. (medicinenet.com)
- The change in the percent stenosis of the most severe proximal lesions increased in association with higher concentrations of the small LDL subfractions LDL-IIIb (24.2-24.6 nm) and LDL-IVa (23.3-24.1 nm) before (both P = 0.002) and after (P = 0.01 and P = 0.03 respectively) adjustment for treatment group and on-study HDL-cholesterol, LDL-cholesterol, and triglyceride concentrations. (plos.org)
- If you want to know how to lower your cholesterol with exercise, here are some great workouts that can help you start dropping those dangerous fats today! (projectswole.com)
Blood cholesterol levels1
- There are several notable factors that can dramatically influence blood cholesterol levels. (projectswole.com)
- Research shows that LDL and total cholesterol levels rise around and after your final period. (medicinenet.com)
- Research shows that nephrotic syndrome, a type of kidney disorder, increases your LDL and total cholesterol levels. (medicinenet.com)
- Obese women had a higher chance of being hypertensive and having high total TC, high TG, high LDL-C and low HDL-C levels than non-obese females. (who.int)
- High cholesterol can be inherited, but it's often the result of unhealthy lifestyle choices, which make it preventable and treatable. (mayoclinic.org)
- Taking certain medicines can lower HDL levels in some people. (medlineplus.gov)
- However, in young and otherwise healthy people, cholesterol levels are rarely determined. (eso-stroke.org)
- For some people, high HDL levels are just a part of their genetic makeup. (healthreporter.com)
- People over 65 should receive cholesterol tests annually. (mayoclinic.org)
- Cholesterol and its role in our body is not something most people think about regularly, but it should be. (projectswole.com)
- Second, you should try to lose weight since overweight individuals tend to exhibit higher cholesterol readings than thinner people due to the excess lipids floating around in their bodies. (projectswole.com)
- Results: HDL-C regression equations obtained with CDC (x) and Osaka (y) were y=0.992x+0.542 (R 2 =0.996) for Osaka UC and y=1.004x-0.181 (R 2 =0.998) for DCM. (elsevier.com)
- Higher levels of HDL, in contrast, have been associated with a lower risk of cardiovascular disease. (nih.gov)
- The team confirmed that carriers of the LIPG 396Ser allele had higher HDL cholesterol than non-carriers but similar levels of other risk factors. (nih.gov)
- In all age groups, a higher percentage of men had low levels of HDL cholesterol than women. (cdc.gov)
- A higher percentage of men aged 40-59 years had low levels of HDL cholesterol than men aged ≥60 years. (cdc.gov)
- There are a few ways your HDL levels can reach a point where they stop being protective and become dangerous. (healthreporter.com)
- Having a excessive blood HDL stage is "no longer regarded as protective. (healthyfountain.com)
- They also have lower amounts of protective HDL cholesterol. (medicinenet.com)
- All patients received simvastatin, 40 to 80 mg per day, plus ezetimibe, 10 mg per day, if needed, to maintain an LDL cholesterol level of 40 to 80 mg per deciliter (1.03 to 2.07 mmol per liter). (nih.gov)
- This makes cholesterol more harmful. (medicinenet.com)
- If your doctor suspects that your 119mg/dL HDL levels are caused by your diet, they will likely suggest making lifestyle changes first. (healthreporter.com)
- This is to find out whether your high HDL levels are caused by your diet or other factors. (healthreporter.com)
- A healthy diet, regular exercise and sometimes medication can help reduce high cholesterol. (mayoclinic.org)
- We reported previously that a very low carbohydrate diet favorably affected fasting and postprandial triacylglycerols, LDL subclasses and HDL cholesterol (HDL-C) in men but the effects in women are unclear. (edu.au)