All About Cholesterol

Lower Your Cholesterol Ebook

Scott Davis' e-Book Beat Cholesterol in 30 Days is a useful compendium of information about natural methods and foods to avoid to lower LDL (bad) cholesterol. While the book is extremely useful in categorizing what helps and harms people in terms of diet, it's not so much a full-fledged system as opposed to a guidebook on foods that will improve and worsen your cholesterol levels. This program reveals to people some main factors that cause their hypercholesterolemia such as smoking, high blood pressure, diabetes, obesity, and family history of heart disease. The program also covers tips to prevent the recurrence of hypercholesterolemia such as eating a low-fat and low-salt diet, stopping smoking, losing extra pounds, and maintaining a healthy weight. In addition to the program you get a few extra bonuses when you download the e-book. You also get 10 recipes to get you started, an appendix with the symptoms of a heart attack, and an appendix of foods that you cant eat. These are a great addition to the rest of the information provided in this e-book. Continue reading...

Natural Cholesterol Guide Summary


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Author: Scott Davis
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My Natural Cholesterol Guide Review

Highly Recommended

I've really worked on the chapters in this ebook and can only say that if you put in the time you will never revert back to your old methods.

All the modules inside this ebook are very detailed and explanatory, there is nothing as comprehensive as this guide.

Crunch Cholesterol Program by Colin Carmichael

Crunch Cholesterol created by Colin Carmichael is a newly updated high cholesterol treatment program that provides people with step-by-step instructions on how to lower cholesterol naturally. The book provides people with a list of low cholesterol foods that people should have in their meal plans, and a list of high cholesterol foods that people should avoid in their meal plans. Moreover, the book contains a lot of delicious recipes that help people get more choice in their diet. Crunch Cholesterol is the unique program that provides people with an exclusive cholesterol lowering diet, and detailed instructions on how to reduce cholesterol quickly and naturally without bad side effects. This program will help people avoid diseases linked to high cholesterol such as coronary heart disease, Diabetes, cardiovascular disease, and some other diseases. Continue reading...

Natural Secrets For High Cholesterol Summary

Contents: EBook
Author: Colin Carmichael
Price: $37.00

The Great Cholesterol Lie

Dr. Dwight Lundell's book reveals why inflammation causes heart disease and how the cholesterol lies and myths began forty years ago. What Will You Learn Inside The Great Cholesterol Lie? The most famous long-term study in heart research. and how it led to the most devastating mistake in health care! Why so many people who undergo bypass surgery are right back on that table ten years later. still not obese. still not smoking. and still with no elevated cholesterol. The essential response your body has to a foreign substance anywhere. and how it can turn against you, when it occurs in your arteries! How 41% of All deaths in America could be prevented easily, simply, and virtually cost-free! Why lowering your cholesterol intake is not helping lower your risk of heart attack. and may actually be doing you more harm! How a healthy heart is meant to function. and how you can keep it that way, simply and easily! How to recognize the signs of a heart attack and the best course of action to ensure you survive! Continue reading...

The Great Cholesterol Lie Summary

Contents: Ebook
Author: Dr. Dwight Lundell
Official Website:
Price: $49.95

2525 Cholestyramine and other lipid reducers

Cholestyramine is an anion-cxchangc resin which is not absorbed systemically. It binds bile acids, producing an insoluble complex which is excreted in the stool. This leads to a reduction of cholesterol and the low-density (LD) lipoproteins in the serum. Cholestyramine is used in pregnancy for the treatment of obstetric cholestasis to relieve the itching. Ursodeoxycholic acid is, however, more effective than cholestyramine in intrahepatic cholestasis of pregnancy (see ursodeoxycholic acid Kondrackiene 2005). There is at least a theoretical risk for the fetus because, in addition to bile acids, cholestyramine also binds other lipophile substances - such as fat-soluble vitamins and medications. One case report concerning the gestational use of cholestyramine has described severe intracranial hemorrhage in a fetus vitamin K deficiency was suspccted (Sadler 1995). Recommendation. Cholestyramine - and, as a second choice, colestipol -may be used for intrahepatic cholestasis of pregnancy or...

3I have high cholesterol level during pregnancy Is this a problem

There are no conclusive studies that show harmful effects of high cholesterol levels to the mother or the developing baby. However, as a high cholesterol level is a risk factor for heart disease and stroke in the long term, we advise you to look into changing your lifestyle if your cholesterol level remains high after delivery. Consider a diet low in cholesterol, consisting of bread, fruits, vegetables and small amounts of lean meat, fish and olive oil. Avoid smoking. See your doctor regularly to check your cholesterol level.

Plasma lipid changes during pregnancy

During gestation there are also relevant changes in lipid metabolism (Figure 6.1B), changes most marked in the second half of pregnancy, when both the plasma triglycerides and cholesterol reach the highest levels.1,2,10,11 The high plasma levels of triglycerides seem to be secondary to both an increased hepatic synthesis of VLDL-TG, as well as a decreased lipoprotein lipase (LPL) activity in the adipose tissue in late gestation.10,11 These changes are due to some of the hormonal changes observed during pregnancy. The increased production of VLDL-TG is secondary to the elevation of estradiol that takes place during gestation, as increased levels of estradiol stimulate the hepatic synthesis of triglycerides.12,13 Both the placental lactogen (hPL), which reaches its maximum concentration by the end of pregnancy, and the insulin resistance that increases adipose tissue lipolysis, lead to an abundant supply of fatty acids to the liver.14,15 The lower levels of adiponectin observed as...

Mechanisms leading to the development of gestational diabetes

Although diagnosed during pregnancy, is secondary to auto-inmune processes or to the diagnosis of mature onset diabetes of the young (MODY) during pregnancy. Regarding the beta-cell dysfunction, several mechanisms could be involved in this process. High progesterone levels may play a relevant role.30,31 Recently, in models of knock-out mice,31 it has been shown that the lack of progesterone receptors is associated with a higher insulin secretion by beta-cells. Therefore the high levels of progesterone that develop during pregnancy may damage these cells. The hyperlipidemia observed during pregnancy may also decrease the capability of beta-cells to secrete insulin.32,33 Although fatty acids may induce insulin secretion,34 under certain circumstances, prolonged high levels of fatty acids may damage the beta-cell, decreasing insulin secretion. In fact, in an experimental animal model during pregnancy, a decrease in plasma free fatty acids and triglycerides increases insulin secretion...

Lipid alterations in gestational diabetes mellitus

In gestational diabetes, as occurs in other conditions of insulin resistance and beta-cell dysfunction, there is an increase in plasma levels of triglycerides and cholesterol. This effect should be added to the physiological hyperlypidemia induced by pregnancy (Figure 6.1C).10,11 Therefore, women with GDM have higher plasma levels of triglycerides and cholesterol than found in normal pregnancies (Figure 6.2).44,45 The hyper-triglyceridemia found in gestational diabetes may also play a role in the fetal macrosomia observed in these pregnancies, as several authors have shown a positive correlation between the plasma levels of triglycerides and birthweight.20,21 Increased plasma levels of both triglycerides and cholesterol have been associated to structural alterations in LDL.46,47 High triglycerides make LDL particles small and more dense. Such particles are more susceptible to oxidation. Nevertheless, as pregnancy advances, the maternal milieu changes and conditions that both increase...

Lipids and fatty acids

At delivery of a normal pregnancy the concentrations of cholesterol, triglycerides, total free fatty acids and lipid soluble vitamins is higher in the maternal than umbilical circulation.19 However, individual fatty acids in the total plasma compartments such as total saturated fatty acids and arachidonic acid are selectively enriched in the umbilical cord blood. GDM does not significantly alter maternal cholesterol levels, but maternal as well as fetal hypertriglyceridemia particularly in the VLDL and HDL fraction has been a well known feature of GDM.22-25

Kinetics of the glucose utilization rate in the fetus

In this situation, substrate supply (amino acids, glucose, fatty acids and triglycerides, and glycerol) is probably as or more important than insulin itself. The capacity for glucose utilization in the human fetus can only be estimated from measurements in prematurely born infants or in animal models such as the sheep. In preterm humans, doubling or even tripling of glucose utilization rate (GUR) from basal is possible.34 GUR in fetal sheep follows MichaelisMenten kinetics,8 and is relatively limited to a doubling of basal GUR. This capacity is variable, however, as increased entry of glucose into the fetal plasma from the placenta increases fetal glucose concentration and insulin secretion, which, in turn, augments fetal glucose utilization, thus limiting further increases in the fetal glucose concentration. Glucose and insulin clamp experiments in fetal sheep, in which glucose or insulin or both are infused until GUR reaches maximal rates, have shown that plasma...

2523 Clofibrine acid derivatives and analogs

Clofibrate is a lipid reducer that acts on the triglycerides and, to a limited extent, on cholesterol It is used for primary hyperlipidemia. Clofibrate has been withdrawn from the market in some countries because of serious side effects. In animal studies, clofibrate was identified in fetal tissue and was capable of inducing fetal hepatic enzymes. Because of the reduced glucuronide conjugation of clofibrate in the fetus, it is possible that fetal accumulation of the drug could occur with treatment towards the end of pregnancy.

2524 Cholesterol synthesisenzyme inhibitors

The lipophylic statins atorvastatin.fluvastatin, lovastatin (mevinolinic acid), pravastatin, simvastatin, and hydrophilic statins pravastatin and rosuvastatin, are used to treat hyperlipidemia and hypercholesterolemia. These agents reduce the biosynthesis of cholesterol through a competitive inhibition of the rate-limiting enzyme, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase. A collection of human malformations - including the aforementioned cases, holoprocencephaly, other CNS malformations, and limb anomalies - involving first-trimester exposure to the lipophylic HMG-CoA reductase inhibitors atorvastatin, cerivastatin, lovastatin, and simvastatin has been published. The authors suggest a possible link to abnormal Sonic Hedgehog signaling. Cholesterol binding to Sonic Hedgehog protein is required for this protein to play a signaling role in embryonic development. The same authors hypothesized that statins may affect fetal development by lowering in utero cholesterol...

Hyaline Membrane Disease

Subcostal And Intercostal Retractions

Comparisons of the clarity of chylous fluid at (a) the age of 4 hours, and prior to feeding, (b) 48 hours and after several milk feeds, and (c) after feeding has been well established. Note the progressive increase in turbidity associated with appearance of fat-laden chylomi-crons after initiation of oral dietary fat intake. Chylous fluid is also high in protein and white blood cells. Management of this infant would include feeds with medium-chain triglycerides and total parenteral nutrition rather than the use of regular formula.

Fetal hyperinsulinemia as a cause of macrosomia in pregnancy

The activities of fetal hepatic enzymes concerned with glycolysis were not affected by the hyperinsulinemia gluco-neogenic enzymes were suppressed but lipogenic enzymes became enhanced, indicating an increased de novo fetal fat synthesis.78 Additional evidence that diabetic macrosomia entails an enhanced cholesterol and lipoprotein metabolism has recently been provided.79 Macrosomic pups of mildly hyperglycemic STZ pregnant rats had elevated plasma low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol associated with increased lecithin-cholesterol acyl transferase activity compared with normal birthweight controls. There was no change in hepatic cholesterol content, but hepatic HMG-CoA reductase and cholesterol 7a-hydroxylase activities were higher in both macrosomic males and females. By 3 months, macrosomic rats had developed hypercholesterolemia with a rise in all lipoproteins. These findings demonstrate that macrosomia throughout adulthood is associated with...

65 Nephrotic Syndrome

Most patients also have high cholesterol and high triglyceride levels. The loss of protein into the urine results in a fall in plasma albumin concentration, but other circulating proteins are also lost. Falling plasma oncotic pressure encourages fluid to leave the circulation, and this results in oedema.

Fetal Risk Summary

Atorvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, is indicated as an adjunct to diet to reduce total cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein B, and triglyceride levels in patients with primary hypercholesterolemia and mixed dyslipidemia (1). It has the same mechanism of action as cerivastatin, fluvastatin, lovastatin, pravastatin, and simvastatin. The parent drug and some of the metabolites are pharmacologically active in humans (1). No published cases involving the use of atorvastatin during human pregnancy have been located. The interruption of cholesterol-lowering therapy during pregnancy should have no effect on the long-term treatment of hyperlipidemia. Moreover, because cholesterol and products synthesized by cholesterol are important during fetal development, the use of atorvastatin is contraindicated during pregnancy.

The dyslipidemia component

Several other metabolic disturbances, such as elevated levels of triglycerides, decreased levels of high-density lipoproteins (HDL), high cholesterol level, glucose intolerance, and hyperuricemia, have also been related to hyperinsulinemia.56 The metabolic consequences of these disturbances include changes in the lipid profile resulting in atherosclerosis, increased deposition of body fat, and proliferation of vascular smooth muscle cells, which place the hypertensive, hyperinsu-linemic individual at increased risk of cardiac complications and stroke.57 Studies of the evolution of the clinical and biological disturbances in women with a polycystic ovary (PCO) support the view that insulin resistance, dyslipidemia, and hypertension are all manifestations of a single syndrome. Often obese, these women have hyperinsulinemia which disrupts sex hormone production,58 resulting in androgenization and clinical manifestations of hirsutism and infertility. During pregnancy, they have more...

Pathophysiology and treatment of diabetic nephropathy

Combination with other antihypertensive has improved the poor prognosis considerably. Progression of manifest diabetic nephropathy can be slowed down by strict antihypertensive treatment with angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers as first line drugs. It is often necessary to combine the treatment with diuretics, beta-blockers and or calcium antagonists in order to control the blood pressure and the albumin excretion sufficiently. Strict antihypertensive treament in patients with diabetic nephropathy results in preservation of kidney function documented by a reduction in the decline in glomerular filtration rate to less than one-third of the decline in untreated patients.4 Inhibition of the rennin angiotensin system with i.e. ACE inhibitors already at the stage of microalbuminuria prior to development of hypertension is also demonstrated effect-full in delaying the progression of the disease and might even reduce the albumin excretion to...

Effect of HRT on blood lipids

Many studies show beneficial effect of HRT on lipid profile in postmenopausal diabetic women. Data from a large survey conducted between 1988 and 1994, presented a better lipoprotein profile and glycemic control among current HRT users postmenopausal diabetic women if compared to never users or previous users of HRT.81 Overall, HRT increased HDL cholesterol and reduced LDL cholesterol, LDL HDL ratio and lipoprotein-A compared to placebo or no treatment. Combined HRT had no effect on triglycerides.52 Recent data from the Diabetes Heart Study,68 related HRT use to a significant reduction of LDL cholesterol levels in Type 2 DM patients. Apolipoprotein A1levels are increased by c. 20 in diabetic subjects and can be reduced by HRT.82 In one study, short-term oral estradiol treatment of postmenopausal diabetic women increased high-density lipoprotein (HDL) cholesterol and its subfraction HDL2 and apolipoprotein A1, whereas low-density lipoprotein (LDL) cholesterol and apolipoprotein B...

Effect of type and mode of delivery of HRT

In diabetics, oral CEE only treatment reduced total and LDL cholesterol and increased HDL cholesterol. There was some increase in triglycerides and reduction of fasting glucose and HBAlc. There was an increase in coagulation factors along with some augmentation of the fibrinolytic activity.87-89 No data was found for either oral or transdermal E2 only treatments. Adding continuous progestins to oral estrogens, mostly CEE MPA57,89 or E2 NETA90-92 usually resulted in a reduction of total cholesterol and LDL cholesterol. Though, HDL cholesterol remained unchanged instead of increasing as in estrogen only treatment. No significant change was observed for triglycerides, fasting glucose, inflammatory biomarkers, and blood pressure measurements. Continuous combined E2 NETA formulations reduced total cholesterol, triglycerides and coagulation factors II, VIII and XI, while keeping LDL and HDL cholesterol, fasting glucose, and plasminogen activity unchanged.92,93 It was therefore hypothesized...

European Diab Care quality network

Network Information Sheet

Equipment, logistics), the process (the way the care is organized - from the first call to treatment plan the annual measurements of indicators - HbAlc, blood pressure, etc the way the treatment is initiated - use of antihypertensive drugs, cholesterol lowering agents, etc).


No clear-cut changes have been identified in the transport of amino acids, but studies using the perfusion system are pending. The mechanisms accounting for lipid transport across the placenta are far from being understood. Alterations in fatty acid uptake, metabolism and transport are known, but no information is available for more complex lipids such as triglycerides, phospholipids and lipoprotein-cholesterol.


Adiponectin is an adipose tissue hormone, which is a specific plasma protein that is secreted by adipocytes. It may facilitate the regulation of the glucose and lipid metabolism. Adiponectin decreases the hepatic glucose production and insulin resistance by up-regulating fatty acid oxidation.47 Adiponectin also suppresses the secretion of TNF-a by adipose tissue, a factor that is known to contribute to insulin resistance.48 Studies have shown that adiponectin serum levels were decreased in obese subjects49 and patients with Type 2 diabetes.50 In studies with rhesus monkeys, adiponectin plasma levels were significantly decreased with the progression of obesity and insulin resistance.51 In all probability, adiponectin increases insulin sensitivity by enhancing the beta oxidation of free fatty acids and by decreasing the intracellular concentrations of triglycerides.52,53 In patients with Type 2 diabetes, who have the same risk factors for GDM, i.e. obesity, maternal age, ethnic origin,...


The immediate effect of lowered inositol concentration would be decreased levels of the phosphoinositides (PI, PIP and PIP2) and their products in the embryonic tissue.51 A lack of PIP2 would subsequently yield less IP3 and diacylglycerol, both of which are stimulators of protein kinase C (PKC) activity. A lowered PKC activity would exert a number of effects, including lowered activity of phospholipase A2, the key enzyme in the metabolism of triglycerides and phospho-lipids.59 A decrease of phospholipase A2 activity would subsequently diminish the availability of free arachidonic acid, and thereby diminish the production and metabolism of prostaglandins, as discussed below.

1241 Macronutrients

The Acceptable Macronutrient Distribution Range (AMDR) for fat for normal pregnancy and lactation is 20-35 of kilocalories for all women from 18 to 50 years of age 28 . Structural and functional changes in the gastrointestinal tract in HIV often affect the absorption of fat, leading to fat malabsorption 16 . In this setting, the use of medium chain triglyceride (MCT) oils may be beneficial. MCT are more easily digested than long-chain triglycerides (LCT) and can be absorbed across the small intestinal mucosa in the absence of pancreatic enzymes 30 . MCT oil can be used as a supplement and added to foods. Also, many enteral feeding formulas designed for patients with fat malabsorption contain MCT oil.

Treatment strategies

In the prevention of asymmetric fetal overgrowth in mothers with abnormal glucose metabolism, treatment strategies must be targeted to prevent overnutrition of the fetus.23 The goal of management in pregnancy complicated by altered glucose tolerance must be to maintain the blood glucose level as near to normal as possible in order to achieve normalization of fetal growth. Indeed, glycemia is the single maternal metabolic parameter routinely assessed in diabetic pregnancies, and the criteria for metabolic control and therapeutic strategies of diabetes in pregnancy are based on maternal glucose levels,24 since normoglycemia in pregnancy is associated with normal levels of other nutrients such as aminoacids and lipids.25 However perhaps 'glucose is merely an easily assessed covari-ate among other more dominant fetal growth determinants.'26 Maternal plasma amino acid levels are important for fetal growth, because they provide essential substrate. For example, a study has shown that...

Ascites Color Fluid

Bulging Flanks

Ascitic fluid obtained before (left) and after (right) feedings. The change from a straw-colored fluid to a milky-white opaque fluid after feeds is consistent with a diagnosis of chylous ascites. Today, such an infant would not be placed on regular feedings but would be fed formula containing medium-chain triglycerides and these changes would not occur.

Nutritional Values

The fat of human milk, which provides about one half of the milk's calories, is its most variable component. The total fat content of human milk ranges from 30 to 50 g L. The energy density of preterm mother's milk is much greater than that of full-term mother's milk, owing to a 30 percent higher fat concentration (Atkinson, Anderson, & Bryan, 1980). Triglycerides, the main constituent (98-99 percent)


The peak plasma level when the drug is given as a single agent occurs within 4 h. The extent of absorption is reduced with food intake however, it should be administered with meals to minimize gastrointestinal intolerance. Metformin is not metabolized and is eliminated unchanged in the urine. It has been effective in reducing plasma triglyceride and cholesterol levels, as well as in promoting weight loss in obese diabetic patients. Hypoglycemia is not an overt side effect of its use. Metformin does not stimulate the fetal pancreas to over-secrete insulin. The efficacy of the drug to reverse known defects responsible for insulin resistance in Type 2 diabetes and its safety with regard to hypoglycemia suggests that it may be an ideal drug for a primary prevention study in GDM.

Lower Your Cholesterol In Just 33 Days

Lower Your Cholesterol In Just 33 Days

Discover secrets, myths, truths, lies and strategies for dealing effectively with cholesterol, now and forever! Uncover techniques, remedies and alternative for lowering your cholesterol quickly and significantly in just ONE MONTH! Find insights into the screenings, meanings and numbers involved in lowering cholesterol and the implications, consideration it has for your lifestyle and future!

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