Restoring patient wellness. Building physician practices.

Cardiovascular Disease

The following conditions put people at increased risk for cardiovascular disease and dyslipidemia.1

• Family history of cardiovascular disease
• Diabetes
• Obesity
• Insulin resistance
• Hypertension
• Thyroid disorders
• Stress
• Chronic illness, including chronic fatigue
• Diets high in meat and saturated fats
• Diets low in essential fatty acids
• Lack of exercise
• Prescription drugs: oral contraceptives, Accutane, glucocorticoids, diuretics
• Hormone imbalances: estradiol, cortisol, melatonin, insulin
• Renal disease

 

Atherosclerosis

Atherosclerosis is a complex disorder arising from the combined interaction of hormones, lipids, and cell proliferation, involving many cells, including arterial medial smooth muscle cells, endothelial cells, and macrophages. Atherosclerosis occurs when fat deposits form on the walls of major arteries throughout the body, particularly on the walls of coronary arteries. The process actually seems to develop in childhood with fatty streaks (atheromas) developing into fat debris at about age 25.2
The highest risk factor for atherosclerosis is LDL cholesterol. Patients who have highest risk factors for cardiovascular disease ideally need to bring down the LDL level to under 100 mg/dl. Patients who have moderate risk factors need to get it under 130 mg/dl.

Hypercholesterolemia

High cholesterol levels are a significant risk factor for cardiovascular disease. For each 1% reduction in cholesterol, it is estimated that there is a 2% reduction in risk of coronary artery disease.
Cholesterol is synthesized in virtually all human tissues and therefore is found throughout the body. Higher concentrations are found in tissues that have essential roles in metabolism of cholesterol, such as the liver, adrenals, ovaries, and testes. The cytosol (the area) within the cell takes HMG-CoA, the building block for cholesterol, into a chemical reaction that converts mevalonic acid into cholesterol. The main enzyme necessary for this reaction involves the HMG Co A reductase. Lipitor and other drugs under the classification of statin drugs inhibit this pathway. Statin drugs are named after a compound synthesized from fungus that inhibits HMG Co A reductase. Insulin acts as a positive stimulus to increase the formation of cholesterol, while catabolic hormones, such as glucagon, inhibit this pathway.
In patients with hypercholesterolemia, it is important that HDL levels are increased. The formation of bile acids needs to be supported, while simultaneously inhibiting the deposition and oxidation of LDL. A holistic approach needs to be considered, in which the cholesterol formation by HMG Co A is not the only concern.

Hypercholesterolemia Causes

In treating high cholesterol levels, it is important to determine the cause. Causes of elevated serum cholesterol can be found in a variety of illnesses and conditions.

• — Lipoproteineimia
• — Nephrotic Syndrome
• — Hypothyroidism
• — Wilson’s Temperature Syndrome
• — Oral Contraceptives
• — Normal Pregnancy
• — Acute Intermittent Porphyria
• — Cholestasis Intra and Extra Hepatic

 

Hypocholesterolemia

Patients with low levels of cholesterol are relatively rare in the Western world, but hypocholesterolemia is found in a variety of serious conditions as well. Just as in treating patients with hypercholesterolemia, a holistic approach needs to be taken and the root causes need to be addressed.

• — Liver disease
• — Malabsorption ex. Inflammatory Bowel Disease
• — Malnutrition
• — Hyperthryoidism
• — Anemia
• — Abetaliproteinemia

 

Conventional Pharmaceutical Treatment [SH]

Statin Drugs

HMG CoA reductase inhibitors, more commonly known as statins, are the most common prescription for dyslipedemia. However, the voluntary withdrawal of cerivastatin (Baycol) from the U.S. market on August 8, 2001, by the manufacturer, in agreement with the Food and Drug Administration, has prompted concern. This drug, when removed from the market, had resulted in 31 deaths from rhabdomyolysis (muscle symptoms with marked CK elevation).3

Side Effects: In general, it is estimated that 5% of patients taking statins will experience general muscle aches and joint pain. Some of these patients will go on to develop rhabdomyolysis, a serious condition in which death may occur due to kidney failure. This is believed to occur because the statins, while blocking cholesterol synthesis in the liver, may also block the synthesis of nutrients important to cellular respiration in the mitochondrion, especially ubiquinone (Co-enzyme Q10).4 100 mg CoQ10 supplementation prevents plasma reduction of Co Q 10 levels while taking statin drugs. Whether this happens with red yeast extract is not known. However many compounds which naturally occur and is taken as a whole plant, does not have the same side effects of taking one isolated compound. For example the red yeast contains numerous different types of statins and antioxidants and flavanoids.
It is also estimated that up to 2% of all patients receiving statin therapy will develop elevated liver enzymes (hepatic transaminases), a blood marker of hepatotoxicity. This may progress to liver failure. Patients taking statins should therefore have their liver enzymes checked every 3 to 6 months.
Because of these side effects and adverse reactions, the FDA recommends prescribing cholesterol medications and statins only when cholesterol levels are markedly elevated or in those who have significant other risks of developing (or already have) coronary heart disease. Even when statins are prescribed, only 40 % of people treated with cholesterol drugs actually achieve target goals within the United States national guidelines.
Finally, it must be noted that a number of medications, such as glucocorticoids, diuretics, and thiazides, have been shown to affect lipid levels negatively. For some patients, their statin prescription is deemed necessary only to manage the side effects of these other medications.

Coumadin and Natural Medicine

Conventional doctors will usually forbid the use of Siberian ginseng, vitamin E, and ginger while taking Coumadin because of its ability to lower levels of prothrombin. Coumadin is one of the most dangerous drugs; however, when administered in conjunction with natural medicines, lower doses of Coumadin can be used. By simply adding high levels of vitamin E at levels of 3200 E, one would be able to monitor the prothrombin time and adjust or eliminate Coumadin dosages.

Naturopathic Prevention and Treatment [SH]

The aim of naturopathic treatments of dyslipidemia is to lower LDL cholesterol, raise HDL cholesterol, and support the organs, specifically the liver, involved in lipid metabolism. Lipid disorders can be effectively treated with natural medicine especially if one takes in consideration all the different pathways of cholesterol metabolism. It is also important to note that most of the prescription drugs currently used for dyslipidemia originate from natural medicines. Patients will normally have a minimum 20% to 30 % decrease in cholesterol and triglycerides, usually within 6 weeks with the use of a comprehensive program in natural medicine.

Lowering LDL

The liver’s production of LDL (low density lipoproteins) is the body’s way of sending cholesterol to the rest of the body for deposition. In patients with high cholesterol, the formation of LDL needs to be inhibited. Botanical medicine and clinical nutrition are helpful in limiting this pathway.

Botanical Medicine

Nopal (Opuntia streptacanthe): This herb is effective not only in the treatment of diabetes but also with hyperlipidemia. One study on healthy and diabetic subjects found that nopal intake before every meal for 10 days reduced body weight, as well as total cholesterol and triglycerides. Nopal also increases liver apolipoprotein receptors while decreasing LDL cholesterol in guinea pigs. The mechanism of action may be similar to bile acid sequestrants.
In another trial of 29 subjects who ere administered nopal, including 8 healthy subjects, 14 obese subjects and 7 diabetic subjects, total cholesterol decreased a mean of 31 mg-dl in 26 out of 29 cases, and decreased in all nine cases with values higher than 240 mg/dl (6.2 mmol/l). Triglycerides also diminished in obese and in diabetic patients, while no changes occurred in healthy subjects with lower triglyceride levels. This is another example of how herbs seem to have their own intrinsic wisdom. In this case, nopal lowered triglyceride levels only when needed. The highest reductions were seen in subjects with highest triglyceride levels. In obese subjects, the mean initial value of 162 mg/dl decreased to 43.8 mg/dl. In the diabetic group, the mean value of 376 mg/dl was reduced to 93.5 mg/dl.5-6
Excessive cholesterol in the form of LDL will be partly excreted in bile and thus a high fiber diet, supplemented with nopal, will support the elimination of these bile acids into stools..

Traditional Chinese Medicine [C]

Hong Qu: A pulverized strain of rice called red yeast has been consumed for over 2,000 years as a culinary ingredient and a medicine to improve blood circulation. It contains over nine different statin compounds inhibiting HMG Co A reductase. In four studies with patient bases between 70 and 446, it has shown to decrease total cholesterol by 16.4% to 25.9%. Red yeast does not damage the liver, unlike prescription drugs containing statin.7

Clinical Nutrition

Vitamin B-3 (Niacin): Nicotinic acid has been shown to decrease LDL cholesterol by about 23% and lipoprotein A by 35%. The decrease of lipoprotein A is significant because it has been shown that high levels are correlated with premature coronary artery disease. This is a unique aspect of nicotinic acid since allopathic drugs, such as Lovastatin, increase these levels.8-9
Unlike many cholesterol drugs that have shown to reduce life expectancy, niacin has been shown to increase life expectancy. The Coronary drug project conducted in the seventies showed that long term death rate for patients treated was only reduced with niacin. Negative risk factors include HDL over 60 mg/dl. Thus a high HDL can outweigh the risk of high LDL.
About 20 to 30 minutes after first taking niacin, patients will notice harmless skin flushing. Occasionally, patients also notice nausea and liver enzyme increase. However, most reports of high levels of liver enzymes were found only in people taking sustained release. Sustained release is a preparation of niacin that is absorbed slowly in order to prevent flushing. The Journal of the American Medical Associaiton has reported cases in which 52% of people using sustained release had elevated liver enzyme increase, while no cases of liver damage were found with niacin in itself.
There haven’t been any reports of damage with Inositol hexaniacinate (INH), another form of nicotinic acid, even at levels of 4 g daily. Patients may choose to take inositol hexanaicinate instead of niacin.10

Clinical Studies

Lovastatin vs. Niacin
In a study reported in The Annals of Internal Medicine, Lovastatin (prescription statin drug) and vitamin B-3 (niacin) were evaluated for their effect on LDL cholesterol. The results indicated that while Lovastatin produced a greater effect on LDL cholesterol, niacin was able to produce better over all results when all the lipid parameters were measured.
The 33% increase in HDL cholesterol found with the niacin group versus the 7% found with the Lovastatin group was indicative of the greater benefit of niacin, since HDL level is a more significant indicator for coronary heart disease than total cholesterol. Lipoprotein A is an independent risk factor for coronary heart disease, especially with patients with high LDL. The niacin group showed a 35% decrease while Lovastatin had no effect. This study correlated well with another previous study in which niacin at 4 g per day reduced lipoprotein A levels by 38.11

Lovastatin vs. Niacin Cholesterol Reductions in Percentages

 

Group	Week 10	Week 18	Week 26
LDL Cholesterol Lovastatin Niacin	26 5	28 16	32 23
HDL Cholesterol Increase Lovastatin Niacin	6 20	8 29	7 33
LP (A) Lipoprotein Reduction Lovastatin Niacin	0 14	0 30	0 35

Inositol Hexaniacinate: Inositol hexaniacinate (INH) consists of six molecules of nicotinic acid (niacin with an inositol molecule in the center). It reaches maximum serum levels 10 hours after ingestion. As with niacin it decreases lipid deposition, decreases VLDL synthesis in the liver, resulting in a decrease in LDL, total cholesterol, and triglycerides. It also increases HDL by inhibiting its breakdown and further inhibits cholesterol synthesis in the liver. Studies have found INH to be more effective than niacin in its hypocholesterolemic action. Significant hypocholesterolemic effect took place at doses as low as 400 mg, 3-4 times a day.12

L-carnitine: This enzyme has been shown to be particularly effective in patients with fatty liver. This is a condition in which the liver is not able to handle effectively the metabolism of cholesterol, thus increasing an excessive amount of VLDL production.13

Beta-sitosterols: Liver function must be working at its optimal level when treating patients with dyslipidemia. Dietary cholesterol is the only pathway where exogenous cholesterol goes to the liver. Beta-sitosterols found in soy and red yeast extracts, fiber, and curcumin inhibits the absorption of cholesterol in the small intestine, thereby inhibiting the formation of chylomicron remnants.14

Bile Acid Resins: Approximately 25% of cholesterol is secreted in the bile every day and is reabsorbed in the intestines. Bile acid resins will support the excretion of cholesterol. However, they will also decrease all the fat vitamins: D,A,K,E and folic acid. The decreased absorption of vitamin D will consequently result in decreased calcium absorption.
The combined use of niacin or nicotinic acid with HMG Co-A reductase inhibitor may increase the likelihood of developing rhabdomyolysis and myopathy. HMG Co-A reductase inhibitors, such as statin drugs, decrease vitamin B12 and folate absorption and deplete CoQ10 (a necessary cofactor in cardiovascular health.) CoQ10 supports all the cells of the body, especially cells that require a lot of energy, such as heart muscle.15

Antioxidants: Superoxide, nitrous oxide, hydrogen peroxide, and other oxidants cause LDL to become oxidized, which in turn causes a cascade of reactions leading to the formation of plaques. Monocytes a type of WBC that attach to the oxidized LDL in the endothelial wall of the artery are called macrophages. These macrophages eat up the LDL and form foam cells (lipid laden macrophages), which in turn cause platelet aggregation. Antioxidants, such as vitamin E, vitamin C, B carotenes, flavonoids, and garlic, have shown to inhibit this pathway.16

Other Supplements: Curcumin (turmeric), a common Indian spice, has been shown to inhibit platelet aggregation by decreasing thromboxane and increasing prostacyclin.17 Capsicum, bromelain, Omega 3 oils, and garlic have shown to increase in fibrolytic activity. Siberian ginseng and vitamin E increase prothrombin time, thus inhibiting the ability for the body to produce plaques.18

Calcium Caution: Lipids are negatively charged ions and so is the phosphate PO4- and chondroitin sulfate, which is inside the endothelial tissue. Calcium, a positive ion, can make these two negative ions connect and thus increase the chance of forming plaques in arteries. This is one reason that calcium should not be taken in megadosages.