Re: OT: High Cholesterol

[Guest guest]

I happen to have some info here, since I was looking this up for my Uncle. LEF has alot of good info on their site about it . . . just search high cholesterol (www.lef.org). Here's the first of 3 emails...

http://www.webmd.com/content/Article/87/99306.htm

Tangerine Peels May Lower Cholesterol

Peels Contain 20 Times the Flavonoids of Juice

By Jeanie Lerche WebMD Medical News

Reviewed By Charlotte Mathis, MDon Wednesday, May 12, 2004

May 12, 2004 -- Tangerine peels have more potent health benefits than the juice and could have powerful cholesterol-lowering potential, a new study shows.

Previous studies have shown numerous health benefits from drinking citrus juices like orange and grapefruit juice -- including their anti-inflammatory and anticancer properties. Studies have also hinted at a cholesterol-lowering capability in juices.

But disease-fighting flavonoids -- antioxidants found in foods -- are packed in higher concentrations in citrus peels than in juice, writes lead researcher Elzbieta M. Kurowska, PhD, with KGK Synergize Inc., in London, Ontario. Her study appears in the current issue of the Journal of Agricultural and Food Chemistry.

A few researchers, including Kurowska, have examined flavonoids found in citrus peels. The compounds, known to researchers as polymethoxylated flavonoids, are similar to plant pigment antioxidants found in citrus fruits.

The most common of these super-flavonoids -- tangeretin and nobiletin -- exist in orange and tangerine peels, and in smaller amounts in the fruits' juices, explains Kurowska.

Previous animal studies have shown that similar flavonoids -- herperidin from oranges and naringin from grapefruit -- may have cholesterol-lowering ability. However, those flavonoids are not as potent as the super-flavonoids, she says.

Hers is the first study looking at the super-flavonoids' cholesterol-lowering potential, she writes.

"Our study has shown that [super-flavonoids] have the most potent cholesterol-lowering effect of any other citrus flavonoid," says Kurowska in a news release. "We believe that [super-flavonoids] have the potential to rival or even beat the cholesterol-lowering effect of some prescription drugs, without the risk of side effects."

Taking super-flavonoid supplements could be an easier way to lower cholesterol than drinking 20 or more cups of juice daily -- the equivalent of the peel's amount of flavonoids, she says.

Save the Peel

Kurowska's study focuses on the super-flavonoids tangeretin and nobiletin found in tangerines. In the study, she fed hamsters a cholesterol-boosting diet -- the hamsters' LDL (bad) cholesterol levels jumped about 40%. Then, she fed hamsters with either a tangeretin supplement, a tangeretin/nobiletin mixture, or a commercially available tangerine flavonoid supplement.

Eureka! The hamsters benefited from all the tangeretin and nobiletin flavonoids. Total cholesterol and LDL cholesterol were significantly reduced -- without altering the HDL "good" cholesterol level, writes Kurowska.

Even much smaller amounts of the two flavonoids helped cholesterol significantly, she writes.

In fact, the peel flavonoids had three times higher cholesterol-lowering power than the juice, she writes. Her earlier studies have shown similar potential for peels.

These peel-derived compounds are more concentrated and easily absorbed and metabolized, she writes.

A long-term study involving humans is in progress to test the supplements' ability to lower cholesterol, Kurowska reports

Qadoshyah

*Got Down Syndrome?

www.gotdownsyndrome.net

From: Down Syndrome Treatment [mailto:Down Syndrome Treatment ] On Behalf Of ~Patty~Sent: Friday, September 15, 2006 10:11 AMDown Syndrome Treatment Subject: OT: High Cholesterol

This is off topic, but you all are such a wealth of info I wanted to ask in you can recommend any supplements for lowering high cholesterol. My dr wants me to take vytorin but I would like to explore some other options first.

TIA, Patty

[Guest guest]

This looks like it has some pretty good info in it. It mentions several things that lower LDL (bad) cholesterol & Trigycerides - Fish Oil, Curcumin (Turmeric), Garlic, etc.

Cholesterol Reduction

Integrated and Alternative Medical Approaches

Some people with high cholesterol are able to reduce to safe levels by using combinations of dietary supplements that have been shown to lower serum cholesterol, protect against LDL cholesterol oxidation, and reduce the risk of an abnormal arterial blood clot formation.

Benefits of PolicosanolPolicosanol is a natural supplement derived from sugar cane. The main ingredient is octacosanol. Octacosanol is an alcohol found in the waxy film that plants have over their leaves and fruit. The leaves and rinds of citrus fruits contain octacosanol, as does wheat germ oil.

Policosanol has been shown to normalize cholesterol as well or better than cholesterol-lowering drugs, without side effects such as liver dysfunction and muscle atrophy (Mas et al. 1999). Efficacy and safety have been proven in numerous clinical trials, and it has been used by millions of people in other countries. Policosanol lowers harmful LDL-cholesterol and raises protective HDL-cholesterol. HDL-cholesterol removes plaque from arterial walls.

Policosanol helps stop the formation of artery lesions (Noa et al. 1995), an effect similar to that of statin drugs. This was proven in studies on rabbits fed a diet designed to create high cholesterol. According to researchers “in most policosanol-treated animals, atherosclerotic lesions were not present, and in others, thickness of fatty streaks had less foam cell layers than in controls” (Arruzazabala et al. 2000).

Policosanol also inhibits the oxidation of dangerous LDL-cholesterol (Menendez et al. 1999), which promotes the destruction of blood vessels by creating a chronic inflammatory response. Oxidized LDL can also provoke metalloproteinase enzymes. (Xu et al. 1999). These enzymes promote blood vessel destruction, partly by interfering with HDL’s protective effect. Studies show that rats treated with policosanol have fewer foam cells, reflecting less inflammatory response and blood vessel destruction (Noa et al. 1996; Lindstedt et al. 1999).

Healthy arteries are lined with a smooth layer of cells so that blood can race through with no resistance. This layer becomes thick and overgrown with cells as a consequence of diseased arteries. As the artery narrows, blood flow slows down or is blocked completely. Policosanol can stop the proliferation of these cells in much the same way as lipid-lowering drugs (Noa et al. 1998; Negre-Aminou et al. 1996).

Policosanol also inhibits the formation of clots, and may work synergistically with aspirin in this respect. In a comparison of aspirin and policosanol, aspirin was better at reducing one type of platelet aggregation (clumping together of blood cells). But policosanol was better at inhibiting another type. Together, policosanol and aspirin worked better than either alone (Arruzazabala et al. 1997; Stusser et al. 1998).

Policosanol has also been shown to inhibit thromboxane, a blood vessel-constricting agent that contributes to abnormal platelet aggregation that can lead to heart attack or stroke. One study showed significant reductions in the level of thromboxane in humans after two weeks on policosanol (Carbajal et al. 1998).

Benefits of FiberHigh intake of soluble fiber is a very effective way of lowering serum cholesterol. Most people, however, find that high amounts of fiber produce gastrointestinal upset, and therefore do not consistently take enough fiber to lower cholesterol levels.

In populations with reported higher incidence of elevated cholesterol, fiber may be of benefit as found in a 1998 study conducted in Mexico City.

Psyllium and oat bran have been shown to lower plasma LDL cholesterol levels in different populations. Hypercholesterolemia is prevalent in the Northern part of Mexico and might be associated to dietary habits and sedentary lifestyle. These results indicate that psyllium and oat bran are efficacious in lowering plasma LDL cholesterol in both normal and hypercholesterolemic individuals from this population (Journal of the American College of Nutrition, Dec. 1998, 17(6):601-8).

Another study contradicts this as follows:

Various soluble fibers reduce total and LDL cholesterol by similar amounts. The effect is small within the practical range of intake. For example, 3 grams soluble fiber from oats (3 servings of oatmeal, 28 grams each) can decrease total and LDL cholesterol by approximately 0.13 mmol/L. Increasing soluble fiber can make only a small contribution to dietary therapy to lower cholesterol (Am. J. Clin. Nutr., (United States), Jan. 1999, 69(1):30-42).

Caution: DO NOT take psyllium if you are presently taking the prescription drugs digitalis or nitrofurantoin.

Chitosan is a fiber composed of chitin, which is a component of the shell of shellfish. Scientists in Norway have processed chitin to provide a magnetic binding affinity for fat and cholesterol in the digestive tract. Chitosan can absorb as much as seven to eight times its weight of fat and bile in the digestive tract. The fat and cholesterol are then excreted through the bowel, thereby improving bowel function and reducing cholesterol levels in the body.

One of the first studies to show a direct correlation between lowering of serum cholesterol with chitosan-suggesting that the agent could be used to inhibit the development of atherosclerosis in individuals with hypercholesterolemia-appeared in the June 1998 issue of the journal Atherosclerosis. Researchers at the Department of Medicine, University of Auckland, New Zealand, found that animals fed for 20 weeks on a diet containing 5% chitosan or on a control diet attained blood cholesterol levels significantly lower in the chitosan-fed animals throughout the study and at 20 weeks were 64% below that of control animals. That's right, 64%!

Additionally, when the area of aortic plaque in the two groups of animals were compared, a highly significant inhibition of plaque deposits was observed in the chitosan-fed animals-42% and 50%, compared to 42% in the control animals.

Earlier in the August-October 1994 issue of the journal ARM Medicina, Helsinki, clinical studies with chitosan demonstrated that in 5 weeks total cholesterol (LDL) was reduced by 32%, HDL increased by 7.5%, and triglycerides were lowered by 18%.

Another study done almost 20 years ago in the April 1980 American Journal of Clinical Nutrition reported a 25 to 30% reduction in cholesterol over a several-month period, initially documenting chitosan's potential cholesterol-lowering effectiveness.

Because of chitosan's ability to bind fat, chitosan is also an excellent aid in weight loss as well as normalization of cholesterol levels in the body.

Caution: Chitosan, like other fibers, can reduce absorption of trace minerals as well as dietary fat. For that reason, it is recommended that trace minerals be taken at a separate time than when the fiber is consumed.

Benefits of NiacinNiacin (vitamin B3) improves cholesterol profiles when given in doses well above the vitamin requirement. Nicotinic acid lowers total cholesterol, LDL-cholesterol, and triglyceride levels, while raising HDL-cholesterol levels. Most people cannot use the doses (1000 to 3000 mg a day) of niacin required to suppress cholesterol levels. Niacin causes a flushing effect, resembling an acute allergic reaction that many people find intolerable. While niacin is considered relatively safe, like other cholesterol-lowering drugs, it can cause liver toxicity when taken in high doses. Monitoring liver enzymes every 6 months is important when taking more than 1000 mg of niacin a day. Those with hepatitis should avoid niacin.

Flush-free niacin may lower cholesterol while boosting the beneficial HDL fraction. In a report on the antiatherogenic role of HDL (high density lipoprotein) cholesterol, flush-free niacin (inositol hexanicotinate) "appears to have the greatest potential to increase HDL cholesterol [by] 30%." This study was made over a 5-year period and focused on the effect of high LDL numbers exhibited before a patient's first coronary event(s).

As reported in a November 1998 American Journal of Cardiology research study, "Nicotinic acid (niacin) has been shown to decrease triglyceride, increase HDL cholesterol, lower LDL cholesterol, and decrease lipoprotein (a); it also decreases fibrinogen," an additional benefit that reduces the risk of related cardiovascular disease.

To determine whether lower doses of nicotinic acid are as effective and better-tolerated than the typical regimen currently used, researchers at the University of Texas Southwestern Medical Center in Dallas, as reported and described in the Archives of Internal Medicine, 1996, conducted a trial using two different doses (1.5 g and 3.0 g) of nicotinic acid.

The results showed that the lower dose (1.5 g ) nicotinic acid treatment significantly lowered triglyceride levels, raised HDL concentrations by approximately 22%, and favorably altered the ratio of total cholesterol: HDL cholesterol in both normal patients and those with abnormal lipid levels at baseline. Further improvement in lipid levels was also observed in those patients who tolerated the higher dose of nicotinic acid.

In this study, significant improvement in blood lipids levels was observed among the 75% of patients who tolerated low-dose nicotinic acid therapy. The authors conclude that use of nicotinic acid in lower doses than traditionally prescribed is both well-tolerated and effective in altering blood lipid levels. In addition, they suggest that this vitamin may be particularly worthwhile when combined with other lipid-lowering medications.

Note: Nicotinamide, another form of the vitamin B3, does not lower cholesterol levels and should not be used in the place of niacin.

Benefits of ArtichokeThe discovery that artichoke leaf extract reduces elevated cholesterol levels opens up exciting perspectives in the prevention and treatment of arteriosclerosis and coronary heart disease.

It was as early as the 1930s that scientists first discovered that artichoke extract had a favorable effect on atherosclerotic plaques in the arteries (Tixier, 1939). Later animal studies, in which rats were fed a high-fat diet, also showed that artichoke extract prevented a rise in serum cholesterol levels and the manifestation of atherosclerotic plaque (Samochowiec, 1959 and 1962).

In addition to findings in animal experiments (Samochowiec et al., 1971; Frohlich and Ziegler, 1973; Wojcicki 1976; Lietti 1977 and 1978), a study by Fintelmann in 1996 of 553 outpatients demonstrated a significant effect of the extract on fat (lipid) metabolism. The researchers found a significant decline in both the cholesterol and triglyceride levels in the blood, which confirmed a discovery made as early as the 1930s.

Recent research confirms these earlier findings. The study by Fintelmann demonstrated a significant reduction in cholesterol and triglyceride levels in spite of the relatively short duration of the study (6 weeks). On an average, there was an 11.5% reduction in serum cholesterol from 264 mg/dL initially to 234 mg/dL. Serum triglycerides were similarly reduced from 215 mg/dL initially to 188 mg/dL, corresponding to a decrease of 12.5%. Although this was an open study, its reliability is buttressed by the relatively large number of patients (302) and the very high level of statistical significance attained for the main results.

Very fascinating results came out of an excellent double-blind clinical trial conducted by Petrowicz in 1996. He studied the cholesterol-lowering effect of artichoke leaf extract on 44 healthy individuals under strictly controlled conditions over a 12-week period. There was a significant decrease of cholesterol levels in the volunteers who had high initial levels (greater than 220 mg/dL). In fact, the higher the initial cholesterol value, the more significant was the reduction in cholesterol levels. It was moreover observed that the protective HDL cholesterol levels showed a tendency to increase.

The restricting effect of artichoke leaf extract on cholesterol synthesis was demonstrated in some very interesting studies by Gebhardt (1995, 1996, and 1997) on rat hepatocytes (liver cells). A highly significant concentration-dependent inhibition of cholesterol synthesis was found. The 1997 study indicates that artichoke leaf extract reduces the formation of cholesterol in a physiologically favorable, long-lasting manner. This reduction of cholesterol synthesis persisted for hours following the period of exposure.

The study further indicates that artichoke extract may work through indirect inhibition of the enzyme HMGCoA-reductase, which might avoid problems known to occur with strong direct inhibitors of HMGCoA-reductase during long-term treatment. The indirect inhibition was supported by the fact that artichoke leaf extract effectively blocked insulin-dependent stimulation of HMGCoA-reductase without affecting insulin in general. HMGCoA-reductase is a key enzyme in cholesterol synthesis, and HMGCoA-reductase inhibitors generally reduce total cholesterol, LDL cholesterol and triglyceride levels

The International Antioxidant Research Centre, UMDS-Guy's Hospital, London, UK, published its research in September 1998 in Free-Radical Research, in which investigators stated, "Artichoke extract retarded LDL oxidation. . . and . . . overall, the results demonstrate the antioxidant activity of the artichoke extract."

Benefits of GarlicA study published in the Journal Nutrition Research (1987, 7:139-49) showed that a liquid garlic extract made by Kyolic caused a 12 to 31% reduction in cholesterol levels in the majority of test subjects after 6 months. The study showed that 73% of the subjects given the Kyolic garlic experienced a greater than 10% reduction in cholesterol, compared with only 17% of the subjects in the placebo group showing the same improvement.

If you have high LDL cholesterol levels, garlic supplementation is especially important because LDL cholesterol oxidation causes atherosclerosis, and garlic specifically inhibits LDL oxidation. And garlic helps protect the arterial lining against oxidation. Most importantly, garlic prevents abnormal platelet aggregation (thrombosis) via several different mechanisms. The formation of arterial blood clots is the primary cause of most heart attacks and strokes.

Investigators reported in a study published in the American Journal of Clinical Nutrition (1996, 64:866-70) that the daily administration of 7.2 grams of Kyolic garlic powder for 6 months produced a modest reduction (of between 6.1 and 7%) in total cholesterol, compared with the placebo group. The more dangerous LDL cholesterol was reduced 4 to 4.6% in the Kyolic group.

The heart-healthy benefits of garlic include protecting the endothelial lining of the arterial system against oxidative damage. A study published in Atherosclerosis (1999, 144:237-49) shows an actual reduction in buildup of fatty plaque in arteries in garlic-supplement users. Fatty plaque is comprised of many substances, including cholesterol. When plaque accumulates in the coronary arteries, the condition can lead to heart attack. In a study of 280 adults, German researchers reported that participants who took 900 mg of garlic powder a day had up to 18% less plaque in their arteries than those who took a placebo, or "dummy," powder. Male study participants who took a placebo had a 5.5% increase in plaque volume, while those who took the garlic powder experienced just a 1.1% increase in plaque buildup during the 4-year study period. By comparison, women who took the garlic showed a 4.6% decrease in plaque volume, while those who took the placebo powder had a 5.3% increase. Garlic may affect plaque buildup by reducing blood platelet stickiness (aggregation) and specifically preventing the oxidation of LDL cholesterol onto the lining of the arteries. Platelet aggregation helps plaque cling to the arteries.

An April 1998 study reported on the effect of garlic on blood lipids, blood sugar fibrogen, and fibrinogenic activity of 30 patients who received 4 grams of garlic daily for 3 months. The patients were monitored at 1.5 and 3 months when it was determined that garlic had "significantly reduced total serum cholesterol and triglycerides, and significantly increased HDL cholesterol." With regard to fibrinogenic activity, it was determined that the garlic inhibited platelet aggregation (Prostagland. Leuk. Essent. Fatty Acids, April 1998, 58[4]:257-63).

An earlier study in June 1994, the University of Massachusetts Medical School published a report that found that those U.S. adults who consumed one-half to one clove of garlic each day showed cholesterol levels that were reduced by 9% (JAMA, June 1, 1994, 271[21]:1660-61). A survey of 7 out of 8 studies on garlic showed that dosages of between 600 to 900 mg of garlic powder (Allium sativum L.) produced a 5 to 20% reduction in cholesterol and triglycerides. (Fortschr. Med. (Germany) 1990, 108[36]:49-54). Other studies have shown that much higher doses of garlic were required for cholesterol reduction.

Human patients fed a daily dose of Kyolic ("Aged Garlic Extract") over a 10-month study showed that "adhesion to fibrinogen was reduced by 30%-compared to placebo . . . and that . . . the beneficial effect of garlic preparations on lipids and blood pressure extends also to platelet function" (Journal of Cardiovascular Pharmacology [united States], 1998, 31[6]:904-8).

Note: Overall studies seem to indicate that dosages of garlic may be a factor in its efficacy. The suggested dose of high allicin garlic extract should be between 6000 mg and 8000 mg daily taken with meals. Since large amounts of garlic may cause stomach upset, we recommend that garlic be taken with the largest meal of the day.

In summary, the mechanisms by which garlic have shown to protect against cardiovascular disease include the following: cholesterol reduction, preventing abnormal blood clot formation inside of blood vessels; protecting against LDL cholesterol oxidation; and protecting the endothelial lining of the arterial system against oxidation. A review of all the studies on garlic indicates that high doses are required for effective cholesterol reduction. If you were to use garlic alone to lower serum cholesterol, you should take 6000 to 8000 mg a day. When used in combination with other cholesterol-lowering nutrients, lower doses of garlic may be effective.

Cholesterol Reduction

Benefits of CurcuminCurcumin, also known as turmeric root, an ancient spice in the ginger family, is gaining attention for its positive impact on a number of diseases, including cholesterol reduction. Scientific evidence has been building since the mid-1980s of curcumin's potential cholesterol-lowering capabilities.

For example, animals fed small doses of curcumin had their cholesterol levels drop by one half (50%) over those that did not receive curcumin. Curcumin reduces cholesterol by interfering with intestinal cholesterol uptake, increasing the conversion of cholesterol into bile acids, and increasing the excretion of bile acids, according to the International Journal of Vitamin Nutritional Research (1991, 61:364-69).

The 1992 Indian Journal of Physiology reported that ten human volunteers taking curcumin showed a 29% increase in beneficial HDL cholesterol in only 7 days. Total cholesterol also fell 11.6% and lipid peroxidation was reduced by 33%.

In January of 1997, the Journal of Molecular Cell Biochemistry reported curcumin has demonstrated, in vivo, the ability to decrease total cholesterol and LDL cholesterol levels in serum and to increase the beneficial HDL cholesterol. "Blood cholesterol was lowered significantly by dietary curcumin in these diabetic animals. Significant decrease in blood triglyceride and phospholipids was also brought about by dietary curcumin in diabetic rats."

The research has continued and curcumin's ability to lower blood cholesterol levels was reported in the April 1998 issue of Molecular Cell Biochemistry, and again, later that year, researchers in Biofactors (1998, 8:1-2, 51-57) reported that "curcumin extract may be protective in preventing lipoperoxidation of subcellular membranes."

Curcumin also provides an additional benefit by potentially reducing the risk of cardiovascular-related disease as it inhibits platelet aggregation and significantly decreases the level of lipid (LDL) peroxidation. "Observation of curcumin's mechanism of action shows that it blocks the formation of thromboxane A2, a promoter of platelet aggregation, thereby inhibiting abnormal blood clot formation. Curcumin also increases a prostacyclin, a natural inhibitor of platelet aggregation" (Arzneim. Forsch., 1986, 36:715-17).

Benefits of Gugulipid (Commiphora mukul)This powerful ancient remedy has been re-discovered by Western culture. Gugulipid is made from the resin of the commiphora mukul tree of north central India. Gugulipid (gugulesterones) has been used for thousands of years to alleviate problems associated with obesity, acne, viral infections, and other ailments.

In a study published in 1989 by the Journal of Associated Physicians-India, 125 patients receiving gugulipid showed an 11% decrease in total serum cholesterol, a drop of 16.8% in triglycerides, and a 60% increase in HDL cholesterol within 3 to 4 weeks. Patients with elevated cholesterol levels showed much greater improvement than normal patients.

The study quoted a second trial (included in the article noted above) where 205 patients receiving gugulipid at a dose rate of 25 mg administered 3 times daily showed a 70 to 80% reduction of serum cholesterol, whereas no response was found in the placebo group (Journal of Associated Physicians-India, 1989, 37[5]:328).

A placebo-controlled trial of 40 patients with high blood-fat levels showed a serum cholesterol reduction of 21.75%, with triglycerides being reduced by 27.1% in only 3 weeks, and after continuing the study for 16 weeks it was learned that HDL cholesterol was increased by 35.8% (Journal of Associated Physicians-India, 1989, 37[5]:328).

Benefits of Green TeaGreen tea has been shown to lower "bad" LDL cholesterol and serum triglyceride levels. Further, green tea's potent antioxidant effects inhibit the oxidation of LDL cholesterol in the arteries, which plays a major contributory role in the formation of atherosclerosis. "There is considerable epidemiological evidence that tea drinking lowers the risk of heart disease" (FEBS Lett., Aug. 1998, 433(1-2):44-46).

The cholesterol-lowering (hypocholesterolemic) effects of green tea (as well as black tea) have been confirmed by both animal and human epidemiological studies. High consumption of green tea by humans, especially more than 10 cups a day, was found to be associated with higher HDLs and lower LDL and VLDL cholesterol, as well as with various biomarkers indicating better liver health. Lower levels of lipid peroxides in the liver are one well-confirmed benefit of green-tea supplementation found in study after study.

A Japanese study relates, "Green tea catechin acts to limit the excessive rise in blood cholesterol" based on a series of studies reported in 1996 (Journal Nutritional Science Vitaminol., 32:613).

Additionally, some very exciting results were found when rats were fed 2.5% green tea leaves in their diet. The experimental group showed a drop in total cholesterol, low-density cholesterol, and triglycerides. The body weight of green tea-fed rats was 10 to 18% lower than that of rats not consuming green tea. In addition, the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase, and of anticarcinogenic phase-II enzyme glutathione S-transferase (GST), were significantly higher in the green tea group, as was the glutathione level in the liver. There was no liver or kidney toxicity. Thus, the study demonstrated combined cardiovascular and anticancer effects of green tea.

The relation between green tea consumption and serum lipid concentrations were examined using cross-sectional data on 1306 males in Japan. Results indicated that total cholesterol levels were found to be inversely related to the consumption of green tea. "Adjusted mean concentrations of total cholesterol were significantly lower in men drinking nine cups or more a day than in those consuming zero to two cups a day" (Prev. Med. July 1992, 21(4):526-31). No wonder the Japanese people have the longest life span. Most Japanese sip tea all day long.

Green tea also has been shown to elevate levels of HDL, the good cholesterol that helps remove atherosclerotic plaque from arterial walls. Green tea is a natural ACE inhibitor. This is an extra benefit for those with high cholesterol and blood pressure, as published studies show lowered blood pressure in animals and humans given green tea extracts. We recommend one capsule (350 mg) of green tea 95% extract daily, or drinking one to ten cups of green or black tea a day.

Benefits of Fish OilFish oil has been shown to reduce high levels of triglycerides by an average of 35%. Fish oil does not appear to reduce cholesterol to that extent, but does offer benefits when consumed as part of an integrated therapy.

A study conducted in The Netherlands on mice and published in June 1998 stated, "Triglyceride turnover studies revealed that fish oil significantly decreased the hepatic VLDL-triglyceride production rate (down 60%)" (Journal of Lipid Research (United States), June 1998, 39(6):1181-88).

Another study indicates, "Our results suggest that fish oil lowers plasma lipid levels significantly" (J. Formos. Med. Assoc., Sept. 1997, 96(9):718-26). Investigations published in the American Journal of Clinical Nutrition in 1997 examined the effects of n-3 fatty acids on serum lipid and lipoprotein concentrations in seven species of experimental animals. n-3 Fatty acids consistently lower serum triglyceride concentrations in humans, but not in most animals. These differences between animals and humans may arise from underlying species differences in lipoprotein metabolism.

Scientific studies have demonstrated that alpha-linolenic acid (from flax or perilla oil) reduces the incidence of atherosclerosis, stroke, and second heart attacks. One study showed a 70% reduction in second heart attacks in those consuming this type of fatty acid. Additionally, perilla oil suppresses platelet-activating factor (PAF), a major cause of arterial blood clots that cause heart attacks and strokes. Perilla oil was shown to decrease PAF by 50% in rats, compared with the administration of safflower oil (Journal of Lipid Mediators and Cell Signaling (Netherlands), 1997, 17/3:207-20).

Fish oil and garlic is a beneficial combination: Forty subjects, all with cholesterol over 200 mg/dL, were enrolled in a single-blind, placebo-controlled crossover study to evaluate both fish oil and garlic extract used in a synergistic regimen. Each patient received 1800 mg of fish oil plus 1200 mg of garlic for 1 month. Crossovers were then made to placebos for 1 month. This study found an 11% decrease in cholesterol, a 34% decrease in triglycerides, and a 10% decrease in LDL levels as well as a 19% decrease in HDL risk. Although not significant, there was a trend toward increase in HDL. The doctors concluded by stating

These results suggest that in addition to the known anticoagulant and antioxidant properties of both fish oil and garlic, the combination causes favorable shifts in the lipid subfractions within 1 month. Triglycerides are affected to the largest extent. The cholesterol lowering and improvement in lipid/HDL risk ratios suggests that these combinations may have antiatherosclerotic properties and may protect against the development of coronary artery disease (J. Natl. Med. Assoc., [united States], Oct. 1997, 89[10]:673-78).

Although fish oil appears to be beneficial for cholesterol reduction, there is a remaining problem: fish and flax oil, traditional sources of omega-3 fatty acids, can cause gastrointestinal side effects as well a stomach upset. There is good news in this regard; a new source of essential fatty acids, perilla oil, is showing superior health benefits without adverse gastrointestinal side effects. For cardiovascular disease risk reduction, we recommend 6000 mg of perilla oil a day.

Benefits of Vitamin ETo say that vitamin E is very important to our health is an understatement: it is protective against approximately 80 diseases.

The National Institute of Aging, Tufts University, and the University of Arizona, College of Medicine have found that vitamin E may help inhibit and slow the development of LDL oxidation, the progression of cardiovascular-related diseases, and possibly slow aging.

Oxidation of low density lipoprotein is involved in the development of atherosclerotic disease. An extensive study by the National Institute of Aging of 11,178 seniors aged 67 to 109 found that seniors who supplement with vitamin E are less likely to die prematurely. The research, reported in the American Journal of Clinical Nutrition late in 1997, discovered that vitamin E has the ability to stabilize free radicals. Free radicals are unstable oxygen molecules that can break down and degenerate cells, much as oxygen causes rust on iron. Partly caused by increased LDL cholesterol oxidation, free radicals result in increased plaque deposits and restricted blood flow, making them extremely dangerous to the interior of arteries.

A study by the National Institute of Aging found that people who took vitamin E supplementation over a 9-year period (1984 to 1993) had a 27% lower risk of all-cause mortality, a 41% reduction in heart disease risk!

Similarly, Dr. Blumberg, professor of nutrition at Tufts University in Boston, who heads the Antioxidant Research NIH Laboratories found that vitamin E helped prevent exercise-induced muscular damage based on many of the same mechanisms mentioned above, in the publication Advanced Nutrition, 1997. "The potential benefit is great, data are consistent and compelling, and the risk of side effects is essentially nil. It makes a clear case for recommending supplements," Dr. Blumberg said.

Increased blood cell adhesion to human aortic endothelial cells (ECs) lining veins and arteries is one of the early events in the development of atherogenesis. Investigators in 1997, in the Journal of Thrombosis and Vascular Biology (United States), indicate that vitamin E has an "inhibitory effect" on LDL-induced production of adhesion molecules and adhesion of blood cell to ECs via its antioxidant function and/or its direct regulatory effect on cell adhesion and arteriosclerosis.

The elderly may receive extra value from vitamin E supplementation, as supplementation with 100 IU vitamin E in the elderly has been reported as beneficial in lowering the rate of oxidation of LDL, slowing the progression of atherosclerosis (Atherosclerosis, Sept. 1997, 133[2]:255-63).

Smokers may benefit from long-term vitamin E supplementation, as it has been reported to improve endothelium-dependent relaxation in forearm resistance in vessels of hypercholesterolemic smokers which are characterized by increased levels of auto-antibodies against oxidized LDL. These findings suggest the beneficial effect of vitamin E for subjects with increased exposure to oxidized LDL such as smokers (J. Am. Coll. Cardiol., Feb., 1999, 33[2]:499-505).

Vitamin E may even work as well as some hypocholesterolemic drugs. Results of a study in the Journal of Circulation Research, August 1998, suggest that vitamin E and selenium inhibited atherosclerosis as effectively as an equally hypocholesterolemic dose of the drug probucol.

The recommended dose of vitamin E ranges from 400 to 800 IU a day. Minimum effective dose for selenium supplementation is 200 mcg a day. Selenium works with vitamin E to protect against LDL oxidation.

Benefits of SoyThe FDA has approved soy as a method of lowering the risk of coronary heart disease. For this dietary supplement, one research abstract says it all:

Soy has been a staple part of the Southeastern diet for nearly 5,000 years and is associated with a reduction in the rates of cardiovascular disease, and certain types of cancer. The research is now showing that phyto-chemicals in soy are the mechanism of action responsible (Society for Experimental Biology and Medicine [united States], 1998, 217[3]:386-92).

Diets rich in soy protein can protect against the development of atherosclerosis. The mechanisms of action of soy protein include cholesterol lowering, inhibition of LDL oxidation, protection against the development of atherosclerosis, and reduction in risk of thrombosis. The active constituents in soy responsible for these benefits are the isoflavones genistein, daidzein, and glycitein. In a study to determine whether soy isoflavones would protect against atherosclerosis in mice, it was reported that mice fed a soy diet averaged 30% lower cholesterol (J. Nutr. [united States], June 1998, 128[6]:954-59).

In a study in Metabolism, June 1997, investigations suggest that dietary soybean protein has a beneficial effect on cardiovascular risk factors. According to another study completed at about the same time, "Potential mechanisms by which soy isoflavones might prevent atherosclerosis include a beneficial effect on plasma lipid concentrations, antioxidant effects, antiproliferative and antimigratory effects on smooth muscle cells, effects on thrombus formation, and maintenance of normal vascular reactivity" (American Journal of Clinical Nutrition, Dec. 1988, 68[6] Suppl., 1390S-93S).

Postmenopausal women may also benefit from intake of soy protein, and it is suggested to be beneficial by researchers in a 1998 issue of American Journal of Clinical Nutrition for diseases and the risk factors (cholesterol) associated with cardiovascular disease.

Adding to the evidence that soy is beneficial, conclusions of a September 1998 Journal of Nutrition study are that "the efficacy of the American Hospital Association Step I cholesterol-lowering diet can be improved with the addition of soy protein." If you want to reduce your disease risk to heart disease and avoid elevated cholesterol levels, it is recommended that you take soy.

Summary

Diseases associated with high cholesterol (and fats) are the number one killer. Fats also play a key role in the incidence of cancers and many other degenerative diseases. Cholesterol exists only in animal tissues, therefore, one's diet is an important first step in its control. For some people, however, limiting fat and cholesterol intake alone is not enough to reduce serum cholesterol to safe levels because of their own liver's production of excess cholesterol. The use of supplements to augment dietary modification can help reduce cholesterol without the side effects of many drugs.

The effectiveness of any cholesterol-reduction therapy varies considerably between individuals. The nutrients we recommend have not only been shown to lower cholesterol, but also protect against cardiovascular disease by other mechanisms such as inhibition of cholesterol-oxidizing free radicals and abnormal blood clots inside arteries (thrombosis).

The following nutritional supplements offer synergistic benefits to assist dietary modification to reduce total serum cholesterol and elevate HDL cholesterol:

Policosanol, take one tablet twice per day with meals: one in the afternoon and one in the evening. Or Sytrinol, one capsule twice daily. Note:Do not take if it causes your cholesterol to drop below 180 mg/dL

Fiber, 4 to 6 grams before any high-fat meal.

Chitosan, three to six 500-mg chitosan capsules and one 1000 mg ascorbic acid capsule right before a high-fat meal.

Niacin, 1500 to 3000 mg a day (if tolerable). Consider flush-free niacin (inositol hexanicotinate) to avoid a "red face."

Artichoke extract, 300 mg, 3 times a day.

Garlic, 600 to 48000 mg a day.

Curcumin, 900 to 1800 mg a day.

Gugulipid, 140 mg 1 to 2 times a day.

Green tea, 750 mg a day of green tea, 93% polyphenol extract.

Perilla oil, 6000 mg a day. We suggest taking six 1000-mg gel caps daily. If triglycerides are high, consider taking 4-8 softgels of fish oil (EPA/DHA).

Vitamin E, 400 to 800 IU daily

Soy protein extract, 2 heaping teaspoons (5 to 6 grams) of soy powder daily. Soy powder can be easily dispersed and has a light peanut butter taste. For those who want to avoid powders, consider taking one-five capsules of the Ultra Soy Extract (40% isoflavones) daily.

Selenium, 200 to 600 mcg daily.

Herbal Cardiovascular Formula, two-six capsules daily with food in divided doses.

Caution: Anyone who is seeking to use dietary supplements to lower high cholesterol must verify efficacy by having a cholesterol blood test 45 to 60 days after initiating a nutritional regimen. If supplements fail to work, cholesterol-lowering drugs should be considered. While blood testing is not mandatory for healthy people seeking to reduce their risk of heart attack or stroke, it is recommended that everyone have an annual blood test to establish a benchmark giving you the ability to monitor and optimize your life extension program.

For more information

Contact the National Heart, Lung, & Blood Institute (301) 251-1222.

Product availability

Policosanol, Sytrinol, Herbal Cardiovascular Formula - containing curcumin, ginger, bromelain and gugulipid. Flush-Free Niacin, Ultra Soy extract, & Soy Power powder, vitamin E, kyolic garlic perilla oil,Super EPA/DHA w/Sesame Lignans, PGX fiber, chitosan, and artichoke extract, are available by phoning 1-800-544-4440 or order online.

From: Down Syndrome Treatment [mailto:Down Syndrome Treatment ] On Behalf Of ~Patty~Sent: Friday, September 15, 2006 10:11 AMDown Syndrome Treatment Subject: OT: High Cholesterol

This is off topic, but you all are such a wealth of info I wanted to ask in you can recommend any supplements for lowering high cholesterol. My dr wants me to take vytorin but I would like to explore some other options first.

TIA, Patty

[Guest guest]

This sounds pretty good. The place I got this info from is www.lef.org. They are a pretty reliable source, from what I have found.

You can order the supplement they are talking about at -

http://www.lef.org/newshop/items/item00674.html?source=mag1104 - they are a bit more expensive.

http://www.herbsmd.com/shop/productdetail.asp?pid=27604 - this place is much cheaper

http://www.lef.org/magazine/mag2004/nov2004_report_sytrinol_01.htm

Novel Dietary Supplement Shows Dramatic Effects in Lowering Cholesterol, LDL, and TriglyceridesBy Jim English

According to the federal Centers for Disease Control and Prevention, 61 million Americans currently suffer from cardiovascular disease. Cardiovascular disease covers a broad spectrum of disorders, including high blood pressure, coronary heart disease (heart attack and chest pain), stroke, congestive heart failure, and birth defects of the heart and blood vessels.

Every year, heart attacks and stroke cause more than 930,000 deaths in the US, accounting for 40% of deaths from all causes and making cardiovascular disease the nation’s number-one killer. While cardiovascular disease primarily kills people aged 65 and older, the incidence of sudden death from heart disease is rising in people aged 15 to 34.1

Reducing serum cholesterol levels—especially low-density lipoprotein (LDL)—is an effective, well-established strategy for preventing cardiovascular disease and reducing coronary events and mortality.2,3 Unfortunately, a recent report in the journal Circulation found that between 1988 and 2000, average total serum cholesterol concentrations in the US population declined by only 1%.4 And while 91% of those surveyed by the American Heart Association (AHA) felt it was “important to them personally to have a healthy cholesterol level,” fewer than 50% knew their own cholesterol levels, and 53% either did not know or overestimated the recommended cholesterol levels for a healthy adult.5

Compounding the problem, only a fraction of those at risk for cardiovascular disease are using pharmaceutical and nutritional strategies known to reduce cholesterol levels. According to estimates based on data gathered from the National Health and Nutrition Examination Survey III (NHANES III), only 6.6% of the 21.1 million Americans eligible for cholesterol-lowering drug therapy under National Cholesterol Education Program (NCEP) guidelines were using such therapy.6 When researchers examined responses gathered from 13,990 patients, they discovered that fewer than 4% of those diagnosed with hypercholesterolemia (elevated cholesterol) were taking vitamins or supplements known to reduce cholesterol.7

Concerned with the persistent failure of conventional strategies to significantly improve cholesterol profiles and reduce the incidence of cardiovascular disease, a broad coalition of medical researchers and scientists is now calling for a massive increase in the use of cholesterol-lowering drugs, particularly the family of pharmaceuticals known as statins.8

Unfortunately, the statin drugs, while very effective, also have side effects that understandably compromise patient compliance. Additionally, statin drugs are expensive to use; depending on the drug and dosage, the cost of statin therapy ranges from $63 to $228 a month.9

A newly available, all-natural supplement has been shown in human studies to significantly lower cholesterol levels—particularly of LDL, triglycerides, and apolipoprotein B—thus helping to reduce the risk of developing cardiovascular disease. This supplement, called Sytrinol™, is an important option for health-conscious people seeking a safe, effective, and convenient way to lower cholesterol levels without the side effects and expense of drugs.

Cholesterol and Human HealthCholesterol is a fatty (lipid) component found in virtually all cell membranes. In addition to supporting cellular integrity, cholesterol is also required for the transport of phospholipids and the biosynthesis of mineralocorticoids (aldosterone), glucocorticoids (cortisol), and sex hormones (progesterone, pregnenolone, testosterone, and estradiol). Far from endangering health, cholesterol is essential to life. In fact, Italian researchers have shown that when serum cholesterol levels are too low (less than 160 mg/dL), mortality in older adults actually increases.10,11

LDL, popularly known as “bad cholesterol,” is the primary transporter of cholesterol in the blood. In atherosclerosis, LDL is taken up in lesions in endothelial cells lining the inner walls of blood vessels, forming deposits in the arterial walls. The deposited LDL undergoes modification, as free radicals oxidize LDL to form foam cells that create a thick, hard plaque.

Over time, plaque accumulation can constrict vessels, inhibiting blood flow and reducing the supply of oxygen reaching the heart, brain, and other organs.12 If a clot (thrombus) blocks an artery already restricted by plaque, blood and oxygen flow can be cut off entirely, leading to a heart attack (if the occlusion occurs in the heart) or a stroke (if it occurs in the brain).

HDL is commonly referred to as “good” cholesterol because it helps remove excess cholesterol from atherosclerotic deposits and retard the growth of new plaque. Low HDL levels have been shown to be an additional risk factor for increased mortality from coronary artery disease and strokes in the elderly.13

How the Body Manages Cholesterol LevelsWhile cholesterol levels can be modestly influenced by dietary modification about 80% of cholesterol does not come from dietary sources, but is synthesized by the liver.2 The rate-limiting enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase controls the biosynthesis of cholesterol.

Normally, the liver regulates cholesterol levels via a biochemical feedback loop. When cholesterol levels are low, liver production of HMG-CoA reductase increases to speed biosynthesis of cholesterol. Conversely, when cholesterol levels are too high, the liver limits HMG-CoA reductase production to reduce cholesterol production. Proper functioning of this feedback mechanism is vital for the maintenance of healthy cholesterol levels.

Unfortunately, modern dietary habits (such as excess intake of saturated and trans fatty acids) and lifestyle contribute to the disruption of this system, leading to elevated cholesterol levels and increased risks for developing cardiovascular disease. Additionally, certain genetic disorders, such as familial hyper-cholesterolemia and autosomal recessive hypercholesterolemia, are known to increase LDL levels and risk for developing cardiovascular disease.14

Not All LDL Is Created EqualTo bind with other molecules for transport through the circulatory system, lipids rely on a specialized class of structural proteins, called apoproteins. LDL exists in two versions, differentiated by their protein components. The first, apolipoprotein A, consists of a large, “fluffy” protein called apoprotein A that is cardioprotective when bound to LDL. The second, apolipoprotein B, consists of a small, dense protein called apoprotein B that plays a major role in cardiovascular disease when bound to LDL. Apolipoprotein-B particles enable cholesterol to penetrate and lodge in vascular walls, an important step in initiating the formation of atherosclerotic plaque.15 Apo-lipoprotein B is the predominant form of apolipoprotein, and over 90% of all LDL cholesterol particles in the blood carry apolipoprotein B, making it an especially accurate (and convenient) marker for measuring the cholesterol-depositing capacity of blood.16-18

The importance of apolipoprotein B was highlighted in a report published in 2001 in the British medical journal The Lancet. In the AMORIS study, researchers evaluated cardiovascular markers in over 175,000 men and women over a period of five and a half years. In addition to conventional lipid markers, such as triglycerides, total cholesterol, and LDL:HDL ratios, the researchers also measured apolipoprotein-B levels. Their findings revealed that those with the highest ratios of apolipoprotein B to apolipoprotein A were at the greatest risk of dying from a heart attack.19

These findings were supported by a second study, published in 2003 in the journal Circulation. In the IRAS study, researchers again measured apolipoprotein-B levels in 1,522 individuals and compared them with an array of standard lipid markers (such as C-reactive protein, fibrinogen, and carotid artery intima-media thickness) to assess cardiovascular disease risks. They found that elevated apolipoprotein-B levels were strongly associated with cardiovascular disease, and concluded that apolipoprotein-B levels are a better predictor of vascular risk than are LDL levels.20

Given the well-documented link between apolipoprotein B and cardiovascular disease, measuring apolipoprotein-B levels offers clinicians and patients a new, highly specific marker for assessing the precise level of LDL in serum and determining individual risk for developing cardiovascular disease.

Continued on Page 2 of 3

LE Magazine November 2004

Novel Dietary Supplement Shows Dramatic Effects in Lowering Cholesterol, LDL, and TriglyceridesBy Jim English

Statin Drugs: the New Aspirin?Due to the failure of previous public health programs to substantially lower cholesterol levels in the general population, medical researchers and health experts are seeking a new approach to better manage the problem. For the last decade, physicians and patients have relied on cholesterol guidelines published by the AHA. According to the AHA, a total cholesterol level of 200 mg/dL or less is considered optimal. Levels of 200-239 mg/dL are considered borderline high risk, and levels above 240 mg/dL are considered high risk.

In May 2001, the National Institutes of Health published new federal guidelines calling for aggressive expansion of the use of statin drugs to treat cholesterol.21 Statin drugs such as atorvastatin (Lipitor®), lovastatin (Mevacor®), pravastatin (Pravachol®), and simvastatin (Zocor®) are among the most potent lipid-lowering agents currently available.

Statins lower cholesterol levels by inhibiting the production of HMG-CoA reductase, resulting in a decrease in cholesterol synthesis in the liver. To compensate for the resulting reduction of cholesterol production, the liver begins to remove LDL circulating in the blood, further reducing overall LDL levels. Statin therapy has been proven to contribute to a decrease in cardiovascular disease morbidity and mortality in recent years, as documented in a number of controlled clinical trials.22 In addition to improvements in lipid profile, statins also appear to confer other benefits, including improved endothelial function, decreased platelet thrombus formation, improved fibrinolytic activity, and reduced frequency of transient myocardial ischemia.23

Although statin therapy was initially used to treat patients suffering from severe hypercholesterolemia, health experts are now pushing to expand statin use to patients with only moderately elevated cholesterol. Moreover, health authorities have called for the use of statins to treat conditions such as diabetes, high blood pressure, high serum triglycerides, and low HDL, as well as for those with a strong family history of heart disease.

Most recently, in July 2004, the journal Circulation published an updated version of the NCEP guidelines, encouraging physicians to aggressively increase the use of statin drugs to lower cholesterol levels. In particular, the report recommends that target LDL levels be reduced from the current 100 mg/dL to 70 mg/dL in patients considered at high risk for a heart attack or death from cardiovascular disease. Additionally, patients at only moderate risk of a heart attack—those with heart disease, diabetes, or other risk factors—are now being encouraged to reduce their cholesterol levels by 30-40%.24

Not surprisingly, the new guidelines could dramatically increase the number of patients on statin drugs to as many as 50 million.25 In an embarrassing oversight, the same government panel drafting the new guidelines failed to mention in its report that most of its panelists are linked to pharmaceutical companies that manufacture statin drugs. Six of the nine panelists had either received grants from or were paid consulting or speakers’ fees by the companies that make some of the most popular statins, including Pfizer’s Lipitor®, Bristol-Myers Squibb’s Pravachol®, Merck’s Mevacor®, and AstraZeneca’s Crestor®.26

Statins and Side EffectsWhile statin drugs effectively lower LDL, they also produce serious side effects. In 1990, Folkers theorized that inhibition of HMG-CoA reductase would also inhibit intrinsic biosynthesis of coenzyme Q10 (CoQ10), a central compound in the mitochondrial respiratory chain. Dr. Folkers’ researchers stated, “If lovastatin were to reduce levels of CoQ10, this reduction would constitute a new risk of cardiac disease, since it is established that CoQ10 is indispensable for cardiac function.”

When the researchers examined five hospitalized patients aged 43 to 72, they found that lovastatin did in fact cause CoQ10 levels to drop. Furthermore, the patients showed evidence of increased cardiac distress, a potentially life-threatening situation for patients hospitalized with class IV cardiomyopathy. The researchers concluded, “Although a successful drug, lovastatin does have side effects, particularly including liver dysfunction, which presumably can be caused by the lovastatin-induced deficiency of CoQ10.”27 Taking supplemental CoQ10 may potentially offset this side effect, but other, more serious side effects cannot be so easily resolved.

For example, rhabdomyolysis is a rare but potentially deadly condition that occurs when large numbers of skeletal muscle cells die. As the rapidly dying cells deteriorate, they release large quantities of muscle proteins into the bloodstream, quickly overwhelming the kidneys. An analysis of the Food and Drug Administration’s side-effect registry, conducted in 2001 by the consumer watchdog group Public Citizen, discovered that statin drugs were linked to 72 fatal and 772 non-fatal cases of rhabdomyolysis between October 1997 and December 2000. In August 2001, pharmaceutical giant Bayer AG was forced to remove its statin drug Baycol® (cerivastatin) from the market after it was found to be responsible for killing at least 31 people.28

More recently, an article in the June 26, 2004, issue of The Lancet raised concerns about the FDA’s approval of one of the newest statin drugs, Crestor®, citing pre-approval evidence that the drug caused rhabdomyolysis. According to the author, Dr. Sidney Wolfe, director of Public Citizen’s Health Research Group, Crestor® was approved despite an FDA claim that new cholesterol drugs would be approved only if they presented a comparable or lower risk of rhabdomyolysis than drugs already on the market.

According to Wolfe, patients taking Crestor® experienced severe muscle deterioration at higher rates than patients taking other cholesterol-lowering drugs. In fact, the incidence of post-marketing reports of rhabdomyolysis for Crestor® appears to exceed that of all other currently marketed statins. From its approval in August 2003 to mid-April 2004,18 patients using Crestor®, including 11 in the US, suffered severe muscle deterioration. In addition, eight cases of acute kidney failure and four cases of kidney insufficiency related to the use of Crestor® have been reported.29

Unknown Long-Term EffectsWhile the cardioprotective benefits of statin drugs outweigh the known side effects, the most recent NCEP recommendations may result in tens of millions of new patients taking statins for a period of decades, and possibly for a lifetime. Unfortunately, data on the long-term use of statins are scant. In one paper published in the Journal of the American Medical Association in 1996, researchers set off a furious round of debate by raising the possibility of long-term statin use causing cancer. In the original paper, authors Newman and Hulley pointed out that all statin drugs have been shown to induce cancer in experimental lab rodents, and in some cases, the amount of statins causing cancer in the animals matched dosages being prescribed to humans. While conceding that extrapolating the incidence of cancer in rodents to humans is “an uncertain process,” the authors wrote that “lipid-lowering drug treatment, especially with the fibrates and statins, should be avoided except in patients at high short-term risk of coronary heart disease.”30 Interestingly, more recent studies indicate that statin drugs might actually reduce the incidence of certain cancers.31-37

Another potentially serious long-term problem appeared in a case study initiated after several reports and a single epidemiological study suggested that statins cause damage to the peripheral nervous system. After reviewing patient records from 1994 to 1998, the authors verified diagnosis of idiopathic polyneuropathy in 166 patients receiving statin therapy for at least two years, concluding in their 2002 paper that “long-term exposure to statins may substantially increase the risk of polyneuropathy.”38

Healthy Options for Lowering CholesterolIn their enthusiasm to reduce premature deaths from heart attack and strokes, the authors of the new cholesterol guidelines are recommending that millions of Americans start taking statin drugs. This recommendation ignores the danger of potential side effects from the long-term use of statins. Would informed health consumers willingly choose to lower their risk of cardiovascular disease if it meant substantially increasing their chances of developing health problems after a decade or two?

In a recent opinion piece published in the Washington Post, Dean Ornish, MD, clinical professor of medicine at the University of California, San Francisco, and president of the nonprofit Preventive Medicine Research Institute, wrote, “As tens of millions of people begin taking these medications for decades, more long-term side effects are likely to become apparent.” Dr. Ornish also questioned why the panel failed to recommend other options, such as diet and lifestyle changes, that for most people “can be a safe and effective alternative to a lifetime of cholesterol-lowering drugs.”39

One of the newest and most effective alternatives to statin drugs is a patented, proprietary formula comprising citrus and palm fruit extracts that contain polymethoxylated flavones and tocotrienols. It has been shown in human trials to significantly reduce total cholesterol, LDL, and triglycerides. Additionally, the powerful antioxidant and anti-inflammatory properties of the extracts in this natural formulation (trademarked under the name SytrinolTM) are known to contribute to managing additional cardiovascular disease risk factors.

Continued on Page 3 of 3

LE Magazine November 2004

Novel Dietary Supplement Shows Dramatic Effects in Lowering Cholesterol, LDL, and TriglyceridesBy Jim English

Safety and Effects of Sytrinol™Sytrinol™ was developed after 12 years of extensive research on the cardiovascular effects of polymethoxylated flavonoids and tocotrienols. The health benefits of Sytrinol™ have been demonstrated in in-vitro, in-vivo, and human clinical studies. Animal toxicity studies have shown that Sytrinol™ is well tolerated, with no toxic effects following consumption of polymethoxylated flavones in amounts of up to 1% of total dietary intake, or the equivalent of a 150-pound individual consuming almost 14 grams per day.

The cholesterol-lowering effects of Sytrinol™ were documented in a recent animal study published in the May 2004 issue of the Journal of Agricultural and Food Chemistry. Canadian researchers first induced high blood levels of cholesterol in hamsters. The animals were then treated with either polymethoxylated flavonoids (tangeretin) or a combination of flavones (hesperidin and naringin). While the flavones were shown to lower cholesterol levels, the tangeretin formulation proved to be almost three times as effective. In hamsters receiving the tangeretin formula, total cholesterol declined by up to 27% and LDL was reduced by 40%. While HDL levels were unchanged, the net result was a significant improvement in the LDL:HDL ratio.70

The cardioprotective and cholesterol-lowering claims for Sytrinol™ are also supported by human studies. Two early trials, each using 10 subjects, measured the effects of Sytrinol™ in men and women diagnosed with hyper-cholesterolemia and screened to eliminate thyroid disorders, kidney disorders, and diabetes. Subjects were instructed to maintain normal dietary habits and discontinue using vitamins, supplements, and cholesterol-lowering medications for at least six weeks before and during the study. Fasting blood samples were drawn at the onset and at the end of each four-week trial, and plasma lipid profiles and other metabolic parameters were analyzed using standard methods.

The results from the first trial (Table 1) show that four weeks of treatment with 300 mg of Sytrinol™ daily significantly reduced levels of total cholesterol (-25%), LDL (-19%), and triglycerides (-24%). HDL levels were unchanged and body mass remained relatively stable.

In the second trial, subjects with elevated cholesterol again benefited after only four weeks of treatment with 300 mg per day of Sytrinol™. As shown in Table 2, treatment with Sytrinol™ substantially cut levels of plasma total cholesterol (-20%), LDL (-22%), apolipoprotein B (-21%), and triglycerides (-28%). Additionally, subjects in the second trial benefited from a significant 5% increase in apolipoprotein A1, an important structural protein of HDL.

Sytrinol™ is currently being tested in a long-term, double-blind, crossover randomized study involving 120 men and women with moderately elevated cholesterol levels (total cholesterol above 230 mg/dL and LDL greater than 155 mg/dL). For 12 weeks, subjects will receive either 300 mg per day of Sytrinol™ or placebo, followed by a washout period of four weeks and another 12 weeks during which the groups receiving the active compound or placebo will be crossed over.

Only the first 12 weeks (phase 1) of the long-term study have been completed, yet already the results are compelling. As shown in Table 3, compared to placebo, the Sytrinol™ subjects saw reductions of 30% in total cholesterol, 27% in LDL, and 34% in total triglycerides. In addition, HDL levels increased 4%, resulting in a significant 29% reduction in the LDL:HDL ratio.

Table 1: Sytrinol™ Clinical Study I Results

Measured Endpoints

Treatment Group

Sytrinol™ Clinical Study I % Change at 4 weeks

Total Cholesterol

Sytrinol™

-25% b

LDL

Sytrinol™

-19% b

Triglycerides

Sytrinol™

-24% b

HDL

Sytrinol™

no change

Means ± SEM. Statistical analysis by ANOVA plus post test by Dunnett’s method b – Significantly different within same group, P 0.05 Source: SourceOne Global Partner

Table 2: Sytrinol™ Clinical Study II Results

Measured Endpoints

Treatment Group

Sytrinol™ Clinical Study II % Change at 4 weeks

Total Cholesterol

Sytrinol™

-20% b

LDL

Sytrinol™

-22% b

Triglycerides

Sytrinol™

-28% b

HDL

Sytrinol™

+3% b

Apolipoprotein A

Sytrinol™

+5% b

Apolipoprotein B

Sytrinol™

-21% b

Means ± SEM. Statistical analysis by ANOVA plus post test by Dunnett’s method b – Significantly different within same group, P 0.05 Source: SourceOne Global Partner

Table 3: Sytrinol™ Clinical Study III Results

Measured Endpoints

Treatment Group

Sytrinol™ Clinical Study II % Change at 4 weeks

Total Cholesterol

Sytrinol™

-30% b

LDL

Sytrinol™

-27% b

Triglycerides

Sytrinol™

-34% b

HDL

Sytrinol™

+4% b

LDL: HDL Ratio

Sytrinol™

-29% b

Means ± SEM. Statistical analysis by ANOVA plus post test by Dunnett’s method b – Significantly different within same group, P 0.05 Source: SourceOne Global Partner

ConclusionCholesterol management is a well-established means of maintaining health and preventing premature death from cardiovascular disease. Many people can maintain desirable cholesterol profiles by natural means, including lifestyle modifications, exercise, dietary strategies, and natural hormone replacement protocols. For those in need of additional cholesterol-lowering strategies, Sytrinol™ is an important new option that can help achieve substantial reductions in total cholesterol, LDL, and triglyceride levels, while improving the LDL:HDL ratio. Its lack of the side effects associated with statin drugs makes Sytrinol™ an especially attractive therapy for maintaining healthy cholesterol levels.

References

1. Available at: http://www.cdc.gov/nccdphp/aag/aag_cvd.htm). Accessed September 7, 2004.

2. Wald NJ, Law MR. Serum cholesterol and ischaemic heart disease. Atherosclerosis. 1995 Dec;118 Suppl:S1-5.

3. Barter P. Treatment of dyslipidaemia in high-risk patients: too little, too late. Int J Clin Pract Suppl. 2002 Jul;(130):15-9.

4. Ford ES, Mokdad AH, Giles WH, Mensah GA. Serum total cholesterol concentrations and awareness, treatment, and control of hypercholesterolemia among US adults: findings from the National Health and Nutrition Examination Survey, 1999 to 2000. Circulation. 2003 May 6;107(17):2185-9.

5. Nash IS, Mosca L, Blumenthal RS, son MH, SC Jr, Pasternak RC. Contemporary awareness and understanding of cholesterol as a risk factor: results of an American Heart Association national survey. Arch Intern Med. 2003 Jul 14;163(13):1597- 600.

6. Gotto AM Jr. Lipid management in patients at moderate risk for coronary heart disease: insights from the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). Am J Med. 1999 Aug 23;107(2A):36S-39S.

7. Steyer TE, King DE, Mainous AG 3rd, Gilbert G. Use of nutritional supplements for the prevention and treatment of hypercholesterolemia. Nutrition. 2003 May;19(5):415-8.

8. Kassirer JP. Why should we swallow what these studies say? Washington Post. August 1, 2004:B03. Available at: http://www.washingtonpost.com/wp-dyn/articles/A29456-2004Jul31.html. Accessed August 30, 2004.

9. Perreault S, Hamilton VH, Lavoie F, Grover S. Treating hyperlipidemia for the primary prevention of coronary disease. Are higher doses of lovastatin cost-effective? Arch Intern Med 1998 Feb 23;158(4):375-81.

10. Onder G, Landi F, Volpato S, et al. Serum cholesterol levels and in-hospital mortality in the elderly. Am J Med. 2003 Sep;115(4):265-71.

11. Brescianini S, Maggi S, Farchi G, tti, et al. Low total cholesterol and increased risk of dying: are low levels clinical warning signs in the elderly? Results from the Italian Longitudinal Study on Aging. J Am Geriatr Soc. 2003 Jul;51(7):991-6.

12. Brown MD, Jin L, Jien ML, et al. Lipid retention in the arterial wall of two mouse strains with different atherosclerosis suscep- tibility. J Lipid Res. 2004 Jun;45(6):1155-61.

13. Weverling-Rijnsburger AW, Jonkers IJ, van Exel E, Gussekloo J, Westendorp RG. High- density vs low-density lipoprotein choles- terol as the risk factor for coronary artery disease and stroke in old age. Arch Intern Med. 2003 Jul 14;163(13):1549-54.

14. Pullinger CR, Kane JP, Malloy MJ. Primary hypercholesterolemia: genetic causes and treatment of five monogenic disorders. Expert Rev Cardiovasc Ther. 2003 May;1(1):107-19.

15. Gustafsson M, Flood C, Jirholt P, Boren J. Retention of atherogenic lipoproteins in atherogenesis. Cell Mol Life Sci. 2004 Jan;61(1):4-9.

16. Cabezas Castro M, Liem A. The use of apolipoprotein B in clinical practice to determine the risk for atherosclerosis. Ned Tijdschr Geneeskd. 2003 Jul 26;147(30):1445-8.

17. Walldius G, Jungner I. Apolipoproteins are new and better risk indicators of myocardial infarction. Lakartidningen. 2004 Mar 25;101(13):1188-94.

18. Walldius G, Jungner I. Apolipoprotein B and apolipoprotein A-I: risk indicators of coronary heart disease and targets for lipid- modifying therapy. J Intern Med. 2004 Feb;255(2):188-205.

19. Walldius G, Jungner I, Holme I, Aastveit AH, Kolar W, Steiner E. High apolipoprotein B, low apolipoprotein A-I, and improve- ment in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet. 2001 Dec 15;358(9298):2026-33.

20. K, Sniderman AD, Sattar N, D’Agostino R Jr, Wagenknecht LE, Haffner SM. Comparison of the associations of apolipoprotein B and low-density lipoprotein cholesterol with other cardiovascular risk factors in the Insulin Resistance Atherosclerosis Study (IRAS). Circulation. 2003 Nov 11;108(19):2312-6.

21. National Health and Nutrition Examination Study III (NHANES III, 1988–94) (CDC) NCHS.

22. Farmer JA. Aggressive lipid therapy in the statin era. Prog Cardiovasc Dis 1998 Sep;41(2):71-94.

23. Farnier M, Davignon J. Current and future treatment of hyperlipidemia: the role of statins. Am J Cardio .l 1998 Aug 27;82(4B):3J- 10J.

24. Grundy SM, Cleeman JI, Bairey Merz CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004 Jul 13;110(2):227-39.

25. Herper M. Cholesterol guidelines a gift for Merck, Pfizer. Forbes. July 12, 2004.

26. Ricks D, Rabin R. Panel’s ties to drugmakers not cited in new cholesterol guidelines. Newsday. July 15, 2004.

27. Folkers K, Langsjoen P, Willis R, et al. Lovastatin decreases coenzyme Q levels in humans. Proc Natl Acad Sci U S A. 1990 Nov;87(22):8931-4.

28. Bayer voluntarily withdraws Baycol. FDA Talk Papers T01-34. August 8, 2001.

29. Wolfe SM. Dangers of rosuvastatin identified before and after FDA approval. Lancet. 2004 Jun 26;363(9427):2189-90.

30. Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA. 1996 Jan 3;275(1):55-60.

31. Graaf MR, Beiderbeck AB, Egberts AC, Richel DJ, Guchelaar HJ. The risk of cancer in users of statins. Clin Oncol. 2004 Jun 15;22(12):2388-94.

32. Esserman L, M, Shoemaker M, Lobo M, Marx C, Benz C. Breast cancer inhibition by statins. J Clin Oncol. 2004 Jul 15;22(14 Suppl):1003.

33. J, Garzotto M, Palma AJ. Statin use and prostate cancer risk. J Clin Oncol. 2004 Jul 15;22(14 Suppl):4596.

34. Poynter J, Rennert G, Bonner J, et al. HMG CoA reductase inhibitors and the risk of colorectal cancer. Proceedings from the 40th annual meeting of the American Society of Clinical Oncology. New Orleans, LA. June 2004.

35. Boudreau DM, Gardner JS, Malone KE, Heckbert SR, Blough DK, Daling JR. The association between 3-hydroxy-3-methylglu- taryl coenzyme A inhibitor use and breast carcinoma risk among postmenopausal women: a case-control study. Cancer. 2004 Jun 1;100(11):2308-16.

36. Katano H, Pesnicak L, Cohen JI. Simvastatin induces apoptosis of Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and delays development of EBV lymphomas. Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4960-5

37. Jiang Z, Zheng X, Lytle RA, Higashikubo R, Rich KM. Lovastatin-induced up-regulation of the BH3-only protein, Bim, and cell death in glioblastoma cells. Neurochem. 2004 Apr;89(1):168-78.

38. Gaist D, Jeppesen U, Andersen M, García Rodríguez LA, Hallas J, Sindrup SH. Statins and risk of polyneuropathy: A case-control study. Neurology 2002 May 14;58(9):1333-7.

39. Ornish D. Lower cholesterol without drugs. Washington Post. August 8, 2004:B07.

40. Buening MK, Chang RL, Huang MT, Fortner JG, Wood AW, Conney AH. Activation and inhibition of benzo(a)pyrene and aflatoxin B1 metabolism in human liver microsomes by naturally occurring flavonoid. Cancer Res. 1981 Jan;41(1):67-72.

41. Siess MH, Guillermic M, Le Bon AM, Suschetet M. Induction of monooxygenase and transferase activities in rat by dietary administration of flavonoids. Xenobiotica. 1989 Dec;19(12):1379-86.

42. Guengerich FP, Kim DH. In vitro inhibition of dihydropyridine oxidation and aflatoxin B1 activation in human liver microsomes by naringenin and other flavonoids. Carcinogenesis. 1990 Dec;11(12):2275-9.

43. Mukhtar H, Das M, Khan WA, Wang ZY, Bik DP, Bickers DR. Exceptional activity of tannic acid among naturally occurring plant phenols in protecting against 7,12-dimethyl- benz(a) anthracene-, benzo(a)pyrene-, 3- methylcholanthrene-, and N-methyl-N- nitrosourea-induced skin tumorigenesis in mice. Cancer Res. 1988 May 1;48(9):2361-5.

44. Verma AK, JA, Gould MN, Tanner MA. Inhibition of 7,12- dimethylbenz(a)anthracene and N-nitro somethylurea induced rat mammary cancer by dietary flavonol quercetin. Cancer Res. 1988 Oct 15;48(20):5754-8.

45. Firenzuoli F, Gori L, Crupi A, Neri D. Flavonoids: risks or therapeutic opportunities? Recenti Prog Med. 2004 Jul-Aug;95(7- 8):345-51.

46. Middleton E, Kandaswami C. Effects of flavonoids on immune and inflammatory cell functions. Biochem Pharmacol. 1992 Mar 17;43(6):1167-79.

47. Maron DJ. Flavonoids for reduction of atherosclerotic risk. Curr Atheroscler Rep. 2004 Jan;6(1):73-8.

48. Milde J, Elstner EF, Grassmann J. Synergistic inhibition of low-density lipoprotein oxidation by rutin, gamma-terpinene, and ascorbic acid. Phytomedicine. 2004 Feb;11(2-3):105-13.

49. Monforte MT, Trovato A, Kirjavainen S, Forestieri AM, Galati EM, Lo Curto RB. Biological effects of hesperidin, a citrus flavonoid. (note II): hypolipidemic activity on experimental hypercholesterolemia in rat. Farmaco. 1995 Sep;50(9):595-9.

50. Tseng KF. Nobiletin. Part I., an oil extracted by cold methyl alcohol from Citrus nobilis, Lour, affords nobiletin, a hexam- ethoxyflavone containing a veratryl nucleus. Chem Soc. 1938;1003-4.

51. Manthey JA, Grohmann K, Guthrie N. Biological properties of citrus flavonoids pertaining to cancer and inflammation. Curr Med Chem. 2001 Feb;8(2):135-53.

52. Murakami A, Nakamura Y, Torikai K, et al. Inhibitory effect of citrus nobiletin on phor- bol ester-induced skin inflammation, oxidative stress, and tumor promotion in mice. Cancer Res. 2000 Sep 15;60(18):5059-66.

53. Minagawa A, Otani Y, Kubota T, et al. The citrus flavonoid, nobiletin, inhibits peritoneal dissemination of human gastric carcinoma in SCID mice. Jpn J Cancer Res. 2001 Dec;92(12):1322-8.

54. O'Leary KA, de Pascual-Tereasa S, Needs PW, Bao YP, O'Brien NM, on G. Effect of flavonoids and vitamin E on cyclooxygenase-2 (COX-2) transcription. Mutat Res. 2004 Jul 13;551(1-2):245-54.

55. Lin N, Sato T, Takayama Y, et al. Novel anti- inflammatory actions of nobiletin, a citrus polymethoxy flavonoid, on human synovial fibroblasts and mouse macrophages. Biochem Pharmacol. 2003 Jun 15;65(12):2065-71.

56. Murakami A, Nakamura Y, Ohto Y, et al. Suppressive effects of citrus fruits on free radical generation and nobiletin, an anti- inflammatory polymethoxyflavonoid. Biofactors. 2000;12(1-4):187-92.

57. EK. The occurrence of a pentamethyl flavonol in tangerine peel. J Am Chem Soc. 1934;56:1392.

58. Kawaii S, Tomono Y, Katase E, Ogawa K, Yano M. Effect of citrus flavonoids on HL-60 cell differentiation. Anticancer Res. 1999 Mar-Apr;19(2A):1261-9.

59. Kawaii S, Tomono Y, Katase E, Ogawa K, Yano M. Antiproliferative activity of flavonoids on several cancer cell lines. Biosci Biotechnol Biochem. 1999 May;63(5):896-9.

60. Manthey JA, Guthrie N. Antiproliferative activities of citrus flavonoids against six human cancer cell lines. J Agric Food Chem. 2002 Oct 9;50(21):5837-43.

61. Datla KP, Christidou M, Widmer WW, Rooprai HK, Dexter DT. Tissue distribution and neuroprotective effects of citrus flavonoid tangeretin in a rat model of Parkinson's disease. Neuroreport. 2001 Dec 4;12(17):3871-5.

62. Kurowska EM, Manthey JA, Casaschi A, Theriault AG. Modulation of HepG2 cell net apolipoprotein B secretion by the citrus polymethoxyflavone, tangeretin. Lipids. 2004 Feb;39(2):143-51.

63. Gordon DA. Recent advances in elucidating the role of the microsomal triglyceride transfer protein in apolipoprotein B lipoprotein assembly. Curr Opin Lipidol. 1997 Jun;8(3):131-7.

64. Jamil H, Gordon DA, Eustice DC, et al. An inhibitor of the microsomal triglyceride transfer protein inhibits apoB secretion from HepG2 cells. Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11991-5.

65. Osiecki H. The role of chronic inflammation in cardiovascular disease and its regulation by nutrients. Altern Med Rev. 2004 Mar;9(1):32-53.

66. Sun W, Yan Y, Dong F. Progression of tocotrienols. Wei Sheng Yan Jiu. 2004 Mar;33(2):243-5.

67. Ong AS, Goh SH. Palm oil: a healthful and cost-effective dietary component. Food Nutr Bull. 2002 Mar;23(1):11-22.

68. Iqbal J, Minhajuddin M, Beg ZH. Suppression of 7,12-dimethylbenz[alpha]anthracene-induced carcinogenesis and hypercholesterolaemia in rats by tocotrienol-rich fraction isolated from rice bran oil. Eur J Cancer Prev. 2003 Dec;12(6):447-53.

69. Qureshi AA, Sami SA, Salser WA, Khan FA. Dose-dependent suppression of serum cholesterol by tocotrienol-rich fraction (TRF25) of rice bran in hypercholesterolemic humans. Atherosclerosis. 2002 Mar;161(1):199-207.

70. Kurowska EM, Manthey JA. Hypolipidemic effects and absorption of citrus polymethoxylated flavones in hamsters with diet-induced hypercholesterolemia. J Agric Food Chem. 2004 May 19;52(10):2879-86.

From: Down Syndrome Treatment [mailto:Down Syndrome Treatment ] On Behalf Of ~Patty~Sent: Friday, September 15, 2006 10:11 AMDown Syndrome Treatment Subject: OT: High Cholesterol

This is off topic, but you all are such a wealth of info I wanted to ask in you can recommend any supplements for lowering high cholesterol. My dr wants me to take vytorin but I would like to explore some other options first.

TIA, Patty

[Guest guest]

Thanks to all of you for taking time to send me some great information!! It is very much appreciated.

Patty