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Cardiovascular
Disease Protocol
Cardiovascular
Recommended Products: The following examples exemplify the breadth of CoQ10's credits: CoQ10 therapy is
associated with a mean 25.4% increase in exercise duration and a 14.3%
increase in workload (Sacher et al. 1997). Reader's guide to
CoQ10 food sources
CLA appears reliable in reducing body fat, while preserving lean body tissue. CLA accomplishes this by increasing the basal metabolic rate and impacting the distribution of fat, especially abdominal obesity. (Recall that apple-shaped bodies are considered vulnerable in regard to heart disease.) A Norwegian human study found that CLA-supplemented subjects lost up to 20% of their body fat in 3 months without changing their diet, while the control subjects on an average gained a slight amount of body fat during the same period (Health-N-Energy 2000). CLA displays hypolipidemic properties as well as the ability to reduce arachidonic acid levels, an initiator of inflammatory leukotrienes (Liu 1998). (Leukotrienes are considered 1000 times more reactive than histamine.) Researchers set out to determine the effects of CLA on the establishment and progression of experimentally induced atherosclerosis in rabbits. To establish atherosclerosis, New Zealand white rabbits were fed a diet containing 0.1-0.2% of cholesterol for 90 days. Some groups were fed the atherogenic diet and CLA. For effects on progression of atherosclerosis, rabbits with established atherosclerosis were also included in the study. At dietary levels as low as 0.1%, CLA inhibited atherogenesis; at dietary levels of 1%, CLA caused substantial (30%) regression of established atherosclerosis. This is the first example of substantial regression of atherosclerosis being caused by diet alone (Kritchevsky et al. 2000). Some question whether linoleic acid and CLA accomplish the same tasks. Although the two acids are related, they appear to oppose one another on factors that influence cardiac performance. While the linoleic acid cascade has a greater tendency to stimulate fat formation, CLA inhibits it. Cholesterol is more likely to be oxidized by various factors working off the linoleic cascade, whereas CLA appears to stabilize cholesterol. Laboratory animals, supplemented with CLA for 36 weeks at a dose 50 times higher than the suggested upper range for human consumption, completed the study without signs of toxicity. A suggested dosage is three to four 1000-mg capsules taken early in the day.
Curcumin is such a powerful antioxidant (comparable to vitamins C and E) that it is considered protective to smokers, lessening free-radical attack and cellular damage. Yet, its cardioprotection extends to reducing blood lipid levels, particularly cholesterol. Rats fed 0.1% curcumin, along with a cholesterol diet, had about one-half of the blood cholesterol as rats fed equal amounts of cholesterol but without curcumin (Rao et al. 1970). Curcumin also possesses potent anti-inflammatory activity. It is, in fact, comparable to cortisone and phenylbutazone in acute inflammatory conditions and about one-half as effective in chronic models. As curcumin reduces inflammation (a more recently established risk factor for cardiovascular disease), fibrinolysis is promoted and leukotriene formation inhibited (Arora et al. 1971; Chandra et al. 1972; Murray 1994). A recommended dosage is 900 mg 1-2 times a day.
Dehydroepiandrosterone
(DHEA)--is anti-inflammatory and antilipidemic, increases hormonal levels,
and is beneficial in diabetes and Syndrome X Other antiatherogenic properties of DHEA include inhibiting the activity of fibroblasts (cells that proliferate at the site of chronic inflammation), encouraging proinflammatory cytokine production. An imbalance of the cytokine network appears to be involved in the development and progression of congestive heart failure (CHF) (Yang et al. 2001). The greater the cardiac debility, the more pronounced the imbalance. Note: A cytokine imbalance refers to a shift toward greater levels of inflammatory cytokines combined with inadequately raised or decreased levels of anti-inflammatory cytokines. Proinflammatory cytokines interleukin-1b (IL-1b), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) typically rise with age. High levels of TNF-alpha are destructive to the heart muscle, while excesses of IL-6 are associated with fibrinogen production and the instability of atheromatous plaque (di Minno et al. 1992; Ikeda et al. 2001; Lindmark et al. 2001). As DHEA suppresses the activity of IL-6 and TNF-alpha, inflammation and the risk of clot formation significantly decrease (Kipper-Galperin et al. 1999; Kaiser 2001). Japanese researchers suggest screening for pro-inflammatory cytokines and using the appropriate anti-inflammatory treatment to reduce the risk of heart disease (Ikeda et al. 2001). By contrast, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) actually increases the likelihood of CHF. The use of NSAIDs (other than low-dose aspirin) in the previous week was associated with a doubling of the odds of a hospital admission with CHF. The use of NSAIDs by patients with a history of heart disease was associated with an odds ratio of 10.5 for first admission with heart failure, compared with 1.6 in those without such a history (Page et al. 2000). Improved glucose control among diabetic rats supplemented with DHEA indicates it may be of value to patients with diabetes and Syndrome X. Research shows that serum DHEA levels fall when serum insulin levels rise (Lukaczer 2000). Reducing carbohydrates to less than 40 grams a day (lessening the incidence of an insulin surge) resulted in a 34% increase in DHEA. Scientists thus speculate that DHEA might be the missing link in the insulin resistance/hyperinsulinemia epidemic. Insulin appears to deliver its blow to DHEA by inhibiting production and stimulating clearance (Nestler et al. 1992). DHEA, by incorporating into HDL and LDL cholesterol, protects against oxidation. With age, cholesterol-bound DHEA becomes scarce, and compared to younger people with adequate levels of DHEA, oxidation spirals. Another hindrance to antioxidant defense occurs as superoxide dismutase (a powerful antioxidant) becomes lethargic as DHEA levels dwindle (Bednarek-Tupikowska et al. 2000). Japanese researchers also showed that DHEA prevented aggression from increasing during times of mental stress, significantly reducing levels of norepinephrine, a hormone synthesized by the adrenal medulla (Sawazaki et al. 1999). The Massachusetts Male Aging Study determined that in a sample analysis of 1167 men, those with serum DHEA-S (DHEA-sulfate) in the lowest quartile at baseline (< 1.6 mcg/mL) were significantly more likely to incur ischemic heart disease (Feldman et al. 2001). Most studies show DHEA supplementation to be of value in regard to the cardiac health of men, but the Rancho Bernardo Study found DHEA-S levels were not significantly associated with cardiovascular mortality in women (Khaw 1996). A suggested DHEA dosage is 15-75 mg, taken early in the day (50 mg represents a typical daily dose). Blood tests are valuable 3-6 weeks into therapy to assist in assigning appropriate dosages. (Optimal DHEA levels for men are between 400-560 mcg/dL; for women, the range is considered ideal at 350-430 mcg/dL.) It has been suggested that antioxidants such as green tea, vitamin E, and N-acetyl-cysteine should accompany DHEA supplementation. Yet, the threat of potentiating free-radical activity in the liver appears roused only at much higher doses than are needed to provide the desired effects. Because DHEA invigorates hormonal systems, DHEA is not recommended for men with prostate cancer or for women with estrogen-dependent cancer without physician approval. (Recall that DHEA can be converted into testosterone and estrogen.) Before starting DHEA therapy, men should know their serum PSA (prostate specific antigen) level and should have passed a digital rectal examination. DHEA does not cause prostate cancer, but since DHEA can cause an increase in testosterone levels, the presence of an undetected cancer should be ruled out before initiating the therapy.
Essential
Fatty Acids--inhibits platelet clumping; has antispasmodic activity;
improves HDL-LDL ratio; lessens risk of second heart attack, stroke,
and restenosis following angioplasty; inhibits cardiac arrhythmias;
is hypotensive; reduces fibrinogen, Lp(a), C-reactive protein (CRP),
total cholesterol, and homocysteine; improves insulin sensitivity; and
is beneficial to dieters Some individuals support the premise that fats do little more than make you fat and that they can be eliminated without upsetting metabolic processes. In truth, fats initiate the transmission of vital messages, in part by programming activity in the omega-6 and omega-3 fatty acid cascades. Instructions received by prostaglandins (hormone-like substances produced from fatty acids) encourage some prostaglandins to oppose and others to neutralize, a process that holds the entire family in check. Prostaglandins are found in virtually all cell membranes and control most metabolic functions. Vital as they are, when out of balance, they can prove the undoing of the host. For example, PGE2 is generally regarded as a less desirable (even destructive) prostaglandin. (Although PGE2 can provoke an inflammatory response, the body does need some PGE2 to maintain the mucosal integrity of the intestinal wall.) On the other hand, PGE1 and PGE3 are good prostaglandins, meaning they decrease the likelihood of platelets clumping and dilate blood vessels, while exerting anti-inflammatory activity (Braly 1985). Standard
American Diet Dr. James Braley, M.D., cautions that a dietary departure from the omega-3 fatty acids can lead to an overproduction of PGE2, a pro-inflammatory, platelet-aggregating prostaglandin. For this reason, diet and supplementation should most often favor the lagging omega-3 fatty acids. When the omega-3s are emphasized, arachidonic acid, the precursor to PGE2, is reduced (Braly 1985). Illustrative of the importance of having more good prostaglandins than bad, some researchers estimate that 30% or more of heart attacks occur as a result of smooth muscles in the walls of the coronary arteries going into spasm, causing disruption of oxygen supply to the heart. If oxygen cutoff is not long lasting, a renewed delivery of oxygen begins and the spasm ceases. PGE1 dilates the blood vessels, making them less prone to spasm; conversely, PGE2 constricts blood vessels. Compounding the problem, PGE2 is often released during heart spasm, further constricting the blood vessels (Braly 1985). Figure 5 illustrates the omega-6 and omega-3 cascades and the enzymes delta-6- and delta-5-desaturase (rate controlling enzymes) that spur sequential movement through the series. Recall that from arachidonic acid, the parent of PGE2, leukotrienes are formed. A functional delta-6-desaturase enzyme appears to be crucial to blood pressure management. An example of this occurred when two trial groups, selected from 25 nonobese participants with mild to moderate hypertension, were given either linoleic acid (sunflower oil) and alpha-linolenic acid (linseed oil) or their reduced forms, GLA (360 mg a day) and EPA (180 mg a day). The first group was delta-6-desaturase dependent; the second group was not. After 8-12 weeks, the group receiving the GLA and EPA had reduced their blood pressure by about 10%. Those in the first group, who lacked the activity of delta-6-desaturase, experienced no significant hypotensive benefit. This observation may indicate that the defective desaturation of the essential fatty acids by the enzyme delta-6-desaturase plays an important role in the etiology of essential hypertension (Venter et al. 1988). Diabetes, hypercholesterolemia, and nutritional deficiencies (zinc, vitamin B6, and magnesium) can inhibit delta-6-desaturase activity. At Comprehensive Cancer Care 2001, Joseph Pizzorno, N.D., prominent educator and cofounder of Bastyr University, cited obesity, viral assaults, stress, aging, alcohol, smoking, and trans fats as additional factors retarding the efficacy of delta-6-desaturase (Pizzorno 2001). Individuals with a sluggish delta-6-desaturase enzyme (about 10-20% of the population) should use the fatty acid appearing downstream from the enzyme. (Figure 5 illustrates this sequence.)
A number of studies have shown the protective value of fish consumption in regard to averting coronary heart disease and the incidence of sudden cardiac death. For example, a recent study reported data collected from the Physicians' Health Study involving more than 22,000 men followed over a 17-year time frame. Researchers tested the blood of 94 male study volunteers who experienced an episode of sudden cardiac death (but in whom there was no prior history of heart disease) against 184 matched control study participants who did not experience a cardiac event. On an average, men who died suddenly had lower levels of omega-3 fatty acids. Among the men with the highest levels of omega-3 fatty acids in the blood, there was a 72% reduction in the risk of sudden cardiac death when compared to the men with the lowest levels of these substances in their blood (Albert et al. 2002; Wascher 2002). Recall that 50% of people who die suddenly of cardiac causes have no signs or symptoms of heart disease; poor omega-3 representation may explain this worrisome statistic. JAMA reported that women receive a similar cardiac advantage when eating fish or using omega-3 fatty acids (Hu et al. 2002). During 16 years of follow-up, there were 1513 incident cases of coronary heart disease (484 deaths and 1029 nonfatal myocardial infarctions) among 84,688 women (ages 34-59) participating in the Nurses' Health Study. Those who ate fish once a week had a 30% lower risk of heart attack or death compared to those who never ate fish. Interestingly, eating fish 5 times a week was only slightly more beneficial, decreasing risk to 34%. JAMA also cited a 40-50% reduction in strokes among middle-aged women who did not use aspirin but regularly included fish in their diet (Iso et al. 2001a). A meta-analysis (a method of evaluating statistical data based on results of several independent studies) showed that omega-3 fatty acids reduce the incidence of fatal heart attacks, even in patients with established coronary heart disease (Bucher et al. 2002). Obviously, there are mechanisms released through fatty acid consumption that go beyond regulating cholesterol and triglycerides. Dr. Kilmer McCully,
pioneer of the homocysteine-heart disease theory, determined that fish
oil lowers homocysteine levels. Clinicians and researchers now affirm
his work (Culp 2000). A Texas researcher reported that GLA mitigates the growth of atherosclerotic plaque in the arterial walls of animals. The research holds promise that GLA supplementation (borage oil and evening primrose oil) may be equally important in halting the atherosclerotic process in humans (Nigam 1999).
Hydrogenation turns liquid oils, such as corn, soybean, sunflower, sesame, and cotton, into a semisolid shortening or margarine. (The harder the fat, the more trans fats it contains.) This process changes a cis (a beneficial fat) to a nonfunctional form (a trans fat) that can no longer participate in prostaglandin production. Hydrogenated fats deliver a serious blow by reducing activity in the omega-6 and omega-3 cascades (probably by inhibiting the enzymes delta-6-desaturase and delta-5-desaturase). This suggests that the consumption of partially hydrogenated vegetable oils may have an adverse impact upon the relative distribution of the final end products of the essential acids in terms of prostaglandin concentrations. Also, as trans fatty acids increase in the diet (replacing cis unsaturated fatty acids), LDL cholesterol is (typically) raised, but the beneficial HDL cholesterol is decreased. Trans fatty acids also increase Lp(a) levels relative to other fatty acids (Mensink et al. 1990, 1992; Zock et al. 1996). A study involving 600 men (ages 64-87), determined that every 2% increase in trans fatty acids increased the risk of developing coronary heart disease 25% over the next 10 years (Oomen el al. 2001). The influence of different types of fats can also be observed in the progression of diabetes. For example, the risk of diabetes was not increased among 84,204 women whose intake of fats came chiefly from nuts, seeds, and avocados, but a 2% increase in calories from trans fatty acids raised the risk of diabetes by about 39%. Conversely, a 5% increase in calories from polyunsaturated fats lowered the risk of diabetes 37% (Salmeron et al. 2001; Mercola 2001b). In 1993, doctors at Harvard Medical School found that women who ate 4 or more tsp of margarine a day had a 50% greater risk of developing heart disease compared to women who ate margarine only rarely (Harvard School of Public Health 2002). Although the amount of trans fatty acids appearing in margarine and shortening has been reduced in the United States, these damaging fats are still found in many other foods such as bakery items and fast food products. Trans fats become a major part of American diets when the 30 pounds of French fries consumed per capita are factored into dietary analysis. Trans fats often hide on dietary labels as partially hydrogenated fats. Learn to read labels and avoid trans fats. Growing public awareness regarding the dangers imposed by trans fats has prompted a reduction in their consumption. An example of the benefits of eliminating trans fatty acids from the diet comes by way of a study released from The Netherlands. An average 2.4% drop in trans fatty acid consumption prompted a 23% decrease in coronary deaths and saved, it is speculated, about 4600 lives (Oomen et al. 2001; Reuters Health 2001).
Evening primrose oil, rich in gamma-linolenic acid, appears to stimulate brown fat cells by producing PGE1. Brown fat is of particular advantage in maintaining a desirable weight because it uses extra calories to provide heat, preventing the deposit of unsightly white fat (Braly 1985). Individual differences in amounts of brown fat have been theorized to account for the ability (or inability) to maintain a desirable weight. Brown fat is found primarily attached to large blood vessels in the thoracic cavity, along certain ribs, the nape of the neck, armpits, and between and below the shoulder blades. Without sufficient amounts of brown fat, calories are not burned and as a result, overweight individuals may actually gain weight on fewer calories. As a weight-deterrent, essential fatty acids most benefit those who are more than 20% overweight (Braly 1985).
The Iowa Women's Health Study examined the relationship between dietary fatty acids and Type II diabetes in a cohort of over 35,000 nondiabetic women (ages 55-69). The study showed that women with the highest intake of vegetable fat had a 22% lower risk of developing diabetes during the 11-year follow-up. Substituting polyunsaturated fats for saturated fats reduced the incidence of diabetes by an average of 16%, regardless of fiber intake, magnesium levels, obesity, physical exercise, or smoking status (Meyer et al. 2001; LEF 2001). Researchers (reporting in JAMA) showed that 120 nondiabetic, hypercholesterolemic men receiving sim-vastatin (20 mg a day for 12 weeks) reduced their total cholesterol 20.8%; LDL cholesterol 29.7%; triglycerides 13.6%; and apolipoprotein B 22.4%. A 13% increase in insulin levels and a 14% increase in insulin resistance, along with a loss of antioxidants (alpha-tocopherol dropped 16.2%, beta-carotene plummeted 19.5%, and CoQ10 fell 22%), minimized the cardioprotective effects of simvastatin. Consuming a modified Mediterranean diet (containing at least 4 grams a day of omega-3 fatty acids) potentiated the cholesterol-lowering effects of simvastatin and counteracted the rise in insulin levels. In addition, beta-carotene and CoQ10 levels were protected (Jula et al. 2002).
Poultry Science reported that three omega-3 enriched eggs provide about the same amount of n-3 PUFAs as one meal containing fish. Researchers found that the 3 eggs a day did not significantly increase total cholesterol or LDL in most subjects. Typically, plasma triglycerides as well as platelet aggregation decrease. LDL particle size tended to shift toward a less atherogenic dimension, appearing less small and dense (Lewis et al. 2000). Olive oil, an omega-9 fatty acid (a monounsaturated fat), is an excellent choice for both salads and cooking. However, it is extremely difficult to purchase oils in an ideal state, if shopping from a supermarket; a better choice appears to be extra virgin olive oil in a lightproof container. (Refrigerate the oil immediately after purchase.) Other sources of omega-9 fatty acids are almonds, pecans, cashews, filberts, and macadamias. Omega-9 contributes primarily to the structural elements of phosphatides. Phosphatides, in turn, are necessary for cell membrane integrity. Almond oil is currently reviewed better than canola oil (rape seed) by various practitioners and researchers. Canola oil, belonging to the mustard family, is derived from seeds of a plant considered (by some) to be toxic. Canola oil, when processed, appears to become rancid very quickly and may over time increase the incidence of heart disease. Refrigeration does not appear to retard its oxidation (Fallon 2002). Canola oil proponents still uphold its value, but until more questions are answered regarding its safety, it seems wiser to select the tried and true olive oil. According to Robert
Erdmann, Ph.D., butter, in small amounts, is a better choice than margarine.
He added: "Butter may not only be highly nutritious but may be
an underexploited form of alternative health therapy" (Erdmann
1990). Cardiovascular Disease Protocol Pg (1) (2) (3) (4) (5) (6) (7) (8) (9) (10) (11) (12) (13) (14)
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These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease
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