~Cardiovascular Disease Comprehensive 9 - Therapeutic D-E
Dehydroepiandrosterone (DHEA)-- is anti-inflammatory and antilipidemic, increases hormonal levels, and is beneficial in diabetes and Syndrome X
Low levels of DHEA, a steroid normally freely expressed in the human body, are associated with inflammation and heart disease in men. DHEA delivers much of its protection by acting as a prohormone, meaning it can bolster lagging estrogenic or androgenic hormones. In fact, DHEA's value as an antilipidemic appears due in part to its ability to increase estrogen and testosterone levels. Studies show that DHEA reduced by 50% the expected atherosclerotic buildup in rabbits fed a high-cholesterol diet. In men, DHEA lowered total cholesterol and bad low-density-lipoprotein cholesterol better than and more safely than the drugs clofibrate and gemfibrozil (Smith 1998) (read about tes-tosterone as a cardioprotector later in this protocol).
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
The current mania regarding low fat diets is contributing to deficiencies and imbalances of the essential fatty acids linoleic acid and alpha-linolenic acid. The body cannot synthesize these fats and is dependent upon the diet for their supply.
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
The standard American diet is high in saturated fats and arachidonic acid but frequently is deficient in alpha-linolenic acid, an omega-3 fatty acid. Many Americans have an omega-6-omega-3 ratio of about 20-30:1. Clarifying our departure from primitive diets, ancient kinsmen maintained a ratio nearer 1:1. A more realistic ratio, according to Joseph Pizzorno, N.D., may be nearer 2:1 (Simopoulos 1999; Pizzorno 2001).
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).
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.
Modulates Lipids, but so Much More
Typically, both men and women observe an increase in HDL2, the most beneficial of the HDL subtypes, after 6 months of omega-3 fatty acid supplementation. The protective role of total HDL against coronary artery disease appears primarily mediated through the HDL2 fraction (Bakogianni et al. 2001). During the course of a recent study, HDL2 cholesterol rose 24% among those eating a daily omega-3-rich fish meal and adhering to a restricted calorie diet. Those who did not lose weight nonetheless experienced a 21% rise in HDL2 cholesterol on the fish diet (Diets 2000). Recall that individuals achieving longevity frequently display elevations in HDL2b cholesterol, suggesting better cardiac function.
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.
Information presented at the International Symposium on Gamma-Linolenic Acid, San Diego (April 2000), showed that GLA (an omega-6 fatty acid) lowered blood pressure in animal studies. According to French researcher Jean Pierre Poisson, "Usually in pharmaceutical therapies we see about a 10% reduction. In our case we saw blood pressure drop 6-16%." Future research on humans is still needed, but Poisson concluded: "It appears GLA is a very potent blood-pressure-reducing nutrient" (Engler et al. 1998; Bioriginal Food and Science 2001).
- 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).
- English researchers reported that fish oil decreased fibrinogen, addressing a major pathological process leading to thrombotic occlusion. A 7-year MAXEPA study concluded without indication of adverse side effects (Saynor et al. 1992).
- Omega-3 fatty acids have been shown to lower Lp(a) (Herrmann et al. 1995; Shinozaki et al. 1996). Note: Cardiologists confess that (in some cases) Lp(a) can be difficult to reduce. A targeted intervention program often includes fish oil (1400 mg EPA and DHA), vitamin C (2-6 grams daily), CoQ10 (60-120 mg daily), L-lysine (1000-3000 mg daily), L-proline (500-1000 mg daily), and niacin. See the Niacin subsection of this section for details regarding dosing instructions and caveats.
- Dr. Robert Atkins, a complementary physician with a background in cardiology, believed that fatty acids are natural defibrillators, lessening the incidence of cardiac arrhythmias and atrial fibrillation. Several years ago, the Life Extension Foundation reported that omega-3 fatty acids reduced the risk of second heart attack and stroke by inhibiting cardiac arrhythmias, maintaining cardiac energy output, and reducing thrombosis.
- DHA reduced 24-hour blood pressure (5.8 mmHg systolic and 3.3 mmHg diastolic) and daytime/ambulatory blood pressure (3.5 mmHg systolic and 2.0 mmHg diastolic) (Mori et al. 1999). For every absolute 1% increase in blood alpha-linolenic acid, systolic and diastolic blood pressure typically drop by about 5 mmHg.
- DHA lowered norepinephrine, a gesture that may protect the cardiovascular system by reducing vasoconstriction and blood pressure (Sawazaki et al. 1999).
- Data suggest that C-reactive protein (CRP) levels can be kept in check by frequent consumption of fish or fish oils. For example, 269 patients underwent angiography for suspected coronary artery disease. The subjects were also evaluated regarding CRP levels and fish consumption. In addition, EPA and DHA levels were assayed in granulocytes (a type of white blood cell). The researchers found that patients with one or more coronary arteries blocked (50% or more) had significantly higher CRP levels in their blood than patients with no significant blockages. They also observed that high CRP levels correlated with low levels of DHA in granulocytes. The level of DHA in granulocytes in turn was closely related to fish consumption. The researchers concluded that DHA has an anti-inflammatory effect that results in lower CRP levels and that fish consumption may decrease the risk of coronary artery disease (Madsen et al. 2001; International Health News)
- After angioplasty, 194 patients were randomly assigned to receive either 4.5 grams a day of fish oil (3150 mg of EPA and 1350 mg of DHA for 6 months) or instructions to eat a low fat (25% of total calories), low cholesterol diet (100 mg a day) without fish oil. At the end of the trial, 36% of those not receiving the fish oil showed signs of restenosis (closure of previously opened arteries). The rate of re-stenosis in the fish oil group was about 19%. The study suggests, as do other trials, that high-dose fish oil supplements may reduce the frequency of re-stenosis following successful coronary angioplasty. Nonetheless, Mark Milner, M.D., the lead researcher, said his preference for supplying omega-3 fatty acids is fish consumption, not fish oil. Milner cited concern for (potentially) hypocoagulative blood states as the mitigating factor (Milner et al. 1989).
- The omega-3 fatty acids in fish oil help to balance the omega-6 fatty acids normally abundantly supplied in Western diets. When these two groups of fatty acids are out of balance, the body releases chemicals that promote inflammation. People appear to produce more inflammatory chemicals when experiencing psychological stress. With a fatty acid imbalance, the inflammatory response to stress appears to be amplified (Maes et al. 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).
Balance: Always the Key
The need for balance regarding dietary fats is clearly evidenced in a report appearing in the journal Circulation. Researchers found that low levels of animal fat and protein increased the risk of hemorrhagic stroke in hypertensive women 370% over women eating more dietary fat. The researchers also noted that individuals with a very low intake of saturated fat may develop structural impairment of the arteries. Although saturated fats have been maligned for years, it now appears that some saturated fats, that is, a balance among the family of fats is required for healthy arteries and a reduced risk of hemorrhagic stroke (Iso et al. 2001b).
Technology can transform a benign fat into a dangerous food product. This occurs when fats are exposed to the hydrogenation process, saturating the oil with hydrogen to improve stability, taste, and odor. Heating oils at temperatures above 300°F has the same effect.
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).
Beneficial to Those on Diets
Studies have shown that genetically obese people profit from essential fatty acid supplementation. The weight loss in these individuals is gradual, but reliable, even among those considered intractably obese.
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).
Essential Fatty Acids and Syndrome X and Diabetes
Omega-3 fatty acids help maintain flexible cell membranes (Igal et al. 1997). This is important, for healthy membranes contain large numbers of insulin receptors, increasing the surface areas available for insulin binding. This is extremely important in diabetes and Syndrome X.
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).
What Are the Good Fats?
Individuals wishing to increase their consumption of beneficial fish and marine life should consider scallops, shrimp, herring, mackerel, sea bass, salmon, cod, sardines, tuna (fresh), whitefish, coldwater halibut, and anchovies, varieties containing varying amounts of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). From the plant kingdom, walnuts, most beans, and according to Joseph Pizzorno, N.D. (Comprehensive Cancer Care 2001), Brussels sprouts and all varieties of squash are also sources of omega-3 fatty acids (Pizzorno 2001).
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).
Supplemental Omega-6 and Omega-3 Fatty Acids: What to Buy
To introduce the reader to various omega-6 and omega-3 fatty acids, the following examples are given:
Note: Prothrombin time usually remains within a normal range when using omega-3. As the number of platelets decreases, platelet size typically increases; therefore, there is no overall decrease in platelet mass. The New England Journal of Medicine reported that the blood-thinning functions of fish oil are small compared to aspirin, but other researchers caution that bleeding time could increase to inappropriate levels if baseline platelet activity is impaired or fibrinogen concentrations are low (Katan 1995).
- Perilla oil, 1000-mg per capsule, provides 550-620 mg of alpha-linolenic acid, a precursor to EPA and DHA. Use 6 softgels daily.
- Flaxseed oil (1000-mg softgels) provides 520-570 mg per capsule of gamma-linolenic acid. Use 6 softgels a day.
- Super GLA/DHA provides 920 mg of GLA, 1000 mg of DHA, and 400 mg of EPA. Use 6 capsules daily.
- Evening primrose oil is a source of GLA. Use one to two 1300-mg softgels daily.
- Borage oil also supplies GLA. A 1300-mg softgel supplies 300 mg of GLA. As a preventive, use 1-2 softgels a day and up to 5 a day as a therapeutic.
Continued . . .
Free Shipping in the CONTINENTAL UNITED STATES - All Orders over $40
The statements made here have not been evaluated by the FDA. The foregoing statements are based upon sound and reliable studies, and are meant for informational purposes. Consult with your medical practitioner to determine the underlying cause of your symptoms. Please always check your purchase for possible allergins and correct dosage on the bottle before use.
While we work to ensure that product information is correct, on occasion manufacturers may alter their ingredient lists. Actual product packaging and materials may contain more and/or different information than that shown on our Web site. We recommend that you do not solely rely on the information presented and that you always read labels, warnings, and directions before using or consuming a product. For additional information about a product, please contact the manufacturer. Content on this site is for reference purposes and is not intended to substitute for advice given by a physician, pharmacist, or other licensed health-care professional. You should not use this information as self-diagnosis or for treating a health problem or disease. Contact your health-care provider immediately if you suspect that you have a medical problem. Information and statements regarding dietary supplements have not been evaluated by the Food and Drug Administration and are not intended to diagnose, treat, cure, or prevent any disease or health condition. Life Extension Institute assumes no liability for inaccuracies or misstatements about products.