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Supplements Boost Cardioprotective Nitric Oxide

August 2004

LE Magazine August 2004
Supplements Boost Cardioprotective Nitric Oxide

Antioxidants, L-arginine, and exercise reduce the risk of atherosclerosis in mice bred to have elevated cholesterol levels, according to research conducted by Nobel Laureate Louis J. Ignarro and his colleagues at the University of California, Los Angeles.

The researchers administered a high-cholesterol diet, the same diet with vitamins C and E, or the diet with the vitamins and the amino acid L-arginine to hypercholesterolemic mice for 18 weeks. Two weeks into their various diets, some of the mice in each group were also put on a moderate exercise regimen.*

All of the mice that exercised experienced weight loss and decreased total cholesterol compared to mice that did not exercise or receive supplements. While the mice that exercised and did not receive supplements experienced a 35% reduction in atherosclerotic lesions, those that did not exercise but received supplements experienced a 40% reduction. Dr Ignarro noted this shows that “the supplements work well even in the absence of exercise.”

The effect was magnified in mice that exercised and received antioxidants combined with L-arginine; these mice experienced a significant regression of their atherosclerotic lesions compared to the other groups. The researchers attributed this to the increased nitric oxide produced by exercise and arginine. Nitric oxide lowers blood pressure, prevents excessive clotting and inflammation associated with coronary artery disease, and protects against heart attack and stroke.

By removing oxidants from the blood, vitamins C and E stabilize the nitric oxide, which allows it to rise to higher levels, producing greater benefits. “This is the first study that shows that if you exercise in addition to taking dietary supplements, you have a markedly enhanced production of nitric oxide,” said Dr. Ignarro. He recommends moderate exercise and a low-fat diet enhanced with dietary supplements: “I would say just do it. It works in mice, it’ll work in humans.”

—Dayna Dye


* Napoli C, Williams-Ignarro S, de Nigris F, et al. Long–term combined beneficial effects of physical training and metabolic treatment on atherosclerosis in hypercholesterolemic mice. Proc Natl Acad Sci USA. 2004

Glucosamine Relieves Osteoarthritis Symptoms

Glucosamine, an amino derivative of glucose, has been shown for the first time to slow and even stop the progression of debilitating osteoarthritis, according to newly published research.

Osteoarthritis, the most common form of joint disease, affects 85% of American adults over the age of 65 and more than 50 million Americans altogether. While not a normal consequence of aging, osteoarthritis is a frequent accompaniment of aging.

Osteoarthritis chiefly affects weight-bearing joints in areas such as the ankles, knees, hips, and spine, as well as the hands. The goal of treatment is generally the relief of pain and restoration of physical activity, most often achieved with non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin. Joint replacement has been the treatment of last resort.

Glucosamine is a building block for glycosaminoglycans and proteoglycans, which are constituents of articular cartilage along with water, cellular elements, and proteins such as collagen, elastin, and fibronectin. Although its mechanism of action is not precisely known, glucosamine is known to be an anti-inflammatory agent. In a systematic review and meta-analysis of randomized clinical trials, glucosamine was found to be effective in ameliorating painful symptoms associated with osteoarthritis.1

Newly published research has shown for the first time that glucosamine slows and even stops the progression of osteoarthritis.2 Study participants received 1500 mg per day of glucosamine sulfate (as has long been recommended by Life Extension) for three years and were permitted to use NSAIDs as well. While the group that received placebo experienced a worsening of clinical symptoms, those who received glucosamine reported a significant improvement in symptoms.

—Dean S. Cunningham, MD, PhD


1. McAlindon TE, LaValley MP, Gulin JP, Felson DT. Glucosamine and chondroitin for treatment of osteoarthritis: a systematic quality assessment and meta-anaylsis. JAMA. 2000 Mar 15;283(11):1469-75.

2. Bruyere O, Pavelka K, Rovati LC, et al. Glucosamine sulfate reduces osteoarthritis progression in postmenopausal women with knee osteoarthritis: evidence from two 3-year studies. Menopause. 2004 Mar- Apr;11(2):138-43.

US Faces “Tidal Wave of Chronic Ocular Disease”

More than 28 million Americans over the age of 40 have eye ailments that put them at risk for vision loss and blindness, a number that is expected to rise rapidly as the population ages, according to research published in the Archives of Ophthalmology.

An estimated 20.5 million American adults have cataracts, a figure expected to climb to 30.1 million in the next 20 years.1 Cataracts are the leading cause of blindness worldwide and of poor vision in the US. Like other major causes of blindness and vision loss such as macular degeneration, glaucoma, and diabetic retinopathy, cataracts are strongly linked with aging.

Macular degeneration affects about 1.8 million adults. Another 2.2 million US adults suffer from glaucoma, while 4 million are afflicted with diabetic retinopathy.

The numbers are alarming in part “because of the substantial increases in health care costs they spell,” said Dr. Nathan Congdon, an associate professor of ophthalmology at Johns Hopkins University. The US spends more than $3 billion yearly on cataract treatment alone, Congdon noted.

In the absence of a significant investment in prevention and treatment to reverse this trend, the US faces a “tidal wave of chronic ocular disease over the next few decades,” fellow Johns Hopkins University researcher James Tielsch wrote in an accompanying editorial.


1. Kempen JH, Mitchell P, Lee KE, et al. The preva- lence of refractive errors among adults in the United States, Western Europe, and Australia. Arch Ophthalmol. 2004 Apr;122(4):495-505.

2. Ferris FL 3rd, Tielsch JM. Blindness and visual impairment: a public health issue for the future as well as today. Arch Ophthalmol. 2004 Apr;122(4):451-2.

Meat Consumption Tied to Risk of Gout

Newly published research has found that diets high in meat raise one’s risk of contracting gout.

Gout is an inflammatory arthritis that affects several million men and women in the US. Gout develops when elevated serum levels of uric acid lead to the deposition of urate crystals in the joints and tissues. The clinical manifestations of gout include recurrent attacks of arthritis, joint deformation, the formation of kidney stones, and kidney damage. The incidence of gout is increasing in the US and has reached epidemic proportions in some groups, such as the Maori of New Zealand.1

Obesity, alcohol consumption, and the use of diuretics generally are considered the dominant predisposing factors for gout. While genetic differences underlie the magnitude of uric acid levels to some degree, diet appears to correlate most strongly with the risk of developing gout.

A recent study clearly demonstrated that diets high in meats (more than 1.92 servings per day compared with less than 0.81 servings per day) led to an increase in the risk of gout.2 In fact, the relative risk increased by as much as 21% with each additional portion of meat consumed daily. In like manner, increased seafood consumption (of greater than 0.56 servings per day compared with less than 0.15 servings per day) also increased the risk for gout, and even more so in men with a body mass index (BMI) of less than 25. No relationship was found to exist between total protein intake and the risk of gout, or between consumption of purine-rich vegetables and the risk of gout.

—Dean S. Cunningham, MD, PhD


1. Lennane GA, Rose BS, Isdale IC. Gout in the Maori. Ann Rheum Dis. 1960 Jun;19:120-5.

2. Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004 Mar 11;350(11):1093-103.