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Homocysteine Raises Risk of Osteoporosis

August 2004

LE Magazine August 2004
Homocysteine Raises Risk of Osteoporosis

Although preventable, osteoporosis or “brittle bones” afflicts one of every two American women and one of every four American men over the age of 50. A new study suggests a clear link between osteoporosis and high blood levels of the amino acid homocysteine.

The complications of osteoporosis take the form of noticeable height loss and fractures of the hip, spine, and wrist. Osteoporosis is implicated in more than 300,000 hip fractures in the US each year; of those affected, approximately 25% will die within one year and another 25% will no longer be able to walk without assistance.

Homocysteine is involved in methionine metabolism, and normally is recycled into methionine or converted into cysteine. An excessive accumulation of homocysteine in the body, however, entails a heightened risk for heart disease and stroke, among other diseases.

In the study, 2,406 men and women over the age of 55 were followed prospectively. Those with homocysteine levels in the highest quartile had twice the risk of osteoporotic fracture compared to those in the other three quartiles.1 This increased risk is comparable to that of acquiring cardiovascular disease or dementia for those with high levels of homocysteine.

In a second study of 1,999 men and women recruited as part of the Framingham Study, men whose homocysteine levels placed them in the highest quartile were nearly four times more likely to sustain an osteoporotic fracture compared to other subjects.2 Women whose homocysteine placed them in the highest quartile were twice as likely to sustain a fracture as other female subjects.

Dietary supplementation with folate and vitamins B6 and B12, even in the absence of measurable deficiencies of these nutrients, helps lower homocysteine levels and may help protect against osteoporosis.

—Dean S. Cunningham, MD, PhD


1. van Meurs JB, Dhonukshe-Rutten RA, Pluijm SM, et al. Homocysteine levels and the risk of osteoporotic fracture. N Engl J Med. 2004 May 13;350(20):2033-41.

2. McLean RR, Jacques PF, Selhub J, et al. Homocysteine as a predictive factor for hip fracture in older persons. N Engl J Med. 2004 May 13;350(20):2042-9.

Curcumin Corrects Cystic Fibrosis Defects

The spice pigment curcumin, a powerful antioxidant and anticarcinogenic agent, has properties that correct for a defective protein implicated in cystic fibrosis, according to newly published research.

Cystic fibrosis is a genetic disease affecting approximately 30,000 children and adults in the US. A defective gene causes the body to produce an abnormally thick, sticky mucus that clogs the lungs, leads to life-threatening lung infections, and obstructs the pancreas, preventing digestive enzymes from reaching the intestines to help break down and absorb food. Cystic fibrosis is uniformly fatal, with a median survival time of 30 years.

The molecular basis of cystic fibrosis involves a defective protein called CFTR, which is required for energy transport. The defective CFTR protein is not delivered to the cell membrane, its site of action. When human cells with the cystic fibrosis mutation are treated in the laboratory with calcium-pump inhibitors, normal movement of CFTR to the cell membrane results.1

Curcumin is a calcium-pump inhibitor, albeit a weak one. Recently, researchers at Yale University demonstrated that administering curcumin orally to mice homozygous for the defective CFTR protein resulted in the expression of normal CFTR activity in both the respiratory and gastrointestinal tracts.2

Mice that are homozygous for the defective CFTR protein have a 60% mortality rate within 10 weeks, with death caused by intestinal obstruction and characterized by progressive weight loss. When such mice were administered curcumin, the mortality rate dropped to 10% and the surviving mice gained weight, as did their normal littermates.2

—Dean S. Cunningham, MD, PhD


1. Egan ME, Glockner-Pagel J, Ambrose C, et al. Calcium-pump inhibitors induce function- al surface expression of Delta F508-CFTR protein in cystic fibrosis epithelial cells. Nat Med. 2002 May;8(5):485-92.

2. Egan ME, Pearson M, Weiner SA, et al. Curcumin, a major constituent of turmeric, corrects cystic fibrosis defects. Science. 2004 Apr 23;304(5670):600-2.

Acetyl-L-Carnitine Improves Andropause Symptoms

New research suggests that the supplement acetyl-L-carnitine relieves the depression, fatigue, and sexual dysfunction that often accompany andropause, or male aging.

Multiple studies have shown that levels of bioavailable carnitine decrease with age in both men and women.1 Carnitine, and its more bioavailable forms such as acetyl-L-carnitine, are essential cofactors for transporting fatty acids into the mitochondria, the cellular engines that produce energy for the body.

Italian researchers conducted a randomized study to determine whether supplemental acetyl-L-carnitine could improve these symptoms in aging men. Over a six-month period, 120 men aged 60-74 received either 160 mg per day of testosterone undecanoate,2 grams per day of acetyl-L-carnitine and propionyl-L-carnitine, or placebo.2 The men treated with testosterone reported significant improvements in erectile capability and sexual desire, and a decrease in fatigue and depression; no improvement was noted in orgasm or general sexual well-being. Men who received the carnitine supplements saw significant improvements in erectile capability, sexual desire, orgasm, and general sexual well-being, along with fewer complaints of fatigue and depression.

These impressive findings led the study authors to conclude: “Testosterone and, especially, carnitine proved to be active drugs for the therapy of symptoms associated with male aging.”

—Edward R. Rosick, DO, MPH, MS


1. Chiu KM, Schmidt MJ, Havighurst TC, et al. Correlation of serum L-carnitine and dehydroepiandrosterone sulphate levels with age and sex in healthy adults. Age Ageing. 1999 Mar;28(2):211-6.

2. Cavallini G, Caracciolo S, Vitali G, Modenini F, Biagiotti G. Carnitine versus androgen administration in the treatment of sexual dysfunction, depressed mood, and fatigue associated with male aging. Urology. 2004 Apr;63(4):641-6.

Green Tea Inhibits Esophageal Cancer

Green tea contains a mechanism that inhibits esophageal cancer associated with Barrett’s esophagus, according to a study presented at the Digestive Disease Week convention held in New Orleans last May.

Barrett’s esophagus is a precancerous condition resulting from chronic irritation of the esophagus that occurs with gastroesophageal reflux disorder. Drinking tea has been linked with a lower risk of several cancers of the gastrointestinal tract. Consuming green tea is believed to expose the esophagus to high levels of green tea polyphenols such as epigallocatechin gallate (EGCG).

Howard Y. Chang, MD, and colleagues at Harvard Medical School and the Veterans Administration Boston Healthcare System administered varying concentrations of EGCG to cultured human Barrett’s esophagus-associated adenocarcinoma cells and compared them to untreated cells. They found that cell growth was inhibited in a dose-dependent manner within 72 hours of exposure to EGCG.

The team concluded that EGCG induces the programmed cell death known as apoptosis, which occurred in as little as 24 hours in the cells exposed to the compound. Further research found an elevation of caspase 3 (an enzyme involved in apoptosis) in the treated cells compared to the untreated cells, as well as increased cleaved PARP protein levels, another indicator of apoptosis.

According to Dr Chang, “Research suggests that drinking green tea may be both a valuable chemopreventive therapy as well as a treatment for esophageal adenocarcinoma. Our results suggest that extracts in green tea may help to lower the prevalence of esophageal adenocarcinoma, one of the fastest growing cancers in Western countries.”

—Dayna Dye