Osteoporosis has emerged as a major public health concern during the past few decades as the population of older Americans has rapidly expanded. Each
year, Americans experience more than 1.5 million fractures due to osteoporosis, resulting in more than 500,000 hospitalizations with a direct cost of more than 20 billion dollars.1
Enormous strides have been made in treating osteoporosis with medication classes such as the bisphosphonates, synthetic estrogens, calcitonin, and, most recently, parathyroid hormone derivatives.2 Although these are excellent medications for treatment of osteoporosis, no current medications are approved by the Food and Drug Administration for the prevention of osteoporosis.
For years, calcium plus vitamin D supplementation and exercise have been the mainstays of preventive therapy, but studies have indicated only marginal improvement in slowing of bone loss.3<8 Recent laboratory experiments have examined the possible role of plant-derived compounds known as phytochemicals in bone remodeling. Conceptually, the idea is that certain phytochemicals increase the rate of bone deposition by osteoblasts and decrease the rate of bone breakdown by osteoclasts. Perhaps the most impressive of these experiments demonstrated that rats fed a diet high in onions experienced a 17.4% increase in bone mineralization for 4 weeks relative to a control group.9,10 At least three
compounds that may be responsible for increasing bone density have been isolated from onions. The first compound is known as F-L-glutamyl-trans-S-1-propenyl-L-cysteine sulfoxide.11
It is believed to work by inhibiting the osteoclasts that normally break down bone.12 Specifically, F-L-glutamyltrans-S-1-propenyl-L-cysteine sulfoxide seems to inhibit osteoclastogensis via attenuation of osteoclast-differentiating factor. The other two compounds that may be responsible for increasing bone density are the flavonoids quercetin and kaempferol. Several experiments performed using human cell cultures have demonstrated that these compounds cause premature apoptosis, or programmed cell death in mature osteoclasts.13