Diet (what you eat) affects osteoporosis, but we do not know the extent to which “dieting” (eating less for weight reduction) affects osteoporosis.
Many risk factors for osteoporosis have been identified. With the exception of an early menopause, premenopausal removal of ovaries, chronic steroid use, and prolonged bed rest, these risk factors are useful only in looking at the population as a whole from an epidemiologic viewpoint and cannot be used clinically to identify individuals at risk of developing osteoporosis. For that reason, the relative importance of one risk factor versus another is very difficult to establish and are a matter of degree. For example, smoking an average of three cigarettes a day for six years will probably have much less effect than severe calcium restriction; but smoking an average of three packs a day for forty years will probably have a much greater effect than ingesting an average 800 mg. (instead of 1,000 mg.) of calcium per day.
Unavoidable factors include: race (Caucasians and Asians are at greatest risk), family history, menopause, Turner’s syndrome, and genetics (e.g. small, fine bones). Nutritional factors include reduced calcium, vitamin D, and fiber intake, and increased caffeine, protein, and alcohol intake. Physical inactivity and smoking are important risk factors as are menstrual dysfunction such as late onset of menstruation, infrequent menstruation and exercise-induced amenorrhea. Having had a hysterectomy, or an eating disorder like anorexia or medical conditions such as chronic renal failure, intestinal bypass, malabsorption syndromes, hyperprolactinemia, hyperparathyroidism, and diabetes are also known risks. Even medications have been implicated, including antacids (with aluminum), anticonvulsants, and thyroid.
Fractures, the most important consequence of osteoporosis, are best predicted by older age, history of maternal hip fracture, less weight gain since age 25, greater height at age 25, overall health status, previous hyperthyroidism, current use of anti-anxiety or anticonvulsant drugs, current caffeine intake, not walking for exercise, on feet less than four hours per day, inability to rise from a chair without using one’s arms, poor depth perception, poor contrast sensitivity, resting pulse rate greater than 80 beats per minute, and any fracture since age 50.
There is evidence that high protein can increase a woman’s risk of developing osteoarthritis. It is difficult to determine whether it is the proportion of protein intake (relative to carbs or fats) or the total amount of protein consumed. It is important to recognize that there are health consequences to weight loss as there are to exercise, having a blood test, or driving. You should always weigh the relative risks of one course of action versus another.
At Lindora Medical Clinics, we are taking steps to learn whether there is a risk for developing osteoarthritis in association with moderate protein intake (such as is found on the ‘Lean for Life’ program) and preventing its occurrence by providing calcium and magnesium supplements. Summaries of studies that demonstrate an association between high protein diets and osteoporosis follow:
– In one study, five untreated osteoporotic patients were studied in a metabolic unit for 30 days while receiving low (0.8 gm/kg) and high (2.0 gm/kg) protein diets. The high protein diet produced a calcium loss. Whether this temporarily increased dietary protein causes continued calcium loss or leads to osteoporosis could not be determined. (J Gerontol 1981 Jan;36(1):14-9 Acute effects of dietary protein on calcium metabolism in patients with osteoporosis. Licata AA, Bou E, Bartter FC, West F)
– Animal studies are often more helpful in that precise amounts and proportions of protein can be given. The hamster was used as a model for investigating the effect of low, moderate, and high protein intake (12, 18, and 36 percent casein) on bone mineral content. Animals fed the low level of protein between 3 and 8 months of age had a reduction in the weight of all skeletal components measured, with the exception of one portion of the long bones. Ingesting a high protein diet resulted in a significant increase in calcium loss, and a reduced amount mineral content in the long bones. Long-term consumption of a high protein diet led to the development of a mild osteoporotic condition in the hamster which was limited to the diaphyseal portions of the long bones. (Proc Soc Exp Biol Med 1983 Mar;172(3):324-9 Dietary protein level and skeletal development in the golden Syrian hamster. Allen LH, Wood RJ, Bartlett RS)
– Another study recognized that the age-adjusted female hip fracture incidence has been higher in industrialized countries than in nonindustrialized countries. To better understand whether the risk is associated with a high animal protein diet, cross-cultural variations in animal protein consumption and hip fracture incidence were examined. When female fracture rates derived from 34 published studies in 16 countries were regressed against estimates of dietary animal protein, a strong, positive association was found. This association could not plausibly be explained by either dietary calcium or total caloric intake. Recent studies suggest that the animal protein-hip fracture association could have a biologically tenable basis. The authors concluded that further study of the metabolic acid-osteoporosis hypothesis is warranted. (Calcif Tissue Int 1992 Jan;50(1):14-8 Cross-cultural association between dietary animal protein and hip fracture: a hypothesis. Abelow BJ, Holford TR, Insogna KL)