How to Build Strong Bones: Get Milk, Lose the Booze

  • Alcohol consumption contributes to bone loss, and is a likely risk factor for osteoporosis
  • Alcohol-induced bone loss seems primarily due to reduced bone formation
  • An experimental drug treatment for osteoporosis called parathyroid hormone may reverse alcohol-induced bone loss in younger drinkers
  • Chronic adult drinkers remain at high risk of earlier and more severe osteoporosis

A popular bar and eatery in Austin, Texas sells T-shirts that say "Beer: It’s not just for breakfast any more." While the play on words may be initially amusing, osteoporosis is not. Alcohol consumption is known to be a significant contributing factor to bone loss, and is believed to be a risk factor for osteoporosis. Two rodent studies in the May issue of Alcoholism: Clinical & Experimental Research (ACER) examine alcohol’s effects on bone. Specifically, one study investigates if these effects are reversible; another explores what difference may exist between the effects of drinking during youth versus adulthood.

"The most common form of osteoporosis occurs in elderly women and is caused by estrogen deficiency," said Russell T. Turner, professor of orthopedics at the Mayo Clinic, and lead author of one of the studies. "Bone thinning occurs as a result of a large increase in bone resorption (a loss of substance). In contrast, alcohol-induced osteoporosis is caused by decreased bone formation and is frequently observed in middle-aged men."

Alcoholics often have bones that are less dense than normal. Less bone density means less bone strength, which can increase an individual’s risk of bone fracture. In fact, alcoholics have a high rate of non-traumatic and trauma-induced bone fractures, especially in the femoral neck. Although good nutrition is essential for maintaining bone health - and alcoholics usually have poor nutritional habits - animal studies have shown that alcohol can slow bone growth even when nutrition is maintained. This indicates that alcohol is directly responsible for at least some detrimental effects on bone health.

"Drinking cessation does not result in a spontaneous reversal of alcohol-induced bone loss," said Turner. "This may mean that alcohol has an irreversible toxic effect on bone cells, or that alcohol interferes with the normal communication between bone cells which governs the delicate balance between how much bone is formed and how much bone is resorbed." Turner and his colleagues tested the effects of parathyroid hormone (PTH), an experimental drug treatment for osteoporosis, on rats whose bone formation had been suppressed by alcohol. The animals were the human equivalent of young adults. "The fact that they responded so vigorously indicates that alcohol-induced bone loss can be reversed," he said.

James R. West, professor and head of the department of anatomy and neurobiology in the College of Medicine, and interim vice-president for research, at the Texas A&M University System Health Science Center, calls this finding very interesting. However, he cautions, "PTH is also known to take calcium out of bone. So the fact that PTH can, under certain conditions, actually stimulate bone growth is a little bit unusual." He called for longer-term studies.

Both Turner and H. Wayne Sampson, professor of human anatomy and neurobiology in the College of Medicine at the Texas A&M University System Health Science Center, and lead author of the second study published in ACER, cautioned against adolescent drinking.

"The issue of bone loss is especially critical for young people today since it is now reported that problem drinkers begin as pre-teens," said Sampson. "Animal studies of an age comparable to human youth have repeatedly shown shorter bones, weaker bones and decreased bone density. Except for length, these qualities do not recover with age and, should osteoporosis occur, the bones would reach fracture threshold sooner."

Most studies of the effects of alcohol on bone use animals that are still growing. Sampson’s study is one of the first to demonstrate actual bone loss in animals that begin drinking as adults. This is an important distinction because if, as believed, alcohol has a direct effect upon osteoblasts (bone forming cells), then adults who drink heavily are causing potentially irreversible damage to their bones.

"In the younger animals tested," said West, "you still had growth. The alcohol interferes with the growth and bone development, but when you stop the alcohol, growth resumes. Alcohol doesn’t prevent or stop the growth; it simply interrupts it. Of course, one of the dangers of growth resumption is that it gives the impression that alcohol exposure is really not a risk." In adults, however, a grave risk of cumulative, alcohol-induced bone damage is that bone growth does not resume.

"After eight weeks," said Sampson, "we saw nothing. But after 14 weeks, results were very dramatic. With time, alcohol had deleterious effects on adult bones. These findings indicate that if adults begin drinking chronically, they will weaken their bones and run the risk of earlier and more severe osteoporosis, should they develop the disease."

"Demographics are changing," said West, "and we’re seeing more osteoporosis. We need to ask ‘to what extent is alcohol abuse playing a role in this?’ People tend to think of someone who misuses or abuses alcohol as kind of a skid-row bum, but that’s not necessarily the case. There are some people out there who are drinking enough to cause organ damage, and yet they’re going to work and keeping up a regular job. The cumulative, toxic effects of alcohol would surprise a lot of people."


Articles were written based on the following published research:

Hogan, H.A., Argueta, F., Moe, L., Nguyen, L.P., & Sampson, H.W. (2001, May). Adult-onset alcohol consumption induces osteopenia in female rats. Alcoholism: Clinical and Experimental Research, 25(5), 746-754.

Turner, R.T., Evans, G.L., Zhang, M., & Sibonga, J.D. (2001, May). Effects of parathyroid hormone on bone formation in a rat model for chronic alcohol abuse. Alcoholism: Clinical and Experimental Research, 25(5), 667-671.

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