Osteoporosis Treatment. Spine Fractures. Kyphoplasty Surgery. The effect of moderate alcohol use on bone health is unclear, and some studies suggest moderate alcohol intake usually defined as up to one drink per day for women and up to two drinks per day for men is beneficial. However, the damaging effects of heavy alcohol use are fairly consistently supported.
As with smoking, excessive alcohol use has a wide range of damaging health effects for any person, but is particularly damaging for persons at risk for osteoporosis. But human and animal studies clearly indicate that chronic heavy drinking, particularly during adolescence and the young adult years, can dramatically compromise bone quality and may increase osteoporosis risk.
Further, research indicates that the effects of heavy alcohol use on bone cannot be reversed, even if alcohol consumption is terminated.
Research suggests that in addition to alcohol, other lifestyle factors—such as tobacco use, nutrition, weight—bearing exercise, increased body weight, and hormone replacement therapy—affect bone development and osteoporosis risk in women. However, there has been little examination of how alcohol interacts with these factors to influence bone health.
Key words: osteoporosis; bone mass density; risk factors; female; AODE alcohol and other drug effects ; alcoholic beverage; tobacco in any form; lifestyle; physical exercise; obesity; nutrition; estrogens; hormone therapy; literature review.
Osteoporosis is a skeletal disorder characterized by low bone mass, increased bone fragility, and susceptibility to fracture see figure 1. Primary osteoporosis is subdivided into two types: Postmenopausal [Type I] osteoporosis occurs 15 to 20 years after menopause in females, following a decline in estrogen levels.
Age—associated, or senile [Type II] osteoporosis occurs after approximately age 70 in both genders. In contrast to these two types of primary osteoporosis, secondary osteoporosis is the result of specific conditions such as disease, surgery, and drugs [Riggs and Melton ]. Figure 1 Normal bone top and bone from an alcohol—treated rat bottom. Note that lighter—colored specules of bone are missing in the bottom image.
After age 35, women lose 0. At menopause, when the ovaries stop producing estrogen, the rate of bone loss increases, in the absence of estrogen replacement therapy, from 3 percent to 7 percent per year, building to 15 percent to 35 percent loss in bone mass in the first 5 years after menopause Bonnick For middle—aged and older adults to have healthy bones, they need to have developed a strong bone structure and an adequate peak bone mass during their younger years.
Bone structure and peak bone mass are greatly affected by lifestyle factors, including alcohol use, especially during the adolescent and young adult years see figure 2. This article reviews research on how alcohol use and other factors affect bone health and osteoporosis risk in women. Figure 2 Peak bone mass is affected not only by genetic and other biological factors but also by lifestyle variables such as nutrition, exercise, tobacco use, and drinking.
In this figure, factors along the steeper line contribute to higher peak bone mass. Federal guidelines consider moderate drinking to be no more than one drink per day for women and no more than two drinks per day for men [U. Department of Agriculture and the U. Department of Health and Human Services ]. A few epidemiological studies in humans have indicated that moderate alcohol consumption may be associated with decreased fracture risk in postmenopausal women Hansen et al.
One large study Diaz et al. This apparent beneficial effect of moderate drinking on bone health has not been found in animal studies, which can control for the amount of alcohol consumed as well as for other lifestyle factors see figure 2. For example, Sampson and Shipley gave ovariectomized and sham animals animals in which abdominal surgery was performed but the ovaries were not removed 0.
Removal of the ovaries led to decreased bone density and bone volume compared with control animals, but comparisons with animals that were not fed alcohol showed that these changes were not significantly altered by alcohol consumption. In contrast, in a study of rats administered alcohol for 4 months, Turner and colleagues reported a decrease in the replacement of old bone with new bone tissue i. These studies found no beneficial effect of moderate alcohol use on bone quality.
Effects of Alcohol on Growing Bone. Almost all epidemiological studies of alcohol use and human bone health indicate that chronic heavy alcohol consumption, particularly during adolescence and young adulthood, can dramatically affect bone health and may increase the risk of developing osteoporosis later. Although alcohol appears to have an effect on bone—forming cells i. Studies in female animals have also demonstrated unequivocally that early chronic alcohol consumption compromises bone health, including decrements in bone length, dry weight weight of the bone with the water removed , and mineral content.
Research has shown that young, actively growing rats chronically consuming alcohol had reduced femur lengths when compared with pair—fed control rats until they were approximately 9 months of age see figure 3 for a comparison of rat and human ages. Eventually, the femurs of alcohol—fed animals caught up with the growth in length of animals in the control group Sampson et al.
Figure 3 Comparison of rat and human ages. In further examinations of these same animals, computer analyses of microscope slides of the upper tibia revealed greatly reduced bone volume in alcohol—fed rats compared with control rats Sampson et al. In particular, the analyses showed a reduction in the number of thin plates trabeculae that form the soft, inner part of the bone. Further, after the animals had stopped growing, the overall thickness of the inner cancellous bone was also reduced in alcohol—fed rats compared with rats in a control group.
Additional evidence that alcohol causes bone—growth deficiencies in actively growing animals is provided by studies of the developing tissue, known as growth plates, near the ends of long bones Sampson et al.
These studies revealed that alcohol severely slowed the proliferation of cartilage cells, important precursors to bone development, and arrested longitudinal bone growth. Studies of rats fed alcohol from 1 month of age throughout their lives indicate that alcohol—induced bone deficiencies may stem from a lag in growth, rather than from a loss of bone content Sampson That is, the animals may not be losing bone per se, but they may not be growing and maturing as they should.
This conclusion is supported by measurements of blood levels of a hormone, known as insulin—like growth factor 1 IGF—1 , that helps maintain bone density. In both groups of rats, IGF—1 values were greatest in younger animals and diminished until the animals stopped growing at 9 months old. Over the long term, alcohol—fed animals seemed to adapt, at least partially, to these reductions in tissue quality and strength by producing generally larger bones with thinner cortical walls Sampson Nevertheless, the effects of alcohol consumption on bone could not be reversed, regardless of whether alcohol consumption continued or was terminated Sampson et al.
Effects of Alcohol on Adult Bone. For information on how light—to—moderate drinking affects bone health in older women, see the article in this issue by Register and colleagues. In addition to such research in human adults, studies of animals that began consuming alcohol as elderly animals also revealed deficiencies in bone volume and density Hogan et al.
These studies in adult animals agreed with cell—culture studies, suggesting that in these adult animals, alcohol consumption has greater deleterious effects on bone formation than on the breakdown i. In addition to alcohol use, lifestyle factors such as tobacco use, exercise and body weight, nutrition, and hormone replacement appear to play a role in bone health and osteoporosis risk, although the magnitude of these roles is not well understood.
Brief summaries of research on such osteoporosis risk factors are provided below, followed by a discussion of how alcohol might interact with each factor.
Donohue said. It also has been shown epidemiologically, because during the years of prohibition, the liver cirrhosis rate declined, which means that people were drinking less and therefore the incidence of liver disease was less. Then, when prohibition was repealed, the rate of liver cirrhosis went back up as drinking increased. Chakkalakal, author of the review. Chakkalakal said. The researchers found differences between the control group and the alcohol-exposed group in the hard bony tissue that forms around the ends of a fractured bone, called the callus.
In the mice exposed to alcohol, the callus was less mineralized, meaning not as much bone was forming. Moreover, the bone that did form was not as strong. Also, the alcohol-exposed group had signs of oxidative stress, a process that produces chemicals called free radicals that, when at the wrong place at the wrong time, can impair normal cellular functions.
Free radicals are highly chemically reactive. Beyond this, the alcohol-exposed group had significantly lower levels of a protein called osteopontin. Osteopontin, along with a second protein called SDF-1, are involved in recruiting stem cells to the injury site. These stem cells mature into bone cells.
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