Alcohol could cause several detrimental effects on the bone. Alcohol inhibits liver enzymes that convert vitamin-D into active form; which can hamper calcium absorption. As a result, chronic alcoholism leads to poor mineral absorption and increased excretion of important bone-building nutrients like calcium, magnesium, vitamin-C, zinc and copper. Alcohol also blocks vitamin-B6 function. Alcohol is directly toxic to bone cells, and cause a decline in the spongy inner matrix of the trabecular bone [Schapira 1990].
Currently, there is conflicting evidence on beneficial effects of moderate alcohol consumption on the bone health. Alcohol derived from wine has favorable effects on the level of high-density lipoprotein (HDL) cholesterol and inhibition of platelet aggregation. In the elderly population, there seems to be a direct correlation between wine consumption and preservation of BMD. Red wine has high levels of polyphenols that positively influence multiple biochemical systems, such as increased HDL cholesterol, antioxidant activity, decreased platelet aggregation and endothelial adhesion, suppression of cancer cell growth, and promotion of nitric oxide production.
In contrast, higher levels of alcohol intake – more than two standard units of alcohol per day, could significantly increase the risk of hip and other osteoporotic fractures. Excess alcohol intake has direct detrimental effects on bone-forming cells and on hormones that regulate calcium metabolism [Sampson 2002]. In addition, chronic, heavy alcohol consumption is associated with reduced food intake (including low calcium, vitamin-D and protein intakes) and overall poor nutritional status, which in turn have adverse effects on skeletal health. Excess alcohol use could influence body balance and predispose the dangers of trip over, thereby increases the risk of fractures. However, available data is insufficient to indicate the precise range of alcohol consumption that would maximize bone density and minimize hip fracture risk [Felson et al 1995].
Smoking and its relation to the onset of bone disorders is complex; also various risk factors often co-exist. Body wise, smokers are thinner than non-smokers, physically less active and consume poor diet. Women smokers tend to reach early menopause than non-smokers. Among smokers, fractures take longer time to repair with several complications during the healing process. Regular tobacco use and smoking cause a significant decrease in blood total alkaline phosphatase, an indicator of bone metabolism. Although not confirmed yet, exposure to second-hand smoke during youth and early adulthood may increase the risk of acquiring low bone mass.
Smoking elevates nicotine levels in the body that cause blood vessels to constrict by approximately 25% of the normal diameter. Due to this constriction, the blood flow is reduced; consequently the supply of nutrients, minerals, and oxygen to bone tissue is diminished, which may slow down the production of bone-forming cells. In post-menopausal women, it reduces the protective effect of estrogen replacement therapy and may double the risk of rheumatoid arthritis.
Nicotine and other harmful chemicals in cigarettes affect bone health in several ways. Cigarette smoke generates huge amounts of free radicals with devastating effects on the body’s natural defenses. Free radicals trigger a chain-reaction that damage tissue, organs, and hormones (e.g. estrogen) that regulate bones health. Other bone-damaging effects of smoking include elevation of the cortisol levels (hormone that regulates bone breakdown); and slowing down the calcitonin (hormone that helps to build bones). Nicotine and free radicals generated by smoking also kill the osteoblasts (bone making cells). Nicotine can also damage nerves in toes and feet, which may increase the risk of falls and fractures. [Law and Hackshaw 1997, Brot et al 1999, Krall et al 1999, Kanis et al 2005].
Caffeine is a stimulant present in a variety of drinks including tea and coffee. Although linked to a number of possible health benefits for heart and memory; caffeine is often implicated in the development of osteoporosis, due to its effect on calcium absorption. Caffeine can temporarily increase calcium excretion and may modestly decrease calcium absorption, but these effects are easily offset by increasing calcium consumption in the diet. Controlled clinical studies show that although caffeine ingestion results in a small, temporary increase in calcium excretion, it has no effect on 24-hour urinary calcium loss. One cup of regular brewed coffee causes a loss of only 2-3 mg of calcium which is easily offset by adding a tablespoon of milk. Moderate caffeine consumption, (1 cup of coffee or 2 cups of tea per day), in young women who have adequate calcium intakes would not have any negative effects on their bones. Studies that examined the effects of caffeine on rates of bone loss in post-menopausal women showed that caffeine intake had no detrimental effects, as long as calcium intake is sufficient (above 800 mg/day). However, if calcium intake is low, caffeine intake equivalent to about 3 cups of brewed coffee per day is associated with significant bone loss. A standard can of Cola drink contains 34-38 mg of caffeine. The potential risk of an acute caffeine toxicity may be greater with the consumption of “energy drinks” (stimulants and boosters) than conventional dietary sources of caffeine, like coffee and tea. Caffeine intoxication has been linked to a number of symptoms like nervousness, anxiety, restlessness, insomnia, gastrointestinal upset etc. which closely resemble symptoms of anxiety and mood disorders. [Massey 2001, Sakamoto et al 2001, Heaney 2002].
Soda drinks, high in phosphate content, are perhaps the most pervasive habit that promotes a calcium drain in the body. Phosphorus, an acid-forming mineral in the cola drinks, can interfere with calcium absorption by the bone and set off calcium loss through urinary excretion. Some studies have reported that high carbonated soft drink consumption either increased the fracture risk or decreased the bone mineral density. A recent study of soft drink consumption in adolescents suggested that teenage girls who drink lots of soda are predisposed to the risk of developing bone fractures and osteoporosis. These drinks also contain large amounts of refined sugar or equally dangerous sugar substitutes, which can trigger bone loss. During the teenage years, 40 to 60 per cent of peak bone mass is built, and therefore, it is very important to avoid or limit soda intake and change to a natural calcium-rich diet.
On the other hand, studies done with controlled calcium-metabolic methods indicated that the net effect of carbonated soft drinks, including those colas with phosphoric acid on calcium retention is low. An ‘acidic diet’ causes minerals to be drawn from the bones to neutralize the impact of the acid on blood pH. The body normally produces 50 to 100 mEq of acid a day during metabolism. The acid load imposed by a 20-ounce cola is only about 4.5 to 5.0 mEq, substantially less than the amount produced by eating a moderate protein breakfast. Phosphorus is a key constituent of bone mineral along with calcium, and there is no evidence for detrimental effects of phosphorus intake on bone health or osteoporosis risk in healthy individuals. The possible adverse effect of carbonated beverages may be due to substitution of milk in the diet by these drinks, which reduces calcium intake. Carbonation itself is also not responsible for the calcium depletion, as many commercial mineral waters are carbonated, and some are rich in calcium and other minerals. [Heaney et al 2001, Fitzpatrick and Heaney 2003].