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COFFEE, CAFFEINE, CALCIUM BALANCE ANDBONE HEALTH

GENERAL

A 2002 review of the scientific literature by Professor Heaney concluded that “There is no evidence that caffeine has any harmful effect on bone status or on the calcium economy in individuals who ingest the currently recommended daily allowances of calcium" (1).

CALCIUM BALANCE

It is generally assumed that a decrease in the supply of calcium, an essential mineral for bone formation, would be likely to decrease bone mass and hence increase the risk of fracture. A number of intervention trials have focused on the effects of coffee, tea or caffeine on calcium balance. Although such studies can show cause effect relationships they cannot establish whether the magnitude of the effects on calcium balance observed are large enough to influence bone health.

A careful study of calcium balance in 170 healthy middle-aged women examined the effects of tea and coffee consumption (2). Multiple regression analysis showed that caffeine consumption in the form of tea or coffee was significantly associated with a small negative calcium balance. It was calculated that for every cup of coffee consumed less than 5 mg calcium was lost, probably due to increased urinary or faecal excretion.

This trial was followed by a series of studies (3, 4, 5) from a second laboratory showing that caffeine induced a loss of calcium in the urine. For example, it was shown that when 37 healthy women consumed 6 mg caffeine/kg body weight the urinary calcium loss increased in the two hour period following caffeine consumption (5). However, it should be noted that these caffeine intakes were unrealistically high and that the two-hour study period was too short. A further study from the same laboratory (6) looked at the effects of 6 mg caffeine/kg body weight in 17 healthy males and females on calcium excretion over a longer time period. They found that caffeine significantly increased urinary calcium excretion for six hours after intake, had no effect in the subsequent nine hours and significantly decreased urinary calcium excretion in the following three hours. Although there was an overall net increase in urinary calcium excretion in response to high intakes of caffeine it is clear that two-hour study periods seriously overestimate calcium loss in response to caffeine.

Two studies were unable to reveal any effects of more moderate doses of caffeine on 24-hour calcium loss (7, 8, 9). A double-blind placebo controlled crossover study with a 37-day washout compared the effects of 400 mg caffeine/day for 19 days with placebo in 16 healthy pre-menopausal women (7). There were no significant effects of caffeine on calcium absorption, urinary calcium excretion or faecal calcium excretion. This is an important study as it looks at the effects of caffeine consumption over the longer-term i.e. 19 days. Most other studies have only looked at the effects of caffeine over periods ranging from two hours to twenty-four hours.

The original calcium balance study (2) has since been expanded by examining 191 healthy perimenopausal women on two or three occasions over a 15-year period, generating a total of 518 balance studies (8, 9). There were no significant effects of caffeine-containing beverages on either urinary calcium loss (8) or faecal calcium loss (9). However, the negative calcium balance observed in the original study (2) persisted in the expanded study (8,9). It was estimated that 4 mg calcium were lost for every cup of coffee consumed and multivariate analysis suggested that this was due to a small but significant decrease in calcium absorption efficiency. However, calcium intakes in the study population were only 660 mg/day or about half the recommended intake in the USA so the effects of caffeine observed on calcium balance may only be relevant to women with inadequate calcium intakes.

Three other studies of effects of caffeine on 24-hour urinary calcium excretion have given mixed results (10,11,12). In eight pre-menopausal women given 1.4 l diet cola per day (equivalent to approximately four and a half cans) as the sole source of caffeine for two weeks, there were no effects on 24-hour calcium excretion (10). In twenty-five pre- and postmenopausal women normally consuming at least 5.8 mg caffeine/kg body weight, abstinence for 2 weeks had no effect on urinary calcium excretion (11). By contrast, in eighty-five postmenopausal women suffering from osteoporosis, multiple regression analysis showed that coffee intake was inversely associated with calcium balance (12). It was calculated that for every 100 ml coffee consumed 6 mg calcium/day was lost. 

It can be concluded that the consumption of caffeine is associated with a small negative calcium balance probably arising from reduced calcium absorption efficiency. The negative balance has been variously estimated as between 4 and 6 mg calcium/day. However, this effect is seen only in women with inadequate calcium intakes. In addition, it has been estimated that this small calcium deficit can be compensated for by the addition of only 1-2 tablespoons of milk to a caffeine-containing beverage such as coffee (8).

BONE HEALTH

Osteoporosis has been defined as “a disease characterised by low bone mass and micro-architectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk”. Like many chronic diseases it is multifactorial. Risk factors for osteoporosis include age, cigarette smoking, alcohol consumption, level of physical activity and calcium intake.

As reviewed recently (13), there are at least 31 cross-sectional, case control and cohort studies of associations between caffeine intake and bone health involving many thousands of subjects. The aspects of bone health measured include bone mineral density, change in bone mineral density, fracture rate and osteoporosis. Although these studies have the advantage of measuring aspects of bone health directly, such observational epidemiological studies can only demonstrate associations and not cause effect relationships. All such studies are subject to confounding.

Twenty-two studies have looked at associations between bone mineral density or change in bone mineral density and caffeine intake. Four cross-sectional studies have shown inverse associations between bone mineral density and caffeine intake which were weak (14), present at one skeletal site but not at others (15) or present in the hip but not in the spine (16, 17). By contrast, a further ten cross-sectional studies were unable to find any associations between caffeine intake and bone mineral density at any skeletal site (18-27). A fifteenth cross-sectional study was able to show a negative association between caffeine intake and bone mineral density but only in subjects consuming inadequate amounts of calcium (28). This finding is supported by the results of a cohort study which found a negative association between change in bone mineral density and caffeine intake (29). By contrast, four other cohort studies failed to find any associations between caffeine intake and change in bone mineral density (30, 31, 32,33) and two other cohort studies failed to find any associations between caffeine intake and bone mineral density (34,35).

Eight studies have looked at associations between risk of fracture and intake of caffeine. Four case control studies were unable to find any associations between risk of fracture and caffeine intake (36, 37, 38,39). A fifth case control study used osteoporosis as an endpoint but was unable to find any association with caffeine intake (40). By contrast, four cohort studies reported a significant association between caffeine intake and risk of fracture. In a subset of the Framingham cohort, there was an incremental increase in fracture risk for coffee consumption above two cups per day (41). In the Nurses Health Study, the risk of hip fracture increased three-fold with caffeine intake but only in women younger than 65 years old (42). In the Study of Fractures cohort, the investigators identified 17 independent risk factors and found that caffeine intake was one of the weakest (43). In a Norwegian study, fracture risk increased with caffeine intake but only when coffee consumption was greater than nine cups per day .

Out of the 31 studies cited above, 10 showed an inverse association between consumption of caffeine- containing beverages and some aspect of bone health and 21 found no association. Although the available evidence is contradictory, the weight of evidence does not support the idea that caffeine-containing beverages adversely affect bone health. One reason for the contradictory results is confounding. Taking one study as an example, the inverse association observed before adjustment for confounders between intake of caffeine containing beverages and bone mass disappeared after adjustment for other risk factors (20). It is also possible that intake of caffeine- containing beverages is acting as a marker for a true causal factor. It is known that there is an inverse relationship between the intake of milk and consumption of caffeine-containing beverages (8). It is possible, therefore, that a low intake of milk rather than a high intake of caffeine-containing beverages is a true cause of impaired bone health. This positon was supported by Hallstrom et al (44) who examined the relationship between consumption of coffee and tea and total caffeine intake associated with osteoporotic fracture risk. They found that a daily intake of 330 mg caffeine, or more, may be associated with a modestly increased risk of osteoporotic fractures, especially in those women with a low calcium intake.

References:

1. Heaney, R.P. Food and Chemical Toxicology, 40, 1263-1270, 2002

2. Heaney, R.P. and Recker, R.R. Journal of Laboratory and Clinical Medicine, 99, 46-55, 1982.

3. Massey, L.K. and Wise, K.J. Nutrition Research, 4, 43-50, 1984. 

4. Massey, L.K. and Hollingberry, P.W. Nutrition Research, 8, 1005-1012, 1988.

5. Bergman, E.A. et al. Life Sciences, 47, 557-564, 1990.

6. Kynast-Gales, S.A. and Massey, L.K. Journal of the American College of Nutrition, 13, 467-472, 1994.

7. Barger-Lux, M.J. et al. American Journal of Clinical Nutrition, 52, 722-725, 1990.

8. Barger-Lux, M.J. and Heaney, R.P. Osteoporosis International, 5, 97-102, 1995.

9. Heaney, R.P. and Recker, R.R. Journal of Bone and Mineral Research, 9, 1621-1627, 1994.

10. Smith, S. et al. Archives of Internal Medicine, 149, 2517-2519, 1989.

11. Massey, L.K. et al. Journal of the American College of Nutrition, 13, 592-596, 1994.

12. Hasling, C. et al. Journal of Nutrition, 122, 1119-1126, 1992.

13. Heaney, R.P. Food and Chemical Toxicology,  40, 1263-1270, 2002.

14. Bauer, D.C. et al. Annals of Internal Medicine, 118, 657-665, 1993.

15. Hernandez-Avila, M. et al. Epidemiology, 4, 128-134, 1993.

16. Krahe, C. et al. Brazilian Journal of Medical and Biological Research, 30, 1061-1066, 1997.

17. Rubin, L.A. et al. Journal of Bone and Mineral Research, 14, 633-643, 1999.

18. Lacey, J.M. et al. Journal of Bone and Mineral Research, 6, 651-659, 1991.

19. Cooper, C. et al. Journal of Bone and Mineral Research, 7, 465-471, 1992.

20. Johansson, C. et al. Age and Ageing, 21, 20-26, 1992.

21.Glynn, N.W. et al. Journal of Bone and Mineral Research, 10, 1769-1777, 1995.

22. Hansen, M.A. Osteoporosis International, 5, 283, 1995.

23. Travers-Gustafson, D. et al. Calcified Tissue International, 57, 267-271, 1995.

24. Lloyd, T. et al. American Journal of Clinical Nutrition, 65, 1826-1830, 1997.

25. Grainge, M.J. et al. Osteoporosis International, 8, 355-363, 1998.

26. Maini, M. et al. Minerva Medicine, 87, 385-399, 1996.

27. Picard, D. et al. Bone Minerals, 4, 299-309, 1988.

28. Barrett-Connor, E. et al. Journal of the American Medical Association, 271, 280-283, 1994.

29. Harris, S.S. and Dawson-Hughes, B. American Journal of Clinical Nutrition, 60, 573-578, 1994.

30. Reid, I.R. et al. Journal of Clinical Endocrinology and Metabolism, 79, 950-954, 1994.

31. Lloyd, T. et al. Journal of the American College of Nutrition, 17, 454-457, 1998.

32. Hannan, M.T. et al. Journal of Bone and Mineral Research, 15, 710-720, 2000.

33. Lloyd, T. et al. Journal of the American College of Nutrition, 19, 256-261, 2000.

34. Hansen, M.A. et al. Osteoporosis International, 1, 95-102, 1991.

35. Packard, P.T. and Recker, R.R. Osteoporosis International, 6, 149-152, 1996.

36. Nieves, J.W. et al. Osteoporosis International, 2, 122-127, 1992.

37. Cummings, R.G. and Klineberg, R.J. American Journal of Epidemiology, 139, 493-503, 1994.

38. Tavani, A. et al. Preventive Medicine, 24, 396-400, 1995.

39. Kanis, J. et al. Osteoporosis International, 9, 45-54, 1999.

40. Blaauw, R. et al. South African Medical Journal, 84, 328-332, 1994.

41. Hernandez-Avila, M. et al. American Journal of Clinical Nutrition, 54, 157-163. 1991.

42. Cummings, R.R. et al. New England Journal of Medicine, 332, 767-773. 1995

43. Meyer,H.E. et al. American Journal of Epidemiology, Volume 145, 117-123. 1997

44. Hallstrom et al, Osteoporosis International, Online Edition, May 2006