To the best of our knowledge, there is no recorded study on the association of caffeine intake with circulating levels of 25-hydroxyvitamin D. Current evidence however relate caffeine intake to calcium metabolism [10–12]. It has been demonstrated that caffeine negatively influences calcium balance by reducing renal reabsorption of calcium, and possibly by reducing intestinal calcium absorption efficiency. High caffeine intake may involve considerable renal and intestinal calcium losses . Results of previous epidemiological studies have suggested a relationship between high caffeine consumption and low bone mineral density (BMD) and osteoporotic fractures, which however may be offset by a high calcium intake [14, 15]. Caffeine intake also reduces inositol levels in the blood. Inositol is a regulating factor in calcium metabolism , and can modestly increase calcium excretion and reduce absorption (Barrett-Connor et al., 1994). Caffeine intake >300 mg/d (≈514 g, or 18 oz, brewed coffee) accelerate bone loss at the spine in elderly postmenopausal women . Furthermore, women who harbor the TT genetic variant of VDR appear to be at a greater risk for this deleterious effect of caffeine on bone . The polymorphisms in the VDR gene correlate with BMD, bone turnover and bone loss [16, 17]. In our study, serum vitamin D level increases as coffee and tea consumption increases. Increased caffeine dose decreases VDR protein expression and alkaline phosphatase enzyme activity, a marker of osteoblast differentiation in osteoblast cells . Caffeine is also metabolized in the liver via the cytochrome P450 oxidase enzyme system [19, 20]. About a dozen metabolites can be recovered in the urine of regular coffee consumers [19, 21]. Methylxanthine, theophylline and caffeine were found to inhibit the conversion of 25 hydroxyvitamin D3, to 1,25 dihydroxyvitamin D3 in isolated renal tubules in vitamin D deficient chicks, which led to increased vitamin D circulating levels .
The role of caffeine as a risk factor for bone loss is controversial. Moderate coffee consumption has no effect on bone health . However, low calcium intake is clearly linked to skeletal fragility, and it is likely that a high caffeine intake is often a marker for low calcium intake . The negative effect of caffeine on calcium absorption is small enough to be fully offset by as little as 1–2 tablespoons of milk. All of these observations implicating caffeine-containing beverages as a risk factor for osteoporosis have been made in populations consuming substantially less than optimal calcium intakes .
Another factor that may contribute to higher vitamin D in the heavy drinkers is the weight reducing effect of coffee. In our study BMI mean value was significantly decreased in heavy drinkers when compared to low and moderate drinkers (mean of BMI =20 ± 5.8 kg/m2, P < 0.05). Both sexes showed a decrease in BMI (appendix). In a study done by Jorde et al. (2001), both gender's serum calcium showed a positive association with body mass index (BMI) and coffee consumption that persisted after correcting for other variables in a multiple regression model (P < 0.05) .
Coffee intake should reduce BMI because coffee consumption decreases the amount of fat tissue by elevating thermogenesis [24–26] and stimulating the sympathoadrenal system . Aside from caffeine's ability to increase fat oxidation and lipolysis [28–30], there is a weak but significant positive association with BMI for coffee intake in both sexes . Coffee may reduce body weight through lipolysis stimulation . Fat loss from adipose tissue is hypothesized to be accompanied by vitamin D withdrawal from its fat store leading to elevated serum vitamin D levels. Studies on weight reduction show that serum 25(OH)D levels rise when obese individuals lose body fat [31–33].
There is consistent epidemiological evidence that consumption of these hot beverages is associated with a reduced risk of diabetes mellitus type 2 (DMT2) and coronary heart disease [34–36]. It has been hypothesized that the protective effect of coffee and tea consumption on DMT2 risk is mediated by a reduction in obesity . This hypothesis is supported by a handful of clinical intervention studies which report that the frequency of coffee or tea consumption is related to weight loss and change in body fat distribution [37, 38].
The study has limitations. Comprehensive data on outdoor physical activity and diet were lacking, and these can be considered major confounders that affect circulating vitamin D levels. The type of coffee and tea were also not taken into consideration. Nevertheless, the number of subjects involved increases the reliability of our results, which shows for the first time a dose-dependent relationship between circulating vitamin D levels in relation to coffee and tea consumption among Saudi adolescents, even after adjustment for physical activity, sun exposure, gender, age and BMI.
In summary, the study suggests that increased coffee and tea consumption elevates circulating vitamin D levels among Saudi Arab adolescents independent of physical activity, sun exposure, age, gender and BMI. Further studies are needed to confirm these findings as assessment of the health risks and benefits of coffee and tea consumption requires reliable data that can accurately for studying relationships between coffee and tea consumption and health-related endpoints.