Caffeine decreases Vitamin D in blood and cells - many studies

4+ Vitamin D Life pages with CAFFINE OR COFFEE in the title

This list is automatically updated

Caffeine deactivates Vitamin D Receptor gene (less D to cells) - Aug 2019

The Effect of Caffeine on Calcitriol-Inducible Vitamin D Receptor-Controlled Gene Expression in Intestinal and Osteoblastic Cells
Calcified Tissue International volume 105, pages651–659 (2019) https://doi.org/10.1007/s00223-019-00602-4
Ondřej Ženata, Adéla Marcalíková & Radim Vrzal

Some epidemiological studies suggested caffeine consumption as the cause for bone mineral density loss. Certain genes involved in this process are regulated by vitamin D receptor (VDR). Therefore, we investigated if caffeine can affect inducible expression of VDR-regulated genes, some of them being involved in bone mineralization process. By employing reporter gene assay, polymerase chain reaction, and western blotting, we monitored the VDR activity and expression in cell cultures of intestinal (LS180), osteosarcoma (HOS), and normal human osteoblasts in vitro. While caffeine stimulated calcitriol-inducible VDR-dependent nanoluciferase activity in stable reporter cell line IZ-VDRE (derived from LS180), it rather modulated mRNA levels of target genes, like CYP24A1, BGLAP, SPP1, and TNSF11 in LS180 and HOS cells. However, caffeine significantly decreased calcitriol-inducible CYP24A1, TNSF11, and SPP1 transcripts in osteoblasts. This decrease had non-linear U-shaped profile. Our in vitro data demonstrate biphasic action of caffeine on the expression of certain calcitriol-inducible VDR-regulated genes in normal human osteoblasts.
 Download the PDF from Vitamin D Life

THE GENETICS OF OSTEOPOROSIS: Vitamin D Receptor Polymorphisms - July 1998

Annual Review of Nutrition Vol. 18:233-258 https://doi.org/10.1146/annurev.nutr.18.1.233

• Richard J. Wood, Mineral Bioavailability Laboratory, Jean Mayer Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts 02111; e-mail: wood_mb at hnrc.tufts.edu
• James C. Fleet. Department of Nutrition and Food Service Systems, School of Human Environmental Sciences, University of North Carolina at Greensboro, Greensboro, North Carolina 27402-6170; e-mail: jcfleet at erickson.uncg.edu

Osteoporosis is a metabolic bone disease characterized by low bone mass and deterioration of bone tissue that leads to bone fragility and an increase in fracture risk. It is a disease with a complex etiology that includes genetic and environmental contributors. Environmental factors that influence bone density include dietary factors—such as intakes of calcium, alcohol, and caffeine—and lifestyle factors—such as exercise and smoking. Ethnic differences in the propensity to nontraumatic bone fracture suggest that genetic factors are important.
Recently, common allelic variations in the vitamin D receptor gene have been found to be associated with bone mineral density in racially diverse population groups, as well as in prepubertal girls, young adult and postmenopausal women, and men. However, many studies have not been able to find this association. Additional approaches, such as sib-pair analysis, will probably be necessary in the future to identify the important genetic determinants of osteoporosis.
 Download the PDF from Sci-hub via Vitamin D Life

High Caffeine intake == > 1.5X more likely to be Vitamin D Deficient - Sept 2021

Higher intakes of dietary caffeine are associated with 25-hydroxyvitamin D deficiency - A cross-sectional study from the NHANES
Published Online:September 20, 2021 https://doi.org/10.1024/0300-9831/a000727 $28 paywall
Qiwei Chen, Hamed Kord-Varkaneh, Heitor O. Santos, Rafael Genario, and Minyan Dang

Low serum 25-hydroxyvitamin D [25(OH)D] levels remain a challenge worldwide. While some in vitro studies show a caffeine-induced decrease in vitamin D receptor expression, there is a paucity of research to define the extent of caffeine intake and effects on 25(OH)D levels. Therefore, we aimed to associate dietary caffeine intake with 25(OH)D deficiency through a recognized dataset. Using data collected from the 2005–2006 National Health and Nutrition Examination Survey (NHANES), 25(OH)D levels and dietary caffeine intake were extracted from 13134 individuals (30–47 years, interquartile range). We used one-way ANOVA and chi-square tests for quantitative and qualitative variables, respectively, and performed multivariate logistic regression for four models to assess the odds ratio (OR) of 25(OH)D deficiency (<20 ng/ml or <50 nmol/L) based on quartiles of dietary caffeine intake. Both crude and multivariable models detected higher OR for 25(OH)D deficiency according to the highest intakes of caffeine (15.8±9.5, 51.9±11.9, and 177±156 mg/d) when compared to the reference category (2.19±1.04 mg/d), in which the OR in the highest category of caffeine intake was 1.24 (95% CI: 1.12 to 1.37) and 1.48 (95% CI: 1.16 to 1.78) for the crude model and the most complete multivariable analysis (adjustment for age, sex, race, body mass index, smoking, physical activity, occupation, energy intake, protein intake, and fat intake), respectively.
sIn conclusion, higher dietary intakes of caffeine were associated with 25(OH)D deficiency in a representative sample of the American population, but further investigation is warranted to determine causation.

The effects of caffeine on bone mineral density and fracture risk - Jan 2022

Osteoporosis International volume 33, pages1235–1241 January 2022
N. K. Berman, S. Honig, B. N. Cronstein & M. H. Pillinger

Caffeine is a regular part of the diet of many adults (coffee, tea, soft drinks, and energy drinks). Multiple molecular effects of caffeine suggest that it may promote bone loss. Given the extensive consumption of caffeine worldwide, any impact of caffeine consumption on bone strength and/or density would have large population health implications. The most well-established pharmacological effect of caffeine is non-specific antagonism of adenosine receptors. Adenosine regulates bone metabolism in a complex manner, with in vitro studies suggesting that direct stimulation of adenosine A2A and A2B receptors induces bone formation by activating osteoblasts and suppressing osteoclast differentiation and function. Thus, competitive inhibition of adenosine A2 receptors by caffeine may inhibit bone formation and promote bone resorption. However, antagonism of adenosine A1 receptors may have opposing effects. Caffeine has also been suggested to affect bone through derangement of calcium metabolism, alteration of vitamin D responses, and other mechanisms. In clinical and population-based studies, the impact of caffeine consumption on bone metabolism offers a mixed picture, with some but not all studies suggesting a potential link between caffeine intake and reduced bone mineral density or increased fracture risk. Differences in methodology, selected populations, and duration/timing of the studies may account for study outcome discrepancies. The in vitro effects of caffeine on cells involved in bone metabolism suggest that caffeine intake may promote osteoporosis, and some but not all clinical studies support a modest adverse caffeine impact. Herein, we describe the basic biology of caffeine as it pertains to bone, review the clinical literature to date, and consider the implications of the current data on clinical practice and future studies.
Clipped from conclusion:

• Caffeine at doses of <400mg/day may not adversely affect bone metabolism
• Effects on calcium metabolism and inhibition of vitamin D receptor activity may also play a role in caffeine effects on bone metabolism__

No such attachment on this page

Vitamin D Life – Vitamin D Receptor is associated in over 58 autoimmune studies

Vitamin D Life - Vitamin D Receptor activation can be increased in many ways

Resveratrol,  Omega-3,  Magnesium,  Zinc,   Quercetin,   non-daily Vit D,  Curcumin,   Berberine,  intense exercise, Butyrate   Sulforaphane   Ginger,   Essential oils, etc  Note: The founder of Vitamin D Life uses 10 of the 16 known VDR activators