Aside from sex hormones, circulating vitamin D – calcidiol – serum levels show a consistent difference between men and women. Ok – I know that
- nuclear receptors are hormone-dependent transcription factors (Drané P, Mol Cell 2004; 16:187)
- 25-OH-D3 hydroxylase is upregulated by estradiol-17 (forgot reference)
- endometrium expresses VDR during cycling (Vigano, J Mol Endo 2006; 36:415)
but what is really responsible for this difference? A new Cell paper now shows that tamoxifen (an estrogen receptor antagonist) disrupts calcium homeostasis in yeast. Yea, yea.
JCI has a paper about resurrection of vitamin D deficiency (more about the author at 1, 2 and 3). The author uses references 46-59 to underpin his opinion that rickets has again become an epidemic. These references are from 1992, 1984, 2005, 2000, 1987, 1987, 1989, 1994, 1989, 2001, 1998, 2001, 1987, 2006. So nothing really new – no prospective study, no systematic survey, just a few isolated reports. Sure, that there might be a rickets problem in a selected areas or in minority groups, but there is no world-wide epidemic. He argues also that many (if not all) studies show “low” serum 25-OH-D3 values. Is this chasing a phantom? A more systematic study concludes that rickets in Africa is more a disease of calcium deficiency. The JCI article is particular poorly written when it comes to immunological effects; asthma is misquoted from the Camargo study (which is subject of my review at Pediatric Allergy. Nay, nay.
… was the title of a recent editorial in JCI. Clearly that’s not true for vitamin D as you may know of the many immunological functions. A new study now shows, that mice get atopic dermatitis by applying vitamin D ointment. A EJCN paper published on the same day concludes that “the national fortification of fluid milks and margarines with vitamin D safely improved the vitamin D status of children”. Nay, nay.