VITAMIN D THE NEW SUPERVITAMIN BUT IS IT A HORMONE?
Should Vitamin D be renamed Sunshine Hormone?
Vitamin D3 is synthesized in the skin during summer under the influence of ultraviolet light of the sun, or it is obtained from food, especially fatty fish. After hydroxylation in the liver into 25-hydroxyvitamin D (25(OH) D) and kidney into 1,25-dihydroxyvitamin D (1,25(OH) 2D), the active metabolite can enter the cell; bind to the vitamin D-receptor and subsequently to a responsive gene such as that of calcium binding protein. After transcription and translation the protein is formed, e.g. osteocalcin or calcium binding protein. The calcium binding protein mediates calcium absorption from the gut. The production of 1,25(OH) 2D is stimulated by parathyroid hormone (PTH) and decreased by calcium. Risk factors for vitamin D deficiency are premature birth, skin pigmentation, low sunshine exposure, obesity, malabsorption and advanced age. Risk groups are immigrants and the elderly. Vitamin D status is dependent upon sunshine exposure but within Europe, serum 25(OH) D levels are higher in Northern than in Southern European countries. Severe vitamin D deficiency causes rickets or osteomalacia, where the new bone, the osteoid, is not mineralized. Less severe vitamin D deficiency causes an increase of serum PTH leading to bone resorption, osteoporosis and fractures. A negative relationship exists between serum 25(OH) D and serum PTH. The threshold of serum 25(OH) D, where serum PTH starts to rise is about 75nmol/l according to most surveys. Vitamin D supplementation to vitamin D-deficient elderly suppresses serum PTH, increases bone mineral density and may decrease fracture incidence especially in nursing home residents. The effects of 1,25(OH) 2D and the vitamin D receptor have been investigated in patients with genetic defects of vitamin D metabolism and in knock-out mouse models. These experiments have demonstrated that for active calcium absorption, longitudinal bone growth and the activity of osteoblasts and osteoclasts both 1,25(OH) 2D and the vitamin D receptor are essential. On the other side, bone mineralization can occur by high ambient calcium concentration, so by high doses of oral calcium or calcium infusion. The active metabolite 1,25(OH) 2D has its effects through the vitamin D receptor leading to gene expression, e.g. the calcium binding protein or osteocalcin or through a plasma membrane receptor and second messengers such as cyclic AMP. The latter responses are very rapid and include the effects on the pancreas, vascular smooth muscle and monocytes. Muscle cells contain vitamin D receptor and several studies have demonstrated that serum 25(OH) D is related to physical performance. The active metabolite 1,25(OH) 2D has an antiproliferative effect and downregulates inflammatory markers. Extra renal synthesis of 1,25(OH) 2D occurs under the influence of cytokines and is important for the paracrine regulation of cell differentiation and function. This may explain that vitamin D deficiency can play a role in the pathogenesis of autoimmune diseases such as multiple sclerosis and diabetes type 1, and cancer. In conclusion, the active metabolite 1,25(OH) 2D has pleiotropic effects through the vitamin D receptor and vitamin D responsive elements of many genes and on the other side rapid non-genomic effects through a membrane receptor and second messengers. Active calcium absorption from the gut depends on adequate formation of 1,25(OH) 2D and an intact vitamin D receptor. Bone mineralization mainly depends on ambient calcium concentration. Vitamin D metabolites may play a role in the prevention of autoimmune disease and cancer.
Prog Biophys Mol Biol. 2006 Sep;92(1):4-8. Epub 2006 Feb 28.
Vitamin D physiology.
Lips P.
Source
Department of Endocrinology, VU University Medical Center, P.O. Box 7057, 1007 MB Amsterdam, Netherlands.
It was not common until recently to measure Vitamin D levels in the blood unless you had a related problem, such as Malabsorption of Calcium or Renal Insufficiency or rare syndromes pertaining to the Bone Metabolism.
In the last twenty years specifically and thirty years generally, there has been a growth in the prevalence, detection and objectification of many measurements. One thing every one can agree about is: People are fatter than before.
It is interesting to note that Vitamin D research attracted pure scientists (PhD) rather than Medical Scientists (MD or MD, PhD), was it perhaps the lack of interest from the Pharmaceutical companies? Who saw no chance of making a killing unlike the one they recognized in STATIN drugs for cholesterol that also increased in the general population during the same period! A few Australian and UK MDs were interested from the beginning and they had published that Vitamin D metabolism was altered in people who are carrying extra weight.
Listening to all the Internet and media hullaballoo about Obesity and its relationship to lower circulating Vitamin D levels, you would think that something great had been discovered. (Please put in vitamin D and obesity and you would see every news media has covered it, as a study was published in the UK about the relationship between Obesity and lower Vitamin D levels).
No one any longer would blindly believe that lack of activity and excess calories as the reason for Obesity, newer research on Microbiome is one interesting diversion as are the chemical poisoning of the population en masse as a cause of obesity.
Can taking Vitamin D in pill form be as good as getting it naturally? My gut reaction is NO..
How to get it naturally? Walk for a few minutes in the sun with your hands and preferably legs exposed (Oh Poor Arabs and other Moslems! You are condemned to suffer for your sartorial habits) and eat salmon and other fatty fish, which would give you omega 3 to counteract the inflammation in the body as well.
We now know that fish oil taken as a food supplement actually may do damage to you, so it would soon follow that vitamin D supplements may also some damage if they are confronted in the ileo jejunal region of the gut by the resident bacteria. Studies from Rochester have pointed out the importance of Vitamin D receptors in the gut and how the microbiota use them to mount anti-inflammatory and anti-infective actions. I know that natural Vitamin D reaches the liver from the skin and then to the kidney, could it be possible that taking too much supplementation orally might saturate these receptors in the gut and make them useless? Quien Sabe?
OR IS IT POSSIBLE?
the chemical interactions/inflammatory processes that give rise to Obesity is interfering with the Vitamin D metabolism as well?
In studies from the Gulf Arab Sheikdom of Qatar, home of Al Jazeera (so so) and Qatar Airways (Excellent), the Vitamin Deficient status was found in over 90 per cent of the population, despite the sliver of the desert having plenty of sunshine..
It may be worth point out that Qatar is now No 1 on the Hit Parade of Obesity around the world !
