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Current research has implicated vitamin D deficiency as a major factor in the pathology of at least 17 varieties of cancer as well as heart disease, stroke, hypertension, autoimmune diseases, diabetes, depression, chronic pain, osteoarthritis, osteoporosis, muscle weakness, muscle wasting, birth defects, periodontal disease, and more.
To read the newspapers and blogs, one would think that vitamin D is the cure-all, the panacea or the snake oil of today (Note that the original snake oil was very effective and high in omega-3 oils.) As with much of today’s medical advice from the media, the problem with our vitamin D metabolism is yesterday’s medical advice. Not only are the previous minimum daily requirements too low by an order of magnitude, but the dietary advice is in conflict with life style suggestions to minimize sun exposure. And all of the advice is prejudiced by commercial considerations. (Note that the way that most sun blocks are used to permit longer time in the sun, actually increases the rate of skin cancer.)
The previous recommendation was to have 200 IU of vitamin D per day in your diet. How can this number make any sense, when 20 minutes of sun exposure can produce 20,000 IU of vitamin D? And what about the storage of vitamin D in fat and the obvious problem that obese people can easily store more vitamin D than they consume in their diet, i.e. they are always deficient even on what appears to be an adequate diet?
It is also confusing to measure vitamin D in the blood. The active form of vitamin D is calcitriol and it is made in the kidney from the short-term stock of vitamin D that is released from the liver. This suggests to me that there are at least three types of protein carriers for vitamin D: 1) point of origin carriers that take vitamin D from fat, skin and intestines to the liver, 2) liver-to-kidney carriers that transport to the kidney and 3) calcitriol carriers that take the active form to organs where it is used for calcium transport, etc. Which form of vitamin D should be measured? The answer is that the major circulating form, not the active, calcitriol, should be measured, because even people with severe deficiencies can have normal levels of calcitriol.
Active vitamin D, calcitriol regulates calcium distribution between diet, serum and bone. The serum calcium level must remain constant or fundamental cellular processes of signaling and secretion will be disrupted. The result of lowered calcium would be loss of neural and muscular function.
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Calcitriol is a prohormone. Calcitriol binds to a cytoplasmic receptor and the calcitrol/receptor complex is transported to and into the nucleus. The hormone complex then acts as a transcription factor by binding to specific control elements of genes and controlling gene expression. Thus, the amount of calcitrol/receptor determines the presence of calcium transporter proteins on the surface of kidney or intestinal epithelial cells and the amount of calcium loaded into the serum.
Since calcitrol is synthesized in the kidney, calcium reuptake by the kidney is directly related to calcitrol production. If there is inadequate calcium in the serum, the calcium level will also lower in the calcitrol synthesizing cells of the kidney and this will increase the activity of the calcitrol/receptor complexes. This should be adequate to produce enough calcitrol in the serum to enhance calcium uptake in the intestines. If the level of calcium is still inadequate, then the parathyroid glands secrete PTH that stimulates both more calcitrol production and release of calcium from bone. Chronic release of bone calcium result in osteoporosis.
Obesity is a problem, because of the solubility of vitamin D in fat. Vitamin D is transported to fat cells, just as it is transported to the liver. Presumably the same carrier protein is used to transport to and from the fat cells. Thus, there is an equilibrium between the vitamin D stored in fat droplets of the fat cells and the vitamin D stored in the liver. Unfortunately, the capacity of the fat cells is much greater than the liver. As a result, a huge quantity of vitamin D is required to saturate the fat storage of an obese person and there is a constant deficiency punctuated by the dietary contributions of vitamin D after each meal. This is one of the reasons for the increased rates of most degenerative and autoimmune diseases for obese individuals.
There is one last point that I want to make about nonsense in the news. It is stated that exclusively breastfed babies are at risk for vitamin D deficiency, because mother’s milk is low in vitamin D by comparison to the higher value in formula. This is ridiculous in the
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The bottom line is that you need to have your arms and face, or arms and legs, exposed to the sun for 15-20 minutes several times a week. This is very important if you carry a few extra pounds and/or show symptoms of chronic inflammation. It may also make sense to supplement your diet with 1-2,000 IU of vitamin D. Don’t forget to follow the rest of the anti-inflammatory diet and lifestyle suggestions.
2 comments:
Excellent stuff! I only found this by expanding every month, as your old posts don't have any labels.
Dr. Ayers: I have a cousin that has had three surgeries to remove extremely large kidney stones. Do you think vitamin D deficiency plays a role? Thanks Ron
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