Vitamin D Deficiency in a Musculoskeletal Practice
 
   

Vitamin D Deficiency in a Musculoskeletal Practice

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:
   Frankp@chiro.org
 
   

FROM:   ACANews ~ January 2012

By David C. Radford, DC, MS


Respond to a primary care challenge to the chiropractic profession.


Vitamin D deficiency is a silent epidemic in our nation, according to Michael F. Holick, MD, PhD, the director of physiology and biophysics at Boston University School of Medicine. Dr. Holick states, “It’s certainly the most common nutritional deficiency and likely the most common medical problem in the world, affecting 1.5 to 2 billion people.” [1]

Patients with vitamin D deficiency are often misdiagnosed with fibromyalgia due to widespread symptoms of nociceptive pain and impaired neuromuscular function. Vitamin D deficiency in chronic pain patients has also been shown to lead to an increased intake of opioid pain medications. [2] It is incumbent on doctors of chiropractic to recognize these issues and to be on the lookout for signs of vitamin D deficiency in patients.

Vitamin D deficiency can occur for a number of reasons. One is lack of adequate sunshine, which can be due to sunscreen, as well as the season, the latitude and the melanin content of the skin acting as a filter for the UVB. Medications and even supplements can decrease serum vitamin D. These include the anti-seizure medications, corticosteroids, the antibiotic Rifampin, highly active antiretroviral therapy for AIDs (HAART), excess vitamin A and the herb St. John’s Wort. Gastrointestinal malabsorption syndromes can prevent vitamin D in foods or supplements from crossing the gut wall; these include irritable bowel syndrome, Crohn’s or Wipple’s disease, cystic fibrosis, celiac disease and sprue, as well as a fatty liver or liver disease. [3]

Normal serum vitamin D levels can be achieved with exposure to ultraviolet light (UVB) from the sun or tanning beds. The clinical response to either UVB light therapy or oral vitamin D supplementation varies based on a patient’s age, skin color, gender, size, percentage of body fat, gastrointestinal absorption, liver and kidney function, geographical latitude and the season of the year. [3]

When exposure to UVB radiation is insufficient for the synthesis of adequate vitamin D3 in the skin, adequate dietary intake is essential for health. [4] While most laboratories give a normal reference range of 30 to 80 or even 100 nanograms per milliliter (10-9 g/mL), current research suggests that a more desirable serum vitamin D level is between 50 and 80 ng/mL3—and that greater than 150 ng/mL is potentially toxic. [1]


Vitamin D Biochemistry

When we go out in the sun, the ultraviolet B light in the wavelength from 290 to 315 nano-meters penetrates our epidermis and converts the 7-dehydrocholesterol in the skin to pre-vitamin D. This endogenous skin production and the vitamin D3 from the diet are indistinguishable in the blood.

Both are metabolized in the liver to form 25-hydroxy-vitamin D, or [25(OH)D], the major circulating form of vitamin D. Reaching the kidney, [25(OH)D] forms [1,25 (OH)2D]—the most potent form of vitamin D, which is responsible for most of the physiological effects of vitamin D in the body. In the kidney, production of [1,25(OH)2D] is tightly regulated by plasma parathyroid hormone levels and serum calcium and phosphorus levels. [3, 5-7]

Vitamin D, a fat-soluble vitamin, is often called a secosteroid (seco, Latin “to cut”), which is a molecule with a “broken” ring. Secosteroids are very similar in structure to steroids, except that in vitamin D, two of the B-ring carbon atoms (C9 and 10) of the typical four steroid rings are not joined, whereas in steroids they are joined. [8]


Clinical Use of Vitamin D

Over 30 years of research, Dr. Holick has demonstrated that the final metabolic product of vitamin D is a potent repair and maintenance secosteroid hormone that affects a wide variety of tissues, targeting more than 2,000 human genes or nearly one-sixth of the entire human genome. Virtually every cell and tissue in the body has a vitamin D nuclear receptor (VDR). The brain, prostate, breast and colon tissues and all the immune system cells contain VDR and respond to the active form of vitamin D, which is involved in regulating cellular proliferation, differentiation, apoptosis and angiogenesis. [3]

A century ago, vitamin D deficiency was associated only with rickets in children, but today it has been implicated in 16 different cancers, most commonly breast, prostate, colorectal and pancreatic cancer. There is a direct association of vitamin D deficiency with coronary artery disease and heart disease, high blood pressure, asthma and wheezing diseases, decreasing FEV1, insulin production in metabolic syndrome X (pre-diabetic state), Type 2 adult-onset diabetes and obesity. [2]

Vitamin D deficiency is associated with many autoimmune diseases, including Type 1 diabetes, Crohn’s disease, multiple sclerosis, rheumatoid arthritis, Behçet’s disease, systemic lupus erythematosus and Hashimoto’s disease, as well as psychiatric problems including Alzheimer’s disease, dementia, autism, depression and even schizophrenia. [3, 9-11] Vitamin D deficiency increases a person’s susceptibility to upper respiratory infection, cold, flu and a host of many other common illnesses—including periodontal disease, cardiomyopathy, osteopenia, osteoporosis, osteomalacia and muscle weakness due to osteomalacic myopathy, resulting in increased susceptibility of falls and injury in the elderly. [2] Chronic vitamin D insufficiency is observed in most patients with Parkinson’s disease, and in virtually all patients with dementia and Alzheimer’s disease. [12]

Vitamin D is essential for maintaining normal calcium, phosphorous, magnesium and bone metabolism, [13] as well as for maintaining the concentration of ionized calcium in the extracellular fluid compartment required for normal neural excitation and relaxation of muscle. Insufficient ionized calcium in the extracellular fluid results in a continuous excitation of the muscle cells, leading to hypocalemic tetany and potentially to a convulsive state. [14]

Chronic vitamin D deficiency leads to a myriad of diseases affecting the soft and bony tissues. It alters endocrine metabolism. It also elevates PTH (parathyroid hormone) and suppresses thyroid function, which can lead to abnormal soft-tissue calcium depositions. In addition, vitamin D deficiency contributes to problems caused by autoimmune disease like rheumatoid arthritis and multiple sclerosis, negatively alters glucose metabolism and contributes to both Type 1 and Type 2 diabetes. [3, 9, 15]


The Spread of Vitamin D Deficiency

Hypovitaminosis D has been shown to be widespread in the United States, especially above the 35th parallel. Consequently, vitamin D deficiency should be considered in virtually every new patient encounter.

After testing and treating more than 1,500 patients with vitamin D deficiency and insufficiency in northeast Ohio, I’ve learned that it affects about 85 percent of the patients I see. In my experience, nearly seven out of eight Caucasian patients have vitamin D insufficiency or deficiency and virtually all dark-skinned patients have a deficiency, because melanin blocks endogenous production through UVB rays. This higher rate of deficiency may contribute to the increased overall illness and shorter life spans in the African-American community. [16]

Cleveland, Ohio, is located at the 41st parallel; consequently, the endogenous production of vitamin D by UVB at this latitude is seasonal, as it is in many other American cities north of Atlanta. In dark-skinned patients, the capacity to endogenously manufacture vitamin D is reduced from one-tenth to one-twentieth of that of white patients. The incidence of vitamin D deficiency in pregnant African-American women is more than 20 times higher than that of pregnant white women. [17]


Identifying Vitamin D Deficiency

During the physical examination, providers should look for symmetrical bone pain on palpation over the more thin-skinned areas—the medial aspect of the proximal tibias, over the distal radii, the clavicles and sternum, where there is often less subcutaneous fat. Palpation of these bony areas may reveal some bone tenderness and a boggy periosteal elevation.

In assessing a patient’s need for a vitamin D blood test, review and discuss:

  • bowel habits in terms of malabsorption issues

  • alcohol and medication use

  • weekly sun exposure

  • dietary sources of vitamin D, such as oily fish or dairy or orange juice enriched with vitamin D.


To confirm a vitamin D deficiency or insufficiency and to make the diagnosis, laboratory measurements of serum 25-hydroxyvitamin D, or [25(OH) D], are used. [18] This testing is essential to differentiate vitamin D deficiency from more commonly seen musculoskeletal complaints and impaired neuromuscular functioning. [19, 20]

The same testing should be used periodically to monitor therapy in the clinical management of the deficient patient. It may be necessary to measure, by label dose, the total vitamin D intake from any supplements, prior to initiating therapy

The ICD-9-CM diagnosis code 268.9 describes unspecified vitamin D deficiency. Supplementation with oral vitamin D3 is used to achieve a normal serum level of 25-hydroxyvitamin D, and repletion often results in dramatic relief of chronic pain symptoms


Treating Vitamin D Deficiency

The current official government recommendations are not effective in preventing or treating vitamin D deficiency. At this time, assessing serum [25(OH)D] is the only way to make the diagnosis of a deficiency state and to ensure that treatment is adequate and remains safe. Vitamin D scientists believe that treatment should be sufficient to maintain levels found in humans living naturally in a sun-rich environment, which are greater than 40 ng/mL, year-round. [13, 21, 22]

Three treatment modalities for vitamin D repletion include reasonable amounts of sunlight, artificial ultraviolet B radiation or oral vitamin D3 supplementation. In the case of vitamin D deficiency, the benefits of all three treatment modalities outweigh potential risks and greatly outweigh the risk of no treatment. As many of us experience a prolonged “vitamin D winter,” at more temperate latitudes, 5,000 IU of vitamin D per day may be required to maintain a normal blood level year-round. Obese, aged or dark-skinned patients may need far more vitamin D to maintain adequate blood levels during the winter; higher dosages may make inexperienced physicians uncomfortable. [11, 13, 21]

Most patients with serious illnesses can benefit from vitamin D supplementation as an adjunctive treatment—never replacing any necessary standard medical care. [2] These patients typically need more aggressive supplementation than well patients. These patients also require more frequent monitoring of their serum [25(OH)D], as well as serum calcium and magnesium levels.

The Vitamin D Council (www.vitaminDCouncil.org) recommends that patients take up to 1,000 IU of vitamin D3 per 25 pounds of body weight. I have found that this will help most patients maintain a normal year-round level of 70 to 80 ng/ml. This dosage is safe for men, women and children, unless there are contraindications; infants need smaller amounts proportional to their size. The council also recommends that pregnant and lactating women take at least 4,000 IU of vitamin D3 per day.


Contraindications

Vitamin D hypersensitivity is a rare syndrome that occurs when abnormal tissue alters the kidney's normal regulation of 1,25-dihydroxyvitamin Dor calcitriolproduction. This can cause an elevation of serum calcium, or hypercalcaemia. The most common contraindications for vitamin D supplementation include sarcodosis, oat cell carcinoma of the lung, non-Hodgkin's lymphoma or other granulomatous illness, or primary hyperparathyroidism. [20]


Conclusion

Helping patients maintain normal year-round serum vitamin D levels above the lower limit of 40 ng/mL is a primary care function that can be easily performed by DCs and is an important public health task. [11, 15, 19, 21, 23]


Dr. David C. Radford is currently the director of Chiropractic Clinic of Solon in Solon, Ohio (www.backtalk.ws). He also works as a member of a multidisciplinary team of spine specialists associated with Lutheran Hospital, a division of the Cleveland Clinic Health System. He can be reached at dradford@backtalk.ws.


References:

1.   Holick MF. Vitamin D and sunlight: Strategies for cancer prevention and other health benefits.
Clin J Am Soc Nephrol 2008;3:1548-1554.

2.   Turner MK, Hooten M, Schmidt JE, Kerkvliet Jl, Townsend CO, Bruce BK. Prevalence and clinical correlates of vitamin D inadequacy among patients with chronic pain.
Pain Med. 2008 Nov;9(8):979-984.

3.   Holick MF. Vitamin D deficiency.
NEJM 2007;357(3):266-81.

4.   Cannell JJ. Autism and vitamin D.
Med Hypotheses. 2008;70(4):750-9.

5.   Lips P. Vitamin D physiology.
Progress Biophysics Mol Biol. 2006 Sep;92(1):4-8.

6.   Stryer L. Biochemistry, 4th ed. W.H. Freeman, 1995. (Chapter 27 pg. 702)

7.   The National Institute of Standards and Technology (NIST). Standard Reference Data Program. NIST, 100 Bureau Drive, Stop 2300, Gaithersburg, MD 20899-2300.

8.   Hollis BW, Wagner CL, Drezner MK, Binkley NC. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status.
J Steroid Biochem Mol Biol. 2007 March;103(3-5):631–634.

9.   Holick MF. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis.
Am J Clin Nutr. 2004;79(3):362-371.

10.   Kumar V. The Pathological Basis of Disease, 7th ed. Robbins and Cotran, 2005. Chapter 9, p. 452.

11.   Turner MK, Hooten WM, Schmidt JE, Kerkvliet JL, Townsend CO, Bruce BK.

Prevalence and clinical correlates of vitamin D inadequacy among patients with chronic pain.
Pain Med. 2008 Mar 11.

12.   Evatt ML, DeLong MR, et al. Prevalence of vitamin D insufficiency in patients with Parkinson disease and Alzheimer disease.
Arch Neurol. 2008;65(10):1348-1352.

13.   Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Diagnosis and treatment of vitamin D deficiency.
Exp Opinn Pharmacother. 2008 Jan;9(1):107-18.

14.   Cannell JJ, Hollis BW. Use of vitamin D in clinical practice.
Alternative Medicine Review. 2008 Mar;13(1):6-20.

15.   Holick MF. High prevalence of vitamin D inadequacy and implications for health.
Mayo Clinic Proceedings. 2006 Mar;81(3):353-73.

16.   Dawson-Hughes B. Racial/ethnic considerations in making recommendations for vitamin D for adult and elderly men and women.
Am J Clin Nutr. 2004 Dec;80 (6 Suppl):1763S-6S.

17.   Nesby-O'Dell S, Scanlon KS, et al. Hypovitaminosis D prevalence and determinants among African American and white women of reproductive age: third National Health and Nutrition Examination Survey, 1988-1994.
Am J Clin Nutr. 2002 Jul;76(1):187-92.

18.   Malabanan A, Veronikis IE, Holick MF, Redefining vitamin D insufficiency.
Lancet.1998 Mar 14;351(9105):805-6.

19.   Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Diagnosis and treatment of vitamin D deficiency.
Exp Opin Pharmacother. 2008 Jan;9(1):107-18.

20.   Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr. 1999 May;69(5):842-856.

21.   Holick MF. Vitamin D: A millennium perspective.
J Cell Biochem. 2003;88 (2):296-307.

22.   Boron WF, Boulpaep EL. Medical Physiology, A Cellular and Molecular Approach, 2003. Chapter 51, pp. 1095-1098.

23.   Holick MF. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis.
Am J Clin Nutr. 2004;79(3):362-371.



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