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Guessing What's Next for Vitamin D

Tracking seasonal changes with certain conditions can shed some light on when to increase vitamin D intake.

By Jacob Schor, ND

In the 30 years since I took Nutrition 101, few changes compare in magnitude to the ones we have seen in vitamin D research. Back then, vitamin D was for rickets. Now, it's good for almost everything.

Dr. Alex Vasquez deserves credit for changing the way I think about vitamin D; when he called D's new status a paradigm shift, he was correct. I now use vitamin D for a wider range of conditions and in higher doses than I ever thought possible.1

Hallmarks of D Deficiency

There are two hallmarks to vitamin D-related conditions; disease incidence varies by latitude and season. This certainly is true with the conditions we already associate with D deficiency. Heart attacks are more common in the winter months.2,3 Multiple sclerosis, the classic example of latitude variability, increases in frequency with distance from the equator. And, of course, MS now is associated with D deficiency.4 Other autoimmune disorders also are linked to low D levels.5 Diabetes is so closely affected by D that blood sugar levels fluctuate by month of the year, hitting their highest point in the late winter and spring, when D status is lowest.6,7 Onset of diabetes also varies seasonally, with the fewest cases diagnosed in August and the most cases diagnosed in March.8 I've been ruminating what other conditions might be related to D deficiency that are not yet on my list. The easiest way to gather data for these ruminations is to rummage on PubMed under the rudimentary headings of "season" and "latitude." It's surprising what comes to light.

Everything Cardio

It's not just heart attacks that fluctuate by season. Apparently, anything that has to do with a person's cardiovascular plumbing is at risk in the winter. This includes atrial fibrillation,9 heart failure,10 DVT,11 pulmonary embolism,12,13 aortic rupture,14,15 cervical artery dissection17 and blood pressure.18 (Though there is an argument that aortic ruptures can be triggered by low air pressure, which probably is more frequent in the winter.16 If this were true, we'd probably hear more about people having serious problems driving west up Interstate 70 from Denver toward the Continental Divide.)

One suggested explanation for these elevated cardiovascular problems in winter is that blood gets thicker because of the higher incidence of colds and flu, triggering hypercoagubility. It turns out this isn't true. When a long list of blood parameters were monitored for seasonal variability, only HDL cholesterol and cortisol showed inverse seasonal patterns, with a maximum during summertime. No statistically significant seasonal variations were seen for red blood cell aggregation, complement factor C4, total cholesterol, ceruloplasmin, haptoglobin, white blood cell count and plasminogen. The researchers who originally posed this question concluded, "These data do not support the hypothesis that increased morbidity and mortality from cardiovascular diseases during winter may be mainly attributable to increased synthesis of acute-phase proteins due to infections."19 So, perhaps it is wintertime decreases in vitamin D levels that trigger all of these cardio problems.

Most Inflammatory Stuff

Many inflammatory conditions fluctuate with season. Pancreatitis20 is seasonal, as it is more common in the spring. So, too, is gout. Frequency of gout attacks vary by season,21 peaking in the spring.22-24 Appendicitis also varies by season but peaks in the summer, July to be exact.25 It's rare for me to treat appendicitis, so I'll hold off trying to rationalize how it can be related to D deficiency. But there is no question my gout patients now take extra vitamin D. Myofascial pain varies with season, peaking during the dark months.26

Inflammatory Bowel Diseases

The inflammatory bowel diseases appear linked to vitamin D. In an Italian study, the onset of Crohn's disease is most common in spring and summer.27 With Crohn's disease, it matters what time of year you were born. If born in May and June, you have less of a chance of developing Crohn's, but being born from September to January increases your chance of getting Crohn's.28-30 Wonder why? Either this has to do with one's mother's vitamin D level just prior to delivery, or the kid's vitamin D level in the first months of life. Maybe it's not the summer low incidence of Crohn's that's important, but the winter increase. Infants born in the winter start out with a lower maternal D donation and will find it difficult to produce their own D during their first months of life. The developing immune system might be handicapped by this early deficiency for the rest of life. What about latitude? Aside from the fact that Crohn's disease incidence is higher in northern Scotland than in southern Scotland,31 not much else came to light. Whatever the explanation, making sure pregnant patients have adequate D when they give birth might change an infant's fate. We already know that supplementing vitamin D to pregnant women lowers the incidence of diabetes in their children.32-33

Ulcerative colitis (UC) also has a seasonal variability, with attacks occurring most often from December to January.34 Curiously, this seasonal variation is not seen on the inside; diagnosing UC via endoscopic exams doesn't show variability with season. Only symptom onset varies.35 Vitamin D suppresses bowel inflammation in animal models. Creating mice missing receptor sites for vitamin D creates mice incredibly susceptible to inflammatory bowel disease.36 In an experiment using these mice bred to develop inflammatory bowel disease (IBD), vitamin D prevented disease development.37 This might have something to do with vitamin D's interaction with interleukin-2. In another one of these animal model experiments, in which mice were bred without the IL-2 gene, D was no longer effective at suppressing ulcerative colitis. D-3 nonetheless did lower the mortality rates of these poor mice.38

Mice bred to get UC do much better if given both D and calcium. Either one of these supplements prevents or reduces the symptoms of disease by inhibiting TNF-alpha, which then suppresses the IBD.39 TNF-alpha is one of those big important things in medicine we are supposed to understand these days and inhibiting it generally is considered a very useful thing to do. The National Institutes of Health Web site (www.nih.gov) links elevated TNF-alpha to a host of conditions, including psoriasis, tuberculosis, insulin resistance, diabetes, obesity, hyperadrogenism, cerebral malaria, alopecia areata, rheumatoid arthritis, ankylosing spondylitis, osteoporosis, osteopenia, asthma, inflammatory bowel disease and hepatitis.40 Drugs such as infiiximab (Remicade) and etanercept (Enbrel), which block TNF-alpha, are all the rage. If vitamin D lowers TNF-alpha, it might help any of these conditions. There is one difference we already are aware of: Blocking TNF-alpha via drugs increases the risk of tuberculosis41 while vitamin D is useful at preventing and treating tuberculosis.42 Inflammatory bowel disease is a disease of the Western world. Perhaps our higher rates simply are due to more time spent indoors and resulting lower vitamin D levels.

Editor's note: Look for part two of "Guessing What's Next for Vitamin D" in the December 2006 issue of Naturopathy Digest.

References

  1. Vasquez, A, et al. The clinical importance of vitamin D (cholecalciferol): a paradigm shift with implications for all healthcare providers. Altern Ther Health Med 2004 Sep-Oct;10(5):28-36.
  2. Manfredini R, et al. Seasonal variation in onset of myocardial infarction - a 7-year single-center study in Italy. Chronobiol Int 2005;22(6):1121-35.
  3. Gonzalez Hernandez E, et al. [Seasonal variations in admissions for acute myocardial infarction. The PRIMVAC study] Rev Esp Cardiol 2004 Jan;57(1):12-9.
  4. Ponsonby, AL, et al. UVR, vitamin D and three autoimmune diseases - multiple sclerosis, type 1 diabetes, rheumatoid arthritis. Photochem Photobiol 2005 Nov/Dec;81(6):1267-75.
  5. Cantorna, MT. Vitamin D and autoimmunity: Is vitamin D status an environmental factor affecting autoimmune disease prevalence? Proc Soc Exp Biol Med, 2000 Mar;223(3):230-3.
  6. American Journal of Epidemiology 2005;161(6):565-574; doi:10.1093/aje/kwi071.
  7. Jarrett RJ, et al. Screening blood glucose values: effects of season and time of day. Diabetologia 1984 Dec;27(6):574-7.
  8. Péter Doró, MPharm, Ria Benk , MPharm, Mária Matuz, MPharm, and Gyöngyvér Soós. PhD. Seasonality in the incidence of type 2 diabetes. Diabetes Care 2006;29:173.
  9. Murphy NF, et al. Seasonal variation in morbidity and mortality related to atrial fibrillation. Int J Cardiol 2004 Nov;97(2):283-8.
  10. Stewart S, et al. Heart failure in a cold climate. Seasonal variation in heart failure-related morbidity and mortality. J Am Coll Cardiol 2002 Mar 6;39(5):760-6.
  11. Gallerani M, et al. Seasonal variation in the occurrence of deep vein thrombosis. Med Sci Monit 2004 May;10(5):CR191-6.
  12. Manfredini R, Gallerani M, et al. Seasonal variation in onset of pulmonary embolism is independent of patients' underlying risk comorbid conditions. Clin Appl Thromb Hemost 2004 Jan;10(1):39-43.
  13. Bilora F, et al. Chronobiology of non fatal pulmonary thromboembolism. Panminerva Med 2001 Mar;43(1):7-10.
  14. Manfredini R, et al. Seasonal variation in the occurrence of nontraumatic rupture of thoracic aorta. Am J Emerg Med 1999 Nov;17(7):672-4.
  15. Mehta RH, et al. Chronobiological patterns of acute aortic dissection. Circulation 2002 Aug 27;106(9):1110-5.
  16. Harkin DW, et al. Periods of low atmospheric pressure are associated with high abdominal aortic aneurysm rupture rates in Northern Ireland. Ulster Med J 2005 Sep;74(2):113-21.
  17. Paciaroni M, et al. Seasonal variability in spontaneous cervical artery dissection J Neurol Neurosurg Psychiatry 2006 May;77(5):677-9.
  18. Rostand SG. Ultraviolet light may contribute to geographic and racial blood pressure differences. Hypertension 1997 Aug;30(2 Pt 1):150-6.
  19. Frohlich M, et al. Seasonal variations of rheological and hemostatic parameters and acute-phase reactants in young, healthy subjects. Arterioscler Thromb Vasc Biol 1997 Nov;17(11):2692-7.
  20. Gallerani M, et al. Seasonal variation in the onset of acute pancreatitis. World J Gastroenterol 2004 Nov 15;10(22):3328-31.
  21. Schlesinger N, et al. Acute gouty arthritis is seasonal: possible clues to understanding the pathogenesis of gouty arthritis. Clin Rheumatol. 2005 Aug;11(4):240-2.
  22. Schlesinger N, et al. Acute gouty arthritis is seasonal. J Rheumatol 1998 Feb;25(2):342-4.
  23. Gallerani M, et al. Seasonal variation in the onset of acute microcrystalline arthritis. Rheumatology (Oxford) 1999 Oct;38(10):1003-6.
  24. Gallerani M, et al. Seasonal variation in onset of acute appendicitis. Clin Ter 2006 Mar-Apr;157(2):123-7.
  25. Gallagher RM, et al. Calcium and 1 alpha, 25-dihydroxyvitamin D3 target the TNF-alpha pathway to suppress experimental inflammatory bowel disease. Pain 1995 Apr;61(1):113-20.
  26. Aratari A, et al. Seasonal variations in onset of symptoms in Crohn's disease. Dig Liver Dis 2006 May;38(5):319-23. Epub 2005 Nov 10.
  27. Mikulecky M, et al. Chronobiological aspects of adult-onset Crohn disease. Wien Klin Wochenschr 2005 Jun;117(11-12):423-8.
  28. Chowers Y, et al. The month of birth is linked to the risk of Crohn's disease in the Israeli population. Am J Gastroenterol 2004 Oct;99(10):1974-6.
  29. Van Ranst M, et al. Crohn's disease and month of birth. Inflamm Bowel Dis 2005 Jun;11(6):597-9.
  30. Armitage EL, et al. Incidence of juvenile-onset Crohn's disease in Scotland: association with northern latitude and affluence. Gastroenterology 2004 Oct;127(4):1051-7.
  31. Stene LC, et al. Use of cod liver oil during pregnancy associated with lower risk of Type I diabetes in the offspring. Diabetologia 2000 Sep;43(9):1093-8.
  32. Hypponen E, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet 2001 Nov 3;358(9292):1500-3.
  33. Moum B, et al. Seasonal variations in the onset of ulcerative colitis. Gut 1996 Mar;38(3):376-8.
  34. Auslander JN, et al. Lack of seasonal variation in the endoscopic diagnoses of Crohn's disease and ulcerative colitis. Am J Gastroenterol 2005 Oct;100(10):2233-8.
  35. Froicu M, et al. A crucial role for the vitamin D receptor in experimental inflammatory bowel diseases. Mol Endocrinol 2003 Dec;17(12):2386-92. Epub 2003 Sep 18.
  36. Cantorna MT, et al. 1, 25-Dihydroxycholecalciferol prevents and ameliorates symptoms of experimental murine inflammatory bowel disease. J Nutr 2000 Nov;130(11):2648-52.
  37. Bemiss CJ, et al. Interleukin-2 is one of the targets of 1, 25-dihydroxy vitamin D3 in the immune system. Arch Biochem Biophys 2002 Jun 15;402(2):249-54.
  38. Zhu Y, et al. Calcium and 1 alpha, 25-dihydroxyvitamin D3 target the TNF-alpha pathway to suppress experimental inflammatory bowel disease. Eur J Immunol 2005 Jan;35(1):217-24.
  39. NIH Web site: www.nih.gov.
  40. "Tuberculosis Associated with Blocking Agents Against Tumor Necrosis Factor-Alpha - California, 2002-2003." Click to view it online.
  41. Liu PT, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science 2006 Mar 24;311(5768):1770-3. Epub 2006 Feb 23.
  42. Cagnacci A, et al. Season of birth influences the timing of menopause. Hum Reprod 2005 May 12.

About the Author: Jacob Schor, ND, graduated with a Bachelor of Science degree from Cornell University and received his naturopathic training at National College of Naturopathic Medicine. He currently practices at the Denver Naturopathic Clinic. E-mail Dr. Schor at DrJacobSchor1@msn.com.



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Date Last Modified - Friday, 17-Oct-2008 12:10:49 PDT