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Alternative Explanation of one aspect of Treatment for CFIDS/FM/RA

The treatment consists of:

  • Reduction of vitamin D intake
  • Use of Benicar, a member of the Angiotensin Receptor Blockers family of drugs
  • Antibiotics

This note examines only the Vitamin D aspect of this protocol.

Impact of Vitamin D reduction

Vitamin D is an important immune system regulator[1]. Its impact on Multiple Sclerosis, an autoimmune disease, has been well studied with the following generally accepted:

  • Low levels are associated with onset[2]
  • Injections of vitamin D hormone could protect against or arrest the animal forms of Multiple Sclerosis[3]
  • Risk of death is significantly reduced with increased Sunlight Exposure[4]

Vitamin D has been identified as a significant factor for incidence of several autoimmune illnesses such as multiple sclerosis, rheumatoid arthritis, insulin-dependent diabetes mellitus, and inflammatory bowel disease[5]. Significant improve from taking vitamin D has been reported for several autoimmune illnesses, for example rheumatoid arthritis[6] and lupus[7]. One studies of Vitamin D in CFIDS patients could be located [See Below], experience CFIDS MD, such as Dr. Teitelbaum, often recommend 600UI of vitamin D[8]. Studies of fibromyalgia and persistent, nonspecific musculoskeletal pain have found that low levels of vitamin D is common[9]. The literature strongly suggests vitamin D supplementation.

The advising an intentional reduction of vitamin D appears to fly in the face of this literature. What is going on?


The anecdotal reports from people trying a new alternative treatment for Chronic Fatigue  have two characteristics:

  • Reduction of symptoms with the reduction of vitamin D
  • Significant Herxheimer reactions occurring from as little as 1-3 mg of antibiotics that did not produce a Herxheimer at 100-300mg prior to the reduction of vitamin D.

Other anecdotal reports of weight gain and muscle weakness are consistent with vitamin 1,25D deficiency.

This suggests the following model may be actually happening with CFIDS patients attempting this treatment:

  1. Reduction of vitamin D results in suppression of the immune system and thus the immune response
    1. Since symptoms in CFIDS appear to be an immune response, shutting down the immune systems should reduce symptom intensity.
  2. Suppression of the immune system allows existing infections to spread with only token resistance from the immune system. Most of the infections associated with CFIDS do not have symptoms directly caused by them; rather the symptoms arise from the immune system response (which has now been suppressed).
    1. When antibiotics are applied, the degree of infection is far more severe than prior producing a far more intense herxheimer reaction.
    2. There may not be any obvious signs of this increase of infection because the infections are not directly producing the symptoms.

If this model is correct, then the patient will be subject to significant growth and establishment of other infections, including virii associated with cancers, as well as increased risk of diabetes from both weight gain and low vitamin D levels.


MDs considering the for any patient should exercise caution about tolerating vitamin D reduction. If there are multiple conditions present, the net result may be counter to the patient’s best interest. Regular monitoring of vitamin D levels in patients prescribed Benicar is strongly recommended since there is a significant risk of non-compliance for prescribed vitamin D supplements.


Ken Lassesen, M.S.



[1] Zhu, Monica Froicu, and Anja Wittke Vitamin D status, 1,25-dihydroxyvitamin D3 and the Immune System, Margherita T Cantorna, Yan Am J Clin Nutr 2004;80(suppl):1717S–20S.

 [2] Goldberg, P., Multiple Sclerosis: vitamin D and calcium as environmental determinants of prevalence. Part 1: Sunlight, dietary factors and epidemiology. Intern. J. Environmental Studies, v. 6, p. 19-27, 1974.  Goldberg, P., Multiple Sclerosis: vitamin D and calcium as environmental determinants of prevalence. Part 2: Biochemical and genetic factors. Intern. J. Environmental Studies, v. 6, p.121-129, 1974.

[3] Lemire, J. and Archer, D., 1991, 1,25-dehydroxyvitamin D3 prevents the in vivo induction of murine experimental autoimmune encephalomyelitis. J. Clin. Invest., v. 87, p. 1103-1107.

[4] D Michal Freedmana, Mustafa Dosemecib, Michael C R Alavanjab Mortality from multiple sclerosis and exposure to residential and occupational solar radiation: a case-control study based on death certificates. Occup Environ Med 2000;57:418-421

[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.

Cantorna MT, Mahon BD. Mounting evidence for vitamin D as an environmental factor affecting autoimmune disease prevalence. Exp Biol Med (Maywood). 2004 Dec;229(11):1136-42.

[6] Cantorna, M., Hayes, C. and DeLuca, H., 1,25-Dihydroxycholecalciferol inhibits the progression of arthritis in murine models of human arthritis. Journal of Nutrition, v. 128, p. 68-72. 1998

[7]  Lemire JM, Ince A, Takashima M. 1,25-Dihydroxyvitamin D3 attenuates the expression of experimental murine lupus of MRL/l mice. Autoimmunity. 1992;12(2):143-8.


[9] Al-Allaf AW, Mole PA, Paterson CR, Pullar T. Bone health in patients with fibromyalgia.

Rheumatology (Oxford). 2003 Oct;42(10):1202-6. Epub 2003 Jun 16.

Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain Mayo Clin Proc. 2003 Dec;78(12):1463-70.

Hack AD. Divalent Cations, Hormones, Psyche and Soma: Four Case Reports Journal of Chronic Fatigue Syndrome 2000; 6(3/4): 117

Objectives: The steroid hormone, vitamin D and the peptide hormone, parathormone are reported to influence not only bone metabolism, but also other metabolic and nervous, cardiovascular and immune functions, and mood. Regular actions of these hormones depend highly on intracellular magnesium content. Although symptoms are recognized, they usually are not correlated to these hormones. Foregoing case studies have revealed that vitamin D and/or parathormone disorders are common causes of CFS-fibromyalgia like symptoms. Methods: Four patients with chronic fatigue-like symptoms and vitamin D (25OHD3) and parathormone (PTH intact) disorders are illustrated to demonstrate conflicting laboratory results. Patients were treated with 5,000 to 10,000 IU cholecalciferol, plus multiminerals and trace elements. Clinical outcome was assessed and treatment difficulties are reported.

Results: Diagnostic pitfalls are shown. Vitamin D and parathormone disorders are not completely detectable by calcium and phosphate screening. In 2 of this 4 demonstrated cases treatable diagnosis would have been missed without endocrinological screening. In the case of undetected long-standing disorder of these hormones, intracellular mineral derangement follows, thus inducing vitamin D resistance and parathormone ineffectiveness which makes therapy difficult. Combining vitamin D therapy with multiminerals possibly may overcome these obstacles.

Conclusions: Vitamin D and parathormone disturbance should not be overlooked in chronic fatigue. Appropriate therapy is easy, inexpensive and harmless. Early diagnosis and treatment might be essential to avoid chronic fatigue syndrome. The complexity of diagnosis, therapy and scientific background may lead to a new understanding of ``psycho-somatic'' disease. The relation between intracellular minerals, trace elements, cellular energy supply and responsible hormones should become clearer.



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