Tag: calcium

Will vitamin D supplementation ameliorate diseases characterized by chronic inflammation and fatigue?

Abstract:

Chronic NF-κB activation has been supposed as a key event in chronic fatigue syndrome (CFS) and many other better-defined pro-inflammatory diseases. Knowledge about the impact of deficiency vitamin D on chronic NF-κB activation could open a new disease approach. Whereas NF-κB activation leads at first to a pro-inflammatory immune response, later on a vitamin D-dependent anti-inflammatory response ensues. Binding of the active vitamin D metabolite 1,25(OH)(2)D(3) to vitamin D receptor (VDR) yields a transcription factor which represses NF-κB activation, and additionally modulates and down-regulates adaptive, but enhances innate immune responses, and improves redox balance, thus counterbalancing inflammation on multiple levels. However, this built-in late counterbalance against inflammation works only when stores of calcium and 25(OH)D(3) are abundant. Therefore a connection between lowered vitamin D-metabolism and persistent NF-κB activation, augmented nitrosative-oxidative stress, redox imbalance, chronic inflammation, and concomitant fatigue can be postulated. In order to confirm this hypothesis, randomized controlled clinical studies about the clinical effects of supplementation of calcium and vitamin D(3) would be necessary in diseases characterized by persistent NF-κB activation and chronic inflammation and fatigue.

Copyright © 2010 Elsevier Ltd. All rights reserved.

 

Source: Hoeck AD, Pall ML. Will vitamin D supplementation ameliorate diseases characterized by chronic inflammation and fatigue? Med Hypotheses. 2011 Feb;76(2):208-13. doi: 10.1016/j.mehy.2010.09.032. Epub 2010 Oct 25. https://www.ncbi.nlm.nih.gov/pubmed/20980105

 

Tired with all those supplements?

A 37 year-old patient, who had a history of chronic fatigue syndrome (CFS), was referred to the Clinical Immunology clinic by her general practitioner (GP). Her chief complaint was of severe fatigue following a viral illness 3 months previously. Concerned by her slow recovery she had sought the advice of a private health professional, who performed a series of blood tests and told her that she had insufficient levels of several vitamins and recommended a variety of supplements. In addition to sertraline prescribed by her GP, she was taking eight nutritional supplements. Her weight was stable and she had no history of cough, night sweats, lymphadenopathy, abdominal pain, joint pain, skin rashes or change in bowel habit. Physical examination was unremarkable.

A worsening of her CFS was considered the likely reason for her increased fatigue, but a range of blood tests were requested to exclude other causes (Table 1). These showed a grossly elevated adjusted calcium (3.93 mmol/l), elevated phosphate (1.65 mmol/l) and high urea and creatinine (10.6 and 162 µmol/l, respectively) with normal alkaline phosphatase (48 u/l), and reduced parathyroid hormone (<5 pmol/l). Calcium and creatinine had been normal in blood processed by the laboratory 10 months previously (2.25 and 77 µmol/l, respectively). The patient was admitted under the care of the acute medical team and treated with intravenous fluids and 90 mg of intravenous pamidronate. Her creatinine normalized within a few days and serum calcium over 3 weeks (Figure 1).

You can read the rest of this report here: http://qjmed.oxfordjournals.org/content/104/6/531.long

 

Source: Manson AL1, Chapman N, Wedatilake Y, Balic M, Marway H, Seneviratne SL, Holloway P. Tired with all those supplements? QJM. 2011 Jun;104(6):531-4. doi: 10.1093/qjmed/hcq140. Epub 2010 Aug 13. http://qjmed.oxfordjournals.org/content/104/6/531.long (Full article)

 

Outcome in the chronic fatigue syndrome

Comment on: Follow up of patients presenting with fatigue to an infectious diseases clinic. [BMJ. 1992]

 

EDITOR,-Michael Sharpe and colleagues’ follow up study of 177 patients with chronic fatigue of uncertain origin raises several important unanswered questions, which require further investigation. Factors such as a belief that their illness followed an infection, intolerance to alcohol, and membership of a support group for patients with myalgic encephalomyelitis were all associated with an adverse prognosis. Could it be that the authors had identified patients belonging to a distinct postinfectious subgroup as many doctors maintain they do? Clearly, if this is the case future studies of this nature will have to include more objective analysis of persisting viral infection (for example, analysis of muscle biopsy specimens with the polymerase chain reaction rather than tests for VP1 antigen); immune function (for example, function of natural killer cells rather than white cell counts); and hypothalamic-pituitary-axis activity (for example, up regulation of serotonin- I receptors and basal cortisol concentrations) to see if there are characteristic abnormalities that distinguish the postinfectious subgroup.

The high incidence of intolerance to alcohol is noted as intriguing, but from personal experience, as well as from seeing many patients with a classic postinfectious fatigue syndrome, I regard this observation as an important diagnostic feature. In these patients even small amounts of alcohol cause a further deterioration in cognitive function, and I suggest that a physiological explanation may lie in the fact that alcohol increases the concentration of the neurotransmitter y-aminobutyric acid, which in turn reduces the availability of calcium ions and hence depresses brain function still further.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1883001/pdf/bmj00086-0047c.pdf

 

Source: Shepherd C. Outcome in the chronic fatigue syndrome. BMJ. 1992 Aug 8;305(6849):365. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1883001/