• Answers to question about restless leg syndrome

    Posted February 14, 2019: by Bill Sardi

    Q: My wife, 66, has suffered for a few years now with sever night-time leg cramps which affect her sleep. We’ve tried a dozen different magnesium supplements, potassium, and other electrolytes all with no affect. Magnesium Chloride baths, foot baths, and sprays—no improvement. Any recommendations?

    REPLY:

    Unabated restless leg is fairly common.

    Requires some further investigation as there are different causes of the same thing.

    1. See reference #1 below — Vitamin D.  Try 10,000 IU/day.  May mean magnesium isn’t working without vitamin D, so take magnesium with D3 (mag oxide is insoluble and almost useless; only 4% absorbed).
    2. Reference #2 below suggests zinc therapy.   30 mg of zinc (zinc oxide is insoluble; use another form). Vitamin B6 improves zinc absorption and selenium releases zinc
    3. Reference #3 below.  Unhealthy gut bacteria may induce lactic acid secretion and induce restless leg.  Try oral vitamin B1 in fat soluble form (benfotiamine) which counters lactic acid buildup.
    4. Reference #4. Restless leg associated with bacterial overgrowth, i.e. Candida (yeast) from refined sugar intake most likely.  Use stevia and/or inositol powder as non-caloric sweeteners.  Embark on natural antibiotic therapy — oil of oregano regimen, 3 capsules 3 times a day for 2 weeks.  Consume fermented foods (sauerkraut, unsweetened pickles, miso soup) and/or probiotics (Dr. Ohira’s is a good brand)
    5. Reference #2 & #5 refer to unavailability of iron and restless leg.  Iron pills are usually problematic and induce nausea and constipation in these instances because chronic inflammation, often in the kidneys, binds up iron in a protein called ferritin.  One would consume iron-rich foods (red meat, highly absorbable) along with ascorbic acid form of vitamin C to improve iron absorption and increase release of iron from the kidneys to produce more red blood cells (erythropoiesis) and therefore halt the iron deprivation which results in a decline in red blood cells and oxygen delivery to leg muscles which then results in leg muscle spasms.

     

    Hope this helps.

    Bill Sardi
    Knowledge of Health

    #1

    Acta Neurol Belg. 2015 Dec;115(4):623-7. doi: 10.1007/s13760-015-0474-4. Epub 2015 Apr 23.

    An evaluation of sleep quality and the prevalence of restless leg syndrome in vitamin D deficiency.

    Abstract

    Vitamin D is known to increase levels of dopamine and its metabolites in the brain and also protects dopaminergic neurons against dopaminergic toxins. The aims of the study were to assess the frequency and symptom severity of restless leg syndrome (RLS) and sleep quality in vitamin D deficiency. A total of 102 patients were enrolled in this cross-sectional study, comprising 57 vitamin D deficient patients as Group 1 and 45 patients with normal levels of vitamin D as Group 2. RLS was diagnosed according to the International RLS Study Group (IRLSSG) diagnostic criteria. Symptom severity was assessed using the IRLSSG rating scale and sleep quality was measured with the Pittsburgh sleep quality index (PSQI). RLS incidence was higher in Group 1 (p = 0.034). The PSQI scores were higher in Group 1 and the difference between the groups was determined as statistically significant (p < 0.05). No statistically significant difference was determined in respect of the clinical evaluation and the IRLSSG Symptom Severity Scale between the patients in Group 1 diagnosed with RLS and the patients in Group 2 diagnosed with RLS (p > 0.05). The findings of this study support the hypothesis that RLS is more frequent and more severe in vitamin D deficiency and indicate a negative effect of vitamin deficiency on sleep parameters.

    #2

    Ann Hematol. 2016 Apr;95(5):751-6. doi: 10.1007/s00277-016-2628-8. Epub 2016 Mar 2.

    Serum zinc levels in patients with iron deficiency anemia and its association with symptoms of iron deficiency anemia.

    Abstract

    Iron deficiency anemia (IDA) is a major public health problem especially in underdeveloped and developing countries. Zinc is the co-factor of several enzymes and plays a role in iron metabolism, so zinc deficiency is associated with IDA. In this study, it was aimed to investigate the relationship of symptoms of IDA and zinc deficiency in adult IDA patients. The study included 43 IDA patients and 43 healthy control subjects. All patients were asked to provide a detailed history and were subjected to a physical examination. The hematological parameters evaluated included hemoglobin (Hb); hematocrit (Ht); red blood cell (erythrocyte) count (RBC); and red cell indices mean corpuscular volume (MCV), mean corpuscular hemoglobin (МСН), mean corpuscular hemoglobin concentration (МСНС), and red cell distribution width (RDW). Anemia was defined according to the criteria defined by the World Health Organization (WHO). Serum zinc levels were measured in the flame unit of atomic absorption spectrophotometer. Symptoms attributed to iron deficiency or depletion, defined as fatigue, cardiopulmonary symptoms, mental manifestations, epithelial manifestations, and neuromuscular symptoms, were also recorded and categorized. Serum zinc levels were lower in anemic patients (103.51 ± 34.64 μ/dL) than in the control subjects (256.92 ± 88.54 μ/dL; <0.001). Patients with zinc level <99 μ/dL had significantly more frequent mental manifestations (p < 0.001), cardiopulmonary symptoms (p = 0.004), restless leg syndrome (p = 0.016), and epithelial manifestations (p < 0.001) than patients with zinc level > 100 μ/dL. When the serum zinc level was compared with pica, no statistically significant correlation was found (p = 0.742). Zinc is a trace element that functions in several processes in the body, and zinc deficiency aggravates IDA symptoms. Measurement of zinc levels and supplementation if necessary should be considered for IDA patients.

    #3

    J Med Food. 2014 Dec;17(12):1261-72. doi: 10.1089/jmf.2014.7000.

    The gut microbiome and the brain.

    Galland L1.

    Author information

    Abstract

    The human gut microbiome impacts human brain health in numerous ways: (1) Structural bacterial components such as lipopolysaccharides provide low-grade tonic stimulation of the innate immune system. Excessive stimulation due to bacterial dysbiosis, small intestinal bacterial overgrowth, or increased intestinal permeability may produce systemic and/or central nervous system inflammation. (2) Bacterial proteins may cross-react with human antigens to stimulate dysfunctional responses of the adaptive immune system. (3) Bacterial enzymes may produce neurotoxic metabolites such as D-lactic acid and ammonia. Even beneficial metabolites such as short-chain fatty acids may exert neurotoxicity. (4) Gut microbes can produce hormones and neurotransmitters that are identical to those produced by humans. Bacterial receptors for these hormones influence microbial growth and virulence. (5) Gut bacteria directly stimulate afferent neurons of the enteric nervous system to send signals to the brain via the vagus nerve. Through these varied mechanisms, gut microbes shape the architecture of sleep and stress reactivity of the hypothalamic-pituitary-adrenal axis. They influence memory, mood, and cognition and are clinically and therapeutically relevant to a range of disorders, including alcoholism, chronic fatigue syndrome, fibromyalgia, and restless legs syndrome. Their role in multiple sclerosis and the neurologic manifestations of celiac disease is being studied. Nutritional tools for altering the gut microbiome therapeutically include changes in diet, probiotics, and prebiotics.

    #4

    Dig Dis Sci. 2008 May;53(5):1252-6. Epub 2007 Oct 13.

    Restless legs syndrome in patients with irritable bowel syndrome: response to small intestinal bacterial overgrowth therapy.

    Abstract

    BACKGROUND: 

    Small intestinal bacterial overgrowth (SIBO) occurs in irritable bowel syndrome (IBS) and fibromyalgia. Since restless legs syndrome (RLS) occurs with fibromyalgia, a link between IBS, SIBO, and RLS was studied.

    METHODS: 

    BS patients with abnormal lactulose breath tests received rifaximin 1,200 mg day(-1) for 10 days, followed by tegaserod 3 mg, long-term, and 1 month of zinc 220 mg day(-1) and once-daily probiotic (N = 11) or rifaximin monotherapy (N = 2). IBS symptom improvement was assessed after rifaximin. RLS symptoms, IBS symptoms, and overall IBS global improvement were assessed at last posttreatment visit: 8/10 patients were followed long-term (mean, 139 days; range, 54-450 days).

    RESULTS: 

    Ten of 13 patients exhibited > or =80% improvement from baseline in RLS symptoms. Five maintained complete resolution of RLS symptoms. Global gastrointestinal symptom improvement was great (n = 6), moderate (n = 5), or mild (n = 2).

    CONCLUSION: 

    This study suggests that SIBO associated with IBS may be a factor in some RLS patients and SIBO therapy provides long-term RLS improvement.

    #5

    Expert Rev Clin Pharmacol. 2018 Dec 2. doi: 10.1080/17512433.2019.1555468. [Epub ahead of print]

    Neurologic conditions and disorders of uremic syndrome of chronic kidney disease: Presentations, causes and treatment strategies.

    Abstract

    Uremic syndrome of chronic kidney disease (CKD) is a term used to describe clinical, metabolic and hormonal abnormalities associated with progressive kidney failure. It is a rapidly growing public health problem worldwide. Nervous system complications occur in every patient with uremic syndrome of CKD. Areas covered: This review summarized central and peripheral nervous system complications of uremic syndrome of CKD and their pathogenic mechanisms. They include cognitive deterioration, encephalopathy, seizures, asterixis, myoclonus, restless legsyndrome, central pontine myelinosis, stroke, extrapyramidal movement disorders, neuropathies and myopathy. Their pathogenic mechanisms are complex and multiple. They include (1) accumulation of uremic toxins resulting in neurotoxicity, blood brain barrier injury, neuroinflammation, oxidative stress, apoptosis, brain neurotransmitters imbalance, ischemic/microvascular changes and brain metabolism dysfunction [e.g. dopamine deficiency], (2) metabolic derangement [as acidosis, hypocalcemia, hyperphosphatemia, hypomagnesemia and hyperkalemia]; (3) secondary hyperparathyroidism, (4) erythropoietin and iron deficiency anemia, (5) thiamin, vitamin D and other nutritional deficiencies, (6) hyperhomocysteinemia, and (7) coagulation problems. Expert Commentary: Nervous system complications of uremia contribute to the patients’ morbidity and mortality. Optimizing renal replacement therapy, correction of associated metabolic and medical conditions and improved understanding of possible pathogenic mechanisms of these complications is a major target for their prevention and treatment.

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