vit D defeicency myopathy?
470821
Correct diagnosis was made initially by a high index of suspicion, following the demonstration of clinical proximal myopathy; confirmation was made by the demonstration of low 25-hydroxyvitamin D and elevated parathyroid hormone concentrations. Treatment with vitamin D caused a resolution of body aches and pains and a restoration of normal muscle strength in 4 to 6 weeks.
617803
I had a total thyroidectomy and the parathyroids came out too (they were stuck to all the scar tissue on my thyroid from all my RAI treatments)  So..my body is totally dependent on calcium and vitamin D supplements.  I take 50 mcg Calcitriol (vit D) and 2000mg OsCal daily.  My levels are monitored every 3 mos but since having a baby, my body has changed quite a bit.  I've had 3 hypercalcemic crisis' since that time, all landing me in the ER and a nice 2 day hospital visit (10 days after birth of my daughter) with calcium levels of 16 each time (normal being 9) between having a baby, losing a lot of weight quickly (IBS) and being dehyrdated when ill I've had my share!  I'm seeing a really good endocrinologist who is supposedly the calcium expert and has run extensive testing on me.  If you live in the NY metro area, email me at mooseny35@yahoo.com and I will gladly provide you with his info.
244656
Kennedy disease (KD) or X-linked spinal-bulbar muscle atrophy is a neuromuscular disease associated with mutations of the androgen receptor (AR). Because of its endocrine manifestations related to the impairment of the AR, it can be viewed as a variation of the disorders of the androgen insensitivity syndrome (AIS). It is named after WR Kennedy, a neurologist who was among the first to describe this disease.\nContents\n[hide]\n\n    * 1 Genetics\n    * 2 Pathology\n    * 3 Signs and symptoms\n          o 3.1 Neuromuscular\n          o 3.2 Endocrine\n          o 3.3 Homozygous females\n    * 4 History\n    * 5 References\n    * 6 External links\n\n[edit]\n\nGenetics\n\nAs a sex-linked disease, KD affects males, while females are carriers. The gene for the AR is located on the X chromosome (Xq11-q12).\n[edit]\n\nPathology\n\nThe distinctive AR mutation of Kennedy disease, reported in 1991, involves multiplied CAG repeats in the first exon (trinucleotide repeats). Such a CAG repeat encodes a polyglutamine tract in a part of the androgen receptor outside of the binding sites. The more CAG repeats are present, the more severe the disease. The mechanism by which this type of mutation causes neuromuscular disease is not completely understood, specifically as complete AIS does not affect neuromuscular activity. KD may share mechanistic features with other neurodegenerative disorders that are caused by polyglutamine expansion, such as Huntington's disease.\n[edit]\n\nSigns and symptoms\n\nAges of onset and severity of manifestations in affected males vary from adolescence to old age, but most commonly develop in middle adult life. The latest onset was described in a male of 84 years of age. KD does not usually compromise longevity. The syndrome has neuromuscular and endocrine manifestations:\n[edit]\n\nNeuromuscular\n\nEarly signs often include weakness of tongue and mouth muscles, fasciculations, and gradually increasing weakness of proximal limb muscles with muscle wasting. In some cases, premature muscle fatigue begins in adolescence. Neuromuscular management is supportive, and the disease progresses very slowly and often does not lead to extreme disability.\n[edit]\n\nEndocrine\n\nEndocrine manifestations of this disorder are variable and rarely include underdevelopment of internal or external genitalia. In other words, most people affected with Kennedy disease are relatively normal XY men with normal fertility. However, exaggerated and persistent gynecomastia is common and often the only symptom, while in more severe forms testicular atrophy and infertility have been described. Many affected men have the mildly high LH, testosterone, and estradiol levels characteristic of other forms of the androgen insensitivity syndrome.\n[edit]\n\nHomozygous females\n\nHomozygous females, whose both X chromosomes have a mutation leading to CAG expansion of the AR gene, show only mild symptoms of muscle cramps and twitching. No endocrinopathy has been described.\n[edit]\n\nHistory\n\nThis disorder was described by Kennedy in 1968. In 1991 it was recognized that the AR is involved in the disease process. The disease is probably more common than originally thought. A study in Scandinavia suggested a prevalence of 1.3/8,500 making KD the most common form of motor neuron disease in the specific area studied; nobody had been diagnosed before 1995. It has been suggested that some men with KS are may be misdiagnosed to have amyotrophic lateral sclerosis (ALS, also Lou Gehrig's disease).\n[edit]\n\nReferences\n\n   1. Kennedy WR, Alter M, Sung JH. Progressive proximal spinal and bulbar muscular atrophy of late onset: a sex-linked recessive trait. Neurology 1968;18:671-680. PMID 4233749.\n   2. La Spada A, Wilson EM, Lubahn DB, Harding AE, Fischbeck KH. Androgen receptor gene mutations in X-linked spinal and bulbar muscular atrophy. Nature 1991;352:77-79.\n   3. Fischbeck KH, Lieberman A, Bailey CK, Abel A, Merry DE. Androgen receptor mutation in
1120888
The condition is called lipodystrophy.\n\nhttp://www.bddiabetes.co.uk/cgi-bin/bd/bdweb/eservices/content/show.bd?Channel=%2fKnowledge+editorials%2fUK+BDM_DC+Documents%2fDB1480B55977328100256E35005C8E1F%2fBCAEF61C34548FF300256E35005E9B1E&BD_SID=UWtSVlN5NUNSRTFmUkVNPTpNQT09Ojo&BD_SID=UWtSVlN5NUNSRTFmUkVNPTpNQT09Ojo%3d&RootChannel=%2fKnowledge+editorials%2fUK+BDM_DC+Documents%2fDB1480B55977328100256E35005C8E1F
849548
Doctor...doctor...doctor....go see your doctor or a nutritionist!\n\nAre you on oral meds?  How long have you been diagnosed with DM?  After a certain amount of time, if your diet doesn't control your blood sugars, your doctor may consider treating you with oral medication.  What is your weight like?  That could be a factor, too.
1148541
I have not explanation for that..an exact one.At any rate that cannot be caused by the intake of your vitamins..You are lucky!
611431
There is no direct relation between diabetes and vit.D deficiency but once you diagnosed with vit.D deficiency you should take a supplement. in some cases of diabetes with renal failure vit.D should be given because kidneys manufacture this vitamin
64978
The Muscular Dystrophy Association is an excellent resource (800-572-1717).\n\nSupport group help
1137553
Une seule solution: Si tu en "veux" VRAIMENT. Body-building, en douceur les premiers mois pour éviter tendinites, ruptures de ligaments et... Concentration d'acide lactique dans les muscles. Prendre un complexe vitaminé, régime en fonction de la corpulence de départ. Demander détails au prof. Ne pas fumer. Huit heures de sommeil. Vélo=bon complément pour le rythme cardiaque et... Beaucoup de sueur, de patience et de souffrance. Mais uniquement les pectos, sans le reste....  Pas très joli! Question d'équilibre, comme disait l'autre
755764
It will not be an overdose. So you are safe.\nVitamin A can accumulate in the liver an cause toxicity. But, this occurs at manyfold higher dose than the RDI. Few other vitamins can cause toxicity. Rarely vit D can. But, you can take a balanced diet and still take vitamin pills.\nMinerals can be toxic but again the dose in pills os extremely low.
2794
can get muscle problems like myositis and myopathy...(muscle pain and weakness)..the way to treat it is to stop the statin and try other ways/medication to lower lipids.
421602
Vitamin D - many cases of Fibromyalgia are actually cases of Vitamin D deficiency.\n\nTake lots of antioxidants: Vitamins C and E, Selenium, Glutathione, NAC (N-acetyl-cysteine: it is converted into glutathione in the body), and Lipoic Acid.\n\nAll of the B-vitamins.\n\nAll of the essential minerals, with special focus on Magnesium, Calcium, Potassium and Zinc.\n\nOmega-3 essential fatty acids as fish oils.\n\nLots of nutrients to help detoxification: Indole-3-Carbinol, MSM, Curcumin, Calcium-D-glucarate.\n\nA quality protein supplement (hydrolyzed whey protein).\n\nA quality probiotic with very high concentrations of bifidobacteria and acidophilus.\n\nA quality multi-vitamin/mineral supplement.\n\nThere are a lot of potential 'causes' of Fibromyalgia.  The listed supplements may help with many of the causes.  However, it may be better if you seek professional guidance to help you properly evaluate what may be the source of your Fibromyalgia.\n\nUnderlying health problems that can produce Fibromyalgia include:\n1) Heavy Metal Toxicities (lead, mercury, arsenic, etc.)\n2) Intestinal dysbiosis (abnormal types of bacteria, fungi/yeasts, parasites) in your gut\n3) Leaky gut syndrome (intestinal hyperpermeability)\n4) A variety of nutrient imbalances/deficiencies (Magnesium, Calcium, Vitamin D, etc.)\n5) Food allergies/intolerances - especially allergies to 'nightshades'\n\nI would also like to suggest an excellent book that may help you.  It is by Sherry Rogers, M.D. and is called:  "Pain Free in 6 Weeks".  It is available at Amazon.com or from the publisher at 1-800-846-6687.  I highly recommend this book (and others by Dr. Rogers).\n\nBest wishes and good luck.
576400
OMG!!!  Reasons for having one of the 40+ forms of MD has nothing to do with diet.  \n\nMuscular Dystrophies are caused from many different reasons as well as genetic problems but has nothing to do with what one eats.\n\nLearn the facts at MDA's website!
838196
I believe you mean Rhabdomyolysis,which is a rare disease in which serious muscle damage results in the release of muscle cell contents into the blood stream. In rare cases, it may result in fatal damage to kidneys and other organs. Some drugs have been withdrawn from the "market" because the "risks" were high.\n\nMuscle problems can occur with statins and other lipid lowering drugs is an accepted problem. While some people seem unable to take statins because of muscle soreness or weakness, the vast majority are unaffected. There is something of a biological progression, from muscle soreness, through more severe muscle problems, to increased levels of creatinine kinase enzymes, to rhabdomyolysis, and even death from rhabdomyolysis (in about 1 in 15 cases). \nMost of the spontaneous reports of rhabdomyolysis to the FDA were associated with cerivastatin, now withdrawnThe problem with spontaneous reporting is that while it may identify cases, there is always uncertainty about denominators, so rates of adverse events are imprecise. Randomised trials are poor at finding rare but serious adverse events, because the events do not occur in sufficient numbers. Only 12 cases of rhabdomyolysis were reported in 30 RCTs reviewed .
503511
Get out in the sun more!  If you're fair-skinned, 45 minutes a week is beneficial.  If dark-skinned, a few hours a week.  \n\nHere's other sources of D:\n\nCod liver oil (best source)\nFatty fish such as salmon, mackerel, tuna, sardines, herring\nVitamin D-fortified milk and cereal\nEggs\n\nWatch out taking supplements, you can OD with serious health consequences.
439109
EATING LOTS OF FRUITS AND VEGETABLES WOULD BE YOUR BETTER BET, YOU DON'T WANT TO DEPRIVE YOUR BODY OF IMPORTANT VITIAMINS AND MINERALS. YOU ARE ACTIVE IN SPORTS SO YOU WILL GET THE EXERCISE YOU NEED ALSO. GOOD LUCK
722748
Sounds like Theramyuildincide (TYD) a mild form of muscle degeneration.\n\nIt won't kill you, but can leave you with useless limbs as the disease ravages tendons and muscle. \n\nEventually your arm will just hang by your side and will have no real form to it. \n\nI'm sorry. But we've got it early, and there are medical advancements every day in this field. Please don't give up, don't give up hope...