Treatment options for Tremors include Pharmaceutical Options, Implantation of electrodes in the brain, modifications to diet, sleep, stress and Nutritional Supplements.
Unfortunately, pharmaceutical options for tremor focus on disease, and typically treat the non-tremor portion of the disease, leaving the tremor portion untreated. (See http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0012001/ ) The conclusion of the author was "In view of this lack of evidence [on efficacy], it is impossible to determine whether beta‐blocker therapy is effective and safe for the treatment of tremor...." You should consult with your health care professionals for their recommendation of pharmaceuticals for tremor treatment. Some pharmaceuticals are effective.
Some Tremor patients elect to have electrodes implanted into their brains in order to generate more ATP and reduce the tremor. [1a]
Non-disease tremors such as Essential Tremor may respond to a variety of non-pharmaceutical and non-surgery strategies which are discussed below:
Elimination of Tremor Triggers- Certain foods can trigger tremors to start or increase in severity. Excess Caffeine or other stimulants should be removed from the diet. It may be helpful to keep a food diary to see if any one type of food results in higher tremor intensity. Eliminate excess alcohol and cigarettes as they add stress that may increase the intensity of Tremors. Small amounts of alcohol can reduce Essential Tremors, but larger amounts of alcohol will decrease quality of life.
Get a Good Night’s sleep- Physical exhaustion can cause or intensify tremors.
Reduce Stress- Many tremors increase in intensity with increases in stress. There are many ways to reduce stress including meditation, exercise, counseling, hot baths, avoiding the stress situation, and setting aside relaxation time.
Nutritional Supplements shown to reduce certain Tremors:
A Case Study with Natural Tremor Treatments
Due to the wide variety of tremors and the variations in causes, no one treatment is effective for all tremors. Below are Nutritional Supplements that have been shown to work on some types of Tremor. Typically, if nutritional supplements are to be effective in with Tremor, they start to show a small beneficial effect after 1 month and a larger effect after 3 months. If you don't feel even a small effect after 1 month, then the nutritional supplement you tried may not be of value to you. If you do feel a positive effect, then continued supplementation may help you further.
Magnesium Oxide- Shortages of magnesium in the diet can cause tremors that can be reversed with magnesium supplementation.[1, 2] Low magnesium levels have been seen in 11% of normal hospital population but in up to 65% of severely ill patients. Magnesium is often used to eliminate tremors associated with alcohol withdrawal. Magnesium shortages can be caused by reduced intake in the foods we eat, reduced absorption (common in chronic diarrhea) or increased excretion from alcoholism, diabetes and stress. An excellent review of magnesium oxide can be found online at http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0000070/
Oxaloacetate- Oxaloacetate is an intermediate in the Citric Acid cycle that is central to and essential for human energy metabolism. There are five potential protective mechanisms that could explain why oxaloacetate supplementation has been of benefit to some persons with Tremor:
• Mimicking Calorie Restriction. Caloric restriction has been shown to attenuate neurochemical and behavioral deficits in a primate model with Tremors. As oxaloacetate supplementation mimics the metabolic response of calorie restriction[6-8], there may be a similar pathway that may help in reducing Tremors.
• Protecting Mitochondrial Function. Multiple lines of evidence suggest mitochondrial issues may cause or intensify tremors. Mitochondrial function, dynamics, and quality control are vital for the maintenance of neuronal integrity. In particular, mitochondrial complex I inhibitors such as Rotenone (a pesticide) have been shown to cause tremors. The effects of rotenone were attenuated by some anti-oxidants, but not by others, indicating a complex effect.  Oxaloacetate is a powerful anti-oxidant that has also been shown to protect neural cells. [13, 14] Perhaps of more interest, oxaloacetate has been shown to protect mitochondrial DNA in the brain from the toxin Kainic Acid  which also causes tremors in laboratory animals.
• Reducing the Impact of Iron and Aluminum Toxicity. Elevated levels of Aluminum and Iron have been found in the brains of some tremors patients. [16, 17] Both Aluminum and Iron (in excess) are neurotoxins, and their presence can increase TBARS production in the brain leading to enhanced neuronal cell death. [18, 19] Iron is thought to be incorporated into the cells through the divalent metal ion transporter DMT1, which is over-expressed in the substantia nigra in animal models with Tremors. In addition, the presence of Aluminum have been shown to negatively affect Iron homeostasis. Oxaloacetate has been shown to reduce TBARS formation in rat brain tissues, and also shows iron-chelating activity.[13, 22, 23] The iron-chelating ability/ reduction of TBARS formation of oxaloacetate may protect neural tissues. It is also interesting that Bacteria excrete oxaloacetate in order to survive in Aluminum-rich waters,  providing additional evidence that oxaloacetate functions as a protective compound from metal toxicity.
• Enhanced ATP Production. It has been postulated that inhibition of mitochondrial complex 1 could reduce ATP levels and lead to neurological death.  Thus, compounds that increase ATP levels could be of benefit to Tremor patients.  Micro-Molar concentrations of oxaloacetate have been shown to increase the time to fatigue in muscle tissue,  presumably due to higher ATP generation, as oxaloacetate has been shown to increase the activity of Pyruvate dehydrogenase by up to 300%.  Thus the increased rate of the Krebs Cycle production of ATP could potentially overcome the inhibition of mitochondrial complex 1.
• Creating More Mitochondria. One of the keys to reducing the impact of mitochondrial issues may be to build new properly functioning mitochondria to preserve neurons. The body continuously builds neurons, and one strategy would be to preserve neurons faster than they are being destroyed. One of the key regulators of mitochondrial biosynthesis is activation of AMP protein activated Kinase (AMPK).  AMPK can be activated by increases in the NAD+/NADH ratio.  Oxaloacetate activates AMPK through its conversion to malate via malate dehydrogenase, which simultaneously converts NADH to NAD+ and thereby increases the NAD+/NADH ratio.  Interestingly, one of the precursors to NAD+, Nicotinamide, has been shown to have broad neuroprotective properties in mouse Tremor models,
A Case Study using Natural Tremor Treatments
1a Bekar, L., et al., Adenosine is crucial for deep brain stimulation-mediated attenuation of tremor. Nat Med, 2008. 14(1): p. 75-80.
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6. Williams, D.S., et al., Oxaloacetate supplementation increases lifespan in Caenorhabditis elegans through an AMPK/FOXO-dependent pathway. Aging Cell, 2009. 8(6): p. 765-8.
7. Cash, A., Oxaloacetic Acid Supplementation as a Mimetic of Calorie Restriction. Open Longevity Science, 2009. 3: p. 22-27.
8. Cash, A., Anti-Aging therapeutics. Modification of the NAD+/NADH Ratio Via Oxaloacetic Acid Supplementation to Mimic Calorie Restriction Metabolic Pathways and Increase Lifespan, ed. R.G. Klatz, R. Vol. XII. 2010: American Academy of Anti-Aging Medicine.
9. Deleted from website due to reference to disease.
10. Deleted from website due to reference to disease as per FDA guidelines for Nutritional Supplements.
11. Deleted from website due to reference to disease as per FDA guidelines for Nutritional Supplements.
12. Chou, A.P., et al., Mechanisms of rotenone-induced proteasome inhibition. Neurotoxicology, 2010. 31(4): p. 367-72.
13. Desagher, S., J. Glowinski, and J. Premont, Pyruvate protects neurons against hydrogen peroxide-induced toxicity. J Neurosci, 1997. 17(23): p. 9060-7.
14. Berry, E.V. and N.J. Toms, Pyruvate and oxaloacetate limit zinc-induced oxidative HT-22 neuronal cell injury. Neurotoxicology, 2006. 27(6): p. 1043-51.
15. Yamamoto, H.A. and P.V. Mohanan, Effect of alpha-ketoglutarate and oxaloacetate on brain mitochondrial DNA damage and seizures induced by kainic acid in mice. Toxicol Lett, 2003. 143(2): p. 115-22.
16. Deleted from website due to reference to disease as per FDA guidelines for Nutritional Supplements.
17. Deleted from website due to reference to disease as per FDA guidelines for Nutritional Supplements.
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21. Contini Mdel, C., et al., Study of iron homeostasis following partial hepatectomy in rats with chronic aluminum intoxication. Biol Trace Elem Res, 2007. 115(1): p. 31-45.
22. Puntel, R.L., et al., Antioxidant properties of Krebs cycle intermediates against malonate pro-oxidant activity in vitro: a comparative study using the colorimetric method and HPLC analysis to determine malondialdehyde in rat brain homogenates. Life Sci, 2007. 81(1): p. 51-62.
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25. Deleted from website due to reference to disease as per FDA guidelines for Nutritional Supplements.
26. Nogueira, L., Acute Oxaloacetate Exposure Enhances Resistance to Fatigue in in vitro Mouse Soleus Muscle. The FASEB Journal, 2011. 25(1104.5).
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