|The Durk Pearson & Sandy Shaw®|
Life Extension NewsTM
Volume 18 No. 7 • November 2015
by Sandy Shaw
My experience with restless legs finds that, at least in my case, it can be brought on or made worse by:
1. Drinking carbonated beverages—Carbon dioxide inhalation can induce arousal by activating serotonin receptors (Richerson, 2004). Certain serotonin receptors surprisingly, induce arousal. “It is now clear that 5-HT [serotonin] actually causes arousal.” (Richerson, 2004, pg. 451) “Serotonergic neurons in the midbrain are also chemosensitive, and might mediate non-respiratory responses to increased carbon dioxide, such as arousal.” (Richerson, 2004) This arousal may be what drinkers of carbonated beverages are looking for. I find that drinking carbonated beverages increases my symptoms of restless legs. How serotonergic activation would do that I do not know. It is known that serotonin receptors can be involved in motor control (Richerson, 2004). The absorption of carbon dioxide from drinking carbonated drinks may be modulated by taking GAS-X or similar remedy to cause the carbon dioxide gas to be “burped” out, reducing the amount that is absorbed in the gastrointestinal tract. (There has to be a reason why humans go to the trouble and expense of getting carbon dioxide into so many drinks. Yes, it is pleasurable, but why? It may have a stimulating effect to increase awareness and arousal via serotonergic receptors. There may be, however, other chemoreceptors involved in the arousal response to carbon dioxide. See (Buchanan, 2010).
2. Eating foods on an empty stomach when the food contains more than about 20 grams of sugar (sucrose). This may be due to the release of insulin and subsequent release of noradrenaline (Watson, 2006). “Thus, changes in insulin levels may modulate synaptic NE [norepinephrine/noradrenaline] levels and behaviors normally associated with noradrenergic activity.” (Watson, 2006). Although noradrenaline levels decrease with aging, there is the possibility of compensatory hypersensitivity (increased reactiveness to NE). (Ah, yes, it is a delicate balancing act to get the dose of noradrenaline just right.)
Eating sugar with a meal should reduce the likelihood of stimulating restless legs because of the dilution of the sugar and the consequent slower absorption of it. Good sweeteners that avoid insulin release include erythritol (unlike other sugar alcohols, doesn’t cause diarrhea), xylitol, other sugar alcohols, palatinose (a natural sugar, found in honey and sugar cane). These slowly releases sugar for a very low glycemic index effect and little increase in insulin). Synthetic sweeteners such as saccharin, aspartame, sucralose, and others have been shown to have a detrimental effect on the gut microbiota. Stevia may also have similar detrimental effects. See below for article on the potential adverse effects of various non-sucrose sweeteners, both natural and synthetic.
3. I speculate (this is purely a speculation) that restless legs may be a symptom of temporal lobe epilepsy (Ottoson, 2015), which I have, and the symptoms of which increase in my own case concurrently in response to the same inducing factors, such as #1 and #2 above. Moreover, the drugs and nutrients I use to control temporal lobe epilepsy, such as gabapentin (with GABA receptor inducing effects), glycine, and taurine, also are effective in controlling restless legs in my case. The latter are personal observations only. I make no claim of cause and effect or generalizability.
4. Drinking very cold drinks can bring it on in my case, perhaps due to adrenergic stimulation. (Rossato, 2014) “In vivo cold sensation is detected by specific sensors for cold temperature expressed on peripheral cutaneous nerve endings leading to adrenergic stimulation.” (Rossato, 2014) (There has to be a reason why humans prefer very cold drinks and throughout history have gone to great lengths and expense to get what is necessary (refrigeration, ice, deep storage in the earth, etc.) to get their drinks cold. One has to presume that there is a preferred psychopharmacological state. I think it may be, in this case, adrenergic activation (Rossato, 2014) —and/or possibly cholinergic activation—by very cold-detecting sensors in the mouth or gastrointestinal tract. People like the effects of being stimulated.)
“The effect of adrenoceptors agonists on the production of other important mediators involved in inflammation have also been investigated. Prostaglandins are produced via the metabolism of AA [arachidonic acid] by a cyclooxygenase (COX) and subsequently by prostaglandin synthases.” “Our laboratory has also demonstrated that NE [norepinephrine, noradrenaline] is able to increase COX-2 expression in LPS-stimulated microglia.” (Schlachetzki, 2010). LPS is lipopolysaccharide, a bacterial cell wall component that activates the immune system and its inflammatory effects. However, noradrenaline levels decline with aging, a detrimental effect on cognition (Schlachetzki, 2010). Clinical trials treating patients with dementia or cognitive impairments with beta adrenergic receptor blockers has resulted in both beneficial results and detrimental results. In other studies, increasing noradrenaline by treatment with insulin resulted in improvement cognition in demented patients but in another study increased the level of inflammatory markers in the CSF (cerebral spinal fluid). The data are conflicting at this point (or as of 2010).
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