Microwave - and other forms of electromagnetic - radiation are major (but conveniently disregarded, ignored, and overlooked) factors in many modern unexplained disease states. Insomnia, anxiety, vision problems, swollen lymph, headaches, extreme thirst, night sweats, fatigue, memory and concentration problems, muscle pain, weakened immunity, allergies, heart problems, and intestinal disturbances are all symptoms found in a disease process the Russians described in the 70's as Microwave Sickness.
Saturday, May 16, 2015
L-Lysine for Electrosensitivity (ES) // Electrohypersensitivity (EHS)?
L-Lysine for Electrosensitivity (ES) // Electrohypersensitivity (EHS)?
Recently I started to take L-lysine supplements and also started to try eat foods high in L-lysine and low in L-arginine and L-glutamine under the premise that EMFs weaken the immune system, which in turn stimulate the activation of a number of viruses in the Herpes family (e.g. Herpes Zoster, Epstein Barr Virus, Cytomegalovirus, etc.), candida, (and other pathogens) — and L-lysine(indirectly) has been shown to inhibit a number of Herpes Family Viruses, while L-arginine, on the other hand, stimulates these Herpes Family viruses, and there is some evidence suggesting that glutamine can stimulate candida. <http://mic.sgmjournals.org/content/80/1/143.full.pdfhttp://mic.sgmjournals.org/content/80/1/143.full.pdf>. <http://www.astrologyzine.com/health/yeast-infections.shtml>Some bakers are known to add MSG when making bread to stimulate the yeast to grow.
Having said that, there are so many factors involved in this condition. While I had pretty much recovered from the most severe symptoms I had been experiencing when I was first got extremely living in the vicinity of a number of cell towers, by having done a number of things, I was still plagued by more minor symptoms like allergies, etc. I think that the L-lysine is now helping with the latter — unless of course it is something else completely. Initially, ten years ago when I was very very sick, I initially did things like chelation therapy, Q-going, acupuncture, Transfer Factors, antioxidants, etc. and all these things helped. Hence, I am not sure how much just taking L-lysine alone might for example help someone who has severe heavy metal toxicity and multiple infections. It would be interesting to see though. I would guess that it might be more beneficial for some people with mild ES and that people with severe ES might not notice any — or just slight — changes.
I am amazed at how good I feel. Symptoms are pretty much all gone. Perhaps this is part of the key to the problem and part of the cure. Something I am adding to my essential supplement list of magnesium, and GABA from sprouted rice milk, tryptophan from bananas, and whey powder (for making glutathione).
Given that nitric oxide (NO) overproduction is a cornerstone of Dr. Martin Pall's research/theory where EMF leads to Calcium Influx leads to nitric oxide production leads to peroxynitrite and other free radical production, the following research study shows that L-lysine indirectly limits NO production, which should in theory help prevent or inhibit the vicious cycle initially stimulated by EMFs.
1Institute of Pathophysiology, University Hospital, Lausanne, Switzerland.
1. An enhanced production of nitric oxide (NO) from L-arginine, related to the diffuse expression of an inducible NO synthase (iNOS), contributes to the pathogenesis of endotoxic shock. Since iNOS activity depends on extracellular L-arginine, we hypothesized that limiting cellular L-arginine uptake would reduce NO production in endotoxic shock. We investigated the effects of L-lysine, an inhibitor of L-arginine uptake through system y+, on NO production, multiple organ dysfunction and lactate levels, in normal and endotoxaemic rats. 2. Anaesthetized rats challenged with intravenous lipopolysaccharide (LPS, 10 mg kg[-1]) received a 5 h infusion of either L-lysine (500 micromol kg(-1) h(-1), n = 12) or isotonic saline (2 ml kg(-1) h(-1), n = 11). In rats treated with saline, LPS produced a large increase in plasma nitrate and L-citrulline concentrations at 5 h, both markers of enhanced NO production. LPS also caused severe hypotension, low cardiac output and marked hyperlactataemia. All these changes were significantly reduced by L-lysine administration. 3. Endotoxaemia also caused a significant rise in the plasma levels of alanine aminotransferase (ALAT), lipase, urea and creatinine, and hence, liver, pancreatic and renal dysfunction. These changes tended to be less pronounced in rats treated with L-lysine, although the differences did not reach statistical significance. 4. Similar experiments were conducted in 10 rats challenged with LPS vehicle in place of LPS and then treated with L-lysine (500 micromol kg(-1) h(-1), n = 5) or saline (2 ml kg(-1) h(-1), n = 5) for 5 h. In these animals, all the haemodynamic and metabolic variables remained stable and not statistically different between both treatment groups, except for a slight rise in ALAT, which was comparable in L-lysine and saline-treated rats. 5. In conclusion, L-lysine, an inhibitor of cellular L-arginine uptake, reduces NO production and exerts beneficial haemodynamic effects in endotoxaemic rats. L-lysine also reduces hyperlactataemia and tends to blunt the development of organ injury in these animals. Contrastingly, L-lysine has no effects in the absence of endotoxin and thus appears to act as a selective modulator of iNOS activity.
Anyway, I am presently taking 1000 mg three times a day (for a total of 3000 mg). I would like to enlist a number of people suffering from ES/EHS to give taking this supplement at this amount (or more) — combined with a strict diet — a try and see if there is any positive benefits to their symptoms. Contact me if you are interested in participating in such an ad-hoc trial.
Some other L-lysine pubmed studies of related interest:
Our earlier observations showed that L-lysine enhanced the activity of diazepam against seizures induced by pentylenetetrazol (PTZ), and increased the affinity of benzodiazepine receptor binding in a manner additive to that caused by gamma-aminobutyric acid (GABA). The present paper provides additional evidence to show that L-lysine has central nervous system depressant-like characteristics. L-lysineenhanced [3H]flunitrazepam (FTZ) binding in brain membranes was dose-dependent and stimulated by chloride, bromide and iodide, but not fluoride. Enhancement of [3H]FTZ binding by L-lysine at a fixed concentration was increased by GABA but inhibited by pentobarbital between 10(-7) to 10(-3)M. While GABA enhancement of [3H]FTZ binding was inhibited by the GABA mimetics imidazole acetic acid and tetrahydroisoxazol pyridinol, the enhancement by pentobarbital and L-lysine of [3H]FTZ binding was dose-dependently increased by these two GABA mimetics. The above results suggest that L-lysine and pentobarbital acted at the same site of the GABA/benzodiazepine receptor complex which was different from the GABA binding site. The benzodiazepine receptor antagonist imidazodiazepine Ro15-1788 blocked the antiseizure activity of diazepam against PTZ. Similar to pentobarbital, the anti-PTZ effect of L-lysine was not blocked by Ro15-1788. Picrotoxinin and the GABA, receptor antagonist bicuculline partially inhibited L-lysine's enhancement of [3H]FTZ binding with the IC50s of 2 microM and 0.1 microM, respectively. The convulsant benzodiazepine Ro5-3663 dose-dependently inhibited the enhancement of [3H]FTZ binding by L-lysine. This article shows the basic amino acid L-lysine to have a central nervous system depressant characteristics with an anti-PTZ seizure activity and an enhancement of [3H]FTZ binding similar to that of barbiturates but different from GABA.
We have previously shown that mice lacking inducible NO synthase are markedly more susceptible to Leishmania major infection but developed a significantly enhanced Th1 cell response compared with wild-type mice. Furthermore, at high concentrations, NO inhibited IL-12 synthesis by activated macrophages, thereby indirectly suppressing the expansion of Th1 cells. We report here that at low concentrations, NO selectively enhanced the induction of Th1 cells and had no effect on Th2 cells. NO exerted this effect in synergy with IL-12 during Th1 cell differentiation and had no effect on fully committed Th1 cells. NO appears to affect CD4(+) T cells directly and not at the antigen-presenting cells. These results therefore provide an additional pathway by which NO modulates the immune response and contributes to the homeostasis of the immune system.