Guest guest Posted February 8, 2006 Report Share Posted February 8, 2006 I posted a last week in regards to PLS and LDN. There have been no responses. Does that mean nobody is familiar with PLS and LDN? PLS is in the same " family " as ALS, are there any persons who have used LDN who have ALS and have had any success? I had taken LDN for 1 1/2 months last year, but I had such a worsening of symptoms I stopped. I was afraid that if I kept taking LDN things would just continue to worsen, but I'd like to investigate it more vs. just giving up entirely. Thanks, Mike Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 9, 2006 Report Share Posted February 9, 2006 > > I posted a last week in regards to PLS and LDN. There have been no > responses. Does that mean nobody is familiar with PLS and LDN? > > PLS is in the same " family " as ALS, are there any persons who have > used LDN who have ALS and have had any success? > > I had taken LDN for 1 1/2 months last year, but I had such a worsening > of symptoms I stopped. I was afraid that if I kept taking LDN things > would just continue to worsen, but I'd like to investigate it more vs. > just giving up entirely. > > Thanks, > > Mike ================== Mike, There used to be a few here with PLS that were doing well on LDN...many do so well they move on with life and on from this board. Their posts have been included on the What Others Are Saying About LDN on the LDN website. Go to the link below and click and once page is loaded click on featured comments and scroll through for to look for copies of the PLS comments. You may need to start with 1.5mg for a month or two and build to 1.75mg for a month, then to 2.0mg for 2 to 4 weeks, then to 2.5mg and so forth. http://www.low dose naltrexone.org/others.htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 9, 2006 Report Share Posted February 9, 2006 Hi Mike, I believe a friend of mine with als answered your post. She has been on the ldn for about a month now and is finding she has more energy and sleeps better. No progression yet. Prayers said and fingers crossed! The worsening you had last time you tried the ldn, was it a worsening of existing symptoms or new symptoms? I have ms and my symptoms seemed a little worse before they got better. No new symptoms. Take Care : > > I posted a last week in regards to PLS and LDN. There have been no > responses. Does that mean nobody is familiar with PLS and LDN? > > PLS is in the same " family " as ALS, are there any persons who have > used LDN who have ALS and have had any success? > > I had taken LDN for 1 1/2 months last year, but I had such a worsening > of symptoms I stopped. I was afraid that if I kept taking LDN things > would just continue to worsen, but I'd like to investigate it more vs. > just giving up entirely. > > Thanks, > > Mike > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 9, 2006 Report Share Posted February 9, 2006 > Hi Mike, below is an out take on naloxone being used as a possible treatment for brain diseases, ALS being one. I see the paper as an independant report on how LDN could be real. Until there is clinical data on how LDN effects people with a serious disease, we are doing our own experiments. Hope Dr. Jill and Dr. Myra Gironi can provide positve reports. The report below sort of confirms naloxone (naltrexone) could help, at least in rats. My guess is that one should be on LDN for about a year before you can get a sense if you're holding your own (unless you're getting worse and then what do you do?). Where did you get your LDN and how much were you taking? Did your symptoms change after you stopped LDN? OPIOIDS, BRAIN INFLAMMATION, AND... REFERENCES Increasing evidence has suggested that inflammation in the brain is closely associated with the pathogenesis of several degenerative neurologic disorders, including Parkinson's disease, Alzheimer's diseases, multiple sclerosis, amyotrophic lateral sclerosis, and AIDS dementia. The hallmark of brain inflammation is the activation of glial cells, especially that of microglia that produce a variety of proinflammatory and neurotoxic factors, including cytokines, fatty acid metabolites, free radicals—such as nitric oxide (NO) and superoxide. Excessive production of NO, as a consequence of nitric oxide synthase induction in activated glia, has been attributed to participate in neurodegeneration. Using primary mixed neuron-glia cultures and glia-enriched cultures prepared from embryonic rodent brain tissues, we have systemically studied the relationship between the production of NO and neurodegeneration in response to stimulation by the inflammagen lipopolysaccharide. This review summarizes our recent findings on the kinetics of NO generation, the relative contribution of microglia and astrocytes to NO accumulation, the relationship between NO production and neurodegeneration, and points of intervention along the pathways associated with NO generation to achieve neuroprotection. We also describe our results relating to the effect of several opioid-related agents on microglial activation and neuroprotection. Among these agents, the opioid receptor antagonist naloxone, especially its non-opioid enantiomer (+)-naloxone, promises to be of potential therapeutic value for the treatment of inflammation-related diseases. http://www.annalsnyas.org/cgi/content/full/962/1/318 > I posted a last week in regards to PLS and LDN. There have been no > responses. Does that mean nobody is familiar with PLS and LDN? > > PLS is in the same " family " as ALS, are there any persons who have > used LDN who have ALS and have had any success? > > I had taken LDN for 1 1/2 months last year, but I had such a worsening > of symptoms I stopped. I was afraid that if I kept taking LDN things > would just continue to worsen, but I'd like to investigate it more vs. > just giving up entirely. > > Thanks, > > Mike > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 10, 2006 Report Share Posted February 10, 2006 Mike, I thought I had answered you previously, but perhaps I hadn't. I have been diagnosed with ALS, and I have now been taking LDN at 3.0 mg. for six weeks. At first I had some problems with getting to sleep and some increased stiffness in my upper arms and shoulders, but since then I have had improvement on ldn. In fact, at my latest appointment with my internist, he noted no progression in the past month. This is the first time that has happened since my diagnosis. I have had increased energy, and my sleep quality has improved since starting the ldn. I have noticed some increased fatigue in my legs over the past week, but I am not sure if it is related to my ALS or to a minor cold I have had. Also, at my appointment in the next few weeks, we will be increasing my dosage to 4.5. If you are also on Baclofen, I would suggest that you DO NOT go off of it. I tried that for the first few days that I started ldn, and found it was very problematic as far as spasticity. As soon as I went back on the Baclofen, that problem stopped. I hope this helps, and if you have any other questions regarding my experience with ALS and ldn, please let me know. Take Care, > > I posted a last week in regards to PLS and LDN. There have been no > responses. Does that mean nobody is familiar with PLS and LDN? > > PLS is in the same " family " as ALS, are there any persons who have > used LDN who have ALS and have had any success? > > I had taken LDN for 1 1/2 months last year, but I had such a worsening > of symptoms I stopped. I was afraid that if I kept taking LDN things > would just continue to worsen, but I'd like to investigate it more vs. > just giving up entirely. > > Thanks, > > Mike > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 10, 2006 Report Share Posted February 10, 2006 , I understand what you are saying about giving ldn time to work. And I am fortunate that is helping me at this time. However, I think you might be a little uninformed regarding the course of ALS. A person with ALS would be unable to wait for a year to get a sense of " holding their own " . It is a progressive, fatal disease in which steady decline is expected on a regular basis. The average length of time between onset and death is 3-5 years. I was diagnosed a year ago, and I am very fortunate to appear to have a slower course than some. However, the difference between my abilities at the date of my diagnosis and now is profound. A friend that was diagnosed with ALS the same month as I was is now starting hospice care. I hope that ldn will be able to keep me from declining over the course of a year, but even as positive as I am about the drug, I would find it pretty unlikely. I am sorry to correct you, but don't want people to misunderstand regarding ALS and waiting for results. Take Care, > > > Hi Mike, below is an out take on naloxone being used as a possible > treatment for brain diseases, ALS being one. I see the paper as an > independant report on how LDN could be real. Until there is clinical > data on how LDN effects people with a serious disease, we are doing > our own experiments. Hope Dr. Jill and Dr. Myra Gironi can > provide positve reports. The report below sort of confirms naloxone > (naltrexone) could help, at least in rats. My guess is that one should > be on LDN for about a year before you can get a sense if you're > holding your own (unless you're getting worse and then what do you > do?). Where did you get your LDN and how much were you taking? Did > your symptoms change after you stopped LDN? > > > OPIOIDS, BRAIN INFLAMMATION, AND... > REFERENCES > > Increasing evidence has suggested that inflammation in the brain is > closely associated with the pathogenesis of several degenerative > neurologic disorders, including Parkinson's disease, Alzheimer's > diseases, multiple sclerosis, amyotrophic lateral sclerosis, and AIDS > dementia. The hallmark of brain inflammation is the activation of > glial cells, especially that of microglia that produce a variety of > proinflammatory and neurotoxic factors, including cytokines, fatty > acid metabolites, free radicals—such as nitric oxide (NO) and > superoxide. Excessive production of NO, as a consequence of nitric > oxide synthase induction in activated glia, has been attributed to > participate in neurodegeneration. Using primary mixed neuron-glia > cultures and glia-enriched cultures prepared from embryonic rodent > brain tissues, we have systemically studied the relationship between > the production of NO and neurodegeneration in response to stimulation > by the inflammagen lipopolysaccharide. This review summarizes our > recent findings on the kinetics of NO generation, the relative > contribution of microglia and astrocytes to NO accumulation, the > relationship between NO production and neurodegeneration, and points > of intervention along the pathways associated with NO generation to > achieve neuroprotection. We also describe our results relating to the > effect of several opioid-related agents on microglial activation and > neuroprotection. Among these agents, the opioid receptor antagonist > naloxone, especially its non-opioid enantiomer (+)-naloxone, promises > to be of potential therapeutic value for the treatment of > inflammation-related diseases. > http://www.annalsnyas.org/cgi/content/full/962/1/318 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 10, 2006 Report Share Posted February 10, 2006 Hi , and Mike, We all care about helping one another on this forum. Any comments that are shared on this form are typically with the intent to help with information and support. Sometimes I give out the wrong info, or not the best info and I am happy to hear back if I am mistaken. Sometimes people mis-understand what I am saying and get in a huff. But that is OK too, I just gently remind them of what I said, or meant. It is great to have so much help, thanks for being here everyone. Aletha [low dose naltrexone] ALS / PLS and LDN > > > > > Hi Mike, below is an out take on naloxone being used as a possible > > treatment for brain diseases, ALS being one. I see the paper as an > > independant report on how LDN could be real. Until there is > clinical > > data on how LDN effects people with a serious disease, we are doing > > our own experiments. Hope Dr. Jill and Dr. Myra Gironi can > > provide positve reports. The report below sort of confirms naloxone > > (naltrexone) could help, at least in rats. My guess is that one > should > > be on LDN for about a year before you can get a sense if you're > > holding your own (unless you're getting worse and then what do you > > do?). Where did you get your LDN and how much were you taking? Did > > your symptoms change after you stopped LDN? > > > > > > OPIOIDS, BRAIN INFLAMMATION, AND... > > REFERENCES > > > > Increasing evidence has suggested that inflammation in the brain is > > closely associated with the pathogenesis of several degenerative > > neurologic disorders, including Parkinson's disease, Alzheimer's > > diseases, multiple sclerosis, amyotrophic lateral sclerosis, and > AIDS > > dementia. The hallmark of brain inflammation is the activation of > > glial cells, especially that of microglia that produce a variety of > > proinflammatory and neurotoxic factors, including cytokines, fatty > > acid metabolites, free radicals-such as nitric oxide (NO) and > > superoxide. Excessive production of NO, as a consequence of nitric > > oxide synthase induction in activated glia, has been attributed to > > participate in neurodegeneration. Using primary mixed neuron-glia > > cultures and glia-enriched cultures prepared from embryonic rodent > > brain tissues, we have systemically studied the relationship > between > > the production of NO and neurodegeneration in response to > stimulation > > by the inflammagen lipopolysaccharide. This review summarizes our > > recent findings on the kinetics of NO generation, the relative > > contribution of microglia and astrocytes to NO accumulation, the > > relationship between NO production and neurodegeneration, and > points > > of intervention along the pathways associated with NO generation to > > achieve neuroprotection. We also describe our results relating to > the > > effect of several opioid-related agents on microglial activation > and > > neuroprotection. Among these agents, the opioid receptor antagonist > > naloxone, especially its non-opioid enantiomer (+)-naloxone, > promises > > to be of potential therapeutic value for the treatment of > > inflammation-related diseases. > > http://www.annalsnyas.org/cgi/content/full/962/1/318 > Quote Link to comment Share on other sites More sharing options...
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