posted
I started LDN a few years ago when I was diagnosed with MS.
Recently was diagnosed as NOT MS, but LYME. I told the LLMD that I was on LDN and he said 'good.'
Posts: 46 | From Wisconsin | Registered: Sep 2006
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posted
How do you know that it is from Naltrexone? You are on abx also right? So what makes you think that it is the LDN therapy? You have only been on it for a month or so according to you posts. I am interested because I know someone personally that is feeling better about 2 months after starting it. She is only on a small amount of Doxy, so I don't think that it is the abx that is helping alone. But she is far from being asymptomatic as you claim that you are.
Kawai.
Do you feel that the LDN has helped significantly? Were you taking abx also before you found out that you really had lyme?
Posts: 132 | Registered: Jul 2005
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posted
Would it help heal nerve pain such as sciatic nerve pain?
-------------------- --Lymetutu-- Opinions, not medical advice! Posts: 96239 | From Texas | Registered: Feb 2001
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LostCityAgent
Unregistered
posted
Hello, It is not designed to help nerve pain, to my knowledge. Kawai, how did it effect your symptoms? There is no sure of telling until you are off of abx. I am on 400mg, doxy.
posted
I started LDN about 2 years ago. I've continued since my LD diagosis and 3 weeks of antibiotics. I never saw any real improvements, but since I didn't have any relapses I sayed on it.
I also take 4-AP which helps my stamina and gait.
Posts: 46 | From Wisconsin | Registered: Sep 2006
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LostCityAgent
Unregistered
posted
Kawai, What is 4-AP? If you have not relapsed, then, you have seen an improvement on that note. I am sorry that perhaps the nerve damage was too severe to heal. I continue to suffer with internal vibration and aggravated parethesias. All other symptoms are gone.
The short version: Fampridine-SR ("4-aminopyridine", "4-AP") is an investigational oral, sustained-release formulation of 4-aminopyridine. In laboratory studies fampridine has improved impulse conduction in nerve fibers in which the insulating layer, called myelin, has been damaged.
It's another drug that needs to be compounded and a pharmacy knowedgeable in that area is highly recommended.
There are many sites about it...just do a search and you'll probably get more than you want to know.
Posts: 46 | From Wisconsin | Registered: Sep 2006
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Truthfinder
Frequent Contributor (1K+ posts)
Member # 8512
posted
Lost City Agent, I'm really glad to hear that you are so much better. You weren't feeling too great about a month ago. And thanks for posting about this.
Unfortunately, there isn't one thing about Lyme Disease on the compounder.com website. Too bad he didn't put something about it on his site. In fact, I can't even tell how he formulates the LDN -whether he uses the pure powder or what.
So are you still at 3 mg., or did you bump up to the 4.5 mg.?
Hope you find a good doc where you are.
Tracy
-------------------- Tracy .... Prayers for the Lyme Community - every day at 6 p.m. Pacific Time and 9 p.m. Eastern Time � just take a few moments to say a prayer wherever you are�. Posts: 2966 | From Colorado | Registered: Dec 2005
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5dana8
Frequent Contributor (1K+ posts)
Member # 7935
posted
Hi Lostcityagent
Thanks for posting the links
I would worry though in the case of lyme some patients that it might over stimulate the immune system
-------------------- 5dana8 Posts: 4432 | From some where over the rainbow | Registered: Sep 2005
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posted
I took it for about 2 years and saw no help of any kind. Kept taking it & hoping.
I talked my gp into giving it to me since there was very little risk and a possible high reward. So if you are sure it helps you keep trying to find a doc who will give you a scrip.
Posts: 561 | From connecticut | Registered: May 2004
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posted
I'm on 3.75 mg since 4 mg made me stiff and 3.5 mg wasn't doing anything.
Your point about the correct pharmacy is most important. I actually have it shipped to me from a pharmacy that's 1-1/2 hours away. Luckily I have refills for a year and just call them for 2-month supplies.
Posts: 46 | From Wisconsin | Registered: Sep 2006
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I am also taking LDN, actualy I started to research it after reading of it from LostCityAgent Its been 4 weeks now and Im at 3.5ml.I have been diagnosed with M.S. for 15 years now and several years ago I found out that I also carry lyme..Is the lyme and the M.S. one in the same? Very well could be. Kawai, I'm very interested in trying the "4-AP could you please tell me how much do you take,dosage.And was it somthing that your Dr.perscribed? Thanks.Terri
Posts: 203 | From tipp city oh.45371 | Registered: Jul 2003
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Jill E.
Frequent Contributor (1K+ posts)
Member # 9121
posted
John,
I really appreciate that you've posted about your improvement on the LDN, both to inform us about the supplement and also to let us know you are doing better.
I have symptoms much like yours - very MS neurological - so I'm interested in learning more about LDN.
I recently corresponded with a Lyme patient in my state whose LLMD recommended LDN, and the patient didn't know what it was, so I told her based on your previous postings.
I'm having major internal vibration and paresthesia problems (and other stuff, myoclonic jerking, tremors, etc) so if you ever find that the LDN starts helping those, please post. But I'm thinking maybe it would help my nerve burning which has been my longest-lasting Lyme problem (although it might be Bartonella).
Take care, Jill
-------------------- If laughter is the best medicine, why hasn't stand-up comedy cured me? Posts: 1773 | From San Diego | Registered: Apr 2006
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posted
It doesn't make any sense to me why it wouldn't work for someone that had only lyme and no MS. The drug helps to restore the immune system. Most lymies have a very low score on their CD-57 test which indicates a very weak immune system. Lyme is not like lupus where you want to suppress the immune system so that it doesn't destroy vital organs. We need our immune systems to be strong and function properly. This could help.
-------------------- You're only a failure when you stop trying. Posts: 945 | From U.S | Registered: Oct 2004
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LostCityAgent
Unregistered
posted
Misul, you are correct, however, it works against preeons differently.
Similar friend: my parethesias has decreased, internal vibration is less, tremors and myoclonic jerking are now non-existent.
My previous doctor (alternative medicine) prescribed it for me when I asked, but I'm sure it's not that easy for most.
The LLMD that I'm seeing now had never heard of it, but has no problem with me continuing it if I feel it helps.
Again, it needs to be compounded and a reputable pharmacy is recommended. I use The Prescription Center in LaCrosse, Wisconsin and they just ship it to me 1 or 2 months at a time.
Good luck!
Posts: 46 | From Wisconsin | Registered: Sep 2006
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LostCityAgent
Unregistered
posted
Kawai, Can you tell us more about AP and what it had done for you?
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LostCityAgent
Unregistered
posted
I do, have something, of hope for those of you who have not benefited from LDN or AP.
It seems to be long term, at least 2 to 5 years, if if succeeds but I would like to link the following information to you.
It is regarding a USC study (new information) that seems to also, "cure" Multiple Sclerosis and reverse effects in a few.
If we can get disease progression to hault and limit our drug intake, then healing is more attainable with our full attention.
As you know, many of use belive that MS and LD are the same thing, holding different presentations. This fight is not important in this regard: a healing is a healing.
I believe that if the vaccine ends up working, if it is coupled with LDN or possibly AP, in a joint operation, a full recovery can be made for most.
Please take a leap of faith and read the following:
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
Positive Results From Phase II Trial Of Rituxan In Relapsing-Remitting Multiple Sclerosis Main Category: Multiple Sclerosis News Article Date: 02 Sep 2006 - 11:00am
Genentech, Inc. (NYSE: DNA) and Biogen Idec, Inc. (Nasdaq: BIIB) announced today that a Phase II study of Rituxan� (Rituximab) for relapsing-remitting multiple sclerosis (RRMS) met its primary endpoint. The study of 104 patients showed a statistically significant reduction in the total number of gadolinium enhancing T1 lesions observed on serial MRI scans of the brain at weeks 12, 16, 20 and 24 in the Rituxan-treated group compared to placebo. Genentech and Biogen Idec will continue to analyze the study results and will submit the data for presentation at an upcoming medical meeting.
"These initial results exceeded our expectations," said Hal Barron, M.D., Genentech senior vice president, development and chief medical officer. "Showing a significant benefit at 24 weeks in this small Phase II trial supports our hypothesis that selective B-cell targeted therapy may play an important role in the treatment of MS."
"Biogen Idec is committed to offering multiple options for people living with MS, a devastating disease. We are very encouraged by these data and look forward to learning more about the potential of Rituxan as a therapy to treat MS," said Alfred Sandrock, M.D., Ph.D., senior vice president, neurology research and development, Biogen Idec.
Rates of overall adverse events and serious adverse events were comparable between the two treatment groups. Serious infectious adverse events occurring in Rituxan-treated patients included gastroenteritis and bronchitis. The overall rates of infection were comparable among the two treatment groups with an increase in the rates of nasopharyngitis, upper respiratory tract infections, urinary tract infections and sinusitis in the Rituxan-treated patients. There were more first infusion-related reactions with Rituxan, the majority of which were mild to moderate and were generally reversible with medical intervention. The companies continue to monitor the long-term safety of Rituxan treatment.
About the Study
This Phase II randomized, double-blind, parallel-group, placebo-controlled, multi-center study was designed to evaluate safety and efficacy of Rituxan in adults with RRMS. A total of 104 patients at 48 sites in the U.S. and Canada were randomized to receive either a single treatment course of Rituxan or placebo. Gadolinium-enhancing lesions visible by MRI scans were assessed at 12, 16, 20 and 24 weeks. Patients will continue to be followed for 48 weeks.
About MS and RRMS
MS is a chronic autoimmune disease in which the immune system is thought to attack the body's own myelin, a fatty substance that surrounds and protects the nerve fibers of the brain, optic nerves and spinal cord. There are four types of MS with a wide variety of symptoms and different courses of disease progression.
MS is the leading cause of neurological disability in young adults. Neurological disability typically accumulates over time and includes muscle weakness and spasticity, balance and coordination problems, as well as memory impairment and depression. Other symptoms include numbness, pain, slurred speech and blurred vision. Many patients experience fatigue and problems with bladder, bowel or sexual function.
RRMS is the most common form of MS and accounts for approximately 65 percent of all MS cases. RRMS is characterized by acute exacerbations with full or partial recovery between attacks. The disease does not progress between attacks.
Rituxan Safety Profile in Oncology and Autoimmune Diseases
The safety profile of Rituxan has been established in more than 960,000 patient exposures over a period of eight years.
In general, the adverse events observed in patients with RA an autoimmune disease, were similar in type to those seen in patients with non-Hodgkin's lymphoma (NHL). The most common adverse events observed in patients treated with Rituxan for RA in clinical trials were infusion reactions and infections. No significant change in average immunoglobulin levels was observed in Rituxan-treated patients in clinical trials. There was no increase in hematologic malignancies, demyelinating events or risk of opportunistic infections (including tuberculosis) in Rituxan-treated patients over 24 weeks of treatment. Although 5 percent of Rituxan-treated patients developed human anti-chimeric antibodies (HACA), this was not associated with loss of clinical response or additional safety observations.
The majority of patients experience infusion-related symptoms with their first Rituxan infusion. These symptoms include but are not limited to: flu-like illness, fever, chills/rigors, nausea, urticaria, headache, bronchospasm, angioedema, hypotension and hypoxia. These symptoms vary in severity and generally are reversible with medical intervention.
Severe infusion reactions have been reported in patients treated with Rituxan, some with fatal outcomes in patients with NHL. These severe reactions typically occur during the first infusion. The most severe manifestations and sequelae include pulmonary infiltrates, acute respiratory distress syndrome, myocardial infarction, ventricular fibrillation, cardiogenic shock, and anaphylactic and anaphylactoid events. Patients who develop clinically significant infusion reactions should have their Rituxan infusion discontinued and receive medical treatment. Acute renal failure requiring dialysis with instances of fatal outcome has been reported in the setting of tumor lysis syndrome following treatment with Rituxan. Severe mucocutaneous skin reactions, some with fatal outcome, have been reported in association with Rituxan treatment. Patients experiencing a severe mucocutaneous reaction should not receive any further infusions and seek prompt medical evaluation. Abdominal pain, bowel obstruction and perforation, in some cases leading to death, were observed in patients receiving Rituxan in combination with chemotherapy for diffuse large B-cell (DLBCL), CD20-positive, non-Hodgkin's lymphoma. Other serious or potentially life-threatening adverse reactions that have been reported following Rituxan therapy include Hepatitis B reactivation with fulminant hepatitis, other viral infections, hypersensitivity reactions, and cardiac arrhythmias.
About Rituxan
Rituxan is a therapeutic antibody that targets and selectively depletes CD20-positive B-cells without targeting stem cells or existing plasma cells. In addition to RRMS, Rituxan is being studied in primary progressive MS, for which there is currently no FDA-approved therapy. Rituxan is being studied in other autoimmune diseases with significant unmet medical needs, including systemic lupus erythematosus, lupus nephritis and ANCA-associated vasculitis.
Rituxan, discovered by Biogen Idec, first received FDA approval in November 1997 for the treatment of relapsed or refractory, low-grade or follicular, CD20-positive, B-cell non-Hodgkin's lymphoma. It was also approved in the European Union under the trade name MabThera� in June 1998. In addition, Rituxan received FDA approval in February 2006 for the treatment of diffuse large B-cell lymphoma (DLBCL) in combination with CHOP (cyclophosphamide, doxorubicin, vincristine and prednisone) or other anthracycline-based chemotherapy regimens in previously untreated patients, as well as in combination with methotrexate to reduce signs and symptoms in adult patients with moderately-to-severely active rheumatoid arthritis who have had an inadequate response to one or more tumor necrosis factor antagonist therapies.
Genentech and Biogen Idec co-market Rituxan in the United States, and Roche markets MabThera in the rest of the world, except Japan, where Rituxan is co-marketed by Chugai and Zenyaku Kogyo Co. Ltd. Rituxan has more than 960,000 patient exposures worldwide. For a copy of the Rituxan full prescribing information, including Boxed Warning, please call 1-800-821-8590 or visit http://www.gene.com.Posts: 1078 | From Fairland | Registered: Apr 2006
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LostCityAgent
Unregistered
posted
Thanks Dave for your contribution!
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So in total you take 30mg.of 4-AP ? Now off to find a Dr. to perscribe it for me !
Posts: 203 | From tipp city oh.45371 | Registered: Jul 2003
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Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
John, you are welcome and you started a very interesting topic.
Because of the low cost, I don't suspect there is any conspiracy behind it.
Low dose naltrexone in multiple sclerosis
While there are no scientific studies documenting the effects of low dose naltrexone (LDN) therapy in MS, the related drug naloxone has been investigated in a variety of neurodegenerative and inflammatory disorders such as septic shock, injuries to brain and spinal cord, myocardial and cerebral stroke and Alzheimer's disease. There is however considerable anecdotal evidence supporting the use of LDN in MS by the lay public.
Anecdotal literature from the United Kingdom and the United States suggests that LDN markedly reduces the frequency of MS relapses and halts the progression of multiple sclerosis. The cult like following of LDN by the lay patient is reflected in the approximately 15,000 hits (48,800 as of today)for ``low dose naltrexone'' on the Google search engine [www.google.com], over 70,000 LDN capsules have been dispensed between Jan and Aug 2004 from just one pharmacy (Dr. Henry Lenz Pharm D, personal communication), an international petition for a clinical trial of LDN in MS has over 5500 signatories (www.thepetitionsite.com), a patent for the use of naltrexone in MS awarded by the US Patent office (#6,586,443 and one ongoing clinical trial of LDN in ulcerative colitis an autoimmune disease http://www.hmc.psu.edu/color ectal/research/naltrexone.htm). Furthermore, MS patients who had been going downhill with conventional therapy have reported their experiences with LDN in five newspaper reports in the British and American press, as well as have organized and participated in a self reported web based survey of 267 LDN users from 16 countries. This patient organized survey, reports an average relapse rate of only 0.2/year in patients with MS. While the patient selfreported survey cannot be equated with a physician organized clinical trial, it begs the question as towhy are there no clinicians investigating this. The patient initiated LDN surveys as well as the media reports have been summarized at www.LDNers.org. While naltrexone has been approved by the US Federal Drug Administration at 10-fold higher doses, it has not been systematically investigated in MS.
Naltrexone is related to naloxone an opioid antagonist with no opioid agonist properties. The activity of naltrexone is due to the parent drug as well as its metabolite 6-b-naltrexol. They have a short half-life of 4 and 13 h, respectively. Naltrexone is used at low doses (3-4.5 mg/day) in clinical Naltrexone is related to naloxone an opioid antagonist with no opioid agonist properties. The activity of naltrexone is due to the parent drug as well as its metabolite 6-b-naltrexol. They have a short half-life of 4 and 13 h, respectively. Naltrexone is used at low doses (3-4.5 mg/day) in clinical practice by private physicians. At these doses, no significant side effects have been reported in the anecdotal literature. Some patients have reported increased stiffness, or increased wakefulness. The increased wakefulness disappears within a few weeks of starting therapy, while decreasing the dose can reduce stiffness.
Posts: 1078 | From Fairland | Registered: Apr 2006
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posted
so does Low Dose Naltrexon work to improve pain--or mostly weakess and sensory loss (i am assuming these are the MS symptoms you refer too, and the tingling etc)
I ask beacuase my friends w/ "ms" (and we have never discussed the posible lyme cnnction) share similiar weakness and sensory problems but NOT the pain.
very interesting and thanks
jif
Posts: 208 | From Santa Fe | Registered: May 2006
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LostCityAgent
Unregistered
posted
David, Thank you for that stunning report. It was truly supportive and exciting to read.
Jif, This refers to any and all symptoms that can be related to Multiple Sclerosis for the simple fact that the culprit is being over taken, much like with meds for HIV. What is under attack and pinned down, cannot attack. I have suffered over 83 symptoms as a LD patient with Multiple Sclerosis, and, around 15 MS symptoms. After 6 weeks of LDN treatment, the only symptoms of these that remain are not bothersome: they are:
Simultaneous quantitation of norepinephrine, dopamine and serotonin in brain during and following chronic naltrexone administration.
Baron SA, Testa FM, Gintzler AR.
The effects of chronic administration of the narcotic antagonist naltrexone on regional brain levels of norepinephrine, dopamine and serotonin were studied in order to determine whether central monoaminergic neurons are tonically modulated by central opioid systems.
Chronic exposure to naltrexone (8 days) is associated with
a significant increase in the content of norepinephrine
in the mesolimbic forebrain and the content of dopamine in the frontal cortex and striatum. Ten days following naltrexone pellet removal the above levels returned to control values but thalamic dopamine content was reduced 10-fold. These data suggest that the affected brain regions receive an opioidergic input that is tonically active.
PMID: 2862958
DATA SYNTHESIS: Naltrexone has been used most commonly at doses ranging from 0.5 to 2 mg/kg/day and found to be predominantly effective in decreasing self-injurious behavior.
Naltrexone may also attenuate hyperactivity, agitation, irritability, temper tantrums, social withdrawal, and stereotyped behaviors. Patients may also exhibit improved attention and eye contact.
Transient sedation was the most commonly reported adverse event. Small sample size, short duration, and inconsistent evaluative methods characterize the available research.
CONCLUSIONS: A child affected by AD may benefit from a trial of naltrexone therapy, particularly if the child exhibits self-injurious behavior and other attempted therapies have failed. Serious adverse effects have not been reported in short-term studies.
Nalmefene (Revex) -Acts like naltrexone but safer for those with liver problems.
Med Hypotheses. 2005;64(4):721-4. Agrawal YP. Department of Pathology, The University of Iowa Roy J. and Lucille A. Carver College of Medicine, Room 153 B MRC, 200 Hawkins Drive, Iowa City, IA 52242-1182, USA. [email protected]
The use of low doses of naltrexone for the treatment of multiple sclerosis (MS) enjoys a worldwide following amongst MS patients. There is overwhelming anecdotal evidence, that in low doses naltrexone not only prevents relapses in MS but also reduces the progression of the disease.
It is proposed that naltrexone acts by reducing apoptosis of oligodendrocytes. It does this by
This results in a decrease in the formation of peroxynitrites, which in turn prevent the inhibition of the glutamate transporters.
Thus, the excitatory neurotoxicity of glutamate on neuronal cells and oligodendrocytes via activation of the alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid class of glutamate receptor is prevented.
It is crucial that the medical community respond to patient needs and investigate this drug in a clinical trial.
All these KLH effects are blocked by naltrexone and/or naloxone which inhibits the IL4 production, the analgesia and the modulation of TH1/TH2 cytokine production. In the latter KLH induces IL-4 production while
These immunostimulatory effects of melatonin could be antagonized by the opioid antagonist naltrexone.
In addition, pinealectomy appeared to reduce
inter- leukin-2 levels in mice,
as well as the associated natural killer cell activity. These findings led to the conclusion that melatonin exerts its effects on the immune system through the
release of opioid peptides and interleukin-2 from T-lymphocytes.
The presence of 2-[ 125 I]-iodomelatonin binding sites on human blood lymphocytes is in support of a direct action of melatonin on T-cells
Abstract We studied the effects of an acute (45 min) exposure to a 60 Hz magnetic field on sodium-dependent, high-affinity choline uptake in the brain of the rat. Decreases in uptake were observed in the frontal cortex and hippocampus after the animals were exposed to a magnetic field at flux densities 0.75 mT.
These effects of the magnetic field were blocked by pretreating the animals with the narcotic antagonist naltrexone, but not by the peripheral opioid antagonist, naloxone methiodide.
These data indicate that the magnetic-field-induced decreases in high-affinity choline uptake in the rat brain were mediated by endogenous opioids in the central nervous systems. � 1993 Wiley-Liss, Inc.
Some evidence has also been provided that melatonin interacts with the opioid peptides.45-46 Melatonin is both utilized and synthesized following acute pain episodes in humans,47
the function of which may be to modulate fluctuations in opioid receptor expression and levels of beta-endorphin.48
The relationship of melatonin with the opioidergic system is complex and not completely understood, although there is evidence that it has mixed opioid receptor agonist-antagonist activity.49
In aggregate these findings lend support to the postulate of a "melatonin-opioid axis"48 possibly serving a variety of protectant functions.
In addition: norepinephrine transport (NET) = a MAO (monoamine transporter)is inhibited by ethanol.
Too much MAO (A)? Block MAO A and increase NE, serotonin and dopamine...tyramine too?
Dopamine INactivation with MAO.
Tyrosine INactivates NFkB.
Another problem: Acetylcholine-gated cation channels at the neuromuscular junction open in response to acetylcholine released by the nerve terminal and
allow Na+ ions to enter the muscle cell,
which causes membrane depolarization and ultimately leads to muscle contraction. The present study tested the hypothesis that, in normal male rats,
chronic changes in salt intake alter the levels of tyrosine hydroxylase and
the norepinephrine transporter
in sympathetic ganglia.(PMID: 12963419)
Another problem:
Many psychotropic drugs interfere with the reuptake of dopamine, norepinephrine, and serotonin. Transport capacity is regulated by kinase-linked pathways, particularly those involving protein kinase C (PKC), resulting in transporter phosphorylation and sequestration.
Bb has a PKC inhibitor.
Back to Naltrexone:
Naltrexone inhibits dopamine neurons in the ventral tegmental area of the brain and decreases dopamine function in the nucleus accumbens.
Dopamine's role in these parts of the brain is to mediate pleasure and urges. A group from the University of Minnesota has done several studies using naltrexone for pathologic gambling. They find that there's a significant improvement, particularly among the more severe gamblers.
The doses required are far greater than those used in alcohol dependence -- at least 100-250 mg per day. The side effects are quite well tolerated and consist of nausea, dry mouth and vivid dreams.
At higher doses, though, naltrexone shouldn't be given with concurrent non-steroidal analgesics as it causes elevations in liver enzymes. It's also important to treat the comorbid anxiety and depressive disorders that commonly accompany gambling, and not just the addiction.
"Morphine, an opioid receptor agonist, increased significantly the activity of N-acetyltransferase in a dose-dependent fashion. In addition, the stimulatory effect of morphine was inhibited by naloxone, an opioid receptor antagonist."
"Alcohol stimulates release of endogenous opioids, which in turn stimulate release of dopamine, which mediates reinforcement."
Tyrosine -> Dopamine -> norepinephrine.
Norepinephrine works with b-adrenergic receptors -> increased levels of cAMP -> activates N-acetyltransferase needed to convert serotonin -> melatonin which then inhibits the synthesis and secretion of other neurotransmitters such as dopamine and GABA.
Tyrosine also takes another path:
"Created from tyrosine, tyramine is a neurotoxic and mildly addicting stimulant. The body has fortunately developed defenses against the substance, and the vast majority of the tyramine found in the average American meal must be neutralized in the gut by a chemical called monoamine oxidase.
In fact, if monoamine oxidase were not present in the body, the average American meal could prove fatal to most people. However, the presence of high amounts of both tyramine and monoamine oxidase in the body can have negative effects on mood.
Tyramine is a stimulant, an agonist at both the noradrenaline and adrenaline receptor sites (while skipping over the dopaminergic ``pleasure'' sites).
Monoamine oxidase (MAO) on the other hand is associated with both aggressive behavior and depression. MAOs find their way into the brain and are used to
permanently break down dopamine and serotonin, the two neurotransmitters most thought to play a role in overall mood."
Another problem: tyrosine nitration (oxidative stress marker)...in several diseases besides lyme too.
Guess why:
Angiotensin II-induced hypertension is accompanied by
increased tyrosine nitration of MnSOD,
which, because it inactivates the enzyme, may contribute to increased oxidant stress in the kidney.
So, if you really want to go after Bb...focus not only on the glyolysis pathway (sugar -> ethanol), but simultaneously the cholesterol pathway to INactivate HMG CoA reductase which is triggered by angiotensin II.
Posts: 9481 | From Sunshine State | Registered: Mar 2001
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I'm glad that you are having some improvement, but it looks to me like you've jumped the gun. You've only been on it for 6 weeks, and there is no way of telling which therapy is working...LDN or Doxy, or a combination.
There have been MANY lymies on here that felt like they were cured after feeling great for a few weeks, only to relapse. I wish you luck, but please keep us informed of your progress, or lack of progress so that others here can make the right choice about LDN therapy
I might add that there are 2 other people that posted that LDN has not done much for them even after years of taking it. So right now the results are only 33% positive for LDN based on 3 peoples results here, and you have only been on it short term.
-------------------- You're only a failure when you stop trying. Posts: 945 | From U.S | Registered: Oct 2004
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posted
RE: 4-AP I took it 2.5yrs ago, had forgot about it. Got info in the mail re: Fampridine SR today. Looking back I think it helped with walking and fatigue. I will call tomorrow to get some from my compounding pharm.
RE: Rituxan - No thanks Dave. It had a different name some yrs back because I remember waiting for it. Well, some people died from it. So, they changed the name and bought it out again. I can't remember what it was called back then.
RE: LDN - I have been on a low dose for yrs. It doesn't help with nerve pain though. I think it helps keep me stable. If I get over 3.0, I get more stiffness, it is cheap and can't hurt anything.
Posts: 315 | From USA | Registered: May 2005
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posted
OK, the title, naltrexone piqued my interest. I have been on 50mg daily (unless I play doctor barb and skip it) for geez, 6,7 years or so. I take it for a completely different (psych) reason. The only thing I thought I noticed related to lyme was an improvement in those dull headaches. they seemed to be less. Back when I started, I probably posted something on this discussion board. I carry a medic-alert tag and a wallet card listing it among my medications. If I am ever in an accident and need pain med's, the naltrexone would cancel the effects of any opiate based pain med. Thus, the danger of no pain relief, or being given too much, over dose. On the subject of off label uses. When they started me on depakote, I think it "cured" my lyme hypersensitivity to light, sound and everything else...might have just been me, weird me.
-------------------- Lyme is like the flu. You can get it and recover, but you can always get it again. Posts: 607 | From (deer tick)Heaven! Angeles National Forest | Registered: Oct 2000
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