***If you are seeing a doctor that is not a part of ILADS (International Lyme and Associated Diseases Society) I highly recommend you get this crucial information into their hands and encourage them to become members, where they will learn the most cutting edge research and treatments. Your very life depends upon it.
Grier, infected himself, has done cutting edge work and we need to listen to it. He shows autopsy results – demonstrating Borrelia Burgdorferi (Bb) in numerous tissues, including the brain (glial cells, neurons, endothelial cells), kidneys, placenta, and much more.
Low Dose Naltrexone (LDN) is widely used for autoimmune disorders such as multiple sclerosis (MS), Crohn’s disease, fibromyalgia, Hashimoto’s thyroiditis, and other inflammatory and chronic disorders. LDNscience produced this video explaining how it works. LDNscience.org, launched in 2009, is a public information project of the MedInsight® Research Institute.
You may remember the use of Naltrexone in the treatment of those with alcohol and opioid addictions; however, those dosages are much higher (50-300mg) than for Low Dose Naltrexone (LDN) (1.5-4.5mg). LDN works by blocking opioid receptors for 3-4 hours, telling your body to increase endorphins that relieve pain and also activate the immune system by directing activity of stem cells, macrophages, killer cells, T and B cells and other immune cells. It also modulates an overactive immune system so there is less inflammation and release of neurotoxins.
Naltrexone at 50 mg prohibits heroin addicts from getting high. Those working with addicts and using Naltrexone uncovered the fact that addicts have low endorphins – which is why addicts reach for things that increase endorphin levels, such as heroin. Heroin works temporarily but it also causes horrific side effects and it ends up lowering endorphin production, which of course causes the addict to keep reaching for a fix, but it takes more and more to achieve the same results.
So what does having low endorphins and addictions have to do with MSIDS(multi systemic infectious disease syndrome – or – Lyme with friends)?
Over 90% of immune cell receptors are endorphin receptors, sowhen we have low endorphin levels, our immune systems are hugely compromised and we feel….well, crappy. Feeling crappy is your body’s way of telling you that something isn’t right. MSIDS patients can’t sleep at night but we are exhausted all day long. We have temperature dysregulation and alternate from sweating to shivering. We suffer with pain that is unbelievable and have cognitive issues such as memory loss and word search, and neurological issues such as tingling, burning, and twitching. (Oh, isn’t it fun when your body acts on its own volition!)
When we are infected with a long train of pathogens that are experts at subverting our immune response, we suffer with a veritable laundry list of symptoms and often need to take various supplements, including neurotransmitters, to help our hijacked immune systems.
According to Cowan, there are 4 ways to increase your endorphins.
1) High intensity exercise – the proverbial “runner’s high,” which frankly isn’t possible when you have MSIDS.
2) Acupuncture
3) Chocolate – the constituent I-Phenylalanine keeps endorphins from breaking down. But it doesn’t last – leading to wanting more chocolate, so this isn’t a great one for MSIDS patients either unless you like gaining weight.
4) LDN – while history found that 50mg blocks endorphin receptors all day making addicts feel lousy, taking only 2-4.5mg right before bed only blocks receptors about an hour. The block wears off which tells the body to make more. LDN is a telegram sent to your body to create more endorphins.
A beautiful connection: The Gut and the Brain (something we can do something about)
Rudolf Steiner once said, “The brain is just smooched up guts.”The brain and the gut both have the same receptors – including serotonin. Dr. Natasha Campbell-McBride has successfully created the Gut and Psychology Syndrome (GAPS) diet.http://www.doctor-natasha.com. Gluteo-morphines (gluten in grains) and caseo-morphines (casein in dairy) alter our immune function and our neurological function by creating imperfect chemicals which ultimately cause immune dysfunction.
What this means is that we can tweak our diets and avoid gluten and casein, talk over LDN with our medical practitioner, and help our guts, our brains, and our immune systems all in one fell swoop.
Cowan states that creating natural endorphins and healing the leaky gut which is causing gut and neurological issues are two key issues.
Dr. Bernard Bihari has treated more than 450 cancer patients with LDN and has noted at least a 75% reduction in tumor size, and nearly 60% of his patients demonstrated disease stability. He also found people with autoimmune diseases such as Lupus often showed quick stabilization. When his HIV/AIDS patients took LDN were typically spared deterioration of helper T cells (CD4+).
Dr. Burton Berkson states: “It is difficult for many to believe that one drug can accomplish so many tasks. But LDN does not treat symptoms as most drugs do. It actually works way ‘upstream’ to modulate the basic mechanisms that result in the disease state.”
Published on Jun 22, 2015 Approx. 1 hour
Hear from several practitioners on how they use LDN with their patients and witness 2 remarkable stories on how LDN has changed the lives of a 8 year old Jacob Valazquez in Miami and Sarah Morton in the UK who was suffering from Fibromyalgia.
LDN helps MS. An Excerpt from “Low Dose Naltrexone Therapy in Multiple Sclerosis,” in Med Hypotheses states: “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 reducing inducible nitric oxide enthuse activity…. It is crucial that the medical community respond the patient needs and investigate tis drug in clinical trial.”
LDN helps PTSD.Post Traumatic Stress Disorder significantly improved with LDN. An Excerpt from “Low Dose Naltrexone in the Treatment of Dissociative Symptoms”:
“The low dose treatment with Naltrexone proved to be effective whereby 11 out of 15 patients reported immediate positive effects and 7 described a lasting helpful effect. The majority of patients who felt positive effects reported a clearer perception of both their surroundings and their inner life.Assessment of reality and dealing with it improved as did the perception of their own body and affects as well as self-regulation. The treatment was very low in side effects….Treatment with low dose naltrexone may be a helpful element in the treatment of patients with complex post traumatic stress disorder.”
Abstract
Complex Regional Pain Syndrome (CRPS) is a neuropathic pain syndrome, which involves glial activation and central sensitization in the central nervous system. Here, we describe positive outcomes of two CRPS patients, after they were treated with low-dose naltrexone (a glial attenuator), in combination with other CRPS therapies. Prominent CRPS symptoms remitted in these two patients, including dystonic spasms and fixed dystonia (respectively), following treatment with low-dose naltrexone (LDN). LDN, which is known to antagonize the Toll-like Receptor 4 pathway and attenuate activated microglia, was utilized in these patients after conventional CRPS pharmacotherapy failed to suppress their recalcitrant CRPS symptoms.
LDN helps Crohn’s Disease. https://www.ncbi.nlm.nih.gov/pubmed/17222320 Dr. Jill Smith found that two-thirds of patients in her pilot study went into remission and 89% responded to treatment to some degree.
Hepatitis C
Lupus
Ulcerative colitis
Autism
Chronic Fatigue
Irritable bowel
Diabetic neuropathies
Dermatomyositis
MS
Crohn’s
Alzheimer’s
Hasimoto’s
Parkinson’s
Tick borne Illness
Common Colds
Emphysema
HIV/AIDS Lyme Disease (Late Stage)
ALS
PTSD
Transverse Myelitis
Behcet’s
Celiac
Dystonia
Endometriosis
Hashimoto’s
Psoriasis
RA
Sjogren’s
Cancers
and more
So why haven’t you or your doctor heard of LDN? Although it has been FDA approved for over two decades, the lower doses used to help the immune system have not been submitted for FDA approval as big pharma wants nothing to do with a drug that costs between $15-$40/month.
“LDN substantially reduces health care costs and improves treatment of a wide array of diseases. Unfortunately, because naltrexone has been without patent protection for many years, no pharmaceutical company will bear the expense of the large clinical trials necessary for FDA approval of LDN’s new special uses. It is now up to public institutions to seize the opportunity that LDN offers.” David Gluck, MD
There are virtually no side-effects; however, occasionally and only during the first week of use, some may have trouble sleeping. Some do report vivid dreams. It’s important to start with the lowest dose (1.5-2mg) for a month before going higher. It’s also important NOT to use the time-release form as you want a spike in the blood stream for therapeutic effect.
The therapeutic dosage range for LDN is from 1.5mg to 4.5mg every night. Dosages below this range are likely to have no effect at all, and dosages above this range are likely to block endorphins for too long a period of time and interfere with its effectiveness.
*Those taking narcotics should NOT take LDN until it is completely out of the body.
*Those taking thyroid hormone for Hashimoto’s thyroiditis with hypothyroidism need to start at the lowest dose as there may be a decrease in their disorder which may necessitate a rapid reduction in thyroid medication in order to avoid hyperthyroidism.
*Folks with organ transplants and taking permanent immunosuppressive drugs should avoid LDN as it will counter the effects of those meds.
*Do not use LDN that has employed the filler calcium carbonate as it has been found to interfere with absorption of the capsule. It is recommended that the fillers be Avicel, lactose (if lactose intolerance is not a problem), or sucrose fillers as useful fast-release fillers.
Irmat Pharmacy, New York, NY
(212) 685-0502
(212) 532-6596
Belmar Pharmacy, Lakewood, CO
(800) 525-9473
(866) 415-2923
The Compounder Pharmacy, Aurora, IL
(630) 859-0333
(800) 679-4667
(630) 859-0114
The Pharmacy Shop and
Compounding Center, Canandaigua, NY
(585) 396-9970
(800) 396-9970
(585) 396-7264
McGuff Compounding Pharmacy,
Santa Ana, CA
(714) 438-0536
(877) 444-1133
(877) 444-1155
Skip’s Pharmacy, Boca Raton, FL
(561) 218-0111
(800) 553-7429
(561) 218-8873
The Medicine Store Pharmacy, Concord, NH
(603) 225-2747
(877) 926-7637
(603) 224-3661
Smith’s Pharmacy, Toronto, Canada
(416) 488-2600
(800) 361-6624
(416) 484-8855
Dickson Chemist, Glasgow, Scotland
+44-141-647-8032
+44-800-027-0673
+44-141-647-8032
**I have successfully used and highly recommend Women’s International Pharmacy in Madison, WI.
Phone: 800.279.5708
Fax: 800.279.8011
They also provide a 24-Hour Automated Phone Service with which you may leave your orders. https://www.womensinternational.com/connections/index.html Excellent articles put out by WIP on hormone-related conditions and therapies. You can also sign up for their monthly e-letter. The pharmacists will be happy to answer any questions you or your practitioner may have.
**The only filler in WIP’s LDN is olive oil. They also sell a compounded form of T3 or (L-triiodothyronine or LT3) much cheaper than the Brand Name Cytomel (which has undesirable fillers such as calcium sulfate, gelatin, starch, stearic acid, sucrose, and talc. Make sure you ask for the compounded form. More info: https://www.restartmed.com/cytomel-side-effects/
The following videos were created by the LDN Research Trust
The spirochaete Borrelia burgdorferi associated with Lyme disease was detected in questing ticks and rodents during a period of 18 years, 1991–2009, at five locations on the Outer Banks of North Carolina. The black-legged tick Ixodes scapularis was collected at varied intervals between 1991 and 2009 and examined for B. burgdorferi. The white-footed mouse Peromyscus leucopus, house mouse Mus musculus marsh rice rat Oryzomys palustris, marsh rabbit Sylvilagus palustris, eastern cottontail Sylvilagus floridanus and six-lined racerunner Cnemidophorus sexlineatus were live-trapped, and their tissues cultured to isolate spirochaetes.
Borrelia burgdorferi isolates were obtained from questing adult I. scapularis and engorged I. scapularis removed from P. leucopus, O. palustris and S. floridanus. The prevalence of B. burgdorferi infection was variable at different times and sites ranging from 7 to 14% of examined questing I. scapularis. Mitochondrial (16S) rRNA gene phylogenetic analysis from 65 adult I. scapularis identified 12 haplotypes in two major clades. Nine haplotypes were associated with northern/Midwestern I. scapularis populations and three with southern I. scapularis populations. Sixteen isolates obtained from tick hosts in 2005 were confirmed to be B. burgdorferi by amplifying and sequencing of 16S rRNA and 5S-23S intergenic spacer fragments. The sequences had 98–99% identity to B. burgdorferi sensu stricto strains B31, JD1 and M11p.
Taken together, these studies indicate that B. burgdorferi sensu stricto is endemic in questing I. scapularis and mammalian tick hosts on the Outer Banks of North Carolina.
Lyme disease is caused by members of the Borrelia burgdorferi sensu lato species complex. Arthritis is a well-known late-stage pathology of Lyme disease, but the effects of B. burgdorferi infection on bone at sites other than articular surfaces are largely unknown. In this study, we investigated whether B. burgdorferi infection affects bone health in mice.
In mice inoculated with B. burgdorferi or vehicle (mock infection), we
measured the presence of B. burgdorferi DNA in bones, bone mineral
density (BMD), bone formation rates, biomechanical properties, cellular
composition, and two- and three-dimensional features of bone
microarchitecture. B. burgdorferi DNA was detected in bone. In the
long bones, increasing B. burgdorferi DNA copy number correlated with
reduction in areal and trabecular volumetric BMD. Trabecular regions of
femora exhibited significant, copy number-correlated microarchitectural
disruption, but BMD, microarchitectural, or biomechanical properties of
cortical bone were not affected.
Bone loss in tibiae was not due to increased osteoclast numbers or
bone-resorbing surface area, but was associated with reduced osteoblast numbers, implying that bone loss in long bones was due to impaired bone building. Osteoid-producing and mineralization activities of existing osteoblasts were unaffected by infection. Therefore, deterioration of trabecular bone was not dependent on inhibition of osteoblast function, but was more likely caused by blockade of osteoblastogenesis, reduced osteoblast survival, and/or induction of osteoblast death.
Together, these data represent the first evidence that B. burgdorferi infection induces bone loss in mice, and suggest that this phenotype results from inhibition of bone building rather than increased bone resorption.
