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Leonardo Myers
Leonardo Myers

Where To Buy Low Dose Naltrexone

Low Dose Naltrexone (LDN) refers to daily dosages of naltrexone that are approximately 10% or less of the typical opioid addiction treatment dosage, commonly up to 5mg. These dosages are compounded at compounding pharmacies and require a prescription. At the low dosage level, naltrexone exhibits paradoxical properties, including analgesia and anti-inflammatory actions, which have not been reported at larger dosages. Studies have shown that it can be beneficial for people with conditions marked by immune system dysfunction.

where to buy low dose naltrexone

LDN is known to be safe and well-tolerated and this is one exciting aspect of LDN. The side effect profile is minimal with most common reports of vivid dreams and interrupted sleep during the initial adjustment they develop rapidly and decrease over time. LDN is compatible with most prescription medications except for narcotics. Low-dose naltrexone blocks the effects of narcotics and could cause withdrawal symptoms, so it should be started only after those drugs are completely out of your system.

Low dose naltrexone may be beneficial for the treatment of various conditions including chronic pain and autoimmune illnesses. Naltrexone is typically used to treat opioid use disorder and alcohol abuse disorder. It is classified as an opioid antagonist blocking the effects of exogenously administered opioids. Naltrexone at low doses (0.5mg - 6mg) has been prescribed for its possible analgesia and anti-inflammatory effects, which have not been observed at higher doses.

Naltrexone, however, exerts its effects on humans via at least two distinct receptor mechanisms. In addition to the antagonist effect on mu-opioid and other opioid receptors, naltrexone simultaneously has an antagonist effect on non-opioid receptors (Toll-like receptor 4 or TLR4) that are found on macrophages such as microglia [17]. It is via the non-opioid antagonist path that LDN is thought to exert its anti-inflammatory effects. Microglia are central nervous system immune cells that are activated by a wide range of triggers [18]. Once activated, microglia produce inflammatory and excitatory factors that can cause sickness behaviors such as pain sensitivity, fatigue, cognitive disruption, sleep disorders, mood disorders, and general malaise [19]. When chronically activated, the resulting proinflammatory cascade may become neurotoxic, causing several deleterious effects [20]. Given the wide variety of inflammatory factors produced by activated microglia (e.g., proinflammatory cytokines, substance P, nitric oxide, and excitatory amino acids) [21], a range of symptoms and medical outcomes could share the pathophysiological mechanism of central inflammation. Conditions such as fibromyalgia may involve chronic glial cell activation and subsequent production of proinflammatory factors. The hypothesis is indirectly and partially supported by the high degree of symptomatic overlap between fibromyalgia and cytokine-induced sickness behaviors.

Both naloxone and naltrexone have been demonstrated to exert neuroprotective and analgesic effects [22]. The neuroprotective action appears to result when microglia activation in the brain and spinal cord is inhibited [23]. By suppressing microglia activation, naloxone reduces the production of reactive oxygen species and other potentially neuroexcitatory and neurotoxic chemicals [24]. The anti-inflammatory effect of opioid antagonists may also extend to the periphery, as evidenced by suppressed TNF-alpha, IL-6, MCP-1, and other inflammatory agents in peripheral macrophages [25]. It should be noted that most animal work has used naloxone, while most human work has used naltrexone (because of its higher oral availability). We cannot discount the possibility that findings from one compound would imperfectly translate to the other.

The hypothesis that naltrexone and naloxone operate via glial cells to exert their beneficial actions is supported by work with dextro-naltrexone. Dextro-naltrexone is a stereoisomer of naltrexone which is active at microglia receptors but has no activity on opioid receptors [26]. Dextro-naltrexone possesses analgesic and neuroprotective properties [27]. Therefore, the analgesic, anti-inflammatory, and neuroprotective effects of naltrexone do not appear to be dependent on opioid receptors.

The typical dosage of LDN in published research is 4.5 mg. The medication is commonly given approximately an hour before bedtime, though some individuals reporting insomnia as a side effect are moved to a morning dosing. Individuals with side effects also have their dosage reduced to 3.0 mg. At the time of writing, naltrexone is commercially available only in a 50-mg tablet form, although one US-based company appears to be gathering regulatory approvals to market the 4.5 mg formulation. Because there is no commercial formulation of LDN, research studies obtain the medication via compounding pharmacies. Standard gelatin capsules and microcrystalline cellulose filler are commonly used.

Dextro-naltrexone, however, may be far more interesting in terms of anti-inflammatory and microglia-modulating properties. Preliminary data in animal models have already suggested that dextro-naltrexone may have a role in reducing pain and inflammation [22]. Not only does it appear to potently suppress microglia but it also exerts little activity on opioid receptors, which could translate into reduced risk of side effects related to systemic opioid blockade. Therefore, dextro-naltrexone might be administered at higher dosages, yielding greater microglia-suppressing activities while minimizing side effects. It is also possible that dextro-naltrexone, co-administered with opioid analgesics, might allow patients to realize the full benefits of opioid analgesia while simultaneously blocking many of the adverse effects.

However, this is naltrexone at regular strength. Studies have shown that lower doses of naltrexone have a variety of uses. Many people take low dose naltrexone for chronic pain, depression, anxiety, and autoimmune diseases.

There is only one way to get low dose naltrexone: with a prescription. Low dose naltrexone is also not available through a traditional pharmacy. Large pharmaceutical companies do not produce naltrexone at lower doses. The regular dosage size used for addiction is around 50-100 mg. In order to get lower doses, your prescription must go to a compounding pharmacy. Compounding pharmacies can develop naltrexone at any dose necessary. Lower doses are usually around 2-5 mg depending on the needs of the patient. Your pharmacist can work with your doctor to determine the optimal dosage size.

Your doctor can give you more information about low dose naltrexone. If you were considering taking this medication for depression, pain, or autoimmune diseases, it may be worth while to bring it up to your provider. They will help you weigh the pros and cons.

However, while naltrexone at regular strength is accepted by the FDA, naltrexone at low doses continues to be studied. Because of this, some doctors may not be as informed about the recent success it has shown helping patients. If your provider is not comfortable with low dose naltrexone, it is possible to seek a second opinion. Functional medicine doctors usually have more experience with and are more open to prescribing low-dose naltrexone. 041b061a72


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