Dosage Strengths of Low Dose Naltrexone (LDN) 
1.5 mg , 3 mg , 4 mg, 4.5 mg   x30 = $25


Naltrexone is an oral opiate receptor antagonist. It is derived from thebaine and is very similar in structure to oxymorphone. Like parenteral naloxone, naltrexone is a pure antagonist (i.e., agonist actions are not apparent), but naltrexone has better oral bioavailability and a much longer duration of action than naloxone. Clinically, naltrexone is used to help maintain an opiate-free state in patients who are known opiate abusers. Naltrexone is of greatest benefit in patients who take the drug as part of a comprehensive occupational rehabilitative program or other compliance-enhancing program. Unlike methadone or LAAM, naltrexone does not reinforce medication compliance and will not prevent withdrawal. Naltrexone has been used as part of rapid and ultrarapid detoxification techniques. These techniques are designed to precipitate withdrawal by administering opiate antagonists. These approaches are thought to minimize the risk of relapse and allow quick initiation of naltrexone maintenance and psychosocial supports. Ultrarapid detoxification is performed under general anesthesia or heavy sedation. While numerous studies have been performed examining the role of these detoxification techniques, a standardized procedure including appropriate medications and dose, safety, and effectiveness have not been determined in relation to standard detoxification techniques.1 Naltrexone supports abstinence, prevents relapse, and decreases alcohol consumption in patients treated for alcoholism. Naltrexone is not beneficial in all alcoholic patients and may only provide a small improvement in outcome when added to conventional therapy. The FDA approved naltrexone in 1984 for the adjuvant treatment of patients dependent on opiate agonists. FDA approval of naltrexone for the treatment of alcoholism was granted January 1995. The FDA approved Vivitrol, a once-monthly intramuscular naltrexone formulation used to help control cravings for alcohol in April 2006, and then in October 2010, the FDA approved Vivitrol for the prevention of relapse to opioid dependence after opioid detoxification


Dosage Strengths of Lipo Injection
Methionine / Choline Chloride 25/50 mg/mL 10 mL Vial

Methionine / Choline Chloride 25/50 mg/mL 30 mL Vial


General Information
Lipotropes are compounds that may aid in the breakdown of body fat by acting on lipid metabolism and synthesis pathways. When used in combination with lifestyle modifications such as exercise and diet, lipotropic compounds may promote fat and weight loss.

Lipotropic compounds including vitamins, nutrients, and other natural or pharmacological agents may be administered as injections or in the form of oral supplements. Injections provide the advantage of better bioavailability by avoiding enzymes in the gastrointestinal tract. In addition, injections may be especially beneficial in individuals with gastrointestinal absorption issues.

The lipotropic agents in this injection are methionine, inositol, and choline. While each may individually affect the mobilization of fats, the combination may provide synergistic benefits.123 The physiological role of each compound and the effects of supplementation are described below.

Methionine
A branched-chain amino acid with sulfur is methionine. Methionine is crucial for immune system function, lipid metabolism, polyamine production, heavy metal chelation, and redox balance since it is a precursor for cellular methylation processes.4 In contrast, methionine limitation in the diet decreased insulin resistance in rodents and promoted adipose tissue lipolysis and fatty acid oxidation.5

The metabolite S-adenosyl methionine (SAM) of methionine, which has lipotropic properties, may be responsible. Methionine is converted into SAM by a process that requires energy. For the treatment of depression, osteoarthritis, and liver conditions, SAM has been studied when taken orally or intravenously.6 SAM may act as a methyl donor in the metabolic processes that control lipid homeostasis, DNA stability, gene expression, and neurotransmitter release, which may account for the benefits it confers.789

Inositol
Inositol is a family of cyclic sugar alcohols consisting of nine stereoisomers of hexahydroxycyclohexane. The stereoisomers of the inositol family are myo-, scyllo-, muco-, neo-, allo-, epi-, cis-, and the enantiomers L- and D-chiro-inositol. Of these, myo-inositol and D-chiro-inositol are among the most abundant biologically active forms. The enzyme epimerase converts myo-inositol to the D-chiro-inositol isomer, maintaining organ-specific ratios of the two isomers. Physiologically, the concentration of myo-inositol is several times higher than D-chiro-inositol in most tissues.10

The myo-inositol derivative phosphatidylinositol is an important component of the lipid bilayer of cell membranes. Phosphatidylinositol and its phosphorylated forms act as second messengers that are involved in a host of cellular functions including membrane trafficking, autophagy, cell migration, and survival. Disruption of phosphoinositide lipid signaling is implicated in cancer, diabetes, and cardiovascular disorders.11

Inositol has shown clinical benefits in treating disorders associated with metabolic syndrome. Inositol supplementation has been effectively used to accelerate weight loss, reduce fat mass,12 improve serum lipid profiles and upregulate the expression of genes involved in lipid metabolism and insulin sensitivity13 in women with polycystic ovarian syndrome. Myo-inositol alone or in combination with D-chiro-inositol significantly reduced weight, BMI, and waist-hip circumference ratios in overweight/obese women with PCOS. Weight loss, reduction in fat mass and increase in lean mass were accelerated when inositol supplementation was accompanied by a low-calorie diet.14 In addition, inositol supplementation was associated with lower rate of gestational diabetes and preterm delivery in pregnant women.12 Currently, research is being performed to assess whether inositol may be used in treating various cancers.

Choline
Choline is an essential nutrient required for optimal functioning of various tissues including the liver, muscles, and brain.15 Since choline breaks down fat as an energy source, choline supplementation caused rapid fat and weight loss in female athletes.16 Only small amounts of choline are synthesized by the human body, necessitating its intake from external sources. In the body, about 95% of the total choline pool is converted to phosphatidylcholine – an essential component of the phospholipid bilayer and the predominant phospholipid in most mammalian cells.17 Choline also undergoes acetylation to form the neurotransmitter acetylcholine. Choline deficiency causes hepatic steatosis (fatty liver disease) and leads to loss of muscle membrane integrity. Chronic choline deficiency may also increase the risk of developing cancer.

Both choline and methionine are a source of methyl groups for the one-carbon transmethylation pathway and serve hepato-protective functions. Culturing hepatocytes in choline and methionine-deficient media impaired VLDL secretion.18 In addition, choline can donate methyl groups to support methionine regeneration, possibly contributing to their synergistic lipotropic effects.
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