Weight Loss


Weight management adheres to a multi-faceted lifestyle model that’s comprised of several interrelated decisions and activities such as: eating healthy foods; understanding portion sizes, nutritional values, and macronutrient ratios; creating a holistic exercise regimen that works with your schedule, incorporates your interests, is dynamic enough to prevent burnout, and sets reasonable goals; and accessing the wealth of safe, clinically proven, prescription weight management medications that are currently available. Formulation Compounding Center is dedicated to providing the resources health professionals need to aid their patients in achieving and maintaining ideal body weight goals, as they strive to improve their health-related conditions and overall quality of life.

Obesity and its many serious comorbidities exert a heavy toll in both human and economic terms. More than one-third of adults in the United States are obese, which exponentially increases their odds of hypertension, dyslipidemia, diabetes, and other cardiovascular disease risk factors. Studies have demonstrated that weight loss of as little as 5% to 10% of baseline body weight, has been shown to result in lower triglyceride and blood pressure levels, and in as much as a 58% reduction in the risk of diabetes in pre-diabetic patients. Unfortunately, the problem of obesity is typically exacerbated by aging, as this condition becomes even more difficult to control for older segments of the population. It is a mistake to merely think of obesity in relation to internal health conditions, because it impacts many other areas of one’s childhood, teen, adult, and especially senior life.  One study of individuals aged 65 years and older found that obese individuals had a 31% higher incidence of falling.

Symptoms and Causes of Obesity

The definitions for being overweight and obese vary depending on the source. The National Heart, Lung, and Blood Institute describes some of the signs of being overweight and possibly obese as: clothes feeling tight and requiring larger size; the development of extra fat around the waist; and possessing a higher than normal body mass index and waist circumference.

More specifically, with regard to defining obesity, the Mayo Clinic quantifies obesity as a body mass index (BMI) of 30 or higher. Your body mass index is calculated by dividing your weight in kilograms (kg) by your height in meters (m) squared.

Causes of Obesity

Although there are genetic components and hormonal influences, obesity occurs when you take in more calories than you burn through normal daily activities and extracurricular exercise. The body stores these excess calories as fat, which if it continues to accumulate results in obesity that can be caused by a combination of contributing factors including:


  • Inactivity – a sedentary lifestyle makes it easy to overeat.
  • Unhealthy diet and eating habits – frequent: high calorie meals; fast food; breakfast skipping; late night eating; drinking high calorie beverages; and eating oversized portions all contribute to weight gain.
  • Pregnancy – Many women view this as a time of overindulgence, which initiates obesity, whereas others simply find this weight difficult to lose after giving birth.
  • Lack of sleep – getting less than seven hours of sleep a night can cause changes in hormones that increase your appetite, and create cravings for high calorie foods.
  • Certain medications – some antidepressants, anti-seizure medications, diabetes medications, antipsychotic medications, steroids, and beta blockers.
  • Medical problems – specific medical diseases and conditions promote weight gain, such as Prader-Willi syndrome, Cushing’s syndrome, polycystic ovary syndrome, metabolic syndrome, etc.

Dangerous Weight Loss Drugs

  • Overweight and obese individuals have been seeking quick fixes for centuries. Called ‘fat reducers’, the first diet pills emerged in the late 1800’s. Based on thyroid extract, which can increase metabolic rate, they were effective but had harsh side effects including abnormal heartbeats, increased heart rate, weakness, chest pains, high blood pressure, and fatalities. In the 1930s, a new medication (though technically a poison) called dinitrophenol became a popular for its thermogenic fat loss property (actually a symptom of phenol poisoning). Once its other poisonous symptoms (severe rashes, cataracts, peripheral neuritis, etc.) turned tragic it was removed from the market.
  • A mid-1950s stimulant used in WWII to keep soldiers alert, amphetamines, promoted energy, suppressed appetite, and provided a slimming effect, but were neurologically and psychological addictive. 1965’s obesity treatment, aminorex fumarate, triggered pulmonary hypertension. By the late 1960s a form of thyroid hormone was introduced, often used in conjunction with diuretics, laxatives, and amphetamines. These drugs proved too toxic. In the 1970s, a Danish physician used ephedrine in combination with caffeine to treat asthma, and eventually weight loss. It was soon banned by several states in the 1990s and finally the U.S. Food and Drug Administration (FDA) on December 31, 2003 for adverse cardiovascular and neurological problems, and implication in several deaths.
  • Later phenylpropanolamine, an ephedra derivative, became popular as an appetite suppressant. It was also discontinued due to hemorrhagic stroke and increased hypertension.
  • In 1973 the FDA approved weight loss drug fenfluramine gained popularity in 1992, when it was combined with another drug, phentermine and came to be known as Fen-Phen. Boasting over 18,000,000 sold bottles in 1996 alone, pulmonary hypertension, heart lesions, and valve abnormalities caused its removal…subsequently fenfluramine was voluntarily removed from the market in 1997.


Methylcobalamin B12 Injection

Dosage Strength

10,000 mcg Lyophilized Vial

50,000 mcg Lyophilized Vial

General Information

Methylcobalamin, or vitamin B12, is a B-vitamin. It is found in a variety of foods such as fish, shellfish, meats, and dairy products. Although methylcobalamin and vitamin B12 are terms used interchangeably, vitamin B12 is also available as hydroxocobalamin, a less commonly prescribed drug product, and methylcobalamin. Methylcobalamin is used to treat pernicious anemia and vitamin B12 deficiency, as well as to determine vitamin B12 absorption in the Schilling test. Vitamin B12 is an essential vitamin found in the foods such as meat, eggs, and dairy products. Deficiency in healthy individuals is rare; the elderly, strict vegetarians (i.e., vegan), and patients with malabsorption problems are more likely to become deficient. If vitamin B12 deficiency is not treated with a vitamin B12 supplement, then anemia, intestinal problems, and irreversible nerve damage may occur.


The most chemically complex of all the vitamins, methylcobalamin is a water-soluble, organometallic compound with a trivalent cobalt ion bound inside a corrin ring which, although similar to the porphyrin ring found in heme, chlorophyll, and cytochrome, has two of the pyrrole rings directly bonded. The central metal ion is Co (cobalt). Methylcobalamin cannot be made by plants or by animals; the only type of organisms that have the enzymes required for the synthesis of methylcobalamin are bacteria and archaea. Higher plants do not concentrate methylcobalamin from the soil, making them a poor source of the substance as compared with animal tissues.

Mechanism of Action

Vitamin B12 is used in the body in two forms, methylcobalamin and 5-deoxyadenosyl cobalamin. The enzyme methionine synthase needs methylcobalamin as a cofactor. This enzyme is involved in the conversion of the amino acid homocysteine into methionine which is, in turn, required for DNA methylation. The other form, 5-deoxyadenosylcobalamin, is a cofactor needed by the enzyme that converts L-methylmalonyl-CoA to succinyl-CoA. This conversion is an important step in the extraction of energy from proteins and fats. Furthermore, succinyl CoA is necessary for the production of hemoglobin, the substance that carries oxygen in red blood cells.

Vitamin B12, or methylcobalamin, is essential to growth, cell reproduction, hematopoiesis, and nucleoprotein and myelin synthesis. Cells characterized by rapid division (epithelial cells, bone marrow, myeloid cells) appear to have the greatest requirement for methylcobalamin. Vitamin B12 can be converted to coenzyme B12 in tissues; in this form it is essential for conversion of methylmalonate to succinate and synthesis of methionine from homocysteine (a reaction which also requires folate). In the absence of coenzyme B12, tetrahydrofolate cannot be regenerated from its inactive storage form, 5-methyl tetrahydrofolate, resulting in functional folate deficiency. Vitamin B12 also may be involved in maintaining sulfhydryl (SH) groups in the reduced form required by many SH-activated enzyme systems. Through these reactions, vitamin B12 is associated with fat and carbohydrate metabolism and protein synthesis. Vitamin B12 deficiency results in megaloblastic anemia, GI lesions, and neurologic damage (which begins with an inability to produce myelin and is followed by gradual degeneration of the axon and nerve head). Vitamin B12 requires an intrinsic factor-mediated active transport for absorption, therefore, lack of or inhibition of intrinsic factor results in pernicious anemia.


Methylcobalamin is administered intranasally, orally, and parenterally, while hydroxocobalamin is administered only parenterally. Once absorbed, vitamin B12 is highly bound to transcobalamin II, a specific B-globulin carrier protein and is distributed and stored primarily in the liver as coenzyme B12. The bone marrow also stores a significant amount of the absorbed vitamin B12. This vitamin crosses the placenta and is distributed into breast milk. Enterohepatic recirculation conserves systemic stores. The half-life is about 6 days (400 days in the liver). Elimination is primarily through the bile; however, excess methylcobalamin is excreted unchanged in the urine.

Intramuscular Route Specific Pharmacokinetics: Bioavailability of the nasal gel and spray forms relative to an IM injection are about 9% and 6%, respectively. Because the intranasal forms have lower absorption than the IM dosage form, intranasal B12 forms are administered once weekly. After 1 month of treatment in pernicious anemia patients, the once weekly dosing of 500 mcg B12 intranasal gel resulted in a statistically significant increase in B12 levels when compared to a once monthly 100 mcg IM dose.

Route-Specific Pharmacokinetics:

Intravenous Route: Peak plasma levels of cyanocobalamin are attained within 1 hour for parenteral doses.

Contraindications/ Precautions

Who should not take this medication? Patients with early hereditary optic nerve atrophy, cyanocobalmin hypersensitivity, and those who are pregnant. Your health care provider needs to know if you have any of these conditions: kidney disease; Leber’s disease; megaloblastic anemia; an unusual or allergic reaction to methylcobalamin, cobalt, other medicines, foods, dyes, or preservatives; pregnant or trying to get pregnant; breast-feeding.

Methylcobalamin is contraindicated in patients with methylcobalamin hypersensitivity or hypersensitivity to any of the medication components. Methylcobalamin is also contraindicated in patients with cobalt hypersensitivity because methylcobalamin contains cobalt. In the case of suspected cobalt hypersensitivity, an intradermal test dose should be administered because anaphylactic shock and death have followed parenteral administration of methylcobalamin.

Methylcobalamin should not be used in patients with early hereditary optic nerve atrophy (Leber’s disease). Optic nerve atrophy can worsen in patients whose methylcobalamin levels are already elevated. Hydroxocobalamin is the preferred agent in this patient population (see separate monograph in Less Common Drugs).

Most formulations of methylcobalamin injection contain benzyl alcohol as a preservative. Benzyl alcohol may cause allergic reactions. Methylcobalamin injections should be used cautiously in those patients with benzyl alcohol hypersensitivity. Methylcobalamin, vitamin B12 preparations containing benzyl alcohol should be avoided in premature neonates because benzyl alcohol has been associated with ‘gasping syndrome,’ a potentially fatal condition characterized by metabolic acidosis and CNS, respiratory, circulatory, and renal dysfunction.

Vitamin B12 deficiency can suppress the symptoms of polycythemia vera. Treatment with methylcobalamin or hydroxocobalamin may unmask this condition.

Folic Acid, vitamin B9 is not a substitute for methylcobalamin, vitamin B12 deficiency, although it may improve vitamin B12 megaloblastic anemia. However, exclusive use of folic acid in treating vitamin B12 deficient megaloblastic anemia could result in progressive and irreversible neurologic damage. Before receiving folic acid or methylcobalamin, patients should be assessed for deficiency and appropriate therapy started concurrently. The intranasal formulations are not approved to treat acute B12 deficiency; all hematologic parameters should be normal before beginning the methylcobalamin intranasal formulations. Concurrent iron-deficiency anemia and folic acid deficiency may result in a blunted or impeded response to methylcobalamin therapy.

Certain conditions may blunt or impede therapeutic response to methylcobalamin therapy. These include serious infection, uremia or renal failure, drugs with bone marrow suppression properties (e.g., chloramphenicol), or concurrent undiagnosed folic acid or iron deficiency anemia. The mechanism appears to be interference with erythropoiesis. Patients with vitamin B12 deficiency and concurrent renal or hepatic disease may require increased doses or more frequent administration of methylcobalamin.

Clinical reports have not identified differences in responses between elderly and younger patients. Generally, dose selection for elderly patients should be done with caution. Elderly patients tend to have a greater frequency of decreased hepatic, renal, or cardiac function, and also have concomitant disease or receiving other drug therapy. Start with doses at the lower end of the dosing range.

Parenteral methylcobalamin is classified as pregnancy category C. Adequate studies in humans have not been conducted; however, no maternal or fetal complications have been associated with doses that are recommended during pregnancy, and appropriate treatment should not be withheld from pregnant women with vitamin B12 responsive anemias. Conversely, pernicious anemia resulting from vitamin B12 deficiency may cause infertility or poor pregnancy outcomes. Vitamin B12 deficiency has occurred in breast-fed infants of vegetarian mothers whose diets contain no animal products (e.g., eggs, dairy), even though the mothers had no symptoms of deficiency at the time. Maternal requirements for vitamin B12 increase during pregnancy. The usual daily recommended amounts of methylcobalamin, vitamin B12 either through dietary intake or supplementation should be taken during pregnancy (see Dosage).
Breast Feeding

Methylcobalamin is distributed into breast milk in amounts similar to those in maternal plasma, and distribution in breast milk allows for adequate intakes of methylcobalamin by breast-feeding infants. Adequate maternal intake is important for both the mother and infant during nursing, and maternal requirements for vitamin B12 increase during lactation. According to the manufacturer, the usual daily recommended amounts of methylcobalamin, vitamin B12 for lactating women should be taken maternally during breast-feeding (see Dosage). The American Academy of Pediatrics considers vitamin B12 to be compatible with breast-feeding. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.


This list may not describe all possible interactions. Give your health care provider a list of all the medicines, herbs, non-prescription drugs, or dietary supplements you use. Also tell them if you smoke, drink alcohol, or use illegal drugs. Some items may interact with your medicine.

Several drugs, including para-aminosalicylic acid, have been reported to reduce the absorption of methylcobalamin, vitamin B12. Monitor for the desired therapeutic response to vitamin B12.

The heavy consumption of ethanol for greater than 2 weeks has been reported to reduce the absorption of Methylcobalamin, vitamin B12. Patients should be aware that heavy, chronic ethanol use may counteract the therapeutic effects of vitamin B12; such patients with regular and chronic ethanol consumption be monitored for the desired therapeutic response to vitamin B12.

Several drugs, including colchicine, have been reported to reduce the absorption of methylcobalamin, vitamin B12. Colchicine has been shown to induce reversible malabsorption of vitamin B12, apparently by altering the function of ileal mucosa. Although further study of these interactions is necessary, patients receiving these agents concurrently should be monitored for the desired therapeutic response to vitamin B12.

In a study of 10 healthy male volunteers, omeprazole, in doses of 20 mg—40 mg per day, caused a significant decrease in the oral absorption of methylcobalamin, vitamin B12. Theoretically this interaction is possible with other proton pump inhibitors (PPIs), although specific clinical data are lacking. Patients receiving long-term therapy with omeprazole or other proton pump inhibitors (PPIs) should be monitored for signs of B12deficiency.

Chloramphenicol can antagonize the hematopoietic response to Methylcobalamin, vitamin B12 through interference with erythrocyte maturation. Chloramphenicol is known to cause bone marrow suppression, especially when serum concentrations exceed 25 mcg/ml. Chloramphenicol should be discontinued if anemia attributable to chloramphenicol is noted during periodic blood studies, which should be done approximately every 2 days during chloramphenicol receipt. Aplastic anemia and hypoplastic anemia are known to occur after chloramphenicol administration. Peripherally, pancytopenia is most often observed, but only 1—2 of the major cell types (erythrocytes, leukocytes, platelets) may be depressed in some cases.

Metformin may result in suboptimal oral vitamin B12 absorption by competitively blocking the calcium-dependent binding of the intrinsic factor-vitamin B12 complex to its receptor. The interaction very rarely results in a pernicious anemia that appears reversible with discontinuation of metformin or with Methylcobalamin, vitamin B12 supplementation. Certain individuals may be predisposed to this interaction. Regular measurement of hematologic parameters is recommended in all patients on chronic metformin treatment; abnormalities should be investigated.

Medications know to cause bone marrow suppression (e.g., myelosuppressive antineoplastic agents) may result in a blunted or impeded response to methylcobalamin, vitamin B12 therapy. Antineoplastics that are antimetabolites for the vitamin may induce inadequate utilization of vitamin B12. However, cancer patients usually benefit from vitamin B12 supplementation. The use of methotrexate may additionally invalidate diagnostic assays for folic acid and vitamin B12; however, this is a diagnostic laboratory test interference and not a drug interaction.

The intranasal forms of methylcobalamin, vitamin B12, should be administered at least 1 hour before or 1 hour after ingestion of hot food or liquids. Hot foods may cause nasal secretions and a resulting loss of medication or medication efficacy. Interactions between foods and oral or injectable forms of methylcobalamin are not expected.

Depressed levels of methylcobalamin, vitamin B12, and abnormal Schilling’s test have been reported in patients receiving octreotide.

The use of antiinfective agents or pyrimethamine may invalidate diagnostic assays for folic acid and vitamin B12; however, these are diagnostic laboratory test interferences and not true drug interactions.

Adverse Reactions

In most cases, methylcobalamin is non-toxic, even in large doses. Adverse reactions reported following methylcobalamin administration include headache, infection, nausea/vomiting, paresthesias, and rhinitis. Adverse reactions following intramuscular (IM) injection have included anxiety, mild transient diarrhea, ataxia, nervousness, pruritus, transitory exanthema, and a feeling of swelling of the entire body. Some patients have also experienced a hypersensitivity reaction following intramuscular injection that has resulted in anaphylactic shock and death. In cases of suspected cobalt hypersensitivity, an intradermal test dose should be administered.

During the initial treatment period with methylcobalamin, pulmonary edema and congestive heart failure have reportedly occurred early in treatment with parenteral methylcobalamin. This is believed to result from the increased blood volume induced by methylcobalamin. Peripheral vascular thrombosis has also occurred. In post-marketing experience, angioedema and angioedema-like reactions were reported with parenteral methylcobalamin.

Hypokalemia and thrombocytosis could occur upon conversion of severe megaloblastic anemia to normal erythropoiesis with methylcobalamin therapy. Therefore, monitoring of the platelet count and serum potassium concentrations are recommended during therapy. Polycythemia vera has also been reported with parenteral methylcobalamin.

Diarrhea and headache.

Call your health care provider immediately if you are experiencing any signs of an allergic reaction: skin rash, itching or hives, swelling of the face, lips, or tongue, blue tint to skin, chest tightness, pain, difficulty breathing, wheezing, dizziness, red, swollen painful area on the leg.


Lipo (MIC) Injection

Dosage Strength

Methionine / Inositol / Choline Chloride 25/50/50 mg/mL 10 mL Vial
Methionine / Inositol / Choline Chloride 25/50/50 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. The physiological role of each compound and the effects of supplementation are described below.


Methionine is a sulfur-containing branched-chain amino acid. A precursor for cellular methylation reactions, methionine plays an important role in lipid metabolism, polyamine synthesis, immune function, heavy metal chelation, and maintenance of redox balance.Conversely, dietary methionine restriction in rodents increased energy expenditure, improved insulin resistance, and enhanced lipolysis and fatty acid oxidation in adipose tissue.

The lipotropic effects of methionine may be attributed to its metabolite S-adenosyl methionine (SAM). SAM is synthesized from methionine via an energy-consuming reaction. SAM administered orally or by injection has been investigated as a treatment for liver diseases, osteoarthritis, and depression. The benefits bestowed by SAM may be due to its role as a methyl donor in biochemical processes governing lipid homeostasis, DNA stability, gene expression, and neurotransmitter release.


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.

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.

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, improve serum lipid profiles and upregulate the expression of genes involved in lipid metabolism and insulin sensitivity  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. In addition, inositol supplementation was associated with lower rate of gestational diabetes and preterm delivery in pregnant women. Currently, research is being performed to assess whether inositol may be used in treating various cancers.


Choline is an essential nutrient required for optimal functioning of various tissues including the liver, muscles, and brain.  Since choline breaks down fat as an energy source, choline supplementation caused rapid fat and weight loss in female athletes. 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. 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.  In addition, choline can donate methyl groups to support methionine regeneration, possibly contributing to their synergistic lipotropic effects.

Mechanism of Action

An essential sulfur-containing amino acid, methionine undergoes transmethylation reactions to generate metabolic by-products including S-adenosyl methionine (SAM) and homocysteine. SAM is a universal methyl group donor that serves as a co-factor in numerous cellular and physiological processes including lipid homeostasis. By donating its methyl group, SAM is converted first to S-adenosyl homocysteine (SAH) and then to homocysteine. As a methyl donor, SAM contributes to the formation of phosphatidylethanolamine and subsequently to phosphatidylcholine. In the liver, phosphatidylcholine is packaged into very low-density lipoproteins (VLDL) and transported to other tissues. Inadequate levels of SAM in the liver disrupts VLDL assembly and leads to hepatic accumulation of triglycerides or fatty liver.

By promoting DNA methylation SAM plays a crucial role in epigenetic regulation. Methylation near gene promoters is a well-known mechanism of transcriptional repression. Therefore, SAM may act as a sensor for cellular nutrient status and epigenetically alter the expression of genes influencing appetite, glucose metabolism, and lipogenesis. SAM also functions as a methyl donor in the synthesis of creatine – a high-energy molecule known to improve exercise.


Structurally, all inositol stereoisomers are 6-carbon sugar alcohols with the same molecular formula as glucose (C6H12O6). Myo-inositol and D-chiro-inositol have insulin-mimetic effects. Inositol administration in diabetic rodents, rhesus monkeys, and humans lowers post-prandial blood glucose levels and improves insulin sensitivity. These benefits may be attributed to the effects of inositol on the insulin signaling pathway. Stimulating the insulin receptor activates the phosphatidylinositol-3-kinase (PI3K) pathway. Phosphorylated forms of phosphatidylinositol act as second messengers that lead to downstream activation of Akt. Akt inactivates the enzyme glycogen synthase kinase-3, enhancing glycogen synthase activity. This increases translocation of the glucose transporter (GLUT4) to the surface of skeletal muscle cells, increasing glucose uptake and lowering blood glucose levels.

Excess circulating glucose is often deposited as fat in the liver and around visceral organs. Dietary supplementation with inositol reduced weight gain and lipid accumulation in the liver of rats. Inositol-mediated activation of PI3K/Akt signaling is believed to play a role in hepatic lipid metabolism and gluconeogenesis. Inositol also affects transcription of SREBP-1 and PPAR-α – genes involved in fatty acid synthesis, oxidation, and lipid transport.


In its unmodified form, or after oxidation to betaine, choline reduces fat deposition and accelerates the lipid transport. Like methionine, betaine can also methylate DNA and influence gene expression. Consequently, choline and betaine methylated the promoter region of PPAR-α, suppressing mRNA expression and possibly the lipogenic actions of the encoded protein. In addition, choline inhibited obesity-induced oxidative stress and prevented hepatic accumulation of triglycerides.

In female athletes, choline supplementation significantly reduced body fat as well as levels of the hunger hormone leptin. Reduction in leptin levels are linked to greater food satiety. Thus, the dual advantage of consuming fewer calories while burning fats as an energy source may contribute to the lipotropic actions of choline.


Methionine is primarily metabolized in the liver. It is transported into hepatocytes via facilitative transport. Methionine metabolism consists of three parts: the methionine cycle, the transsulfuration pathway, and the salvage cycle. In the first step of the methionine cycle, the enzyme methyl adenosyltransferase catalyzes the conversion of methionine to S-adenosyl methionine (SAM). SAM donates its methyl group, generating S-adenosyl homocysteine, which is then hydrolyzed to adenosine and homocysteine. Homocysteine may be remethylated to regenerate methionine. Alternatively, it can be converted to cysteine via the transsulfuration pathway. In the salvage pathway, SAM is decarboxylated and used as an aminopropyl donor for polyamine biosynthesis. In healthy human subjects, 9-15% of methionine was excreted through urine following oral ingestion of 1-1.5 g of methionine. Decrease in urinary excretion occurred when the subjects were on a high-fat diet.

Myo-inositol and inositol phosphate derivatives are primarily absorbed in the gut. Cellular uptake of inositol occurs via sodium ion-coupled transporters as well as sodium-glucose co-transporters. Because they compete for the same transporters for uptake into cells, high glucose levels can significantly inhibit the uptake of inositol. Kidneys are the main sites for breakdown of inositol. Renal cortical tubules express the enzyme myo-inositol oxygenase. This enzyme metabolizes myo-inositol via the glucuronate-xylulose pathway, converting it into the monosaccharides xylulose and ribulose. Inositol that is unmetabolized or not re-absorbed at the renal tubular level is excreted unchanged through urine. Although most studies have evaluated the pharmacokinetics of inositol following oral administration, one study assessed the pharmacokinetics of myo-inositol following intravenous (IV) administration in preterm infants. In this study, the serum half-life of inositol following a single IV dose was 5.22 hours and after multiple IV dosing was 7.9 hours.

Choline obtained through the diet is absorbed by choline transporters in the intestine. Choline is primarily metabolized in the liver. Here, choline is converted to phosphatidylcholine via the cytidine diphosphate (CDP)-choline pathway. It may also be converted to betaine in a two-step irreversible reaction. Betaine contributes methyl groups to the one-carbon pathway, resulting in the regeneration of methionine from homocysteine. The metabolism of choline may be impaired by single nucleotide polymorphisms in genes encoding folate metabolizing enzymes. Furthermore, dietary choline is converted to trimethylamine by gut bacteria. Trimethylamine is oxidized to trimethylamine-N-oxide by flavin monooxygenase 3 (FMO3) in the liver. Trimethylamine-N-oxide is then excreted through urine. Impaired expression or function of FMO3 enzyme manifests as trimethylaminuria or Fish Odor Syndrome

Pregnancy / Breastfeeding

There are no randomized, controlled trials studying the effect of Lipo-MIC injections on pregnant and lactating women or their offspring. Human and animal studies on each constituent compound may offer some insights.

Excess methionine in the maternal diet may be detrimental to fetal development. This is because additional glycine and serine may be required to catabolize the excess methionine, inadvertently resulting in the deficiency of these amino acids. Excess methionine may also be metabolized to homocysteine. Elevated plasma homocysteine levels are associated with preeclampsia, spontaneous abortion, placental rupture, and miscarriage.

Given its use in the treatment of polycystic ovarian syndrome and gestational diabetes, myo-inositol may be considered relatively safe during pregnancy. In a meta-analysis of randomized controlled trials, 2 g of myo-inositol administered orally twice daily was reported to be safe during pregnancy. However, high concentrations of D-chiro-inositol negatively affect the quality of oocytes. Therefore, D-chiro-inositol may not be used by women seeking to get pregnant. Effects of other inositol isomers are not well characterized.

Choline requirements are especially high in pregnant women and nursing mothers. In women of reproductive age, 425 mg/day of choline is considered adequate. Adequate choline intake increases to 450 mg/day during pregnancy and 550 mg/day in lactating women. Choline supplementation had beneficial effects on fetal neurodevelopment and maternal placental function. Randomized controlled studies have reported up to 900 mg/day of choline administered orally to be safe and free of adverse events in healthy pregnant women. However, too low and excessively high levels of choline may adversely affect fetal health and development. Additionally, consuming more than 3.5 g/d of choline may cause fishy odor and hypotension in adults.

Women who are pregnant, planning to be pregnant, or are breastfeeding must consult their physician regarding the use of lipotropic injections for weight loss.


The methionine metabolite S-adenosyl methionine (SAM) may interact with antidepressants, antipsychotics, amphetamines, and narcotics causing excess accumulation of serotonin in the body. It may also interact with the cough suppressant dextromethorphan and the dietary supplement St. John’s wort, leading to an increased risk of serotonin syndrome. Mild symptoms of serotonin syndrome include shivering and diarrhea, while severe symptoms include muscle rigidity, fever, and seizures.

Choline and inositol are not known to have any clinically relevant interactions with drugs, supplements, or foods.

Adverse Reactions / Side Effects

Potential side effects of lipotropic injections include:

  • Pain or soreness at the site of injection
  • Diarrhea
  • Constipation
  • Anxiety
  • Increased heart rate
  • Incontinence
  • Insomnia
  • Dry mouth
  • Fatigue
  • Numbness of hands and feet

This is not a comprehensive list of adverse effects. If you experience rash, hives, itchiness, shortness of breath, or other symptoms of an allergic reaction, please discontinue use immediately and consult your physician. Side effects may vary from person to person.

Contraindications / Precautions

Upcoming evidence indicates that the choline metabolite trimethylamine-N-oxide may be a risk factor for cardiovascular diseases. Studies in animal models suggest that TMAO may be atherogenic and prothrombotic. Therefore, Lipo-MIC injections are contraindicated in individuals with cardiovascular disorders. S-adenosyl methionine may worsen the symptoms of mania in people with bipolar disorder. Consult a physician before use.


Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond-use date. Do not flush unused medications or pour down a sink or drain

LipoB (MIC) Injection


Methionine / Inositol / Choline Chloride / Cyanocobalamin 25/50/50/1 mg/mL 10 mL Vial
Methionine / Inositol / Choline Chloride / Cyanocobalamin 25/50/50/1 mg/mL 30 mL Vial

General Information

The Lipo-B (MIC) injection is a product that contains a combination of compounds that have been shown to exhibit lipotropic effects. The lipotropic effects facilitate the burning of adipose tissue within the human body which may, consequently, result in some degree of weight loss. Lipo-B injections are typically used as fat loss supplements, in combination with diet and exercise, in weight loss plans. The combination of products that make up the Lipo-B (MIC) injection are methionine, inositol, choline, and cyanocobalamin (vitamin B12).


Methionine is one of the four sulfur-containing amino acids; the other three are cysteine, homocysteine, and taurine. Additionally, it is one of the nine essential amino acids in the human body. As an essential amino acid, it cannot be synthesized de novo by the human body due to a lack of the require metabolic pathway needed for its synthesis. Therefore, methionine has to be exogenously introduced into the human body either within the diet or as a supplement.

Methionine serves several key roles in the human body such as:

  • Substrate in the production of critical hormones and proteins including L-cysteine, carnitine, adrenaline, choline, and melatonin, among others.
  • Increasing liver production of lecithin which helps lower serum cholesterol levels.
  • Provides sulfur which aids development of nails and promotes hair growth.
  • Chelating agent which helps get rid of heavy metals such as mercury.
  • Provides protection against hepatotoxins such as acetaminophen.


Originally isolated from muscle extracts in 1850, inositol is a cyclic carbohydrate with six hydroxyl groups. It has nine different stereoisomers, with the most common form being myo-inositol, followed by D-chiro-inositol as the next most common. Most texts, however, use the term inositol to describe its most common variant, myo-inositol. Once considered to be an essential vitamin, it has since been discovered that inositol can be produced by the liver and the kidneys; these organs are able to produce up to 4 grams daily of inositol. Additionally, inositol can be found in food sources such as beans and fruits. It is also synthesized in the placenta in pregnant women and can be found in high concentrations in breast milk.

One of the major roles of inositol in the body is the production of inositol triphosphate, which is an essential second messenger for hormones such as insulin and follicle stimulating hormone.


Choline is an essential nutrient that plays a key role in a number of metabolic pathways in the human body. Even though choline is produced endogenously in the liver, it is still considered an essential nutrient because the quantities produced is not sufficient to meet the body’s metabolic needs; as such, dietary supplementation of choline is necessary. Choline can be found in both animal and plant food sources, with animal food sources generally having more choline per gram of food product.

Some functions that choline serves in the body are:

  • Production of sphingomyelin and phosphatidylcholine, which are needed to maintain cell membrane integrity.
  • Production of acetylcholine, which is one of the major neurotransmitters in the body.
  • Modulation of gene expression and cell membrane signaling.
  • Early brain development in fetuses.


Otherwise known as vitamin B12, cyanocobalamin derives its name from the fact that it has a cyanide group attached to its molecule and also contains the mineral cobalt. It is essential for cellular energy production as well as DNA synthesis. It is an essential water-soluble vitamin and must be obtained from food or as dietary supplements. Some good food sources of vitamin B12 are meat, fish, milk, eggs, and cheese, among others. Some of the roles that cyanocobalamin serves in the body include:

  • Cofactor for methionine synthase and L-methymalonyl-CoA mutase.
  • Synthesis of methionine from homocysteine.
  • Regeneration of tetrahydrofolate from 5-methyltetrahydrofolate.
Mechanism of Action


Methionine exerts its effect in the body through the production of S-adenosylmethionine in the methionine cycle; this process is catalyzed by the enzyme methionine adenosyltransferases. Methionine adenosyltransferases combines methionine, water, and adenosine triphosphate (ATP) to produce S-adenosylmethionine, pyrophosphates, and inorganic phosphates. S-adenosylmethionine participates in a number of processes in the body such as biotin and polyamine synthesis. It is also involved in the synthesis of phospholipids and some neurotransmitters within the body.  These methylation reactions also regulate gene expression during fetal development. One of the by-products of methionine metabolism is homocysteine which, in high serum quantities, has been linked to developmental disorders, learning disabilities, and skeletal deformities, among others.


There are serves means by which inositol exerts its effects in the human body. Inositol is a key substrate in glucose metabolism and is a second messenger in insulin action. It binds to insulin which then initiates a cascading pathway of metabolic events through the action of the enzyme phosphatidylinositol-3-kinase and the activation of insulin-1 receptor substrate. These convert phosphatidylinositol2-phosphate (PIP2) into phosphatidylinositol-3-phosphate (PIP3) and, by so doing, activates protein kinase B (PKB), the metabolic pathway for glycogen synthesis.

In addition to the conversion to phosphatidylinositol-3-phosphate, inositol also acts by activating pyruvate dehydrogenase kinase, isoenzyme 1. This enzyme acts on glucotransporter 4 and facilitates the transport of glucose into cell across the plasma membrane for their use as an energy substrate.


The primary way through which choline acts within the body is through its derivative phosphatidylcholine. The biosynthesis of phosphatidylcholine occurs via the CDP-choline pathway. After absorption from the intestine, choline is transported into cells using choline transporters. Within the cells, choline is phosphorylated into phosphocholine or oxidized into betaine; the phosphorylation of choline is catalyzed by the enzyme choline kinase. The final step in this pathway is the conversion of phosphocholine into phosphatidylcholine, a process catalyzed by the enzyme 1,2-diacylglycerol cholinephosphotransferase. Phosphatidylcholine is a major constituent of all cell membranes within the body and is also required for the biosynthesis of lipoproteins.


After oral ingestion, cyanocobalamin binds to intrinsic factor as well as other cobalamin binding proteins before absorption. Once absorbed, it binds to plasma proteins before it is transported around the body. Within body tissues, the specific B12 binding proteins transcobalamin I and II facilitate the absorption of cyanocobalamin into the cells.

Cyanocobalamin is a cofactor for the synthesis of two major enzymes in the body namely methionine synthase and L-methymalonyl-CoA mutase. L-methymalonyl-CoA mutase converts L-methymalonyl-CoA to succinyl-CoA, which is essential for the metabolism of protein and fat. Methionine synthase plays a role in the production of purines and pyrimidines, which are building blocks in DNA synthesis.



Methionine is typically ingested oral as part of a food source such as eggs, meat, and fish. It can also be orally ingested as a supplement or parenterally as part of a complex compound. After oral ingestion, absorption of methionine occurs in the small intestine through an active transport process. Following absorption, methionine is then transported to the liver where it is then metabolized. As earlier stated, methionine is an important substrate in the development of a number of products within the body. One of the most essential products of methionine metabolism is S-adenosylmethionine which is important in polyamine and biotin synthesis, phospholipid synthesis, and production of some neurotransmitters. While not entirely clear, methionine is believed to be excreted from the body through urine.


After oral ingestion, inositol is actively absorbed and transported by intestinal cells using a sodium-dependent transport mechanism. Following intestinal absorption, it then binds to plasma proteins and is then transported to the cells and tissues around the body where it is then metabolized. If produced endogenously, myo-inositol is derived from glucose-6-phosphate, which is isomerized to inositol-3-phosphate by the enzyme D-3-myo-inositol-phosphate synthase. Inositol may also be produced through the recycling of inositol-1,4,5-triphosphate as well as inositol-1,4-biphosphate. Inositol is catabolized is the kidneys and its metabolites are excreted in urine.


After oral ingestion, choline is absorbed by enterocytes in the small intestine by means of transporter proteins. It is then transported throughout the body where it is absorbed by cells by both diffusion and cell-mediated transport. Within the tissues, choline undergoes phosphorylation to cytidine diphosphocholine, and from there to phosphatidylcholine. Alternatively, phosphatidylcholine may be produced from the methylation of phosphatidylethanolamine. Some choline is also oxidized to form betaine in the liver and kidney.


Cyanocobalamin can be administered orally, intramuscularly, or subcutaneously. After oral ingestion, it binds to intrinsic factor before making its way down the gastrointestinal tract. In the terminal ileum, cyanocobalamin is cleaved from intrinsic factor and is then absorbed by the mucosal cells. In the bloodstream, cyanocobalamin binds to the plasma proteins transcobalamin 1 and 2 before it is transported throughout the body. It has a half-life of about 6 days, with a peak plasma concentration of 8-12 hours after oral administration and is excreted mainly in urine.

Indications For Use

Lipo-B (MIC) injections are mainly used as supplements to help in the reduction of excessive fats from specific areas of the body. They have also been shown to be of benefit in the removal of fats from the liver. Each of the individual components has a lipotropic effect and so they are believed to work synergistically in getting rid of body fat.

Contraindications / Precautions

There are certain clinical conditions under which Lipo-B (MIC) should be avoided or administered with caution. Some of these conditions include:

  • Hypersensitivity: Lipo-B (MIC) is absolutely contraindicated in individuals who have a demonstrated hypersensitivity to any components of the product.
  • Acidosis: This can be worsened by methionine administration.
  • Liver disease: This may impair the metabolism of the product components.
  • Hereditary optic nerve atrophy (Leber’s disease): Individuals with Leber’s disease may experience a worsening of their symptoms if administered products containing cyanocobalamin
Pregnancy/ Breastfeeding

There are insufficient studies available to ascertain the safety as well as efficacy of Lipo-B (MIC) in pregnant and breastfeeding mothers. However, Lipo-B (MIC) should generally not be administered to pregnant or breastfeeding mothers to minimize any risks to the fetus or infant.

Adverse Reactions / Side Effects

Lipo-B (MIC) is generally well tolerated in most individuals. As stated earlier, hypersensitivity to any of the product components is one of the adverse reactions that may occur after Lipo-B (MIC) injections. Additionally, toxic effects may occur if Lipo-B (MIC) is administered to individuals with hepatic diseases due to impaired metabolism. Some individuals may also experience generalized non-specific symptoms such as nausea and vomiting, diarrhea, and dizziness, among others.


Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.

LipoC (MIC) Injection

Dosage Strengths

Methionine / Inositol / Choline Chloride / L-Carnitine / Thiamine HCl / Dexpanthenol 15/50/50/50/15/5 mg/mL 10 mL Vial
Methionine / Inositol / Choline Chloride / L-Carnitine / Thiamine HCl / Dexpanthenol 15/50/50/50/15/5 mg/mL 30 mL Vial

General Information

Lipo-C injection contains a mixture of compounds that may aid in the reduction of adipose tissue (fat). The mixture of compounds individually may be effective, however in combination they may exhibit more lipotropic activity than when administered alone in a synergistic fashion. Injection of this mixture of lipotropic compounds may be more effective than oral supplementation, this is due to the increased bioavailability of parenteral exposure.

These lipotropic agents are structurally and functionally closely related to the B-vitamins, or are involved in the homeostasis of energy production from fat. These compounds are often employed together in the hope of potentiating fat-loss, thus while the MIC mixture and B vitamin(s) are often injected separately, they are part of the same overall injection cycle. The non-vitamin compounds (MIC) that are injected into the body stimulate the liver into optimizing the process of metabolism, elevate the movement of and utilization of fat, and provide the needed metabolic environment of the body for a fatty acid (fat) mobilization and utilization.

Lipotropic compounds are used on the potential for release of fat deposits in some parts of the body. They sometimes go by the names Lipo-Den, Lipo-Plex, Lipo Shot, or MIC Injection. The lipotropic agents included in this injection are:

Methionine: Methionine helps the liver maintain the optimal ability to process fatty acids. Methionine is a major constituent of S-adenosylmethionine which has been shown to be associated in genetic regulation and activation of certain genes. Methionine contributes to methyl donation to histones that activate certain genetic processes that may be involved in the increase in lean tissue. Although indirectly linked to lipolysis, it is believed that the increase in lean tissue increases resting metabolic rate, therefore increasing the overall required calories that must be obtained from storage or dietary intake. Methionine, via S-adenosylmethionine, has been shown in animal models to increase CNS activity, therefore increasing the caloric requirements required by the CNS The downstream effects of this may ultimately lead to increased caloric requirements for the entire organism. Although studies have not been replicated. in humans, there may be an association due to the similarity in pathways shared between organisms.

Inositol: Inositol is a sugar-like molecule, referred to as a sugar alcohol. Even though very similar in molecular structure to glucose, this molecule does not exhibit the traits that simple carbohydrates exhibit. Contrary to simple carbohydrates, this sugar alcohol has been shown to not actively increase adipose storage. In fact, Inositol has been found to decrease fatty acid synthase activity, a multi-enzyme protein that catalyzes fatty acid synthesis. This set of enzymes ultimately enables the body to produce triglycerides fat molecules that reside in adipose tissue (body fat).

Inositol may be effective in reducing insulin resistance, a common condition associated with increase adiposity (body fat). Insulin resistance, a condition to which your body becomes resistant to the activities of the hormone insulin. This condition leads to excess blood glucose levels and a host of symptoms and dysfunctions. A chemical called Inositol phosphoglycan is known to regulate the body’s sensitivity to insulin signaling. Inositol phosphoglycan structurally incorporates Inositol, thus inositol is required for this molecule to exert its regulating behavior.

The proper functioning and sensitivity to insulin is found in most healthy individuals, and is essential in maintaining overall health. Excessive exposure to blood glucose ultimately leads to insulin resistance and poor nutrient transport. Inositol may be effective in reducing this condition while at the same time reducing fatty acid (fat) synthesis.

Choline: Choline is a simple molecule usually classified as a B vitamin. The B vitamin class is usually involved in the generation of energy and support of metabolism. Choline is an important precursor to the neurotransmitter acetylcholine. This neurotransmitter is involved in a host of activities, one of which includes muscular function and contraction. Acetylcholine is a fundamental neurotransmitter that enables the communication between neurons. Increased neural communication results in increased CNS activity which ultimately leads to increased energy expenditure. Energy expenditure requires nutrient input, either from stored energy (fat), or dietary nutrients. Choline exist in a delicate balance and homeostasis with methionine and folate. When these nutrients are not in balance adverse health effects may be present. Along with the increase in CNS activity comes increased cognitive ability, reported by many users. Choline may be effective as a nootropic, or a substance with ability to increase cognition. Increased neural cognition is thought to be due to choline’s role as a precursor to acetylcholine.

The supplementation of choline has been shown to reduce serum and urinary carnitine. The reduction of carnitine in these fluids may indicate carnitine has been partitioned in tissues that utilize it as a fatty acid mitochondrial transport. When carnitine is used in the mitochondria it transports fatty acids to the location which they are broken down and used as energy. It has also been reported that molecular fragments of fat have been found in urine after carnitine and choline supplementation, which may be due to incomplete fatty acid oxidation and the removal of the subsequent byproducts. This means, choline supplementation may increase the utilization of carnitine and increase the removal of fatty acids, even though all fatty acids are not burned as energy. The fragments of fatty acids not burned as energy are extruded in the urine as molecular fragments.

Methionine, which helps the liver maintain the optimal ability to process fatty acids; Choline, which stimulates the mobilization of fatty acids and prevents their deposition in a given part of the body; and, Inositol, which aids in the transport of fat into and out of the liver and intestinal cells, acts synergistically with choline, exhibiting more lipotropic activity than when administered alone.

As soon as the effect of all 6 of these substances wears out, the body gradually begins returning to its normal rate of fat and general metabolism.

Typically, these compounds are administered in concert. Injections can be administered up to twice a week. B12 is purported by its users and practitioners to help speed up overall metabolic processes and create a greater feeling of overall energy & well-being. Because these lipotropics are structurally and functionally closely related to the B-vitams, they are often employed together in the hope of potentiating the potential for fat-loss, thus while the MIC mixture and B vitamin(s) are often injected separately, they are part of the same overall injection cycle. The non-vitamin compounds (MIC) that are injected into the body stimulate the liver into optimizing the process of metabolism, elevate the movement of and utilization of fat, and boost the metabolic power of the body for awhile.

Other compounds are included as an attempt to further potentiate these effects:

  • L-Carnitine
  • Thiamine HCl (Vitamin B1)
  • Dexpanthenol (Vitamin B5)
What Is This Medicine Used For?

Lipotropic injections are used to help release fat deposits in some parts of the body. Some of these areas include the stomach, inner thighs, neck, buttocks, and hips. Lipotropic, or fat burning, substances include methionine which helps the liver remove fat; inositol, similar to methionine; choline, which distributes cholesterol and prevents it from getting deposited in one part of the body. In some cases, a combination of these may be given. Injections can be administered up to twice a week. B12 is purported by its users and practitioners to help speed up the overall metabolic processes and create a greater feeling of overall energy. Because lipotropics directly aid fat breakdown and are closely related to B vitamins, when used together they are thought to intensify each others’ effects. They are usually injected separately but as part of the same overall injection cycle. The amino acids that are injected into the body stimulate the liver into optimizing the process of metabolism. These injections boost the metabolic power of the body. The injections are only effective temporarily. As soon as the effect of these substances wears out, the body starts returning to normal gradually.

Who Should Not Take This Medicine

If you have an allergy to methionine, inositol, choline, or any part of this medicine. Tell your healthcare provider if you are allergic to any medicine. This includes rash; hives; itching; shortness of breath; wheezing; cough; swelling of face, lips, tongue, or throat; or any other symptoms involved.

Side Effects

Potential side effects include stomach upset and urinary problems due to the strain the injections place on the kidneys. Depression is another possible side effect. Some patients are unable to control their urine, and/or have diarrhea. Finally, some patients reported an unpleasant odor. Lipotropic injections change the function of the digestive system temporarily. This can result in extreme exhaustion, since the body is not used to working at this level and condition. Unexplained pain in unrelated parts of the body is another potential side effect. Patients have complained of pain in the neck and parts of the hand. How these injections cause these pains is not clear. Some patients have also experienced joint pains and allergic reactions to the injections. Call your healthcare provider immediately if you are experiencing any signs of an allergic reaction: wheezing; chest tightness; fever; itching; bad cough; blue skin color; fits; or swelling of face, lips, tongue, or throat; also if you experience severe behavioral problems, chest pain or pressure or fast heartbeat, severe dizziness or passing out, nervousness and excitability, or severe headache.


Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.

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