Overview of Hydrate Cream

Dosage Strength

General Information

Acetyl-D Glucosamine
An amino-monosaccharide called acetyl-D glucosamine performs important metabolic tasks both on its own and as a substrate precursor for the manufacture of polymers like glycosaminoglycans (like hyaluronic acid) and proteoglycans. Glucosamine has a very good safety record and has been proven to be helpful in treating a number of clinical conditions. The skin or skin cells have been shown to benefit from a number of glucosamine compound-related benefits. Glucosamine has been demonstrated to hasten wound healing, enhance skin hydration, and lessen wrinkles by stimulating the manufacture of hyaluronic acid. Additionally, as a tyrosinase activation inhibitor, it prevents the synthesis of melanin and is helpful in the treatment of hyperpigmentation disorders. In a similar manner, glucosamine provides chondroprotective and anti-inflammatory properties.

Niacinamide
A B-complex vitamin, niacin is also known as nicotinic acid or 3-pyridinecarboxylic acid. Animal proteins, beans, green vegetables, liver, mushrooms, peanuts, whole wheat, and unpolished rice are excellent dietary sources of niacin. Cereal grains contain niacin as well, although it is primarily attached to plant proteins and is therefore poorly absorbed after consumption. Niacin is one of the ingredients added to refined wheat to enrich it, and enriched grains account for the majority of the preformed niacin we consume each day. The manufacture of niacin from the amino acid tryptophan, however, also satisfies the body’s need for niacin. Niacin, for instance, is absent from milk and eggs but is abundant in tryptophan, which is the precursor of niacin. After protein synthesis, each excess 60 mg of tryptophan is converted to roughly 1 mg of niacin. Roughly half of a man’s niacin requirement is met by the synthesis of the vitamin from tryptophan in proteins. Due to the dependency of coenzymes in the niacin manufacturing route, iron shortage, poor pyridoxine, or riboflavin status will limit the conversion of tryptophan to niacin and may contribute to deficit. Pellagra is a clinical symptom complex that primarily affects the GI tract, skin, and CNS, producing symptoms of diarrhea, dermatitis, and dementia, respectively. It is a late and significant consequence of niacin insufficiency. Niacin and protein deficiencies, isoniazid medication, or specific conditions that cause poor tryptophan usage can all contribute to pellagra. Due to the enrichment of refined flours, pellagra is now uncommon in industrialized nations. Pellagra was the only vitamin deficiency disease to ever reach epidemic proportions in the US.

For both niacin and niacinamide, there are numerous synonyms. Nicotine might be converted into synthetic niacin through oxidation, leading to the development of the name “nicotinic acid.” The terms “nicotinamide” and “niacinamide” were also created by scientists to describe the amide form of nicotinic acid. Since the 1940s, foods have been labeled with the generic name “niacin” to prevent conflating the vitamin with the nicotine alkaloid found in tobacco. As a result, both chemical forms of niacin—which are comparable as vitamins on a weight basis—have been referred to as “niacin.” Nicotinamide and nicotinic acid are both produced for use in dietary supplements. It is crucial to distinguish between the two forms in pharmaceutical products because nicotinic acid and nicotinamide differ in their pharmacologic qualities from their function as vitamins.

Niacinamide, also known as nicotinamide, is ineffective as an antilipemic in clinical medicine; nevertheless, nicotinic acid is. The incidence of subsequent myocardial infarction (MI) and overall mortality in MI patients were both reduced by nicotinic acid, the first hypolipidemic drug to demonstrate these effects. However, no additional advantage of extended-release niacin combined with lovastatin or simvastatin over and above that shown for extended-release niacin, simvastatin, or lovastatin monotherapy on cardiovascular morbidity and mortality has been established. Additionally, the AIM-HIGH trial showed that simvastatin alone does not reduce the risk of cardiovascular events any more than simvastatin combined with extended-release niacin (1500–2000 mg/day PO). 1 These findings are in line with the larger HPS2-THRIVE trial, which found that adding extended-release niacin to efficient statin-based therapy did not lead to a higher decline in the risk of cardiovascular events. Additionally, there was a higher likelihood of major adverse effects, such as an increase in the frequency of diabetes diagnoses and control issues, serious gastrointestinal, musculoskeletal, dermatological, infectious, and bleeding problems. Additionally, the rate of deaths from any cause increased by a statistically insignificant 9 percent in the niacin group. 2 The ARBITER 6-HALTS experiment proved that the addition of extended-release niacin 2000 mg/day to statins is superior to the combination of ezetimibe plus a statin in that it causes a substantial regression in atherosclerosis as evaluated by carotid intima-media thickness. 3 In an MRI investigation, the addition of 2000 mg/day of extended-release niacin to statin medication significantly decreased the carotid wall area when compared to the control group. 4 However, the NIA Plaque study, which was presented at the 2009 Scientific Sessions of the American Heart Association (AHA), did not discover a substantial slowing of atherosclerosis progression linked to the addition of niacin to statin medication as compared to statin monotherapy. Additionally, nicotinic acid has been tried to treat tinnitus, but there are few reliable results. When compared to immediate-release versions, some sustained-release nicotinic acid formulations had a reduced incidence of flushing but a higher incidence of hepatotoxicity. 5 There are some dose forms that are offered over-the-counter. Niacin was formally approved by the FDA in 1938.