Anti-Aging Vita Gel

Overview of Anti-Aging Vita Gel

Dosage Strength

Niacinamide / Tretinoin / Vitamin C / Vitamin E 4/0.03/5/1% 30 mL Pump

General Information

Niacin is a B-complex vitamin (nicotinic acid or 3-pyridinecarboxylic acid). Animal proteins, beans, green vegetables, liver, mushrooms, peanuts, whole wheat, and unpolished rice are all good sources of niacin. Niacin is found in cereal grains as well, although it is primarily attached to plant proteins and so poorly absorbed after ingestion. Niacin is one of the compounds used to enrich refined flour, and we get the majority of our pre-formed niacin from enriched grains. However, the biosynthesis of niacin from tryptophan, an amino acid, also meets the body’s niacin requirement. Milk and eggs, for example, do not contain niacin but do contain high levels of tryptophan, from which niacin is generated. After protein synthesis, each 60 mg of extra tryptophan is converted to approximately 1 mg of niacin. The vitamin is synthesized from tryptophan in proteins, which provides nearly half of the vitamin’s requirement in humans. Due to the interdependence of coenzymes in the niacin manufacturing pathway, iron insufficiency or insufficient pyridoxine or riboflavin status may limit the conversion of tryptophan to niacin and may contribute to deficiency. Pellagra, a clinical symptom complex primarily affecting the GI system, skin, and CNS, presenting symptoms of diarrhea, dermatitis, and dementia, is a late and dangerous manifestation of niacin insufficiency. Pellagra can be caused by a niacin- and protein-deficient diet, isoniazid medication, or certain conditions that cause inadequate tryptophan usage. Pellagra was the only vitamin-deficiency disease to ever reach epidemic proportions in the United States; pellagra is now uncommon in developed countries due to the enrichment of refined flours.

There are several synonyms for niacin and niacinamide. The oxidation of nicotine produced synthetic niacin, and the word “nicotinic acid” developed. For the amide form of nicotinic acid, scientists devised the words ‘nicotinamide’ and ‘niacinamide.’ Since the 1940s, the name “niacin” has been used generally to label goods in order to avoid confusion with the nicotine alkaloid found in tobacco. As a result, the term “niacin” has come to refer to both chemical forms, which are nutritionally identical. Nicotinic acid and nicotinamide are both produced for use in dietary supplements. However, because nicotinic acid and nicotinamide have distinct pharmacologic qualities apart from their usage as vitamins, it is critical to identify the two forms in pharmaceutical goods.

Although nicotinic acid is utilized as an antilipemic in clinical medicine, nicotinamide (niacinamide) is not. Nicotinic acid was the first hypolipidemic medication to be demonstrated to reduce the risk of secondary MI and total mortality in MI patients. However, no additional advantage of coadministration of extended-release niacin with lovastatin or simvastatin on cardiovascular morbidity and mortality has been reported in comparison to extended-release niacin, simvastatin, or lovastatin monotherapy. Furthermore, the AIM-HIGH study indicated that taking simvastatin with extended-release niacin (1500—2000 mg/day PO) does not result in a higher reduction in the risk of cardiovascular events than using simvastatin alone. 1 These findings are consistent with the larger HPS2-THRIVE study, which found that adding extended-release niacin to successful statin-based therapy did not result in a higher reduction in the risk of cardiovascular events. Furthermore, there was an increased risk of significant adverse events, including an increased incidence of diabetes control and diagnosis problems, as well as major gastrointestinal, musculoskeletal, dermatological, infectious, and bleeding problems. In the niacin group, there was also a statistically insignificant 9 percent proportionate increase in the risk of mortality from any cause. 2 The ARBITER 6-HALTS trial found that combining statins with extended-release niacin 2000 mg/day results in considerable regression of atherosclerosis as evaluated by carotid intima-media thickness, and is superior to the combination of ezetimibe and a statin. 3 The addition of extended-release niacin 2000 mg/day to statin medication resulted in a significant reduction in carotid wall area compared to placebo in an MRI investigation. 4 The NIA Plaque study, presented at the American Heart Association (AHA) 2009 Scientific Sessions, did not identify a significant reduction in the progression of atherosclerosis linked with the addition of niacin to statin medication versus statin monotherapy. Furthermore, nicotinic acid has been utilized as a tinnitus treatment, however efficacy data are limited. 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 Some dose forms can be obtained without a prescription. Niacin was first approved by the FDA in 1938.

Tretinoin, also known as all-trans-retinoic acid (ATRA), is a vitamin A derivative that occurs naturally. Retinoids are key regulators of cell reproduction, proliferation, and differentiation as vitamin A (retinol) derivatives; however, unlike vitamin A, retinoids are not transformed into rhodopsin, which is required for night vision. Topical tretinoin is used to treat mild to moderate acne (grades I-III) and photodamaged skin. Topical tretinoin has also been used to treat the symptoms of keratinization disorders such ichthyosis and keratosis follicularis. Tretinoin is a distinguishing agent in a novel class of anticancer medicines. Oral tretinoin is used to treat acute promyelocytic leukemia (APL) and is currently being studied in phase III for the treatment of Kaposi’s sarcoma. Tretinoin is a less harmful way to achieve complete remission in the treatment of APL than traditional chemotherapy; nonetheless, roughly 25% of patients who use tretinoin for the treatment of APL develop acute promyelocytic leukemia differentiation syndrome. 6

Vitamin C
Vitamin C is a water-soluble vitamin, antioxidant, and essential co-factor in the metabolism of carnitine and catecholamines, collagen formation, and iron absorption. Because humans cannot synthesize vitamin C, it must be obtained through fruits and vegetables. Citrus fruits, berries, tomatoes, potatoes, and green leafy vegetables are all high in vitamin C. Although the bulk of vitamin C is completely absorbed in the small intestine, the percentage of absorbed vitamin C decreases as intraluminal concentrations rise. Vitamin C is essential for the hydroxylation of proline residues on procollagen, which leads in the formation of the triple helix of mature collagen. The absence of a stable triple-helical framework jeopardizes the integrity of skin, mucous membranes, blood vessels, and bone. Scurvy develops as a result of a vitamin C deficiency. Scurvy develops as a result, causing bleeding, hyperkeratosis, and hematological abnormalities. Scurvy is caused by a lack of vitamin C. This activity describes the indications, mechanism of action, methods of administration, significant adverse effects, contraindications, and monitoring of vitamin C in order for providers to direct patient therapy in the context of treatment or supplementation when it is indicated as a member of the interprofessional team. 7

 Vitamin E Acetate 
Vitamin E is a fat-soluble vitamin that can be found in a variety of foods such as vegetable oils, wheat germ, cereal grains, fruits, green vegetables, meat, eggs, and certain types of seafood. The name “vitamin E” refers to a set of eight distinct tocopherols, which are lipid-soluble chemicals generated by plants and required by most animals, including humans. The naturally occurring version with the highest vitamin activity is d-alpha-tocopherol. dl-alpha-tocopherol is the synthetic form. Commercial vitamin E preparations primarily contain synthetic dl-alpha-tocopheryl acetate. This acetate ester gives the molecule stability but is less active than the native form. Given the levels present in typical dietary sources, vitamin E deficiency is uncommon. Patients with malabsorptive illnesses such as fat malabsorption syndrome, cystic fibrosis, chronic bowel disease (e.g., Crohn’s, Celiac, and Whipple’s disease), or who have undergone specific gastrointestinal procedures may require supplementation (e.g., gastrectomy or gastric bypass). Vitamin E is typically used in children as a supplement to maintain proper intakes and prevent insufficiency. 8 Pure vitamin E was obtained from wheat germ oil for the first time in 1936, and its molecular structure was characterized and synthesis accomplished in 1938. Vitamin E was initially acknowledged by the Food and Nutrition Board of the National Research Council in 1968. The FDA authorized systemic vitamin E in 1941. In addition to oral vitamin E formulations for supplementing, various topical vitamin E formulations are available. Off-label use of topical vitamin E preparations with claims of antioxidant protection against photoaging has occurred. These claims have not been assessed by the FDA, and the ability of topical Vitamin E preparations to aid in the healing of small burns and sunburns has not been proven.

Although early findings revealed that vitamin E had the ability to prevent cardiovascular disease (CVD),910111213 more recent outcome studies have not found vitamin E to be beneficial. The HOPE research found that vitamin E had no effect on cardiac outcomes in high-risk patients with diabetes or vascular disease. 14 The Women’s Health Study (WHS), which included around 40 thousand women who were given a daily dose of 400 mg (600 International Units), found no overall benefit for major cardiovascular events. 15 The American Heart Association does not suggest vitamin E therapy for women as a CVD prevention strategy. 16 The SU.VI.MAX trial, which included 13,017 patients (including 5,141 men aged 45 to 60 years) and was followed for 7.5 years, found that supplementation with a multivitamin (containing 30 mg of vitamin E) did not reduce the incidence of ischemic CVD in men. 17

The findings of investigations on the off-label use of vitamin E in cancer have been ambiguous and variable. According to the findings of the HOPE-TOO trial, vitamin E supplementation did not prevent cancer, especially prostate cancer. In this trial, high-risk individuals (e.g., diabetes, vascular disease) were given 268 mg (400 International Units) daily and were observed for a median of 7 years. 18 The early positive effects of alpha-tocopherol vanished after post-interventional following in the ATBC Study, according to a post-interventional followup. 19 Some research have suggested that vitamin E supplementation may be beneficial for prostate cancer. A cohort study found an unfavorable relationship between supplemental vitamin E use and the incidence of metastatic or fatal prostate cancer in current or former smokers. 20 Vitamin E (30 mg) conferred protection in men but not women in the SU.VI.MAX research, resulting in a substantial reduction in total cancer incidence. 17 Due to lower baseline antioxidant levels in men, researchers determined that supplementation may be useful in this investigation. A previous controlled clinical experiment found that patients receiving alpha-tocopherol had a 32% lower incidence of prostate cancer than those who did not get alpha-tocopherol. 21 The reduction was observed in clinical prostate cancer but not in latent prostate cancer. In this trial, 29,133 prostate cancer patients who had smoked for 5-8 years were given alpha-tocopherol and beta-carotene supplements either separately or jointly. In contrast, more than 35,000 men 50 years of age and older were randomized to receive either selenium 200 mcg and vitamin E 400 mg, selenium and placebo, vitamin E and placebo, or placebo in the Selenium and Vitamin E Cancer Prevention Trial (SELECT), a long-term, multi-center, placebo-controlled trial. The trial was called off after around 7 years when preliminary data revealed that neither treatment prevented prostate cancer. Furthermore, two preliminary patterns were discovered, with vitamin E marginally raising the risk of prostate cancer and selenium slightly increasing the chance of diabetes. The gathering of follow-up data is still happening. 22


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