Amvi Forte
Amvi Forte Uses, Dosage, Side Effects, Food Interaction and all others data.
Chromium is a transition element with the chemical symbol Cr and atomic number 24 that belongs to Group 6 of the periodic table. It is used in various chemical, industrial and manufacturing applications such as wood preservation and metallurgy. The uses of chromium compounds depend on the valency of chromium, where trivalent Cr (III) compounds are used for dietary Cr supplementation and hexavalent Cr (VI) compounds are used as corrosion inhibitors in commercial settings and are known to be human carcinogens . Humans can be exposed to chromium via ingestion, inhalation, and dermal or ocular exposure . Trivalent chromium (Cr(III)) ion is considered to be an essential dietary trace element as it is involved in metabolism of blood glucose, regulation of insulin resistance and metabolism of lipids. Clinical trials and other studies suggest the evidence of chromium intake improving glucose tolerance in patients with Type I and II diabetes, however its clinical application in the standard management of type II diabetes mellitus is not established. Chromium deficiency has been associated with a diabetic-like state, impaired growth, decreased fertility and increased risk of cardiovascular diseases .
According to the National Institute of Health, the daily dietary reference intake (DRI) of chromium for adult male and non-pregnant female are 35 μg and 25 μg, respectively . Chromium picolinate capsules may be used as nutritional adjuvant in patients with or at risk of type 2 diabetes mellitus (T2DM) to improve blood sugar metabolism and stabilize the levels of serum cholesterol. Chromium chloride is available as an intravenous injection for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN) .
Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity . In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency .
Ginkgo biloba extract contains a group of terpene lactones (notably, ginkgolides and diterpenes) and ginkgo flavone glycosides (notably, ginkgetin, bilobetin, and sciadopitysin) that have antioxidant and vasoactive properties. Most of the studies that investigate the effect of ginkgo biloba use the standardized extract of Ginkgo biloba (EGb) 761 (EGb761), which was developed by a German pharmaceutical company in 1964. EGb761 contains 6% terpene lactones and 24% flavonoid glycosides. Flavonoids include quercetin, rutin, kaempferol, and isorhamnetin. Lactones include ginkgolide A, ginkgolide B, ginkgolide C, bilobalide, and ginkgotoxin, a lactone that is structurally related to pyridoxine. Ginkgo biloba is an herbal plant that is now cultivated worldwide. It is originally native to China, and ginkgo biloba extract has been used in traditional Chinese medicine for centuries.
After its nootropic properties were discovered, ginkgo biloba has gained attention as a therapeutic ingredient for memory and concentration enhancement in cognitive impairment and neurogenerative diseases, such as dementia. Ginkgo biloba was investigated in preliminary studies for a variety of therapeutic purposes such as improving cardiovascular health, sexual dysfunction, psychiatric disorders, skin disorders, and glaucoma. Ginkgo biloba is found in a number of homeopathic and over-the-counter herbal products and dietary supplements, but it has no approved therapeutic indications by regulatory bodies, such as the FDA, EMA, and Health Canada. Ginkgo folium, the leaf extract of Ginkgo biloba, is considered an anti-dementia drug by the World Health Organization.
Ginkgo biloba is a herbal ingredient with demonstrated antioxidant, vasoactive, antiapoptotic, anti-inflammatory, antiplatelet, and fibrinolytic properties. Ginkgo biloba has been investigated for use in a variety of medical conditions, but the most extensively studied area is in the context of cognitive impairment and neurodegenerative disorders. Ginkgo biloba was examined as a potential nootropic agent or cognitive enhancer but research findings supporting the therapeutic efficacy of ginkgo biloba extract (EGb) in dementia remain controversial. Some clinical studies of dementia that were up to one year long showed that EGb improves the cognitive performance and social functioning of patients. However, other studies did not support its clinical benefit for patients with cognitive impairment and dementia. Numerous meta-analysis studies showed insufficient evidence of the effectiveness of EGb in reducing both all-cause dementia incidence and Alzheimer's disease-associated dementia incidence in elderly patients with normal cognition or with mild cognitive impairment. Additionally, there is no up-to-date evidence that demonstrates the benefit of the long-term use of standardized EGb in reducing the risk of progression to Alzheimer's disease. A 2012 meta-analysis did not support the use of EGb in enhancing cognitive function in healthy adults.
Ginseng is promoted as an adaptogen (a product that increases the body's resistance to stress), one which can to a certain extent be supported with reference to its anticarcinogenic and antioxidant properties. Ginseng is also known to contain phytoestrogens.
Bioperine has been used in trials studying the treatment of Multiple Myeloma and Deglutition Disorders.
Selenium is a trace metal in the human body particularly important as a component of glutathione peroxidase, an important enzyme in the prevention of cellular damage by free radicals and reactive oxygen species
Selenium is incorporated into many different selenoproteins which serve various functions throughout the body .
| Trade Name | Amvi Forte |
| Generic | Vitamin D3 / Cholecalciferol + Ginseng + Grape Seed Extract + Selenium + Chromium + Omega 3 Fatty Acid + Piperine + Ginkgo Biloba + Green Tea |
| Weight | 200iu |
| Type | Capsule |
| Therapeutic Class | |
| Manufacturer | Spiritus Healthcare Pvt Ltd |
| Available Country | India |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Chromium is an ingredient found in a variety of supplements and vitamins.
Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms .
Ginkgo biloba is a herbal supplement found in over-the-counter or unapproved homeopathic products for various health conditions, such as cognitive, neurodegenerative, cardiovascular, and reproductive health disorders.
Ginkgo biloba does not currently have any approved therapeutic indications, and there is insufficient evidence to support its unapproved use. It is available in over-the-counter herbal products mostly for oral use, to improve memory and cognitive problems.
Ginseng is a herbal supplement used in many health products.
Selenium is an ingredient found in a variety of supplements and vitamins.
For the supplementation of total parenteral nutrition to prevent hyposelenemia .
Amvi Forte is also used to associated treatment for these conditions: Mineral supplementationCognitive Dysfunctions, Cognitive Function, DepressionDietary and Nutritional Therapies, Vitamin E SupplementationNutritional supplementation
How Amvi Forte works
Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules . Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake . Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt.
Under insulin-resistant conditions, chromium also promotes GLUT-4 transporter translocation that is independent of activity of IR, IRS-1, PI3-kinase, or Akt; chromium mediates cholesterol efflux from the membranes via increasing fluidity of the membrane by decreasing the membrane cholesterol and upregulation of sterol regulatory element-binding protein . As a result, intracellular GLUT-4 transporters are stimulated to translocate from intracellular to the plasma membrane, leading to enhanced glucose uptake in muscle cells . Chromium attenuates the activity of PTP-1B in vitro, which is a negative regulator of insulin signaling. It also alleviates ER stress that is observed to be elevated the suppression of insulin signaling. ER stress is thought to activate c-Jun N-terminal kinase (JNK), which subsequently induces serine phosphorylation of IRS and aberration of insulin signalling . Transient upregulation of AMPK by chromium also leads to increased glucose uptake .
Two key active ingredients in ginkgo biloba are terpene lactones (notably ginkgolides and diterpenes) and ginkgo flavone glycosides (notably ginkgetin, bilobetin, and sciadopitysin), which are present at varying concentrations. Ginkgo biloba extract EGb 761 is the standardized extract of ginkgo biloba used in studies, which contains 6% terpenoids and 24% flavonoid glycosides. Animal studies have shown that ginkgo biloba works on several neurotransmitter pathways and brain structures. Flavones were shown to inhibit lipid peroxidation; inhibit the uptake of serotonin, dopamine, and norepinephrine; and inhibit platelet aggregation. Terpene lactones may also act as potent antagonists of the platelet-activating factor and may possess anti-ischemic and fibrinolytic effects. They were also shown to downregulate adrenal peripheral benzodiazepine receptors and increase adrenocorticotropic hormone levels. Ginkgo biloba also reversibly inhibits monoamine oxidase A; and modestly inhibits anticholinesterase activity, leading to enhanced cholinergic transmission in the brain.
Several studies suggest that ginkgo biloba exerts neuroprotective effects by reducing free radical production in the prefrontal cortex, which may explain its improvement on short-term memory. Ginkgo biloba extract acts as a free radical scavenger, protecting neurons from oxidative damage and apoptosis related to aging, cerebral ischemia, and neurodegenerative disorders. Ginkgo biloba also inhibits amyloid-β neurotoxicity and protects against hypoxic challenges and increased oxidative stress. One study showed that bilobalide, a terpene lactone, delays the onset of hypoxic glycolysis. Ginkgo biloba has the potential to regulate metabolism, stabilize the membrane, and promote vasodilation. In the arterial endothelium, EGb stimulated the release of endogenous relaxing factors, such as endothelium-derived relaxing factor and prostacyclin. In the inflammatory environment that causes tissue damage, EGb promoted nitric oxide production, leading to enhanced peripheral and cerebral blood flow.
Selenium is first metabolized to selenophosphate and selenocysteine. Selenium incorporation is genetically encoded through the RNA sequence UGA . This sequence is recognized by RNA ste loop structures called selenocysteine inserting sequences (SECIS). These structures require the binding of SECIS binding proteins (SBP-2) to recognize selenocystiene. The specialized tRNA is first bound to a serine residue which is then enzymatically processed to a selylcysteyl-tRNA by selenocystiene sythase using selenophosphate as a selenium donor. Other unidentified proteins are required as part of the binding of this tRNA to the ribosome. Selenoproteins appear to be necessary for life as mice with the specialized tRNA gene knocked out exhibited early embryonic lethality .
The most important selenoproteins seem to be the glutathione peroxidases and thioredoxin reductases which are part of the body's defenses againts reactive oxygen species (ROS) . The importance of selenium in these anti-oxidant proteins has been implicated in the reduction of atherosclerosis by preventing the oxidation of low density lipoprotein . Selenium supplementation is also being investigated in the prevention of cancer and has been suggested to be beneficial to immune function .
Toxicity
Oral LD50 for Cr (VI) is 135 - 175 mg/kg in mouse and 46 - 113 mg/kg in rat . Oral LD50 for Cr (III) in rat is >2000 mg/kg . LD50 of chromium (III) oxide in rats is reported to be > 5g/kg . Other LD50 values reported for rats include: 3.5 g/kg (CI 3.19-3.79 g/kg) for chromium sulphate; 11.3 g/kg for chromium (III) acetate; 3.3 g/kg for chromium nitrate; and 1.5 g/kg for chromium nitrate nonahydrate .
Acute overdose of chromium is rare and seriously detrimental effects of hexavalent chromium are primarily the result of chronic low-level exposure . In case of overdose with minimal toxicity following acute ingestion, treatment should be symptomatic and supportive . There is no known antidote for chromium toxicity.
Hexavalent chromium is a Class A carcinogen by the inhalation route of exposure and Class D by the oral route . The oral lethal dose in humans has been estimated to be 1-3 g of Cr (VI); oral toxicity most likely involves gastrointestinal bleeding rather than systemic toxicity . Chronic exposure may cause damage to the following organs: kidneys, lungs, liver, upper respiratory tract . Soluble chromium VI compounds are human carcinogens. Hexavalent chromium compounds were mutagenic in bacteria assays and caused chromosome aberrations in mammalian cells. There have been associations of increased frequencies of chromosome aberrations in lymphocytes from chromate production workers . In human cells in vitro, Cr (VI) caused chromosomal aberrations, sister chromatid exchanges and oxidative DNA damage .
Oral LD50 of standardized extract in mice is 7730 mg/kg, which corresponds to 2300 mg/kg of active ingredients, 1900 mg/kg of flavone glycosides, and 464 mg/kg of terpene lactones. Intravenous LD50 is 1100 mg/kg.
No case of overdose has been reported so far. Cyanogenic glycosides found in raw ginkgo seeds are potentially toxic compounds; thus, contact or ingestion of ginkgo seeds can lead to serious reactions such as allergic skin reaction, including acute generalized exanthematous pustulosis, and convulsions. Ginkgo toxicity can manifest as bleeding, seizure, and serotonin syndrome. As there is no known antidote for ginkgo toxicity, treatment includes discontinuation of ginkgo and symptomatic and supportive care. Seizures may be attributed to ginkgotoxin, which can cause seizures at high doses.
Oral LD50 of 6700mg/kg in rats . Selenium exposure is teratogenic and can result in fetal death as tested in mice. Chronic toxicity is characterized by hair loss, white horizontal streaking on fingernails, paronchyia, fatigue, irritability, hyperreflexia, nausea, vomiting, garlic odor on breath, and metallic taste . Serum selenium correlates weakly with symtoms. Blood chemistry as well as liver and kidney function are normally unnaffected. Acute toxicity presents as stupor, respiratory depression, and hypotension. ST elevations and t-wave changes characteristic of myocardial infarction may be observed.
Volume of Distribution
Absorbed chromium is distributed to all tissues of the body and its distribution in the body depends on the species, age, and chemical form . Circulating Cr (III) following oral or parenteral administration of different compounds can be taken up by tissues and accumulates in the liver, kidney, spleen, soft tissue, and bone .
No data available.
Elimination Route
Chromium compounds are both absorbed by the lung and the gastrointestinal tract. Oral absorption of chromium compounds in humans can range between 0.5% and 10%, with the hexavalent (VI) chromium more easily absorbed than the trivalent (III) form . Absorption of chromium from the intestinal tract is low, ranging from less than 0.4% to 2.5% of the amount consumed . Vitamin C and the vitamin B niacin is reported to enhance chromium absorption .
Most hexavalent Cr (VI) undergoes partial intragastric reduction to Cr (III) upon absorption, which is an action mainly mediated by sulfhydryl groups of amino acids . Cr (VI) readily penetrates cell membranes and chromium can be found in both erythrocytes and plasma after gastrointestinal absorption of Cr (IV). In comparison, the presence of chromium is limited to the plasma as Cr (III) displays poor cell membrane penetration . Once transported through the cell membrane, Cr (VI) is rapidly reduced to Cr (III), which subsequently binds to macromolecules or conjugate with proteins. Cr (III) may be bound to transferrin or other plasma proteins, or as complexes, such as glucose tolerance factor (GTF).
Studies assessed the pharmacokinetic parameters of terpene lactones, the main component of ginkgo biloba. Following oral administration of ginkgo biloba solution, the mean absolute bioavailability was 80% for ginkgolide A, 88% for ginkgolide B and 79% for biloalide. In an early rat study, about 60% of radiolabeled EGb 761 was absorbed with a Tmax of 1.5 hours. The highest amount of radioactivity was measured in the stomach and small intestine.
In another study, after a single oral dose of 120 mg EGb 761 in healthy volunteers, Cmax was 22.22 ± 4.57 ng/mL for ginkgolide A, 8.27 ± 1.82 ng/mL for ginkgolide B, and 54.42 ± 13.62 ng/mL for biloalide. AUC0-∞ was 121.35 ± 22.92 ng × h/mL for ginkgolide A, 59.88 ± 11.39 ng × h/mL for ginkgolide B, and 217.24 ± 44.07 ng × h/mL for biloalide. Tmax ranged from 1.17 to 1.54 hours for those three compounds.
Oral bioavailability of 90% when given as L-selenomethionine . Tmax of 9.17h.
Half Life
The elimination half-life of hexavalent chromium is 15 to 41 hours .
Unpublished human data reports that after oral administration of 80 mg EGb 761, the half-life was four hours for ginkgolides A and six hours for ginkgolides B. The half-life of bilobalide was three hours after administration of 120 mg EGb 761 extract.
Half life was observed to increase with chronic dosing time . For day 1-2 half life was 1.7 days. For day 2-3 half life was 3 days. For day 3-14 half life was 11.1 days.
Clearance
Excretion of chromium is via the kidneys ranges from 3 to 50 μg/day . The 24-hour urinary excretion rates for normal human subjects are reported to be 0.22 μg/day .
No data available.
Elimination Route
Absorbed chromium is excreted mainly in the urine, accounting for 80% of total excretion of chromium; small amounts are lost in hair, perspiration and bile . Chromium is excreted primarily in the urine by glomerular filtration or bound to a low molecular-weight organic transporter .
At 72 hours following oral administration in rats, about 38% of the ginkgo biloba extract was excreted via expiration, 22% was excreted in urine, and 29% was excreted in feces. About 70% of ginkgolides A, 50% of ginkgolides B, and 30% of bilobalide were excreted unchanged in the urine.
Mainly excreted in urine as 1beta-methylseleno-N-acetyl-d-galactosamine and trimethylselenonium . The amount excreted as 1beta-methylseleno-N-acetyl-d-galactosamine plateaus at doses around 2microg after which the amount excreted as trimethylselenonium increases. Some selenium is also excreted in feces when given orally .
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