Illness prevention by boosting your immunity as well as supercharging your overall health and wellness.
This Encompasses: Normal Saline I Vitamin C I Zinc
Vitamin C Information
Ascorbic acid is a water-soluble vitamin found in fruits and vegetables such as citrus fruits and green peppers. It occurs as a white or slightly yellow crystal or powder with a slight acidic taste. It is an antiscorbutic product. On exposure to air and light it gradually darkens. In the dry state it is reasonably stable in air, but in solution it rapidly oxidizes. Ascorbic acid is a free radical, an antioxidant scavenger, and plays a major role in oxidation-reduction reactions. Ascorbic acid is a cofactor for enzymes involved in the biosynthesis of collagen (essential for tissue maintenance and repair), carnitine, and neurotransmitters. Humans cannot synthesize ascorbic acid endogenously and a lack of dietary intake can lead to scurvy. Vitamin C is most frequently used as a nutritional supplement. It also is used as an adjunct treatment of idiopathic methemoglobinemia and with deferoxamine in the treatment of chronic iron toxicity. Ascorbic acid has been used for a variety of ailments including the common cold, gum infections, acne, depression, fertility, and cancer; however, these claims have not been substantiated and vitamin C is not recommended for these purposes (see Mechanism of Action). Ascorbic acid was approved by the FDA in 1939.
No Ascorbic Acid within one week of surgery Zinc toxicity is extremely unlikely at this dose
Loss of taste or metallic taste
Transient flushing, blurred vision and jaundice
Zinc induced copper deficiency can lead to anemia, and thrombocytopenia. Caution CHF, Edema with Hydration
INDICATIONS: Immunity boost. Acute infections. Prior to surgery or travel. Auto-immune conditions.
Mechanism of Action
Ascorbic acid is necessary for collagen formation (e.g., connective tissue, cartilage, tooth dentin, skin, and bone matrix) and tissue repair. It is reversibly oxidized to dehydroascorbic acid. Both forms are involved in oxidation-reduction reactions. Vitamin C is involved in the metabolism of tyrosine, carbohydrates, norepinephrine, histamine, and phenylalanine. Other processes that require ascorbic acid include biosynthesis of corticosteroids and aldosterone, proteins, neuropeptides, and carnitine; hydroxylation of serotonin; conversion of cholesterol to bile acids; maintenance of blood vessel integrity; and cellular respiration. Vitamin C may promote resistance to infection by the activation of leukocytes, production of interferon, and regulation of the inflammatory process. It reduces iron from the ferric to the ferrous state in the intestine to allow absorption, is involved in the transfer of iron from plasma transferrin to liver ferritin, and regulates iron distribution and storage by preventing the oxidation of tetrahydrofolate. Ascorbic acid enhances the chelating action of deferoxamine during treatment of chronic iron toxicity (see Interactions). Vitamin C may have a role in the regeneration of other biological antioxidants such as glutathione and α-tocopherol to their active state.
Ascorbate deficiency lowers the activity of microsomal drug-metabolizing enzymes and cytochrome P-450 electron transport. In the absence of vitamin C, impaired collagen formation occurs due to a deficiency in the hydroxylation of procollagen and collagen. Non-hydroxylated collagen is unstable, and the normal processes of tissue repair cannot occur. This results in the various features of scurvy including capillary fragility manifested as hemorrhagic processes, delayed wound healing, and bony abnormalities.
Ascorbic acid should not be ingested 48—72 hours before amine-dependent stool occult blood tests are conducted because false negatives may occur.
Chronic, excessive doses of ascorbic acid can cause an increase in its own metabolism, which can cause scurvy if normal and supplemental intake are significantly reduced or discontinued. Large doses can also increase the likelihood of oxalate stones in the urinary tract in patients with a history of nephrolithiasis, hyperoxaluria, or oxalosis.
Large IV or oral doses of ascorbic acid have caused hemolytic anemia in some patients with G6PD deficiency (glucose-6-phosphate dehydrogenase deficiency).
High doses of ascorbic acid may interfere with urinary glucose determinations using the glucose oxidase method. Patients with diabetes mellitus should be made aware of the possibility of falsely decreased glucose concentrations with these tests.
Ascorbic acid may increase the risk of iron toxicity in patients with hemochromatosis, therefore, patients with hemochromatosis should limit their intake of ascorbic acid to no more than 500 mg/day. Rarely, ingestion of large quantities of ascorbic acid have been associated with fatal cardiac arrhythmias in patients with iron overload.
Patients with anemia (e.g., sideroblastic anemia, thalassemia) may experience decreased iron absorption during high dose ascorbic acid therapy. High doses of ascorbic acid may precipitate a crisis in patients with sickle cell anemia.
Ascorbic acid, vitamin C is classified as pregnancy category C. Umbilical cord blood concentrations are 2—4 times higher than those of maternal plasma levels. Adverse effects have not been reported with the normal daily intake of ascorbic acid, vitamin C within the recommended dietary daily intakes for a pregnant female. The use of ascorbic acid, vitamin C in excess of the recommended dietary allowance during normal pregnancy should be avoided unless, in the judgment of the physician, potential benefits in a specific, unique case outweigh the significant hazards involved
Ascorbic acid, vitamin C is distributed into breast milk. Use of ascorbic acid, vitamin C within the recommended daily dietary intake for lactating women is generally recognized as safe. In mothers not taking vitamin C supplements, vitamin C in human milk in the first 6 months of lactation varied from 34—83 mg/L. In mothers taking vitamin C supplements ranging from 45 to > 1,000 mg/day, vitamin C content of human milk varied from 45—115 mg/L.2 Consider the benefits of breastfeeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breastfeeding infant experiences an adverse effect related to a maternally administered drug, healthcare providers are encouraged to report the adverse effect to the FDA.
Ascorbic acid is necessary for many physiologic functions, including the metabolism of iron.3 The absorption of nonheme iron (primarily from plant sources) from the intestinal tract depends on iron being in its reduced form. (Heme iron, found in meat, fish, and poultry, appears to be absorbed intact.) Ascorbic acid, by maintaining iron in the ferrous state, can enhance the absorption of oral iron, however, the magnitude of this increase is in the range of 10% and only occurs with doses of ascorbic acid, vitamin C of 500 mg or greater. Healthy individuals usually absorb iron supplements (e.g., iron salts or polysaccharide-iron complex) adequately from the GI tract, but some patients may benefit from receiving supplemental ascorbic acid with each oral iron dose.
Patients should be advised not to take ascorbic acid, vitamin C supplements along with deferoxamine chelation therapy unless such supplements are prescribed with the approval of their health care professional. Patients with iron overload usually become vitamin C deficient, probably because iron oxidizes the vitamin. Vitamin C can be a beneficial adjunct in iron chelation therapy because it facilitates iron chelation and iron complex excretion. As an adjuvant to iron chelation therapy (e.g., deferoxamine), vitamin C (in doses up to 200 mg/day for adults, 50 mg/day in children < 10 years of age or 100 mg/day in older children) may be given in divided doses, starting after an initial month of regular treatment with deferoxamine. However, higher doses of ascorbic acid, vitamin C can facilitate iron deposition, particularly in the heart tissue, causing cardiac decompensation. In patients with severe chronic iron overload, the concomitant use of deferoxamine with > 500 mg/day PO of vitamin C in adults has lead to impairment of cardiac function; the dysfunction was reversible when vitamin C was discontinued. The manufacturer of deferoxamine recommends certain precautions for the coadministration of vitamin C with deferoxamine. First, vitamin C supplements should not be given concurrently with deferoxamine in patients with heart failure. Secondly, in other patients, such supplementation should not be started until 1 month of regular treatment with deferoxamine, and should be given only to patients receiving regular deferoxamine treatments. Do not exceed vitamin C doses of 200 mg/day for adults, 50 mg/day in children < 10 years of age, or 100 mg/day in older children, given in divided doses. Clinically monitor all patients, especially the elderly, for signs or symptoms of decreased cardiac function.
Adverse Reactions/Side Effects
Oxalate, urate, or cystine renal stones causing renal tubular obstruction, characterized by costovertebral pain or lower back pain, can occur following large doses of ascorbic acid. Hyperoxaluria develops in 5% of patients taking large doses. Patients at an increased risk are those with renal disease, on hemodialysis, or with a history of nephrolithiasis.5
Ascorbic acid is generally nontoxic. Adverse reactions that have been reported include flushing, headache, nausea/vomiting, and abdominal cramps. Diarrhea has resulted from oral dosages of more than 1 gram daily. Dizziness and faintness can result from rapid administration of IV ascorbic acid.5
Hemolytic anemia due to hemolysis has been observed in some patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency after receiving large IV or oral doses of ascorbic acid. In rare cases, sickle-cell crisis has occurred in patients with sickle cell disease because of decreased blood pH.6
Excessive use of chewable ascorbic acid formulations can lead to dental caries or sensitivity from the breakdown of dental enamel.
Zinc Sulfate Information
After iron, zinc it the second most abundant trace element in the human body. It is a divalent cation and the 30th element as well as the first element in group 12 of the periodic table. It is an essential micronutrient that plays a key role in the catalysis of over 100 enzymes such as alkaline phosphatase, lactic dehydrogenase, and RNA and DNA polymerase. It assists in the synthesis of RNA and DNA, cell proliferation and differentiation, and the stabilization of cell membranes and cell structures. Zinc exerts its gene regulatory and expressive effects through the formation of zinc finger proteins (ZnF).
The Role of Zinc in the Human Body
Zinc also plays a role in the regulation of the immune system. Being an essential element, it is not synthesized by the human body but must be ingested through food or mineral supplements. Some of the common food sources of zinc include beef, poultry, seafood, and grains, among others. In adults, normal serum zinc levels are between 70 and 250 ug/dl. After oral ingestion, zinc absorption occurs mainly in the ileum and duodenum and its binds to plasma proteins such as albumin in the blood. Following its metabolism, it is excreted mainly in the stool; some metabolites are also excreted in the urine and sweat, but to a significantly lower extent.
Symptoms of Zinc Deficiency
With zinc playing a significant role in many of the body’s key processes, zinc deficiency can result in a variety of illnesses and medical disorders. Some of the clinical manifestations include, but are not limited to, the following:
Hair and weight loss.
Delayed wound healing and skin lesions such as oral lichen planus, pemphigus vulgaris, bullous pemphigoid, and epidermodysplasia verruciformis, among others.
Decreased taste sensation and loss of appetite.
Altered cognitive and motor performance in neonates and infants.
Increased susceptibility to infections due to decreased functionality in monocytes, neutrophils, granulocytes, and phagocytosis.
Exacerbation of hypertension as well as other cardiovascular diseases.
Delayed puberty and growth retardation in adolescents.
Osteoporosis as well as other abnormalities in bone mineralization and development.
Decreased folate absorption which may result in macrocytic megaloblastic anemia.
Mental lethargy and mood disorders.
Mechanism of Action
With zinc playing a prominent role in many major processes within the human body, its mechanism of action varies depending on the organ system as well as the relevant process involved.
Immune System and Anti-Inflammation
In the immune system, zinc functions as a second messenger for immune cells; intracellular zinc participates in signaling events in immunity. It is involved in the development of monocytes and macrophages and regulates macrophagic functions such as phagocytosis and the production of proinflammatory cytokines. Zinc also inhibits phosphodiesterase, resulting in increased levels of guanosine-3′ 5′- cyclic monophosphate which leads to the suppression of Tumor Necrosis Factor alpha (TNF-a), interleukin-1 beta (IL-1B), as well as other inflammatory cytokines. Additionally, zinc increases the expression of peroxisome proliferator-activated receptor- alpha; this results in the downregulation of inflammatory cytokines and adhesion molecules. Due to these and several other actions in the immune system, zinc is considered to be a key anti-inflammatory agent in the human body.56
Zincs Effect on Skin
In the skin, zinc exerts its effects through several means in the development and maintenance of the skin cells. Zinc is most concentrated in the stratum spinosum layer of the skin compared to the other three layers namely basal layer, stratum granulosum, and stratum corneum. Studies have shown that zinc facilitates the proliferation as well as the survival of keratinocytes in the stratum spinosum; it also suppressed the activation of interferon-gamma and tumor necrosis factor-alpha by these keratinocytes. Additionally, zinc plays an active role in the development of Langerhans cells, a type of antigen-presenting cells, within the skin. Furthermore, the expression of melanocytes in the human skin is facilitated by zinc through mechanisms that are not yet fully understood.7
Central Nervous System
In the central nervous system, zinc is essential in the formation and development of the growth factors, hormones, enzymes, and proteins during neurodevelopment; mild zinc deficiency during pregnancy has been shown to result in learning and memory abnormalities. Zinc helps in the development of the neural tube, the first brain structure that develops during pregnancy, the neural crest, and the process of stem cell proliferation during neurogenesis. Furthermore, free zinc is found in synaptic vesicles where it acts to modulate a variety of postsynaptic receptors; in the synaptic cleft it reduces the inhibitory actions of GABA receptors. Free zinc also exerts inhibitory actions on the release of glutamate, an excitatory neurotransmitter.
While exogenous zinc supplements are generally well tolerated, there are some situations or circumstances that may warrant some degree of caution before it is administered. These include:
Renal impairment: Care should be exercised when administering zinc to individuals with renal compromise. As zinc is excreted in the urine, renal disease may impair its excretion in the urine and increase the likelihood of developing zinc toxicity.
Hypersensitivity reactions: Individuals may be hypersensitive to additional substances in the zinc supplement. Individuals with demonstrated hypersensitivity to any of the additional substances should not receive exogenous zinc supplements.
Exogenous zinc sulfate has been assigned to the pregnancy category C by the Food and Drug Administration. Though there is the possibility of fetal harm, the likelihood of this occurring is very remote. Zinc can be used in pregnancy since the dangers of zinc deficiency is substantially greater than any risks that may occur from its administration. Zinc crosses the placenta to the fetus where it plays a role in fetal neurodevelopment, as previously stated.
Zinc crosses from nursing mothers to infants through breast milk during lactation.
Zinc is known to interact with a variety of other medications which may impair their efficacy. Extreme care should be exercised when administering zinc to individuals taking other medications at the same time. Some medications that have the potential to interact with exogenously administered zinc are quinolones, tetracyclines, and penicillamine; zinc inhibits the absorption of these medications from the intestine. Also, thiazide diuretics, when given concurrently with zinc, increases the renal excretion of zinc and may also deplete zinc levels in the tissue. It may be necessary to monitor serum zinc levels when administered in conjunction with other medications.
Adverse Reactions/Side Effects
Apart from the likelihood of developing hypersensitivity reactions to exogenous zinc, the common adverse effect to watch out for is zinc toxicity. This may occur through an increased ingestion of zinc or a reduced excretion. Toxic levels of zinc in the human body is typically associated with a marked decrease in serum copper levels. Some of the clinical features that may arise as a result of zinc toxicity are hematemesis, hematuria, acute tubular necrosis, sideroblastic anemia, granulocytopenia, diarrhea, and myelodysplastic syndrome, among others. If zinc toxicity occurs, the exogenous administration of zinc should be discontinued immediately, and measures should be initiated to bring the zinc levels back down within normal ranges.
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