If you are looking for reckless, irresponsible marketing or abuses to the consumer for the sake of a buck check out, VitaminVape.com.
This company appears to be a shell company of “Youngevity” company’s house of cards.
The concept of “VitaminVape” is to vape (inhale) B12 vitamins. This should give a charge to the system, however the delivery of B12 vitamins to and through the lungs (breathing) is dubious indeed. As this product is developed and launched through joint venture with the founder who also developed RED BULL, we can anticipate financial returns, but HUGE HEALTH RISKS. This is becoming the hallmark it seems of a pseudo nutrition company seeking gain by offering up seemingly dodgy products. If you do not think so, go to a function and look at all the sick people. These are people desperately seeking answers to problems. Many claim to find answers, however observation and communication will reveal many a heartache for these people.
VitaminVape could be the Viagra of the nutrition world, or the RED BULL of the soft drink market. This means it will likely provide financial return, but at certain risk. Note the following:
B12 vitamins put in to public consumption are almost always derived from managed bacteria. If you want to introduce bacteria and sickness into the lungs insert there…..Seem simple. Wikipedia advise: Only bacteria and archaea have the enzymes needed for its synthesis.
A common synthetic form of the vitamin is cyanocobalamin, produced by chemically modifying bacterial hydroxocobalamin. Because of superior stability and low cost this form is used in many pharmaceuticals and supplements as well as for fortification of foods. In the body, it is converted into the human physiological forms methylcobalamin and 5′-deoxyadenosylcobalamin. In this process a cyanide ion, (CN−), is produced, but the amount is very, very small (20 μg from 1,000 μg of cyanocobalamin) compared to what would cause a toxicity risk, and is in fact less than the amount of cyanide consumed daily from food (primarily fruit, nuts, seeds, and legumes). Cyanide-free synthetic forms of the vitamin—hydroxocobalamin, methylcobalamin, and adenosylcobalamin—are being used in some pharmacological products and supplements, but their claimed superiority to cyanocobalamin is debatable.
- Hematologic: Peripheral vascular thrombosis has been reported. Treatment of vitamin B12 deficiency can unmask polycythemia vera, which is characterized by an increase in blood volume and the number of red blood cells. The correction of megaloblastic anemia with vitamin B12 can result in fatal hypokalemia and gout in susceptible individuals, and it can obscure folate deficiency in megaloblastic anemia.
- Leber’s disease: Vitamin B12 in the form of cyanocobalamin is contraindicated in early Leber’s disease, which is hereditary optic nerve atrophy. Cyanocobalamin can cause severe and swift optic atrophy, but other forms of vitamin B12 are available. The sources of this statement are not clear, while an opposing view concludes: “The clinical picture of optic neuropathy associated with vitamin B12 deficiency shows similarity to that of Leber’s disease optic neuropathy. Both involve the nerve fibers of the papillomacular bundle. The present case reports suggest that optic neuropathy in patients carrying a primary LHON mtDNA mutation may be precipitated by vitamin B12 deficiency. Therefore, known carriers should take care to have an adequate dietary intake of vitamin B12 and malabsorption syndromes like those occurring in familial pernicious anaemia or after gastric surgery should be excluded.”
Vitamin B12 supplements in theory should be avoided in people sensitive or allergic to cobalamin, cobalt, or any other product ingredients. Direct allergy to a vitamin or nutrient is extremely rare, and if reported, other causes should be sought.
Elevated plasma B12 (cobalamin) levels
Elevated levels of serum B12 or cobalamin (above about 600 pmol/L) in the absence of supplementation may be a diagnostic sign of serious disease. In such cases B12 is thought to be only a marker for disease, and not a causal agent.
One cause of elevated plasma B12 (cobalamin) is general liver disease, since hepatic cytolysis releases B12, and the affected liver shows decreased cobalamin clearance. Thus, acute hepatitis, cirrhosis, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. Elevated B12 levels have been suggested as a predictor of ICU mortality risk, but a recent study of this found that “[e]levated B12 levels are not a significant predictor of mortality after ICU admission when liver function is controlled for, and may instead be a proxy for poor liver function.” 
A second group of non-supplemented patients with high cobalamin levels have them due to enhanced production of the plasma B12 transporters haptocorrin and transcobalamin II  This happens in hematologic disorders like chronic myelogeneous leukemia, promyelocytic leukemia, polycythemia vera and also the hypereosinophilic syndrome. Increased cobalamin levels are one of the diagnostic criteria for the latter two diseases.
A third group of non-supplemented patients with high cobalamin levels (> 600 pmol/L) may be at immediate (mostly within one year of testing) higher risk for new diagnosis of certain smoking and alcohol-related cancers which are non-hematologic. In a study of 333,000 persons in Denmark, those with elevated B12 had a three to six times higher standard incidence ratio, with respect to those with normal B12 levels, for later development of certain types of cancer.
Thus, one review states: “Altogether it can be concluded that an observed elevation of cobalamin in blood merits a full diagnostic work up to assess the presence of disease.” 
- Aminosalicylic acid (para-aminosalicylic acid, PAS, Paser): Aminosalicylic acid can reduce oral vitamin B12 absorption, possibly by as much as 55%, as part of a general malabsorption syndrome. Megaloblastic changes, and occasional cases of symptomatic anemia have occurred, usually after doses of 8 to 12 g/day for several months. Vitamin B12 levels should be monitored in people taking aminosalicylic acid for more than one month.
- Antibiotics: An increased bacterial load can bind significant amounts of vitamin B12 in the gut, preventing its absorption. In people with bacterial overgrowth of the small bowel, antibiotics such as metronidazole (Flagyl) can actually improve vitamin B12 status. The effects of most antibiotics on gastrointestinal bacteria are unlikely to have clinically significant effects on vitamin B12 levels.
- Hormonal contraception: The data regarding the effects of oral contraceptives on vitamin B12 serum levels are conflicting. Some studies have found reduced serum levels in oral contraceptive users, but others have found no effect despite use of oral contraceptives for up to 6 months. When oral contraceptive use is stopped, normalization of vitamin B12 levels usually occurs. Lower vitamin B12 serum levels seen with oral contraceptives probably are not clinically significant.
- Chloramphenicol (Chloromycetin): Limited case reports suggest that chloramphenicol can delay or interrupt the reticulocyte response to supplemental vitamin B12 in some patients. Blood counts should be monitored closely if this combination cannot be avoided.
- Cobalt irradiation: Cobalt irradiation of the small bowel can decrease gastrointestinal (GI) absorption of vitamin B12.
- Colchicine: Colchicine in doses of 1.9 to 3.9 mg/day can disrupt normal intestinal mucosal function, leading to malabsorption of several nutrients, including vitamin B12. Lower doses do not seem to have a significant effect on vitamin B12 absorption after 3 years of colchicine therapy. The significance of this interaction is unclear. Vitamin B12 levels should be monitored in people taking large doses of colchicine for prolonged periods.
- Colestipol (Colestid), cholestyramine (Questran): These resins used for sequestering bile acids to decrease cholesterol, can decrease gastrointestinal (GI) absorption of vitamin B12. It is unlikely this interaction will deplete body stores of vitamin B12 unless there are other factors contributing to deficiency. In a group of children treated with cholestyramine for up to 2.5 years, there was not any change in serum vitamin B12 levels. Routine supplements are not necessary.
- Folic acid: Folic acid, particularly in large doses, can mask vitamin B12 deficiency by completely correcting hematological abnormalities. In vitamin B12 deficiency, folic acid can produce complete resolution of the characteristic megaloblastic anemia, while allowing potentially irreversible neurological damage (from continued inactivity of methylmalonyl mutase) to progress. Thus, vitamin B12 status should be determined before folic acid is given as monotherapy.
- H2-receptor antagonists: include cimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid), and ranitidine (Zantac). Reduced secretion of gastric acid and pepsin produced by H2 blockers can reduce absorption of protein-bound (dietary) vitamin B12, but not of supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Clinically significant vitamin B12 deficiency and megaloblastic anemia are unlikely, unless H2 blocker therapy is prolonged (2 years or more), or the person’s diet is poor. It is also more likely if the person is rendered achlorhydric(with complete absence of gastric acid secretion), which occurs more frequently with proton pump inhibitors than H2 blockers. Vitamin B12 levels should be monitored in people taking high doses of H2 blockers for prolonged periods.
- Metformin (Glucophage): Metformin may reduce serum folic acid and vitamin B12 levels. Long-term use of metformin substantially increases the risk of B12 deficiency and (in those patients who become deficient) hyperhomocysteinemia, which is “an independent risk factor for cardiovascular disease, especially among individuals with type 2 diabetes“. There are also rare reports of megaloblastic anemia in people who have taken metformin for five years or more. Reduced serum levels of vitamin B12 occur in up to 30% of people taking metformin chronically. Clinically significant deficiency is not likely to develop if dietary intake of vitamin B12 is adequate. Deficiency can be corrected with vitamin B12 supplements even if metformin is continued. The metformin-induced malabsorption of vitamin B12 is reversible by oral calcium supplementation. The general clinical significance of metformin upon B12 levels is as yet unknown.
- Neomycin: Absorption of vitamin B12 can be reduced by neomycin, but prolonged use of large doses is needed to induce pernicious anemia. Supplements are not usually needed with normal doses.
- Nicotine: Nicotine can reduce serum vitamin B12 levels. The need for vitamin B12 supplementation in smokers has not been adequately studied.
- Nitrous oxide: Nitrous oxide inactivates the cobalamin form of vitamin B12 by oxidation. Symptoms of vitamin B12 deficiency, including sensory neuropathy, myelopathy, and encephalopathy, can occur within days or weeks of exposure to nitrous oxide anesthesia in people with subclinical vitamin B12 deficiency. Symptoms are treated with high doses of vitamin B12, but recovery can be slow and incomplete. People with normal vitamin B12 levels have sufficient vitamin B12 stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (such as recreational use). Vitamin B12 levels should be checked in people with risk factors for vitamin B12 deficiency prior to using nitrous oxide anesthesia. Chronic nitrous oxide B12 poisoning (usually from use of nitrous oxide as a recreational drug) may result in B12 functional deficiency even with normal measured blood levels of B12.
- Phenytoin (Dilantin), phenobarbital, primidone (Mysoline): These anticonvulsants have been associated with reduced vitamin B12 absorption, and reduced serum and cerebrospinal fluidlevels in some patients. This may contribute to the megaloblastic anemia, primarily caused by folate deficiency, associated with these drugs. It is also suggested that reduced vitamin B12 levels may contribute to the neuropsychiatric side effects of these drugs. Patients should be encouraged to maintain adequate dietary vitamin B12 intake. Folate and vitamin B12 status should be checked if symptoms of anemia develop.
- Potassium: Potassium supplements can reduce absorption of vitamin B12 in some people. This effect has been reported with potassium chloride and, to a lesser extent, with potassium citrate. Potassium might contribute to vitamin B12 deficiency in some people with other risk factors, but routine supplements are not necessary.
- Proton pump inhibitors (PPIs): The PPIs include omeprazole (Prilosec, Losec), lansoprazole (Prevacid), rabeprazole (Aciphex), pantoprazole (Protonix, Pantoloc), and esomeprazole (Nexium). The reduced secretion of gastric acid and pepsin produced by PPIs can reduce absorption of protein-bound (dietary) vitamin B12, but not supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Reduced vitamin B12 levels may be more common with PPIs than with H2-blockers, because they are more likely to produce achlorhydria (complete absence of gastric acid secretion). Clinically significant vitamin B12 deficiency is unlikely, unless PPI therapy is prolonged (2 years or more) or dietary vitamin intake is low. Vitamin B12 levels should be monitored in people taking high doses of PPIs for prolonged periods.
- Zidovudine (AZT, Combivir, Retrovir): Reduced serum vitamin B12 levels may occur when zidovudine therapy is started. This adds to other factors that cause low vitamin B12 levels in people with HIV, and might contribute to the hematological toxicity associated with zidovudine. The data suggest vitamin B12 supplements are not helpful for people taking zidovudine.
Think long and hard before engaging a product such as this . The risk/reward apparently was considered by the company(s) offering it and their reward outweighed your risk apparently.
If you are seriously looking to recoup your health, get a boost, and heal, then get the book, THE ANSWER TO CANCER: A SIMPLE SOLUTION FOR THE WESTERN CONDITION.