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Laurel Boars
Laurel Boars

Where To Buy Methyl B12 For Cats



The present study sought to determine the spectrum of diseases associated with subnormal concentrations of serum cobalamin in cats undergoing investigation of suspected gastrointestinal problems. The solid-phase boil radioassay (RA) for cobalamin employed in the present study was immunologically specific, precise, and accurate, with a sensitivity of 15 pg/mL. The RA yielded results that strongly correlated with those obtained by bioassay (Spearmann rho = .805; P




where to buy methyl b12 for cats



Even though vitamin B12 is water soluble, tissue half-life (how long it stays in the body) averages 13 days in healthy cats and is reduced to approximately 5 days in cats with gastrointestinal diseases or poor overall health. This means that if your cat has FIP, his B12 reserves can be depleted rather quickly.


B12 oral supplements. Methylcobalamin should be used because it helps the liver function much more efficiently. B12 supplements sold for humans are suitable for cats. A good starting dose would be 500mcg (0.5mg) per day, but you can give up to twice as much. It may sound high, but in reality, only a small percentage is absorbed. Consider a cat-specific multi-vitamins supplement that also contains iron (for anemia).


The improvement of your cat's health can be measured by blood tests, hematology and/or chemistry panels. However, you should notice changes in your cat's everyday behavior: increased energy, less lethargy, better appetite. It is important to remember that cats don't understand they are sick, or why they are sick. They have a vague sense of being unwell, and that is all they know. The addition of B12 to their treatment protocol may help lessen their discomfort and improve their quality of life.


Measurements of vitamin B12 (cobalamine) and folate in serum are useful for diagnosing and characterizing some malabsorptive disorders of the small intestine of dogs. Concentrations of folate in serum depend on absorptive function of the proximal small intestine (jejunum), whereas, concentrations of vitamin B12 reflect absorptive function of the distal small intestine (ileum). Therefore, diffuse intestinal malabsorptive disorders lead to reduced serum B12 and folate concentrations. Diseases of the ileum are characterized by reduced B12 concentrations and diseases of the jejunum are characterized by reduced serum folate concentrations. Elevated folate and reduced B12 concentrations may indicate bacterial overgrowth in the proximal small intestine because certain bacteria synthesize folate and bind B12 making it unavailable for absorption. This pattern (high folate; low B12) also occurs in some dogs with exocrine pancreatic insufficiency. The exocrine pancreas secretes trypsinogen and other zymogens into the small intestine. Because trypsinogen is produced only by the pancreas, a low serum concentration of trypsinogen (i.e., trypsin-like immunoreactivity) is diagnostic for exocrine pancreatic insufficiency (EPI). Elevated TLI concentrations are consistent with acute pancreatitis, renal disease, or malnutrition.


Measurements of vitamin B12 (cobalamine) and folate in serum are useful for diagnosing and characterizing some malabsorptive disorders of the small intestine. Concentrations of folate in serum depend on absorptive function of the proximal small intestine (jejunum), whereas, concentrations of vitamin B12 reflect absorptive function of the distal small intestine (ileum). Cats with malabsorption or maldigestion often have subnormal vitamin B12 levels. Cats being supplemented with Vitamin B12 for deficiencies should have levels assessed regularly as the vitamin B12 half life is less than 3 weeks in cats.


In cats and dogs, the most common cause of cobalamin deficiency is chronic, severe small intestinal disease. In addition to hereditary cobalamin deficiency in certain breeds of dogs (such as Border Collies), exocrine pancreatic insufficiency (EPI) may also be a culprit.As most pets are fed commercially available diets, low dietary sources of B12 contributing to a Vitamin B12 deficiency would be increasingly rare.


Pets fed commercially available diets, or homemade diets with animal products, do not require vitamin B12 supplementation. If your pet has a vitamin B12 deficiency because of an intestinal disorder where they are unable to absorb the vitamin from the diet, oral supplementation will not work as expected. These patients would require vitamin B12 supplementation through subcutaneous injection and is usually administered once monthly.


B12 is a vitamin (Cobalamin) that is important for neurological function, red blood cell production, DNA synthesis, and energy production. B12 is present in commercially available diets. Cats and dogs are unable to produce vitamin B12 in their bodies and must receive it from the foods they eat or from supplementation. Vitamin B12 deficiency causes a number of symptoms in both cats and dogs, and when left untreated can potentially lead to serious health problems. Vitamin B12 deficiency is treatable and carries a good prognosis, so it is important to monitor your pet's vitamin B12 levels to prevent health problems.


A similar association between hypercobalaminaemia and the presence of a solid neoplasm has been recognised in man [23], with the strongest associations for liver tumours and hepatic metastases [14],[15],[17],[24],[25]. Recently, associations with a wider variety of malignancies have been established [9],[13]. Unfortunately, in the current study, there were insufficient cases presenting with a solid neoplasm to enable associations with any particular tumour type. The reason for the hypercobalaminaemia in the cats with a tumour in the current study is not known. In humans, various mechanisms have been proposed, including the direct production of cobalamin binding proteins (transcobalamins) [9], upregulation of folate-centred metabolic pathways and production of cobalamin autoantibodies [13],[26]. In humans, the association between hypercobalaminaemia and neoplasia was first reported for haematopoietic malignancies, particularly chronic myeloid leukaemia [10]-[12]. Increased production of binding proteins (specifically, a transcobalamin derived from granulocyte membranes) is proposed to occur as a result of leucocytosis [21],[27]. No association with either haematogenous neoplasms or leucocytosis was detected in this study. This might be due to differences in human and feline transcobalamins, namely that cats lack transcobalamin I [28], or might reflect the type of haematogenous neoplasms encountered. The vast majority in this study were lymphoma (32/33) and there is conflicting evidence regarding an association with lymphoma in man. Some [17] but not other [11],[15],[16],[21] studies have suggested an association with hypercobalaminaemia. Additionally, as many of the cats with lymphoma had ileal involvement (the site of intestinal cobalamin absorption), this would likely be confounding, even if a true association with lymphoma does exist.


Hypercobalaminaemic cats in this study were also more likely to be diagnosed with liver disease, and similar associations are seen in humans [9],[14],[15]. Possible mechanisms include leakage into the circulation following hepatocellular injury and impaired hepatic uptake of cobalamin. An association with hepatocellular injury is less likely, given that there was no correlation between serum ALT activity and cobalamin concentration. The association between hypercobalaminaemia and hepatobiliary disease in cats is intriguing, since hepatobiliary disease is also associated with hypocobalaminaemia in this species [3],[4],[7],[28]-[30]. This discrepancy might reflect the tendency for concurrent gastrointestinal, pancreatic and hepatobiliary pathology in cats, having counteracting effects on serum cobalamin. Indeed, only 9 of the 17 hypercobalaminaemic cats with confirmed liver disease in this study had a disease confined to the hepatobiliary system. Alternatively, it could reflect differing effects of specific hepatobiliary diseases on cobalamin metabolism. A final observation, with regard to hepatic disease was the fact that one of the cats had portal vein hypoplasia. The reason why hypercobalaminaemia would be associated with a congenital disease is not known. One possibility might be that there are effects on cobalamin metabolism as a result of changes in hepatic function caused by the PVH. However, further work would be required to determine this. 041b061a72


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