Blogs, Doctors, Wikipedia and YouTube are horrible sources of information when researching health and science. The reason for that is the lack of experts who are correcting the information. Peer review is the process by which each scientific paper is sent to professors or researchers in the scientific field who edit and approve the work.
There is a difference between a story and facts. To say that you have e.g. Candida overgrowth is a story you tell but the facts are that there are many species in the Genus Candida and they all can behave differently to certain treatments. What you will find on non-reviewed sources of information are mostly stories. Things that sound logical but where an expert would correct it immediately.
Peer review is not perfect but it guarantees that a study has to at least undergo some scrutiny by experts in the field. Every single word must be correct to the best of the current knowledge. So, you will need two websites to get started:
Google Scholar to find the research
Sci Hub to access the journals (insert the DOI)
Also, do not place too much value on a single study or studies that are over 10 years old. A Review is an article that summarizes the current state of the art in a certain field and you will see that it will often discuss bad methodologies and contradictory results. Science is created over decades and not in a single study. Always add a time filter and, if applicable, the word Review to your search.
Now, to Vitamin B-12.
There are four forms of Vitamin B-12, also known as Cobalamine (Cbl). Cyano-Cbl, Hydroxy-Cbl, Methyl-Cbl and Adenosyl-Cbl (PDF)1. In summary, Cyano- and Hydroxy-Cbl are general forms that the body can convert into what it needs. Methyl- and Adenosyl-Cbl are the forms that are actually utilized by the body. Here are the most important quotes from the article:
Methylcobalamine (MeCbl) is a cofactor for the enzyme methionine synthase involved in the production of methionine from homocysteine. In vitamin B12 deficiency, decreased MeCbl leads to the ‘folate trap’, that is, a functional deficiency of folate.4 This affects the rapidly dividing cells of the bone marrow, which require increased thymidylate for DNA synthesis, eventually leading to macrocytic anaemia.
MeCbl is primarily involved along with folate in hematopiesis and development of the brain during childhood. Whereas deficiency of AdCbl disturbs the carbohydrate, fat and amino-acid metabolism, and hence interferes with the formation of myelin. Thereby, it is important to treat vitamin B12 deficiency with a combination of MeCbl and AdCbl or hydroxocobalamin or Cbl. Regarding the route, it has been proved that the oral route is comparable to the intramuscular route for rectifying vitamin B12 deficiency
AdCbl is the cofactor for the enzyme methylmalonyl-CoA mutase that catalyzes the isomerization of methylmalonyl-CoA to succinyl-CoA, which is a key component of the tricarboxylic acid pathway of carbohydrate metabolism. In vitamin B12 deficiency, decreased AdCbl leads to a decrease in the conversion of methylmalonyl-CoA to succinyl-CoA with a resultant increase in methylmalonyl-CoA, which disturbs the carbohydrate, fat, aminoacid and urea metabolism and thereby affects the synthesis of neuronal myelin.
Concerns have been raised regarding the stability of Cbl. It has also been said that Cbl should not be used in smokers as it has a cyanide moiety and smokers have an excess of thiocyanate in their blood, which can disturb the metabolism of Cbl and increase its excretion.
And also some information on the selective deficiency of either Methyl-Cbl or Adenosyl-Cbl (PDF)2. Take just as a general direction since it is based on a small sample size.
Patients with homocystinuria, isolated or in combination with MMA-emia, present with megaloblastic anemia and various neurological abnormalities and have, at least to some degree, responded biochemically and clinically to vitamin B12 therapy.
Patients with isolated MMA-emia usually present with metabolic decompensation and show lethargy, failure to thrive, feeding problems, and muscular hypotonia but no signs of megaloblastic anemia.