Those experiencing pernicious anemia (an auto-immune reaction to either the parietal cells or intrinsic factor) go on to develop vitamin B12 deficiency through malabsorption if untreated. Deficiency could develop within 1–3 years in those experiencing malabsorption. 

Patients having surgical alteration of the distal ileum, Crohn’s disease, and using metformin are also at an increased risk for malabsorption.

Herbert (1994) estimates that deficiency could take as long as 20–30 years to develop in persons having normal absorption/reabsorption and suddenly ceasing to include substantial amounts of vitamin B12 in their diet during adulthood. This is due to the large amount of vitamin B12 that can be stored in the body and recycled through enterohepatic reabsorption. 

The prevalence of vitamin B12 deficiency increases with age and is associated with a number of conditions and treatments.

The main causes of vitamin B12 deficiency are

• poor dietary intake (as in vegetarianism),
• poor absorption (occurring in achlorhydria, pernicious anemia, Helicobacter pylori (H. pylori) infection, Crohn’s disease, and metformin use),
• poor distribution (genetic predisposition for aberrant proteins that are inefficient in transport or cellular uptake of vitamin B12).