Vitamin B12, also known as cobalamin, is a water-soluble nutrient that plays a significant role in various bodily functions. It is necessary for the formation of red blood cells, the proper functioning of the nervous system, and the synthesis of DNA, the genetic material in all cells. For the body to utilize B12 effectively, it must be absorbed correctly from the diet.
The Journey of B12
The absorption of vitamin B12 begins in the mouth, where food mixes with saliva containing R-proteins. As the B12-containing food reaches the stomach, hydrochloric acid and pepsin, an enzyme, work to detach B12 from the food proteins. Once freed, B12 then binds to these R-proteins, forming a complex that protects it from degradation by stomach acid.
This B12-R-protein complex then travels from the stomach into the duodenum, the first part of the small intestine. In the duodenum, pancreatic enzymes are released, which degrade the R-proteins, releasing B12. The freed vitamin B12 binds to Intrinsic Factor (IF), a specialized protein secreted by parietal cells in the stomach lining.
The B12-Intrinsic Factor complex then continues its journey through the small intestine, specifically to the terminal ileum, its final segment. Here, specialized receptors on the cells lining the ileum recognize and bind to the B12-IF complex, facilitating its absorption into the enterocytes, or intestinal cells.
Once inside the intestinal cells, B12 is released from the Intrinsic Factor and binds to another transport protein. This B12 complex is then transported into the bloodstream, where it circulates throughout the body, delivering B12 to various tissues and organs, including the liver, where a lot of B12 is stored.
Factors Impairing Absorption
Several conditions and factors can interfere with the process of B12 absorption. Gastric issues are common causes, with pernicious anemia being an example. This autoimmune condition involves the immune system attacking the parietal cells in the stomach, leading to a deficiency in Intrinsic Factor. Atrophic gastritis, a thinning of the stomach lining, can reduce the production of both stomach acid and Intrinsic Factor, hindering B12 release and binding.
Surgical procedures like bariatric surgery can also impair B12 absorption. These surgeries reduce stomach capacity and may bypass sections of the stomach that produce Intrinsic Factor, limiting its availability.
Beyond gastric problems, conditions affecting the small intestine can disrupt B12 absorption. Inflammatory bowel diseases such as Crohn’s disease, or celiac disease, can cause inflammation and damage to the terminal ileum. Bacterial overgrowth in the small intestine (SIBO) or parasitic infections can compete for B12, making it unavailable for absorption.
Pancreatic insufficiency can also impede B12 absorption by reducing the release of digestive enzymes. Certain medications also pose a risk. Proton pump inhibitors (PPIs) and H2 blockers, used to reduce stomach acid, can slow the release of B12 from food, impacting its absorption. Metformin, a medication for diabetes, can interfere with B12 absorption.
Recognizing Impaired Absorption
When B12 absorption is impaired, the body’s stores can become depleted, leading to a range of symptoms. Hematological signs are often observed, with megaloblastic anemia being a common outcome. This condition is characterized by abnormally large red blood cells and can manifest as fatigue, generalized weakness, shortness of breath, and pale skin.
Neurological symptoms are also prevalent due to B12’s role in nerve health. Individuals may experience numbness or tingling sensations, often described as “pins and needles,” particularly in the hands and feet. Other neurological symptoms include balance issues, memory problems, confusion, and changes in mood such as depression or irritability.
Gastrointestinal symptoms can also signal impaired B12 absorption. These may include a sore or smooth tongue, a loss of appetite, and unintended weight loss. Muscle weakness can also occur. The onset of these symptoms can be gradual, as the liver stores B12.
Addressing Absorption Challenges
Diagnosing impaired B12 absorption involves blood tests to assess B12 levels. Serum B12 levels are measured, and sometimes additional markers like methylmalonic acid (MMA) and homocysteine are checked, as elevated levels of these can indicate B12 deficiency. Historically, the Schilling test was used to determine the cause of deficiency, but it is less commonly employed today.
Management and treatment strategies depend on the underlying cause and severity of the absorption issue. For mild deficiencies or cases where Intrinsic Factor is not lacking, oral B12 supplementation may be effective. However, for severe deficiencies or when Intrinsic Factor or ileal absorption is compromised, intramuscular injections of B12 are the preferred method of delivery.
These injections bypass the digestive system, ensuring direct delivery of B12 into the bloodstream. Nasal gels are another option for B12 administration. In some cases, addressing the root cause can also help improve B12 absorption.