Vitamin B12, or cobalamin, is a water-soluble nutrient obtained primarily from animal products. This micronutrient is necessary for the proper function of the nervous system, assisting in the maintenance of protective nerve sheaths. It also plays a fundamental role in the formation of healthy red blood cells and the synthesis of DNA. A deficiency in this vitamin can lead to serious health problems, including nerve damage and anemia. Cancer can cause this deficiency through mechanisms involving both the direct effects of the disease and the subsequent treatments used to fight it.
How Specific Cancers Interfere with B12 Absorption
The absorption of vitamin B12 relies heavily on intrinsic factor, a protein produced by the parietal cells lining the stomach. This factor binds to B12 in the stomach, and the resulting complex travels to the small intestine where it is absorbed. Cancers of the digestive tract, particularly gastric (stomach) cancer, can directly disrupt this process.
Tumors in the stomach can destroy the parietal cells responsible for producing intrinsic factor, leading to an inability to absorb B12 from food. This disruption mirrors the mechanism seen in pernicious anemia. The tumor’s physical presence and chronic inflammation can effectively stop the first step of B12 absorption.
Pancreatic cancer also interferes with B12 absorption through a different pathway. The pancreas produces digestive enzymes necessary to break down the food-B12 bonds before intrinsic factor can attach. When pancreatic function is impaired by a tumor, this initial digestive step fails, preventing B12 from being properly prepared for later absorption.
The Role of Cancer Treatments in Causing Deficiency
Many necessary medical treatments for cancer can induce a B12 deficiency, primarily by physically altering the digestive system. Surgical procedures are a major cause, especially those involving the stomach or small intestine. A gastrectomy, which is the removal of all or part of the stomach, eliminates the source of intrinsic factor production.
Patients who undergo a total gastrectomy lose virtually all ability to produce intrinsic factor and are highly likely to develop B12 deficiency. Similarly, surgical resection of the ileum, the last section of the small intestine, removes the site where the B12-intrinsic factor complex is absorbed into the bloodstream. These anatomical changes mean the body can no longer physically take in the vitamin.
Certain chemotherapy agents and extensive radiation therapy to the abdominal region can also impair the gut lining. Chemotherapy targets rapidly dividing cells, inadvertently including the fast-growing cells that line the digestive tract. Damage to this lining (mucosa) can result in malabsorption that limits the uptake of many nutrients, including vitamin B12.
Identifying the Signs of Low B12 Levels
Recognizing the signs of B12 deficiency in cancer patients is often complicated because many symptoms overlap with the side effects of cancer or its treatment. The deficiency can manifest through two main avenues: hematological (blood-related) and neurological (nerve-related).
A common sign is fatigue, which stems from megaloblastic anemia. This is a condition where the body produces abnormally large, immature red blood cells that cannot efficiently carry oxygen.
Neurological symptoms include numbness, tingling, or a “pins and needles” sensation, often starting in the hands and feet. Patients may also experience problems with balance, coordination, and muscle weakness. Cognitive changes, such as confusion or memory issues, can also occur. Prompt diagnosis is essential to prevent permanent nerve damage, as these issues can mimic or worsen chemotherapy-induced peripheral neuropathy.
Clinical Management of B12 Deficiency
Diagnosis of B12 deficiency often begins with a standard blood test to check serum B12 levels, but this test can sometimes be misleading in cancer patients. For a more functional and accurate assessment, doctors rely on measuring levels of methylmalonic acid (MMA) and homocysteine. These substances build up when B12 is lacking because the vitamin is needed to metabolize them.
Elevated MMA and homocysteine levels can indicate a functional deficiency, even when the serum B12 level appears within the normal range. Once a deficiency is confirmed, treatment must account for the underlying cause of malabsorption. Since the deficiency is often due to an absorption problem in the stomach or intestines, oral B12 supplements are typically ineffective.
The standard treatment for these malabsorption cases is intramuscular injection of B12. These injections bypass the entire digestive system, delivering the vitamin directly into the muscle tissue for systemic use. This parenteral route is necessary to replenish the body’s stores and resolve the hematological and neurological symptoms. Patients with ongoing malabsorption problems often require continuous, lifelong B12 injections.