In the United States, nearly 20% of people over the age of 60 have vitamin B12 deficiency.1 Vitamin B12 is required for brain and nervous system function, DNA and RNA synthesis, red blood cell formation, and plays a role in energy metabolism.1,2 Foods rich in B12 include animal sources such as beef liver, clams, oysters, fish, meat, dairy products, and fortified cereals.2 Clinical characteristics of B12 deficiency are known to cause megaloblastic anemia, neurological changes (manifesting as numbness and tingling), vision problems, memory loss, ataxia, depression and developmental delays in infants.2 As a water-soluble vitamin, B12 easily passes through the urine, therefore the Institute of Medicine concludes taking the maximum daily intake is unlikely to cause adverse health effects.2

Elevated levels of vitamin B12, hypercobalaminemia, is often considered irrelevant and the pathophysiology is scarcely studied.2,3 Most laboratories consider B12 deficiency as serum levels less than 250 pg/mL. The lower and upper reference values vary across laboratories. The Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine has not established an upper daily limit for vitamin B12 because of the low potential for toxicity.2 Taking large doses is considered safe since the body does not store excess vitamin B12 and instead, excretes it through the urine. However, 1 case report describes symptoms of acne, palpitations, anxiety, headache, and insomnia following twelve 1 mg doses of cyanocobalamin daily for treatment of severe pernicious anemia.4 The symptoms resolved within two weeks of stopping the medication.4 A retrospective study found a significant relationship between high levels of vitamin B12 and malignant hematological diseases.5

The objective of this case report is to describe the potential effect of hypercobalaminemia and to discuss the continuity of care between a chiropractor and primary care physician working within the same integrated health care system for improved outcomes.

Case Report

A 49-year-old female sought care from her primary care physician (PCP) for symptoms of numbness, tingling and muscle spasms in the arms, legs, and upper back. The patient had a history of Hashimoto’s Thyroiditis and irritable bowel syndrome and was on the low FODMAP diet for 3 years. She had a family history of inflammatory bowel disease, multiple sclerosis, systemic lupus, and thyroid autoimmune disorder. Her daily medications and supplements list included levothyroxine, 500 mcg cyanocobalamin, a multivitamin, turmeric, and zinc sulfate. The multivitamin consisted of 20 mcg of vitamin B12. The PCP ordered MRIs of the brain, and cervical, thoracic, and lumbar spine. The brain and cervical MRI results showed no evidence of demyelination; therefore, multiple sclerosis was ruled out. There was mild central canal narrowing from C4-C7 and mild C5/C6 left and right foraminal narrowing. The results from the thoracic and lumbar MRI revealed spondylosis of the lumbar spine with no compression of the spinal cord or nerve roots. EMG tests for the bilateral arms and legs were negative for evidence of large fiber neuropathy but did indicate a possible right S1 sensory radiculopathy. Overall, the images and nerve conduction studies did not explain the patient’s symptoms.

L:aboratory tests inlcuded a basic metabolic panel, creatine kinase, vitamin B12, antinuclear antibody test, erythrocyte sedimentation rate, Lyme antibody, and protein electrophoresis, all of which were normal except vitamin B12. Normal serum vitamin B12 reference range at this laboratory was 211-911 pg/mL. Her serum vitamin B12 laboratory result was high, at levels over 2,000 pg/mL. She was advised by her family physician to reduce the intake of B12 supplements. Nevertheless, elevated B12 levels were not thought to have causal role for the reported symptoms.

She underwent a physical therapy trial and saw neurology, pain management, and an orthopedic spine specialist before being referred to a chiropractor. Gabapentin was also provided, with no change in symptoms and was discontinued.

At her initial chiropractic visit, she reported symptoms of numbness and tingling in her arms and legs that had been present for 8 months. The paresthesia was random in its location and frequency, sometimes occurring in all extremities, occasionally just in one arm or one leg at a time. Muscle twitches and sharp pain were also present in the arms, legs, and upper back. The patient reported a 0/10 on the Numeric Rating Scale (NRS) because at the time of the appointment, she was not experiencing any pain. She reported a 15/40 on the DoD/VA Pain Supplement Questionnaire.

Her neurological examination revealed normal strength and sensation. The lumbar range of motion was normal except for decreased right lateral flexion. Straight leg raise, Ely’s, and Faber’s tests were negative, and Yeoman’s test was positive on the left. Limited range of motion was found with joint palpation at the spinal levels of L3/L4 and L4/L5 facet joints and left sacroiliac joint. The left hip flexor, right lumbosacral paraspinal, and left quadratus lumborum muscles exhibited hypertonicity and limited flexibility. Although there were musculoskeletal issues found in the examination, no test could reproduce the patient’s feeling of paresthesias. The mechanical deficiencies were treated with spinal manipulative therapy and myofascial therapy.

Following the examination, extended time was spent reviewing her chart, with greater attention to laboratory, neurological, and MRI findings. Her serum B12 levels 6 months before the initial chiropractic examination were elevated at >2,000 pg/mL, over twice the amount of the upper reference range, and recognized by the chiropractor as a potential cause of paresthesia. She discontinued the use of 500 mcg cyanocobalamin supplementation before starting chiropractic treatment ,per request of her PCP. We recognized that another supplement the patient was taking had 20 mcg of B12 and discussed with her discontinuing use of this supplement. We also educated the patient on foods high in B12 and the function of B12. The chiropractor discussed with the PCP the possibility of elevated vitamin B12 levels causing paresthesia and the PCP ordered a retest of vitamin B12 three months following the initial laboratory B12 test. The retest showed B12 levels were still elevated but had significantly decreased to1,270 pg/mL.

As levels of B12 in the blood decreased, her symptoms improved. After 4 visits, she did not follow up with the chiropractor because she was “feeling better” with a decrease in frequency of the numbness and tingling. Two months following the last chiropractic visit, she stated there were “very few issues in the last 4 weeks.” Nine weeks following the last visit, she stated she had a drink with 6.82 mcg B12 and “woke up with paresthesia in arms and legs” the next morning, which took about 7-10 days before the symptoms completely subsided. Upon chiropractor’s request, the PCP ordered another serum B12 test following the first test. The results showed normal serum levels at 617 pg/mL.


Once ingested, vitamin B12 dissociates from its carrier protein, binds with intrinsic factor in the stomach, and is absorbed in the ileum of the small intestine.3 The transport of cobalamin to all tissues of the body requires transcobalamin (TCB) proteins. The 3 main mechanisms found to cause high serum levels of cobalamin are excessive ingestion or administration, liberation of B12 from an internal reservoir, and an increase in TCB or lack of clearance.3 Elevated serum cobalamin levels have also been associated with pathologies that disrupt the metabolism of vitamin B12, such as alcoholism, liver disease, and cancer and has even been suggested as a possible tumor marker for poor prognosis.3 The majority of high serum cobalamin typically involves a disorder of TCBs. Elevated serum cobalamin in inflammatory diseases, such as systemic lupus, may be linked to an increase in TCB II. Our patient had a family history of systemic lupus; however, the most likely explanation for her elevated cobalamin serum levels was excessive oral intake. She had a diet high in fatty fish and was supplementing daily with 520 mcg cyanocobalamin, 216% over the recommended daily allowance.

Effective communication between the providers involved (DC and MD) brought forth the idea that her symptoms of paresthesias and muscle spasms could be correlated to the elevated B12 serum levels. The collaboration of care resulted in monitoring serum B12 levels over a 13-month period. Her initial serum B12 levels were >2000 pg/mL. This means her serum B12 levels could have been significantly higher than 2,000 pg/mL. Thirteen months later, the levels had dropped to 617 pg/mL. Although the mechanical deficiencies were treated with spinal manipulative therapy, the main treatment was education on nutrition. The collaboration of care between the chiropractor and PCP improved patient outcomes and promoted continuity within the patient care team.


This is not a controlled study and there are many variables that may have influenced the outcome. The outcomes reported may have been consequent to the natural history of the patient’s pathology. The outcomes may also be because of combination of several modalities used during chiropractic management that synergistically worked together to improve symptoms. There is limited evidence on the explanation of the physiological response to elevated B12 levels, so more research is needed since specific conclusions cannot be drawn from a solitary case.


Vitamin B12 deficiency results in neurological manifestations. However, clinical manifestations of hypercobalaminemia are less known. Preliminary evidence from this case supports the notion that hypercobalaminemia may be correlated with widespread paresthesia and muscle spasticity. Although there is no upper intake level for vitamin B12, it is wise to exercise caution for potential ramifications of high-dose supplementation. This case also shows the importance of continuity of care within a health care system.