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Review
. 2025 Apr 8;14(8):2550.
doi: 10.3390/jcm14082550.

Unraveling the Enigma: Food Cobalamin Malabsorption and the Persistent Shadow of Cobalamin Deficiency

Emmanuel Andrès  1 , Jean Edouard Terrade  1 , María Belén Alonso Ortiz  2 , Manuel Méndez-Bailón  3 , Cosmina Ghiura  1 , Chalène Habib  1 , Thierry Lavigne  4 , Xavier Jannot  1 , Noel Lorenzo-Villalba  1
Affiliations
Review

Unraveling the Enigma: Food Cobalamin Malabsorption and the Persistent Shadow of Cobalamin Deficiency

Emmanuel Andrès et al. J Clin Med. .

Abstract

Food cobalamin malabsorption (FCM) represents a prevalent, often underdiagnosed, etiology of vitamin B12 deficiency, particularly within an aging population. Unlike pernicious anemia, an autoimmune disorder targeting intrinsic factor, FCM stems from the impaired release of cobalamin from food proteins, primarily due to age-related gastric changes, medication-induced gastric hypochlorhydria, metformin, or non-immune atrophic gastritis. The clinical presentation of FCM mirrors that of general cobalamin deficiency, encompassing a spectrum of neurological (peripheral neuropathy, cognitive decline), hematological (megaloblastic anemia), and gastrointestinal (glossitis, anorexia) manifestations. Given the potential for irreversible neurological sequelae, early detection and intervention are paramount. High-dose oral cobalamin (125-250 mcg daily) has demonstrated efficacy, offering a convenient and cost-effective alternative to parenteral administration.

Keywords: cobalamin deficiency; cobalamin treatment; food cobalamin malabsorption; pernicious anemia; vitamin B12 deficiency.

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Conflict of interest statement

The authors declared no conflicts of interest.

Figures

Figure 1
Figure 1
Pathophysiology of pernicious anemia (Biermer’s disease) and food cobalamin malabsorption [13]. Legend: B: vitamin B12, HCI: hydrochloric acid, I: intrinsic factor, P: animal protein, PPI: proton pump inhibitor, R: protein, TC: transcobalamin.
See this image and copyright information in PMC

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