Depletes Vitamin B12. This medication is commonly used for Stomach Acid
Research suggests that long-term use of medications that reduce stomach acid, like H2 blockers and PPIs, may be linked to vitamin B12 deficiency. Stomach acid plays a role in releasing vitamin B12 from food, and reduced acid levels caused by these medications could hinder proper B12 absorption. Some studies find an increased risk of B12 deficiency, particularly in older adults or those using these medications for extended periods. Individuals taking H2 blockers or PPIs long-term should consider vitamin B12 supplementation.
Miller JW. Proton Pump Inhibitors, H2-Receptor Antagonists, Metformin, and Vitamin B-12 Deficiency: Clinical Implications. Adv Nutr. 2018 Jul 1;9(4):511S-518S. Valuck RJ, Ruscin JM. A case-control study on adverse effects: H2 blocker or proton pump inhibitor use and risk of vitamin B12 deficiency in older adults. J Clin Epidemiol. 2004 Apr;57(4):422-8.
Vitamin B12 (as methylcobalamin) — 0.2 mg
Vitamin B12 deficiency is strongly associated with cognitive impairment, including problems with memory, attention, and executive function, and is considered a reversible cause of dementia when caught early. Low or borderline B12 levels are more common in older adults, particularly those with atrophic gastritis, long-term use of acid-suppressing medications, or vegetarian/vegan diets, and studies show that deficient individuals often perform worse on cognitive tests than those with adequate status. Clinically, correcting B12 deficiency can lead to measurable improvements in cognition and mood in some patients, which is why B12 levels are routinely checked in the evaluation of cognitive decline and suspected dementia.
In older adults, low folate status has been associated with a higher risk of mild cognitive impairment (MCI) and faster cognitive decline over time, likely through effects on one‑carbon metabolism and homocysteine. Several longitudinal cohort studies have found that individuals with lower serum or red‑cell folate and higher homocysteine show steeper declines on memory and global cognition tests, and in some cohorts have a significantly higher incidence of MCI or dementia over follow‑up. The clinically important takeaway is that, when folate deficiency is detected and corrected (usually along with ensuring adequate vitamin B12), some patients demonstrate stabilization or modest improvement in cognitive performance, particularly when interventions are combined with aggressive management of vascular risk factors such as hypertension and diabetes.
Low or deficient vitamin B12 status elevates homocysteine levels by impairing its conversion to methionine, a process that requires B12 as a cofactor. This hyperhomocysteinemia is linked to increased cardiovascular risks, including atherosclerosis, heart disease, and stroke, through vascular inflammation and endothelial damage. Additionally, low B12 contributes to metabolic disturbances like insulin resistance and type 2 diabetes risk, compounding heart health concerns in susceptible individuals.
Vitamin B12 Methylcobalamin by Pure Encapsulations — 0.2 mg