Depletes Vitamin B1. This medication is commonly used for Contraception
Studies suggest a potential for mild thiamine (vitamin B1) deficiency with long-term use of Oral Contraceptives (OCs). One finding showed that red blood cell activity of an enzyme dependent on thiamine (transketolase) decreased during OC treatment. This decrease indicates that the cells might not have enough thiamine to function optimally, suggesting a mild thiamine deficiency induced by the contraceptives. Supplementation with thiamine (vitamin B1) should be considered for women using OCs.
Briggs MH, Briggs M. Thiamine status and oral contraceptives. Contraception. 1975 Feb;11(2):151-4. doi: 10.1016/0010-7824(75)90025-6. PMID: 1112084.Anderson KE, Bodansky O, Kappas A. Effects of oral contraceptives on vitamin metabolism. Adv Clin Chem. 1976;18:247-87. Shikh EV, Makhova AA, Chemeris AV, Tormyshov IA. [Iatrogenic deficits of micronutrients]. Vopr Pitan. 2021;90(4):53-63. Russian. Bielenberg J. Folsäure- und Vitaminmangel durch orale Kontrazeptiva [Folic acid and vitamin deficiency caused by oral contraceptives]. Med Monatsschr Pharm. 1991 Aug;14(8):244-7. German. PMID: 1921842.
Vitamin B1 Thiamine — 10 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.
In susceptible adults, acute thiamine (vitamin B1) deficiency can rapidly trigger an encephalopathy marked by confusion, gait ataxia, and ocular motor abnormalities such as nystagmus or ophthalmoplegia. This classic triad is often incomplete at presentation, and only a minority of patients show all three features together initially, which contributes to delayed diagnosis. Because body stores are quickly exhausted, maintaining adequate ongoing thiamine intake is critical, and can reverse many of the acute neurologic signs if started early, whereas even short delays increase the risk of persistent cognitive impairment and structural brain injury on imaging.
Vitamin B12 Methylcobalamin by Pure Encapsulations — 0.2 mg