A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 40-year-old male presents to the clinic. The patient has begun taking large doses of vitamin E in order to slow down the aging process and increase his sexual output. He has placed himself on this regimen following reading a website that encouraged this, without consulting a healthcare professional. He is interested in knowing if it is alright to continue his supplementation. Which of the following side-effects should he be concerned about should he continue his regimen?
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A
Night blindnessIncorrect. Night blindness is the consequence of vitamin A DEFICIENCY, not vitamin E excess.
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B
Deep venous thrombosisIncorrect. Vitamin E impairs clotting (predisposes to bleeding) and does not cause thrombosis.
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C
Peripheral neuropathyIncorrect. Peripheral neuropathy is a feature of vitamin B6 toxicity and vitamin E deficiency—not vitamin E excess.
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D
HemorrhageCorrect. High-dose vitamin E antagonizes vitamin K–dependent γ-carboxylation and increases the risk of hemorrhage (including hemorrhagic stroke).
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E
Hepatic steatosisIncorrect. Hepatic steatosis is a feature of vitamin A toxicity, alcohol use, and metabolic syndrome; vitamin E excess primarily causes bleeding via interference with vitamin K-dependent coagulation.
↑ Tap an answer to reveal the reasoning
Answer: D. Vitamin E (α-tocopherol) is a lipid-soluble antioxidant that protects polyunsaturated fatty acids in cell membranes from peroxidation. While vitamin E deficiency causes hemolytic anemia and neurologic problems (ataxia, posterior column abnormalities), the most clinically important toxicity of supraphysiologic vitamin E intake is bleeding (hemorrhage).
Mechanistically, high-dose vitamin E inhibits vitamin K–dependent γ-carboxylation of clotting factors II, VII, IX, and X, effectively functioning as a vitamin K antagonist. This effect is amplified in patients also taking warfarin or antiplatelet agents. Large clinical trials have shown an increased risk of hemorrhagic stroke with high-dose vitamin E supplementation.
Key distinctions: night blindness (vitamin A deficiency, not toxicity) — vitamin A toxicity instead causes pseudotumor cerebri, dry skin, hepatotoxicity, and teratogenicity. Deep venous thrombosis is the opposite of what vitamin E does (it predisposes to bleeding, not clotting). Peripheral neuropathy is seen with vitamin B6 toxicity (pyridoxine megadose) and with vitamin E deficiency—but vitamin E excess does not classically cause neuropathy.
**Why each option:**
**A.** Night blindness is the consequence of vitamin A DEFICIENCY, not vitamin E excess.
**B.** Vitamin E impairs clotting (predisposes to bleeding) and does not cause thrombosis.
**C.** Peripheral neuropathy is a feature of vitamin B6 toxicity and vitamin E deficiency—not vitamin E excess.
**D.** Correct. High-dose vitamin E antagonizes vitamin K–dependent γ-carboxylation and increases the risk of hemorrhage (including hemorrhagic stroke).