Vitamin A (retinol)

Vitamin A (retinol) is a fat-soluble vitamin whose biological activity is so tightly coupled with thyroid hormone that they share a single transport protein, transthyretin, and are taken up by cells together. 3 Peat argued that vitamin A is essential for the production of all steroid hormones from cholesterol, for protein synthesis in skin and hair, and for the maintenance of mucous membranes. 4 He noted that a high metabolic rate dramatically increases the requirement for vitamin A because it is consumed in the production of large amounts of pregnenolone and progesterone. 7 This functional partnership means that in hypothyroidism, the precursor carotene cannot be converted to active retinol, leading to its accumulation in steroid-forming tissues and a visible yellowing of the calluses on the palms and soles. 3

The relationship between vitamin A and thyroid function is bidirectional and can be antagonistic in extreme situations. Peat explained that because thyroid hormone and retinol travel on the same protein, taking a massive supplement like 100,000 units can displace thyroid hormone, causing a noticeable dip in thyroid activity in borderline individuals. 2 Dinkov elaborated on this, citing a human dose-escalation study in obese, hypothyroid women which found that up to 25,000 units daily produced no side effects even in severely compromised subjects, establishing a practical upper threshold for sensitive individuals. 8 He further noted that the toxicity symptoms in animal and human studies do not typically manifest until doses reach the hundreds of thousands of units taken for at least six months. 6 To mitigate the risk of vitamin A inhibiting thyroid function or undergoing autoxidation into toxic metabolites, both Peat and Dinkov recommend combining it with vitamin E. 2

Peat directly challenged the conventional narrative of vitamin A toxicity, suggesting that the famous polar bear liver poisoning was likely caused by algae toxins stored in the liver rather than the vitamin itself. 4 He suspected that many toxicity reports were fabricated to promote synthetic retinoids. 4 Dinkov reinforced this distinction, emphasizing that the severe birth defects and liver toxicity associated with "vitamin A" are attributable to synthetic analogs like Accutane (isotretinoin), which have extremely long half-lives and are treated as toxins by the body. 2 In contrast, the natural esters retinyl palmitate and retinyl acetate—which are the body's own preferred storage forms in the liver—have been used in trials at doses up to 500,000 units daily without long-term toxicity. 3

A deficiency or an excess of vitamin A can produce similar symptoms due to a self-catalyzing breakdown process. Peat described a state where an overdose, in the context of a deficiency in other antioxidants, causes retinol to catalyze its own destruction, leading to tissue breakdown such as chapped lips from defective protein synthesis. 1 He recommended interrupting this cycle with vitamin E or progesterone rather than continuing supplementation. 1 Dinkov added that vitamin A is a crucial cofactor for steroidogenesis, and a deficiency can manifest as poor night vision, acne, dandruff, and an inability to produce protective hormones. 2 He noted that vitamin A supplementation often makes vitamin D supplementation smoother and less likely to cause irritability or insomnia, suggesting a synergistic requirement among the fat-soluble vitamins. 2