Vitamin A (Retinol / Carotenoids)

Night vision

Every rod cell in the retina is packed with rhodopsin, a light sensor made of a protein (opsin) holding a bent form of vitamin A, 11-cis-retinal. When a single photon hits it, the retinal straightens to all-trans in less than a trillionth of a second. That shape change switches the opsin on and starts a signalling chain that closes ion channels and sends a signal to the brain. Rods are sensitive enough to respond to a single photon, which is what makes vision in dim light possible.¹

The straightened retinal is then released and has to be recycled. It goes to the retinal pigment epithelium next to the rods, where enzymes bend it back to 11-cis and return it. That is the visual cycle, and it slowly loses vitamin A, which has to be topped up from blood.¹ When supply runs short, rods can't rebuild rhodopsin fast enough after exposure to light. The first symptom is night blindness: slow adjustment to darkness, then no usable vision in dim light. It's one of the oldest known diet-cured diseases. Ancient Egyptian texts recommended eating liver for it.² Cone cells use the same chemistry for colour vision but are less sensitive, so daylight vision lasts longer.

Healthy skin and gut lining

Outside the eye, vitamin A works as a hormone. Cells convert retinol to retinoic acid, which enters the nucleus and binds receptors (RAR and RXR). Those receptors switch hundreds of genes on or off. Among their main jobs is telling epithelial cells, the cells that line skin, eyes, airways, gut and urinary tract, what to become.³

With enough retinoic acid, the lining of airways and gut grows into moist, mucus-making tissue with tiny hair-like cilia that sweep out debris and germs. Without it, those linings turn into dry, flat, keratinised cells like the outer skin (squamous metaplasia). The eye shows it first. The conjunctiva dries and develops foamy Bitot's spots, and then the cornea can soften and dissolve (keratomalacia). Vitamin A deficiency is still the leading preventable cause of childhood blindness worldwide.² In the airways and gut, the same change means less mucus, poor clearance of germs and a leakier barrier. That is a large part of why deficient children get so many lung and gut infections.

Retinoic acid drugs (isotretinoin for acne, tretinoin for sun-damaged skin) use this same pathway at doses far above dietary levels.

Immune defense

Retinoic acid also steers immune cells. Immune cells in the gut wall (dendritic cells) make retinoic acid from dietary vitamin A and use it to "stamp" T and B cells with gut-homing receptors (CCR9 and α4β7). That sends them back to the intestinal lining where they're needed.⁴ Retinoic acid also helps B cells switch to making IgA, the antibody secreted onto mucous surfaces, and supports regulatory T cells that keep the gut from overreacting to food. So vitamin A defends mucous membranes in two ways: the barrier and the immune cells patrolling it.

The human evidence is unusually strong. In the 1980s, Alfred Sommer noticed that Indonesian children with even mild signs of vitamin A deficiency died at much higher rates. Large trials followed.² A 2022 Cochrane review of 47 studies covering over a million children aged 6 months to 5 years found that vitamin A supplements reduced deaths from all causes by 12% and cut diarrhoea and measles, with high-certainty evidence for the mortality result.⁵ Few nutrient interventions have outcome data this solid. The benefit applies to populations where deficiency is common. It doesn't mean people with good vitamin A status gain from more.

Intake: retinol vs carotenoids

The RDA is 700 mcg RAE/day for women and 900 mcg for men. Vitamin A comes in two forms:

• Retinol (preformed vitamin A) from liver, eggs, dairy and oily fish is ready to use and well absorbed.
• Beta-carotene and other carotenoids from orange and dark-green plants have to be split by the enzyme BCO1 in the gut. The official conversion ratio is 12:1 by weight, but people vary a lot. Two common variants of the BCO1 gene cut conversion by 32–69% in carriers.⁶ Some people get a lot of vitamin A from carrots, and others very little.

Top foods

• Beef liver: about 6,600 mcg RAE in 3 oz
• Cod liver oil: about 1,350 mcg per tsp
• Sweet potato, baked: about 1,400 mcg RAE (from beta-carotene, conversion varies)
• Carrots, raw: about 460 mcg RAE per ½ cup (from beta-carotene)
• Eggs: about 80 mcg each; butter about 100 mcg per tbsp; cheese 80–100 mcg per oz
• Spinach and kale, cooked: about 470–570 mcg RAE per ½ cup

Deficiency effects

In order: night blindness, then dry eyes with Bitot's spots, then corneal damage and blindness. Along the way: dry rough skin, more and more severe respiratory and gut infections, and in children, poor growth and higher death rates.² Deficiency is rare in wealthy countries except with fat malabsorption (coeliac disease, cystic fibrosis, pancreatic insufficiency, bariatric surgery), liver disease or very restrictive diets. Vitamin A needs zinc to be transported out of the liver, so zinc deficiency can cause a functional vitamin A shortage (see Zinc).