Beta-Carotene, Vitamin A, and Eye Health

Table of Contents

1. What Beta-Carotene Actually Is
2. How Your Body Turns It Into Vitamin A
3. The Conversion Ratio, and Why It Varies So Much
4. How Vitamin A Makes Sight Possible
5. Night Blindness and What Real Deficiency Looks Like
6. The Honest Limit: Correction, Not Enhancement
7. The Supplement Trials: ATBC, CARET, and Smokers
8. Why Food Beta-Carotene Does Not Cause Vitamin A Toxicity
9. Carotenemia: The Benign Orange Skin
10. Macular Degeneration and the AREDS Story
11. How Much to Eat, and in What Form
12. Key Research Papers
13. Connections
14. Featured Videos

What Beta-Carotene Actually Is

Beta-carotene is a pigment. It is a long, symmetrical hydrocarbon chain with a ring at each end, built out of forty carbon atoms, and its backbone is a run of alternating single and double bonds. That alternating run is what physicists call a conjugated system, and it is the reason the molecule is orange: the electrons in a long conjugated chain absorb blue and green light and let red and yellow pass through to your eye. The same structural feature that makes a carrot orange is the feature that makes it useful to you.

Beta-carotene belongs to a family called the carotenoids, of which several hundred are known in plants. Only a handful matter nutritionally, and they split into two groups. The provitamin A carotenoids — beta-carotene, alpha-carotene, and beta-cryptoxanthin — can be cut apart by human enzymes to make vitamin A. The non-provitamin carotenoids — lutein, zeaxanthin, lycopene — cannot; they do other jobs, several of them in the eye. A carrot supplies mostly beta-carotene, with a substantial amount of alpha-carotene alongside it and small quantities of lutein. Purple carrots add anthocyanins; yellow carrots are richer in lutein; red carrots carry lycopene, the tomato pigment.

Beta-carotene is fat-soluble and essentially insoluble in water. Inside the carrot it is not floating free but packed into crystalline deposits inside plant cells, wrapped in tough cellulose walls. That physical packaging turns out to matter enormously for how much you actually absorb, which is the subject of the companion page on cooking, fat, and absorption.

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How Your Body Turns It Into Vitamin A

Vitamin A is not one molecule but a small family: retinol (the alcohol form, the storage and transport form), retinal (the aldehyde, the form your retina uses to see), and retinoic acid (the acid, which acts like a hormone controlling gene expression in skin, immune cells, and developing tissue). Beta-carotene is the plant precursor of all three.

The key step happens mostly in the cells lining your small intestine. An enzyme called beta-carotene 15,15'-oxygenase — abbreviated BCO1, and in the older literature BCMO1 — snips the beta-carotene molecule exactly in the middle. Because beta-carotene is symmetrical, one clean central cut theoretically yields two molecules of retinal. Lindqvist and Andersson purified the human enzyme in 2002 and showed directly that it performs this central cleavage. The retinal produced is then either reduced to retinol and packaged into chylomicrons for delivery to the liver, or oxidised onward to retinoic acid.

A second enzyme, BCO2, cuts carotenoids off-centre instead of in the middle, producing fragments that are not vitamin A. BCO2 handles carotenoids that BCO1 does not take, and it seems to act partly as a housekeeping system that clears carotenoids out of tissues. The existence of two competing routes is one reason the yield of vitamin A from a given amount of beta-carotene is not a fixed number.

Your liver stores vitamin A, and it stores a lot of it — a well-nourished adult liver holds enough to cover months of zero intake. This is why vitamin A status changes slowly, why a single carrot-heavy week does nothing measurable to a replete person, and why deficiency, when it happens, is the end point of a long slide rather than a sudden event.

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The Conversion Ratio, and Why It Varies So Much

If beta-carotene splits neatly into two retinals, you might expect roughly two units of beta-carotene to buy one unit of vitamin A. In a test tube that is close to right. In a human eating a carrot it is nowhere near right, and the gap is one of the most practically important facts in this whole subject.

The United States Institute of Medicine, when it set the modern reference intakes in 2001, adopted a conversion of 12 micrograms of dietary beta-carotene to 1 microgram of retinol, and 24 to 1 for alpha-carotene and beta-cryptoxanthin. Purified beta-carotene dissolved in oil converts far better — about 2 to 1. The difference between 2 and 12 is not chemistry; it is the food matrix. Beta-carotene locked in crystalline form inside intact plant cells simply never reaches the enzyme.

This is why nutrition labels now use retinol activity equivalents (RAE) rather than the older international units. One microgram RAE means one microgram of actual retinol activity, whatever it came from. A raw carrot supplies roughly 835 micrograms RAE per 100 grams, so a medium carrot of about 60 grams delivers on the order of 500 micrograms RAE — well over half the adult daily requirement, which is 900 micrograms RAE for men and 700 for women. Cooked carrots score slightly higher per 100 grams, partly because cooking concentrates the food as water is lost and partly because the carotene becomes more extractable.

Averages, though, hide a huge spread between individuals. Hickenbottom and colleagues used a double-tracer design in men in 2002 and found conversion efficiency varying several-fold from one person to the next. Leung and colleagues traced part of that variation to its source in 2009: two common single-nucleotide polymorphisms in the BCMO1 gene measurably reduced beta-carotene conversion in female volunteers who carried them. Later work by Lietz, and a broad review by Borel and Desmarchelier in 2017, confirmed that a substantial fraction of the population carries variants that make them relatively poor converters. Nobody is testing you for this, and you do not need to be tested. The practical implication is simply that plant carotenoids alone are a less reliable vitamin A supply for some people than for others, and that a diet containing some preformed vitamin A — eggs, liver, butter, whole dairy, oily fish — covers that uncertainty in a way an all-vegetable diet does not.

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How Vitamin A Makes Sight Possible

Here is the part that genuinely deserves the reputation carrots have. Vitamin A is not merely helpful to vision. It is the molecule that does vision. Nothing else in your body can do its job.

At the back of your eye, the rod and cone cells each carry stacks of membranes packed with a light-sensitive protein. In rods that protein is rhodopsin: a large protein called opsin with a single small molecule tucked into a pocket inside it. That small molecule is 11-cis-retinal — a bent form of vitamin A aldehyde.

When a photon strikes it, the retinal absorbs the energy and straightens: the bent 11-cis form isomerises to the straight all-trans form in a few trillionths of a second. That change of shape is the entire trick. A straightened retinal no longer fits its pocket, so it forces the surrounding opsin protein to change shape too. The altered opsin activates a signalling protein called transducin, which switches on an enzyme that destroys cyclic GMP, which causes ion channels in the cell membrane to close, which changes the cell's voltage — and that voltage change is a nerve signal. George Wald won a share of the 1967 Nobel Prize in Physiology or Medicine for working this out, and his 1968 Science paper is still the clearest short account of it.

The straightened retinal then falls out of the protein and has to be carried to neighbouring cells, bent back into the 11-cis shape, and returned. This recycling loop — the visual cycle — runs continuously, millions of times over, and it leaks. A little retinal is lost on every pass, and that loss has to be made good from the body's vitamin A stores. That is the actual, literal mechanism by which eating vitamin A lets you see. When stores run down, the loop cannot be resupplied fast enough, rhodopsin cannot be regenerated at normal speed, and vision fails — starting in the dark, where the demand on rhodopsin is highest.

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Night Blindness and What Real Deficiency Looks Like

Vitamin A deficiency has a characteristic sequence, and it is worth knowing because it explains exactly where carrots do and do not help.

The first symptom is impaired dark adaptation, then frank night blindness (nyctalopia). Someone in this stage sees perfectly well in daylight and cannot find their way across a dim room. It is a rod-cell problem: rods handle low light and depend most heavily on rhodopsin turnover. This stage is fully reversible, sometimes within days of restoring vitamin A.

If deficiency continues, it moves from the retina to the surface of the eye. The conjunctiva dries and thickens (conjunctival xerosis), and foamy grey-white patches called Bitot's spots appear on the white of the eye. Then the cornea itself dries, ulcerates, and in the final stage liquefies — keratomalacia — which destroys the eye permanently within days. The whole spectrum is called xerophthalmia, and Alfred Sommer's 1998 review in Progress in Retinal and Eye Research remains the standard clinical description.

This is not a historical curiosity. Vitamin A deficiency remains a leading cause of preventable childhood blindness worldwide, and it does more than blind: it cripples immune defence at mucosal surfaces, so deficient children die of measles, diarrhoea, and respiratory infection at higher rates. Sommer's field trials in Indonesia in the 1980s produced the finding that changed global child health policy — that simple vitamin A supplementation reduced child mortality substantially. The 2017 Cochrane review by Imdad and colleagues, pooling trials in children aged six months to five years, put the reduction in all-cause mortality at roughly 12 percent. Wiseman and colleagues described the self-reinforcing loop in 2017: deficiency causes infection, infection depletes vitamin A further, and the cycle tightens.

Against that background, the humble carrot looks different. In populations where provitamin A vegetables are the main dietary source of vitamin A, orange and yellow roots are not a garnish — they are a public health intervention.

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The Honest Limit: Correction, Not Enhancement

Now the correction. Carrots restore vision that vitamin A deficiency has taken away. They do not improve vision that is already normal.

The reason is a ceiling, not a shortage. The visual cycle needs a supply of retinal sufficient to keep rhodopsin regenerating at full speed. Once that supply is adequate, more retinal does not make rhodopsin regenerate faster, does not add rod cells, does not widen your pupil, and does not change the optics of your cornea and lens. A replete person's liver already holds months of reserve; adding to a full tank does not make the engine run better. Someone with normal vitamin A status who eats a kilogram of carrots will have orange palms and unchanged night vision.

It follows that carrots also do nothing for the reasons most people actually see poorly. Myopia, hyperopia, and astigmatism are shape problems — the eyeball is too long, too short, or unevenly curved, so light focuses in the wrong place. No nutrient reshapes an eyeball. Presbyopia is the stiffening of the lens with age. Cataract is clouding of the lens protein. Glaucoma is optic nerve damage, usually with raised pressure. None of these is a vitamin A deficiency, and none is corrected by diet.

Saying this plainly does not diminish carrots. It puts them where they belong: as an excellent, cheap, reliable source of a nutrient your retina cannot function without — keeping a system intact rather than upgrading it.

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The Supplement Trials: ATBC, CARET, and Smokers

This section is the most important on the page, and it is the one place where the beta-carotene story turns genuinely dangerous.

By the late 1980s the observational evidence looked excellent: people who ate more carotenoid-rich vegetables, and people with higher blood beta-carotene, got less lung cancer. The obvious next step was to give beta-carotene as a pill and watch cancer rates fall. Two large randomised trials set out to do exactly that, and both found the opposite.

The ATBC trial (Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study), published in the New England Journal of Medicine in 1994, randomised 29,133 male smokers in Finland to beta-carotene, alpha-tocopherol, both, or neither. Among the men receiving beta-carotene, lung cancer incidence was about 18 percent higher, and total mortality was higher as well.

The CARET trial (Beta-Carotene and Retinol Efficacy Trial), reported by Omenn and colleagues in 1996, gave beta-carotene plus retinyl palmitate to 18,314 smokers, former smokers, and asbestos-exposed workers. It was stopped early, ahead of schedule, because the treated group had roughly 28 percent more lung cancer and higher overall mortality.

A third trial, the Physicians' Health Study reported by Hennekens and colleagues in the same 1996 issue, gave beta-carotene to 22,071 male physicians — a population in which only a small minority smoked — and found no effect on cancer or cardiovascular disease in either direction over twelve years. Taken together the three trials point at the same conclusion, and Druesne-Pecollo's 2010 meta-analysis of randomised trials confirmed it: high-dose beta-carotene supplements raise cancer risk specifically in smokers and asbestos-exposed people, and do nothing measurable in everyone else.

Why would a pigment from vegetables do this? The leading explanation is that beta-carotene behaves differently in a lung full of tobacco smoke. At high concentrations and under the oxidative conditions of a smoker's airway, beta-carotene can break down into products that behave as pro-oxidants rather than antioxidants, and there is evidence they can interfere with normal retinoid signalling in lung tissue. This is a dose-and-environment problem, not a verdict on the molecule.

The distinction that matters for anyone reading this page is sharp and must not be blurred:

• High-dose isolated beta-carotene supplements — typically 20 to 30 milligrams a day — increased lung cancer in smokers in two large randomised trials. If you smoke, or used to smoke, or have had asbestos exposure, do not take beta-carotene supplements, and check the label of any multivitamin or eye-health formula you already take.
• Eating carrots is not that. No trial has ever found harm from carotenoid-rich vegetables. The dietary evidence points the other way: whole-food carotenoid intake is associated with lower, not higher, cancer rates. Whole carrots deliver beta-carotene bound in a food matrix, absorbed slowly and incompletely, alongside alpha-carotene, lutein, polyacetylenes, fibre, and potassium — nothing like a daily 30-milligram bolus of the isolated molecule.

This is the general lesson of the supplement era in one example: an isolated compound at pharmacological dose is a drug, and must be judged as a drug, whatever food it was originally found in. Our section on dangerous supplements covers the same pattern across other products.

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Why Food Beta-Carotene Does Not Cause Vitamin A Toxicity

Preformed vitamin A — retinol and retinyl esters, the form in liver, cod liver oil, and many supplements — genuinely can poison you. Acute overdose causes headache, nausea, and vomiting; chronic excess causes liver damage, bone loss, and hair loss; and high intake in early pregnancy causes birth defects. The tolerable upper intake level for adults is set at 3,000 micrograms of preformed vitamin A per day, and it is a real limit.

Beta-carotene from food does not do this, and the reason is elegant. The conversion is regulated by your own vitamin A status. When stores are full, BCO1 activity is turned down; when stores are low, it is turned up. Novotny and colleagues demonstrated the dose side of the same control directly in 2010: as the dietary dose of beta-carotene rises, the proportion converted to vitamin A falls. The unconverted surplus is simply stored in fat and skin, or excreted, rather than being pushed into the retinol pool.

The practical result is that there is no recorded case of vitamin A toxicity from eating carrots, or from any other provitamin A vegetable, and the Institute of Medicine set no upper limit for provitamin A carotenoids from food. It advised against high-dose beta-carotene supplements — for the smoking-related reasons above — but not against carrots. You can eat carrots freely. The only thing that happens if you eat a great many is that you turn orange, which brings us to the next section.

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Carotenemia: The Benign Orange Skin

Carotenemia — the high blood carotene level — and carotenoderma — the orange skin it produces — are the real, and entirely harmless, consequence of eating a great many carrots.

Because beta-carotene is fat-soluble, surplus that is not converted dissolves into subcutaneous fat and into the lipid-rich outer layer of the skin. Above a sustained intake in the region of 20 to 30 milligrams of carotene a day — roughly four to six large carrots daily, or a habitual glass of carrot juice, kept up for several weeks — the skin takes on a visible yellow-orange cast.

It shows first and most strongly where the skin's outer layer is thickest and sweat glands most numerous: the palms of the hands, the soles of the feet, the nasolabial folds beside the nose, and behind the ears. Maharshak and colleagues reviewed the literature in 2003 and describe exactly this distribution.

The single most useful clinical detail is this: in carotenoderma the whites of the eyes stay white. In jaundice they turn yellow, because bilirubin binds to elastin in the sclera and carotene does not. That one observation separates a person who has eaten a lot of carrots from a person with liver or bile duct disease, and it is the check a clinician makes first.

Carotenoderma is most often seen in infants and toddlers fed a lot of pureed carrot, sweet potato, and squash, and in adults on juice-heavy or very high vegetable diets. It causes no symptoms, damages nothing, and fades over weeks to a few months once intake falls. No treatment is needed beyond reassurance and, if the colour bothers you, eating fewer carrots.

One caveat worth stating: persistent yellow-orange skin is not always carotene. Hypothyroidism, diabetes, kidney disease, and liver disease can all raise blood carotene or produce similar discolouration, so if the colour appears without a corresponding diet, it is worth investigating rather than assuming.

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Macular Degeneration and the AREDS Story

There is one eye condition where carotenoids genuinely change outcomes, and it is instructive that the carotenoid involved is not beta-carotene.

The original AREDS trial, reported in 2001, tested a formula of vitamin C, vitamin E, beta-carotene, zinc, and copper in people with age-related macular degeneration. In participants at high risk, the formula reduced progression to advanced disease by roughly a quarter over five years — a real and clinically meaningful result that put the AREDS formula into ophthalmology practice worldwide.

But the formula contained 15 milligrams of beta-carotene, and by then ATBC and CARET had reported. Prescribing it to a former smoker meant handing them the exact exposure two trials had linked to lung cancer. So AREDS2, published in JAMA in 2013, tested replacing beta-carotene with lutein and zeaxanthin — the two carotenoids that are actually concentrated in the macula, where they form the yellow macular pigment that filters blue light and quenches oxidative damage in the most metabolically stressed patch of the retina. The substitution worked at least as well. The ten-year follow-up reported by Chew and colleagues in 2022 found that the lutein/zeaxanthin version outperformed the beta-carotene version for macular outcomes, while beta-carotene was associated with a substantially higher rate of lung cancer — and nearly all of those cases occurred in former smokers.

The AREDS formula sold today therefore contains no beta-carotene at all. Two lessons follow. First, the carotenoids that protect the retina structurally are lutein and zeaxanthin, found in kale, spinach, egg yolk, and in smaller quantities in yellow carrots — not beta-carotene. Second, AREDS is a treatment for established macular degeneration, not a general eye supplement; it has never been shown to prevent the disease in people who do not have it.

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How Much to Eat, and in What Form

Practical guidance, with the reasoning attached.

One medium carrot a day covers it. A medium raw carrot supplies on the order of 500 micrograms RAE, against an adult requirement of 700 to 900. Add any other orange or dark green vegetable across the week and vitamin A ceases to be a concern. There is no need to eat carrots daily, and no benefit to eating six.

Cook them, and eat them with fat. This is the single biggest lever. Gentle cooking softens the cell walls that trap beta-carotene, and dietary fat is required to get a fat-soluble pigment across the intestinal wall. Rock and colleagues showed in 1998 that beta-carotene bioavailability is lower from raw carrots than from processed ones; Brown and colleagues showed in 2004 that a fat-containing dressing markedly increased carotenoid absorption from salad compared with a fat-reduced one. Carrots roasted in olive oil, or raw carrots eaten with avocado, nuts, cheese, or a full-fat dip, deliver far more usable carotene than plain raw sticks. The companion page on cooking, fat, and absorption goes through the numbers.

Chop or grate before cooking. Breaking cells mechanically does part of the job that heat does. Lemmens and colleagues found in 2010 that particle size reduction mattered more for raw carrots than for cooked ones — grated raw carrot is significantly better than a whole stick.

Do not overcook. Prolonged high heat, especially in the presence of oil, degrades and isomerises beta-carotene. Steaming or brief roasting keeps the pigment; boiling for half an hour and discarding the water does not.

Eat colours other than orange too. Purple carrots add anthocyanins, red add lycopene, yellow add lutein. Arscott and Tanumihardjo's 2010 review makes the case that the heritage colour range is nutritionally broader than the orange monoculture.

Include some preformed vitamin A. Because conversion varies so much between people, a diet that includes eggs, whole dairy, oily fish, or occasional liver is a more robust vitamin A supply than plant carotenoids alone. This matters most for infants, for pregnancy, and for anyone eating no animal foods at all.

Skip the beta-carotene supplement. There is no situation in which a healthy person eating vegetables needs one, and for smokers and former smokers there is a clear reason not to.

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Key Research Papers

1. Wald G. Molecular basis of visual excitation. Science. 1968;162(3850):230-239. — doi:10.1126/science.162.3850.230
2. Lindqvist A, Andersson S. Biochemical properties of purified recombinant human beta-carotene 15,15'-monooxygenase. Journal of Biological Chemistry. 2002;277(26):23942-23948. — doi:10.1074/jbc.M202756200
3. Grune T, Lietz G, et al. Beta-carotene is an important vitamin A source for humans. The Journal of Nutrition. 2010;140(12):2268S-2285S. — doi:10.3945/jn.109.119024
4. Tang G. Bioconversion of dietary provitamin A carotenoids to vitamin A in humans. The American Journal of Clinical Nutrition. 2010;91(5):1468S-1473S. — doi:10.3945/ajcn.2010.28674G
5. Haskell MJ. The challenge to reach nutritional adequacy for vitamin A: beta-carotene bioavailability and conversion — evidence in humans. The American Journal of Clinical Nutrition. 2012;96(5):1193S-1203S. — doi:10.3945/ajcn.112.034850
6. Hickenbottom SJ, Follett JR, et al. Variability in conversion of beta-carotene to vitamin A in men as measured by using a double-tracer study design. The American Journal of Clinical Nutrition. 2002;75(5):900-907. — doi:10.1093/ajcn/75.5.900
7. Leung WC, Hessel S, et al. Two common single nucleotide polymorphisms in the gene encoding beta-carotene 15,15'-monoxygenase alter beta-carotene metabolism in female volunteers. The FASEB Journal. 2009;23(4):1041-1053. — doi:10.1096/fj.08-121962
8. Borel P, Desmarchelier C. Genetic variations associated with vitamin A status and vitamin A bioavailability. Nutrients. 2017;9(3):246. — doi:10.3390/nu9030246
9. Novotny JA, Harrison DJ, et al. Beta-carotene conversion to vitamin A decreases as the dietary dose increases in humans. The Journal of Nutrition. 2010;140(5):915-918. — doi:10.3945/jn.109.116947
10. Lietz G, Lange J, Rimbach G. Molecular and dietary regulation of beta,beta-carotene 15,15'-monooxygenase 1 (BCMO1). Archives of Biochemistry and Biophysics. 2010;502(1):8-16. — doi:10.1016/j.abb.2010.06.032
11. Sommer A. Xerophthalmia and vitamin A status. Progress in Retinal and Eye Research. 1998;17(1):9-31. — doi:10.1016/S1350-9462(97)00001-3
12. Sommer A. Vitamin A deficiency and clinical disease: an historical overview. The Journal of Nutrition. 2008;138(10):1835-1839. — doi:10.1093/jn/138.10.1835
13. Imdad A, Mayo-Wilson E, et al. Vitamin A supplementation for preventing morbidity and mortality in children from six months to five years of age. Cochrane Database of Systematic Reviews. 2017;(3):CD008524. — doi:10.1002/14651858.CD008524.pub3
14. Wiseman EM, Bar-El Dadon S, Reifen R. The vicious cycle of vitamin A deficiency: a review. Critical Reviews in Food Science and Nutrition. 2017;57(17):3703-3714. — doi:10.1080/10408398.2016.1160362
15. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. New England Journal of Medicine. 1994;330(15):1029-1035. — doi:10.1056/NEJM199404143301501
16. Omenn GS, Goodman GE, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. New England Journal of Medicine. 1996;334(18):1150-1155. — doi:10.1056/NEJM199605023341802
17. Hennekens CH, Buring JE, et al. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. New England Journal of Medicine. 1996;334(18):1145-1149. — doi:10.1056/NEJM199605023341801
18. Druesne-Pecollo N, Latino-Martel P, et al. Beta-carotene supplementation and cancer risk: a systematic review and meta-analysis of randomized controlled trials. International Journal of Cancer. 2010;127(1):172-184. — doi:10.1002/ijc.25008
19. Age-Related Eye Disease Study Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Archives of Ophthalmology. 2001;119(10):1417-1436. — doi:10.1001/archopht.119.10.1417
20. Age-Related Eye Disease Study 2 (AREDS2) Research Group. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the AREDS2 randomized clinical trial. JAMA. 2013;309(19):2005-2015. — doi:10.1001/jama.2013.4997
21. Chew EY, Clemons TE, et al. Long-term outcomes of adding lutein/zeaxanthin and omega-3 fatty acids to the AREDS supplements: AREDS2 report 28. JAMA Ophthalmology. 2022;140(7):692-698. — doi:10.1001/jamaophthalmol.2022.1640
22. Maharshak N, Shapiro J, Trau H. Carotenoderma — a review of the current literature. International Journal of Dermatology. 2003;42(3):178-181. — doi:10.1046/j.1365-4362.2003.01657.x
23. Arscott SA, Tanumihardjo SA. Carrots of many colors provide basic nutrition and bioavailable phytochemicals acting as a functional food. Comprehensive Reviews in Food Science and Food Safety. 2010;9(2):223-239. — doi:10.1111/j.1541-4337.2009.00103.x
24. Live topic search — PubMed: beta-carotene vitamin A conversion in humans
25. Live topic search — PubMed: carotenemia and carotenoderma

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Connections

• Carrots
• Cooking, Fat, and Carotenoid Absorption
• Falcarinol and the Carrot Polyacetylenes
• Carrot Fiber, Gut Health, and Cholesterol
• Carrots: History and Origins
• Vitamin A
• Vitamin A Deficiency
• Vitamin A Toxicity
• Beta-Carotene
• Lutein
• Zeaxanthin
• Ophthalmology
• Macular Degeneration
• Cataracts
• Retinitis Pigmentosa
• Lung Cancer
• Dangerous Supplements
• Sweet Potatoes
• Pumpkin
• Kale
• Spinach
• Olive Oil

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