Beta-carotene

Beta-Carotene: A Comprehensive Reference

1. Identity, Chemistry, and Forms

Chemical Identity

Beta-carotene (β,β-Carotene) is a symmetrical tetraterpene belonging to the carotenoid family — specifically the carotene subclass of non-oxygenated carotenoids. It represents the most significant provitamin A compound in the human diet, serving as both a fat-soluble antioxidant and a regulated precursor to vitamin A (retinol). Its molecular formula is C₄₀H₅₆, with a molar mass of 536.87 g/mol. Its IUPAC name is 1,1'-(3,7,12,16-Tetramethyl-1,3,5,7,9,11,13,15,17-octadecanonaene-1,18-diyl)bis[2,6,6-trimethylcyclohexene], registered under CAS number 7235-40-7.

Beta-carotene is an organic, strongly colored red-orange pigment abundant in fungi, plants, and fruits. It is a member of the carotenes, which are terpenoids (isoprenoids), synthesized biochemically from eight isoprene units and thus having 40 carbons. Beta-carotene consists of 8 isoprene units forming an extended conjugated polyene chain with 11 conjugated double bonds. Two identical β-ionone rings flank each end of the molecule — this symmetry distinguishes it from alpha-carotene, which has one β-ionone and one ε-ionone ring. The all-trans isomer is most thermodynamically stable and biologically active.

Being highly conjugated, it is deeply colored, and as a hydrocarbon lacking functional groups, it is lipophilic. The compound is known by numerous synonyms including β,β-Carotene; all-trans-β-Carotene; Provitamin A; Betacarotene; and the food-color designation C.I. Food Orange 5 (E number E160a).

Natural Sources

Plant carotenoids are the primary dietary source of provitamin A worldwide, with β-carotene as the best-known provitamin A carotenoid. Others include α-carotene and β-cryptoxanthin. In foods, it is found in rich content in carrots, pumpkin, spinach, and sweet potato. Beta-carotene is most abundant in carrots, but is also found in pumpkins, apricots and nectarines. Dark green vegetables such as spinach and broccoli are another good source; in these, the orange color is masked by the green color of chlorophyll.

Beta-carotene is present as crystalline formations in the plastids of plant sources like fruits and vegetables, where it makes photosynthetic complex structures with other compounds in these cells. It is industrially extracted from richer sources such as the algae Dunaliella salina. Natural carotenoid extracts can also be obtained by solvent extraction of carrots (Daucus carota), oil of palm fruit (Elaeis guinensis), sweet potato (Ipomoea batatas), and other edible plants, with subsequent purification; the main coloring principles in such extracts are alpha- and beta-carotenes, of which beta-carotene constitutes the major part.

Commercial and Supplement Forms

Beta-carotene, along with alpha-carotene, lutein, zeaxanthin, and lycopene, is available as a dietary supplement. It is used in dietary supplements usually in the form of provitamin A (beta-carotene), sometimes in combination with preformed vitamin A. Supplement forms include soft gelatin capsules (oil-based), vegetarian softgels, hard gelatin or HPMC capsules in beadlet form, tablets, liquid drops in oil solution, and water-dispersible beadlets. Natural extracts containing carotenoids, for example carrot extracts and red palm oil, have been used to color foods for centuries. Synthetic beta-carotene was first marketed as a food coloring by Roche in 1954. There is no biological difference between naturally occurring or chemically synthesized beta-carotene.

2. Historical Discovery and Traditional Use

Discovery

The discovery of carotene from carrot juice is credited to Heinrich Wilhelm Ferdinand Wackenroder, a finding made during a search for antihelminthics, which he published in 1831. He obtained it in small ruby-red flakes soluble in ether, which when dissolved in fats gave "a beautiful yellow colour." The structure was deduced in 1930.

Traditional Dietary and Coloring Uses

Natural extracts containing carotenoids, for example carrot extracts and red palm oil, have been used to color foods for centuries. Synthetic beta-carotene was first marketed as a food coloring by Roche in 1954, and it is mainly used for coloring margarine and butter, with its vitamin A activity regarded as an added benefit. The orange color of modern carrots was bred intentionally by Dutch growers in the 17th century.

Carotenoids are natural pigments synthesized by plants and are responsible for the bright colors of various fruits and vegetables; they act as photosynthesis aids and provide photo protection for their host plants. The historical human use of beta-carotene-rich foods spans all cultures that consumed orange and yellow vegetables and fruits, though the compound itself was not isolated until the 19th century. Red palm oil — a highly concentrated source of carotenoids including beta-carotene — has been a dietary staple in sub-Saharan Africa for millennia, used both as a cooking fat and a source of color and nutrition.

Use as a Vitamin A Source in Public Health

The one clear function of certain carotenoids that is firmly linked to a health outcome is the provitamin A activity of some dietary carotenoids (alpha-carotene, beta-carotene, and beta-cryptoxanthin) and their role in the prevention of vitamin A deficiency. A World Health Organization analysis of data from 83 countries showed that 11,200 child deaths from measles were associated with vitamin A deficiency in 2013, and more than 95% of these deaths occurred in sub-Saharan Africa and south Asia. In these contexts, beta-carotene from food sources has served as the primary accessible vehicle for meeting vitamin A needs.

3. Key Constituents and Mechanisms of Action

Provitamin A Activity

Compared with other carotenoids, the primary role of beta-carotene is its provitamin A activity. Provitamin A activity is the main function of beta-carotene known in humans. The uniqueness of beta-carotene is that, compared with other carotenoids, it has a β-ionone structure as the terminal ring system on each end of the polyene chain, and its central oxidative cleavage in the intestine allows for its conversion to 2 molecules of vitamin A in a physiologically regulated manner.

The oxidative cleavage of beta-carotene is achieved by BCMO1 (also written as BCO1), which cleaves beta-carotene into 2 molecules of all-trans-retinal (retinaldehyde). It is cleaved to form two molecules of retinal, one of which is further metabolized to form retinol and retinoic acid. Retinoids affect gene expression through nuclear receptors (various retinoic acid receptors and retinoid X receptors).

Micelles formed in the intestine are absorbed by enterocytes, where beta-carotene is either cleaved to retinal by the BCO1 enzyme or packaged intact into chylomicrons. Scavenger receptor class B type 1 (SR-B1) facilitates uptake into enterocytes; CD36 also participates in carotenoid uptake.

Antioxidant Mechanisms

Beta-carotene can also act as a lipid radical scavenger and as a singlet oxygen quencher, as demonstrated in vitro. As an antioxidant, the compound quenches singlet molecular oxygen and scavenges reactive oxygen species, especially peroxyl radicals. Singlet oxygen quenching is likely to be restricted to the skin as the only light-exposed tissue that contains higher levels of beta-carotene; other carotenoids demonstrate similar activity.

Possible prooxidant reactions involve the abstraction of a hydrogen atom from an unsaturated fatty acid, resulting in propagation of lipid peroxidation. Carotenoid epoxides and cyclic peroxides may be produced, the latter decomposing upon cleavage of the carotenoid molecule. Oxidative cleavage products, such as apo-carotenals, retain the structure of biologically active signaling molecules (e.g., retinoic acid) and may interfere with or trigger signaling pathways. This dual antioxidant/prooxidant character is relevant to understanding the safety divergence between dietary and supplemental forms at high doses.

Genetic Variation in Conversion Efficiency

A number of single nucleotide polymorphisms (SNPs) have been identified in genes coding for proteins involved in intestinal uptake, transport, and metabolism of carotenoids. Specifically, SNPs within genes coding for SR-BI, CD36, and BCO1 are suspected to affect the expression and/or activity of these proteins and, in turn, individual carotenoid status. Food-related factors that largely influence the bioavailability of beta-carotene include food matrix, food processing, dosage, fat in the meal, other carotenoids in the meal, and dietary fiber. Additional consumer-related factors include polymorphisms related to metabolism, vitamin A status, and gut integrity.

Regulated Conversion

No increase in serum retinol level was found even after long-term beta-carotene supplementation in people with already adequate levels of vitamin A. Reports provide an initial level of support for the idea that the efficiency of absorption and/or cleavage of beta-carotene is somewhat influenced by vitamin A nutritional status and may be directly responsive to the level of retinoic acid.

4. Bioavailability

Absorption of beta-carotene in the GI tract is influenced by numerous factors such as host-related factors (genetic makeup, nutritional status, physiological condition and their interaction), the concentration of consumed beta-carotene, conversion into vitamin A, the nature of the meal, presence of other food components like lipids, rate of digestion, absorption, and metabolism inside the body.

The relative absorption efficiency of supplemental and dietary beta-carotene has been reported to range from 5% (spinach) to 26% (raw carrots). For prolonged serum and tissue accumulation of beta-carotene, its administration must be with dietary fats. Carotenoid absorption is restricted to the duodenum of the small intestine. The dietary source of beta-carotene and adherence to the matrix influence the absorption and bioavailability significantly.

Considering the higher bioavailability of beta-carotene from dietary supplements compared with fruit and vegetables, and the purposeful addition of supplemental amounts of beta-carotene to juices and other foods specifically containing adequate fats and oils, fortified foods have a potentially important role in supplying vitamin A to the population.

5. Scientific Evidence by Area of Use

5.1 Vitamin A Deficiency and Nutritional Support

Currently, the only essential function of carotenoids recognized in humans is that of the provitamin A carotenoids — alpha-carotene, beta-carotene, and beta-cryptoxanthin — to serve as a source of vitamin A. Although consumption of provitamin A carotenoids can prevent vitamin A deficiency, no overt deficiency symptoms have been identified in people consuming low-carotenoid diets if they consume adequate vitamin A. After reviewing the published scientific research in 2000, the Food and Nutrition Board of the Institute of Medicine concluded that the existing evidence was insufficient to establish a recommended dietary allowance (RDA) or adequate intake (AI) for carotenoids.

Studies conducted in Germany show that beta-carotene makes up 25–30% of vitamin A intake, with approximately 10% of the total vitamin A supply coming from nonalcoholic beverages and other fortified food (cheese, butter, etc.). Americans and British are reported to consume up to 2 mg of beta-carotene from dietary sources, while vegan and vegetarian consumption was up to 9 mg/day.

Evidence strength: Well established. Beta-carotene's role as a provitamin A source is the most firmly supported function in humans and forms the basis of global public health nutritional policy.

5.2 Cancer — Lung Cancer and Smoking Risk

Three large-scale clinical trials tested the effects of supplemental beta-carotene on the risk for chronic diseases such as cancer. The populations involved were Finnish male heavy smokers (the Alpha Tocopherol Beta Carotene [ATBC] trial), male asbestos workers and male and female heavy smokers (Beta-Carotene and Retinol Efficacy Trial [CARET]), and U.S. male physicians, 11% of whom were current smokers (Physician's Health Study). All three trials concluded that beta-carotene provided no protection against lung cancer; however, quite unexpectedly, two of the trials found a higher risk for lung cancer for those subjects given beta-carotene compared with those that were not.

In current smokers participating in the Alpha-Tocopherol, Beta-Carotene (ATBC) Cancer Prevention Study, supplementation with 20 mg/day of beta-carotene (with or without 50 mg of alpha-tocopherol) for 5 to 8 years led to a higher incidence of lung cancer but had no effect on the incidence of other major cancers (prostate, bladder, colon or rectum, or stomach) in this population.

The ATBC Study was a randomized, double-blind intervention trial conducted in southwest Finland. A total of 29,133 male smokers, aged 50–69 years, were enrolled and randomly assigned to one of four groups (alpha-tocopherol, beta-carotene, both, or placebo). The ATBC Study reported an 18% excess in cumulative lung cancer incidence and an 8% excess in overall mortality in the beta-carotene arm of the trial, whereas the CARET study showed 28% more lung cancer cases and a 17% increase in overall mortality in the active intervention group.

The CARET study was a double-blind RCT in which 18,314 persons at high risk for lung cancer, including both male and female heavy smokers (defined as a smoking history of ≥20 pack-years) and asbestos-exposed men, were treated with a combination of 30 mg beta-carotene and 25,000 IU of retinyl palmitate.

A meta-analysis, based on data from 109,394 subjects, conclusively demonstrated a 24% increase in the risk of lung cancer among smokers who received high-dose beta-carotene supplements. The averaged dose of beta-carotene in these trials ranged from 20 to 30 mg daily (33,333–50,000 IU) and the median duration of intervention ranged from 2 to 12 years.

There are a number of hypotheses concerning the beta-carotene/tobacco smoke interaction, including alterations of retinoid metabolism and signaling pathways and interaction with CYP enzymes and pro-oxidation/DNA oxidation.

Among nonsmokers, beta-carotene and vitamin A supplements do not appear to affect the risk of cancer. A large body of observational epidemiological evidence suggests that higher blood concentrations of beta-carotene and other carotenoids obtained from foods are associated with lower risk of several chronic diseases. However, this evidence, although consistent, cannot be used to establish a requirement for beta-carotene or carotenoid intake because the observed effects may be due to other substances found in carotenoid-rich food, or to other behavioral correlates of increased fruit and vegetable consumption.

Evidence strength: Strong clinical trial evidence showing no protective effect against lung cancer, and clear harm (increased lung cancer risk and mortality) in current and former smokers and asbestos-exposed workers receiving high supplemental doses. The epidemiological association between dietary beta-carotene and reduced cancer risk likely reflects broader dietary patterns rather than a direct causal role.

5.3 Age-Related Macular Degeneration (AMD)

AMD is the leading cause of significant vision loss in older people. Its etiology involves complex interactions among genetic susceptibility, environmental factors (including exposure to oxidative stress), and normal aging. Because of the role of oxidative stress in AMD pathophysiology, supplements containing carotenoids with antioxidant functions, such as beta-carotene, lutein, and zeaxanthin, might be useful for preventing or treating this condition.

In the Age-Related Eye Disease Study (AREDS), the 4 treatment interventions were double-masked and given as an oral total daily supplementation of antioxidants (500 mg of vitamin C, 400 IU of vitamin E, and 15 mg of beta-carotene), or zinc (80 mg of zinc as zinc oxide and 2 mg of copper as cupric oxide), or the combination of antioxidants and zinc, or placebo.

The Age-Related Eye Disease Study (AREDS) demonstrated that treatment with high-dose antioxidant supplements (vitamin C, vitamin E, and beta carotene) and zinc could reduce the risk of progression to advanced AMD in persons at high risk. A 10-year follow-up study (multicenter, randomized, controlled clinical trial) enrolled 4,757 participants with varying severity of AMD. Participants were randomly assigned to antioxidants C, E, and beta-carotene and/or zinc versus placebo during the clinical trial. For participants with intermediate or advanced AMD in one eye, the AREDS formulation delayed the progression to advanced AMD.

The Age-Related Eye Disease Studies (AREDS and AREDS2) established that dietary supplements can slow progression of AMD, the most common cause of blindness in older Americans. In a new report, scientists analyzed 10 years of AREDS2 data. They showed that the AREDS2 formula, which substituted antioxidants lutein and zeaxanthin for beta-carotene, not only reduces risk of lung cancer due to beta-carotene, but is also more effective at reducing risk of AMD progression, compared to the original formula.

Because beta-carotene increased the risk of lung cancer for current smokers in two NIH-supported studies, the goal with AREDS2 was to create an equally effective supplement formula that could be used by anyone, whether or not they smoke.

Evidence strength: Strong evidence (large RCT) that the original AREDS formulation — which included 15 mg/day beta-carotene — slows progression to advanced AMD in high-risk individuals. However, the updated AREDS2 formula replacing beta-carotene with lutein and zeaxanthin is now preferred as it is equally or more effective and eliminates the lung cancer risk for smokers.

5.4 Erythropoietic Protoporphyria (EPP) and Photoprotection

Erythropoietic protoporphyria is a genetic disease caused by the accumulation of protoporphyrin IX. This molecule absorbs 400-nm light and its presence is at times associated with severe cutaneous photosensitivity. Oral administration of beta-carotene has been described as a treatment for this disease.

Three patients with erythropoietic protoporphyria, with elevated levels of porphyrin in blood and stool and with severe photosensitivity on exposure of skin to both sunlight and artificial light, were treated with an oral preparation of beta-carotene. After treatment, two of the patients were able to tolerate five to eight hours of sun without experiencing photosensitivity, and the third could tolerate exposure to sun with less discomfort than he had experienced before therapy. When the patients were carotenemic, they also reacted less intensely to artificial light. Beta-carotene appears to counteract photosensitization in the skin of these patients.

Beta-carotene has been prescribed and used against photosensitivity in erythropoietic protoporphyria, but its beneficial potential in normal skin remains uncertain. After approximately 10–12 weeks of dietary intervention, a decrease in the sensitivity toward UV-induced erythema was observed in volunteers, and a number of experimental studies have indicated protective effects against acute and chronic manifestations of skin photodamage, but there is a lack of controlled clinical studies demonstrating its beneficial effects.

A systematic review of trials found moderate positive effects of inorganic sunscreen application and subcutaneous implant of afamelanotide, but no effect of organic sunscreen application or oral treatment with beta-carotene for EPP, among controlled trials. This finding suggests that while earlier uncontrolled studies showed benefit, controlled evidence for beta-carotene in EPP is weaker than previously assumed.

Beta-carotene is used as a dietary supplement and may be prescribed to treat erythropoietic protoporphyria, an inherited condition of sunlight sensitivity.

Evidence strength: Early clinical use and uncontrolled studies support oral beta-carotene for EPP-related photosensitivity; more rigorous controlled trial evidence is limited and mixed. Evidence for photoprotection in the general healthy population is weak and relies on small or uncontrolled studies.

5.5 Cardiovascular Disease

Several studies reveal that beta-carotene is a potent antioxidant, able to function against oxidative stress, maintaining health, and preventing diseases such as cancer and cardiovascular disease (CVD). Observational evidence also suggests that a high dietary intake of beta-carotene is associated with a reduced risk of cancer and CVD. However, these associations from observational data have not translated into benefits in clinical intervention trials.

Supplementation with beta-carotene, with or without retinyl palmitate, for 5–8 years has been associated with an increased risk of lung cancer and cardiovascular disease in current and former male and female smokers and in male current and former smokers occupationally exposed to asbestos. In the ATBC study, beta-carotene supplements (20 mg daily) were also associated with increased mortality, mainly due to lung cancer and ischemic heart disease.

A large randomized controlled trial of simvastatin and an antioxidant combination of 297 mg of RRR-alpha-tocopherol, 250 mg of vitamin C, and 20 mg of beta-carotene daily in more than 20,000 men and women with coronary heart disease (CHD) or diabetes mellitus found that the antioxidant combination did not diminish the cardioprotective effects of simvastatin therapy over a five-year period.

Evidence strength: No clinical trial evidence of cardiovascular benefit from beta-carotene supplementation. Supplementation at high doses in smokers was associated with increased cardiovascular mortality. Observational associations may reflect overall dietary patterns.

5.6 Cognitive Function

The Women's Antioxidant Cardiovascular Study was a trial of vitamin E (402 mg every other day), beta-carotene (50 mg every other day), and vitamin C (500 mg daily) for the secondary prevention of cardiovascular disease. Women 40 years and older with CVD or three or more coronary risk factors were randomized from 1995 to 1996, and a cognitive function substudy was initiated among 2,824 participants aged 65 years and older. With 5 cognitive tests, cognition was assessed by telephone four times over 5.4 years. In this randomized placebo-controlled trial, use of antioxidant supplements was not clearly associated with slowing of cognitive decline.

In an observational study of high-functioning older persons, the adjusted odds ratio of high beta-carotene level for cognitive decline was 0.11 (95% CI: 0.02–0.57) in participants with at least one APOE ε4 allele, and 0.89 (95% CI: 0.54–1.47) among those who were APOE ε4 negative. The authors suggested that antioxidants and beta-carotene in particular may offer protection from cognitive decline in persons with greater genetic susceptibility as evidenced by the presence of the APOE ε4 allele.

Evidence strength: RCT evidence does not support beta-carotene supplementation for cognitive protection. Some observational data suggest possible benefit in genetically susceptible individuals, but this is hypothesis-generating only and requires prospective confirmation.

5.7 Immune Function

Beta-carotene offers health benefits other than vitamin A activity. It is described as an effective free radical scavenger that helps boost immunity and prevent and combat antioxidant stress, cancer, metabolic disease, cardiovascular diseases, and ophthalmic diseases. However, most of the clinical immunological evidence comes from studies in vitamin A-deficient populations, where restoration of vitamin A status (via beta-carotene conversion) does restore immune competence, rather than studies of beta-carotene supplementation specifically in replete individuals.

Vitamin A is essential for normal growth and development, immune system function, and vision. Because beta-carotene is the primary dietary precursor to vitamin A, its role in immune function is closely coupled to its provitamin A activity.

Evidence strength: Indirect; the immune benefits attributable to beta-carotene in humans are largely a function of its conversion to vitamin A. Direct supplementation trials for immune endpoints in replete populations show limited evidence.

6. Body Systems Associated With Beta-Carotene

• Visual system: Beta-carotenes serve as precursors of provitamin A, which plays a vital role in eyesight and vision. The AREDS trials directly tested its role in AMD.
• Immune system: Vitamin A, derived from beta-carotene, is essential for normal immune system function.
• Integumentary system (skin): Beta-carotene acts as an antioxidant that quenches singlet molecular oxygen, with this activity likely restricted to the skin as the only light-exposed tissue containing higher levels of beta-carotene.
• Reproductive and developmental systems: Beta-carotenes affect embryonic development and correct growth through their conversion to vitamin A.
• Respiratory system: The lung cancer findings of ATBC and CARET represent the most significant clinical outcome established in this system — one of harm rather than benefit in smokers.
• Cardiovascular system: Serum beta-carotene has also been inversely correlated with systemic inflammation and insulin resistance in observational data, though intervention trials show no benefit.
• Central nervous system: Exploratory observational and limited RCT evidence has examined a possible role in cognitive aging, with no established benefit from supplementation.

7. Dosage Forms and Dosages Reported in Studies

No RDA (Recommended Dietary Allowance) has been established for beta-carotene. The adequate intake for vitamin A from all sources is 700 mcg RAE (women) to 900 mcg RAE (men) daily. There are no established upper limits for beta-carotene and other forms of provitamin A.

A daily dose of 1.5 mg of beta-carotene equalizes 2,500 IU of vitamin A or 250 retinol equivalents.

Doses used in major clinical trials include:

• ATBC trial: 20 mg/day of beta-carotene (with or without 50 mg of alpha-tocopherol) for 5 to 8 years in 29,133 male smokers aged 50–69 years.
• CARET trial: 30 mg/day of beta-carotene combined with 25,000 IU of retinyl palmitate in 18,314 heavy smokers and asbestos-exposed men.
• AREDS trial: 15 mg/day of beta-carotene as part of an antioxidant combination (with 500 mg vitamin C, 400 IU vitamin E), with or without zinc.
• Women's Antioxidant Cardiovascular Study (WACS): 50 mg of beta-carotene every other day in women at cardiovascular risk.
• Large supplemental doses of 20–30 mg/day of beta-carotene or diets with high levels of carotenoid-rich food for long periods are not associated with toxicity in general populations (outside of smokers).

A large dietary survey reported a median dietary beta-carotene intake of 1.3 mg/day among adults responding to a food frequency questionnaire.

8. Safety Considerations and Interactions

Carotenodermia

Large supplemental doses (20–30 mg/day) of beta-carotene or diets with high levels of carotenoid-rich food for long periods are not associated with toxicity. The most significant effect of long-term, excess beta-carotene is carotenodermia, a harmless condition in which the skin becomes yellow-orange. This condition can be reversed by discontinuing beta-carotene ingestion.

Lung Cancer and Mortality Risk in Smokers

Supplementation with beta-carotene, with or without retinyl palmitate, for 5–8 years has been associated with an increased risk of lung cancer and cardiovascular disease in current and former male and female smokers and in male current and former smokers occupationally exposed to asbestos. In the ATBC study, beta-carotene supplements (20 mg daily) were also associated with increased mortality, mainly due to lung cancer and ischemic heart disease.

Intake of natural beta-carotene from the diet is considered safe even at large doses and does not show any toxic effects. Supplemental beta-carotene can exhibit toxicity at higher concentrations, leading to unwanted side effects and disturbances in the human body.

Absence of Preformed Vitamin A Toxicity

No increase in serum retinol level was found even after long-term beta-carotene supplementation in people with already adequate levels of vitamin A. The upper limit (UL) for preformed vitamin A is 3,000 mcg RAE, but no UL has been established for beta-carotene from food.

Alcohol Interaction

Long-term alcohol consumption can interact with beta-carotene, raising the chances of developing liver problems.

Drug Interactions with Fat Absorption Inhibitors

The cholesterol-lowering agents cholestyramine (Questran) and colestipol (Colestid) can reduce absorption of fat-soluble vitamins and carotenoids, as can mineral oil and orlistat (Xenical), a drug used to treat obesity. Orlistat (Xenical, Alli) can undermine the absorption of beta-carotene by up to 30 percent, resulting in lower blood beta-carotene levels. Those choosing to take a multivitamin while on orlistat should take them at least two hours before having their medication.

Cholestyramine, a medication used to lower cholesterol, can lower levels of dietary beta-carotene in the blood by 30 to 40%, according to one study. Colestipol, a cholesterol-lowering medication similar to cholestyramine, may also reduce beta-carotene levels.

Interaction with Statins and Niacin

A large randomized controlled trial of simvastatin and an antioxidant combination including 20 mg of beta-carotene daily in more than 20,000 men and women with CHD or diabetes found that the antioxidant combination did not diminish the cardioprotective effects of simvastatin therapy over a five-year period. These contradictory findings indicate that further research is needed on potential interactions between antioxidant supplements and cholesterol-lowering agents such as niacin and statins.

Proton Pump Inhibitors

Increasing gastric pH through the use of proton-pump inhibitors (omeprazole, lansoprazole) may decrease the absorption of a single dose of a beta-carotene supplement, but the effect is unlikely to be clinically significant.

GRAS Status

Both lycopene and beta-carotene have been generally recognized as safe (GRAS).

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