Palmitate

Palmitate (Retinyl Palmitate / Vitamin A Palmitate): A Comprehensive Reference

1. Identity and Chemical Characterization

1.1 Nomenclature and Synonyms

Retinyl palmitate, or vitamin A palmitate, is the ester of retinol (vitamin A) and palmitic acid, with formula C₃₆H₆₀O₂. In the dietary supplement and pharmaceutical literature, it is also encountered under several alternate names: all-(E)-retinol palmitate, all-trans-retinyl hexadecanoate, all-trans-retinyl palmitate, retinol palmitate, and retinol hexadecanoate. Its CAS registry number is 79-81-2 and its IUPAC name is (2E,4E,6E,8E)-3,7-dimethyl-9-(2,6,6-trimethylcyclohex-1-en-1-yl)nona-2,4,6,8-tetraen-1-yl hexadecanoate. An alternate spelling, retinol palmitate, which violates the -yl organic chemical naming convention for esters, is also frequently seen.

The term palmitate itself refers to the saturated fatty acid component of this molecule — palmitic acid — and also to any salt or ester of palmitic acid. Palmitic acid (hexadecanoic acid in IUPAC nomenclature) is a fatty acid with a 16-carbon chain and is the most common saturated fatty acid found in animals, plants, and microorganisms. Palmitates are the salts and esters of palmitic acid; the palmitate anion is the observed form of palmitic acid at physiologic pH (7.4).

1.2 Chemical Structure and Physical Properties

Chemically, vitamin A palmitate (also called retinyl palmitate) is an ester — a combination of retinol (the active form of vitamin A) bonded to palmitic acid, a fatty acid found naturally in many foods. Vitamin A consists of three structural domains: a cyclic moiety, a polyene side chain, and a polar end group. Palmitic acid itself — the moiety from which palmitate derives — has the chemical formula CH₃(CH₂)₁₄COOH, and its C:D ratio is 16:0, indicating no carbon-carbon double bonds and making it a fully saturated molecule. The esterification product, retinyl palmitate, is more stable than retinol on its own; the oil-based form resists oxidation during storage and holds up better against light exposure.

1.3 Natural Sources

Retinyl palmitate is the most abundant form of vitamin A storage in animals. Animals use long-chain esters of vitamin A, most abundantly the palmitate form, as a form of vitamin A storage. The normal adult liver contains approximately 100 to 300 micrograms per gram, mostly as retinyl palmitate.

Palmitic acid — the fatty acid component — is among the most widespread molecules in the natural world. The most common natural fatty acid, it is abundant in oil extracted from the fruit of oil palms (Elaeis guineensis and E. oleifera), as well as in meats and dairy products. It is a major component of palm oil from the fruit of Elaeis guineensis (oil palms), making up to 44% of total fats. Meats, cheeses, butter, and other dairy products also contain palmitic acid, amounting to 50–60% of total fats. Palmitic acid is the main saturated fatty acid naturally occurring in animal fats and vegetable oil, as well as the main component of human milk fat.

Cod liver oil has long been recognized as one of the most concentrated whole-food sources of vitamin A. In fish liver oils, vitamin A occurs primarily as retinyl esters that are converted to retinol during digestion before absorption.

1.4 Common Preparations and Dosage Forms

Vitamin A palmitate is a common vitamin supplement, available in both oral and injectable forms for treatment of vitamin A deficiency, under the brand names Aquasol A, Palmitate A, and many others. Retinyl palmitate is used as a source of vitamin A added to low-fat milk and other dairy products to replace the vitamin content lost through the removal of milk fat; palmitate is attached to the alcohol form of vitamin A, retinol, to make vitamin A stable in milk. Retinyl palmitate is also a constituent of some topically applied skin care products. It is a constituent of intraocular treatment for dry eyes at a concentration of 138 μg/g (VitA-Pos) by Ursapharm.

Parenteral administration is indicated when oral administration is not feasible, as in anorexia, nausea, vomiting, pre- and postoperative conditions, or in the malabsorption syndrome with accompanying steatorrhea. In fortification programs, vitamin A palmitate is a synthetic ester form of vitamin A commonly used to fortify foods such as milk, cereals, and infant formulas, especially in populations where deficiency is a concern.

2. Historical and Traditional Use

2.1 Pre-Scientific Traditional Use

The use of vitamin A-rich foods predates the isolation of retinyl palmitate as a chemical entity by centuries. Traditional Chinese medicine and folk practices across the globe prescribed animal liver or cod liver oil to promote vision and support overall vitality. In northern European countries, cod liver oil had a long history of folklore medical uses, including applied to the skin and taken orally as a treatment for rheumatism and gout.

Cod liver oil has a long history in both folk and traditional medicine in northern Europe. Considered a delicacy in Scotland and Norway for centuries, fresh cod liver was revered for medicinal purposes long before modern extraction methods were developed. Scandinavian Vikings produced cod liver oil by laying birch tree branches over a kettle of water; fresh livers were laid over the branches, the water was brought to a boil, and as the steam rose, the oil from the liver dripped into the water and was skimmed off.

2.2 Emergence as Medicine (18th–19th Century)

Cod liver oil, rich in vitamin D, was first advocated for the treatment of tuberculosis (TB) in 1770, and it was widely used for this purpose in the nineteenth century. In 1833, Henkel, a German doctor, reported on the successful use of cod liver oil in the treatment of TB. Historically, it was given to children in the United States in the 19th century as a patent medicine and by the end of the century was being praised by doctors in medical journals.

2.3 Scientific Identification and 20th-Century Development

In the early 20th century, when rickets disease was becoming a considerable health concern, cod liver oil was the basis for the discovery of vitamins A and D, essential for healthy growth and development. In the 1910s, biochemists discovered two essential nutrients in cod liver oil — vitamins A and D — and scientists began extracting these vitamins from cod liver oil. The esterification of retinol with palmitic acid to form the stable retinyl palmitate subsequently became the standard pharmaceutical and nutritional preparation of preformed vitamin A used in fortification programs and supplement manufacturing. The knowledge of palmitic acid itself dates to 1840, when French chemist Edmont Frémy made it by saponifying palm oil, a process that is still used to manufacture the compound.

3. Key Constituents and Mechanisms of Action

3.1 Nature as a Retinoid

Vitamin A derivatives include a number of related nutritional hydrophobic compounds, such as retinal, retinol, retinoic acid, and several retinyl esters. Vitamin A derivatives serve essential roles in aiding healthy vision, maintenance of the immune system, embryonic growth and development, and protection of epithelial tissues. Retinyl palmitate belongs to a category of compounds called retinoids, which are chemically similar to vitamin A.

3.2 Intestinal Absorption and Hepatic Storage

Dietary retinyl esters must be hydrolyzed in the lumen of the small intestine, emulsified, and incorporated into lipid micelles before retinol can be absorbed into the mucosa. Several retinyl ester hydrolase (REH) enzymes are present in pancreatic juice or situated on the brush border of duodenal and jejunal enterocytes. For greatest efficiency, these processes require an adequate amount of bile salts and a small quantity of dietary fat, approximately 5%, consumed concomitantly. The retinol molecules then diffuse into the enterocyte where they are bound to CRBP-II and then esterified by the enzyme lecithin:retinol acyltransferase (LRAT).

Once in circulation, when the body requires vitamin A, retinyl esters are hydrolyzed to free retinol, which can then be bound to retinol-binding protein (RBP) for transport to target tissues. The storage reaction is catalyzed by LRAT, and the inverse hydrolysis is catalyzed by retinyl ester hydrolase (REH). Preformed vitamin A is rapidly absorbed and slowly cleared from the body.

3.3 Visual Cycle

In the retinal pigment epithelium, retinol is esterified to all-trans-retinyl ester for storage. When needed, retinyl esters are hydrolyzed to 11-cis-retinol and then isomerized to 11-cis-retinal. Arrows indicate that 11-cis-retinol moves through the interphotoreceptor matrix to the photoreceptor cell, where 11-cis-retinal binds opsin to form rhodopsin (visual purple). The esters are also intermediates in the visual cycle: RPE65 isomerizes the retinyl part to 11-cis-retinal.

3.4 Nuclear Receptor Signaling

Retinoic acid, a metabolite of retinol, is essential for cellular differentiation, growth, and immune function. Retinoic acid modulates gene expression by binding to nuclear receptors such as retinoic acid receptors (RARs) and retinoid X receptors (RXRs), which in turn regulate the transcription of genes involved in cell proliferation, differentiation, and apoptosis.

3.5 Topical Conversion Pathway

The mechanism of action of retinyl esters when applied topically is that they penetrate into the skin and are transformed into retinol by the action of esterases, then into retinal by the action of enzymes, and finally into retinoic acid. This process prevents strong skin irritation and activates cell renewal. However, after its absorption into the skin, retinyl palmitate is converted to retinol, and ultimately to retinoic acid (the active form of vitamin A present in Retin-A), though neither its skin absorption nor its conversion is very effective.

3.6 Palmitic Acid: Metabolic Roles

In living organisms, palmitic acid is a critical component of cell membranes and is involved in numerous biological processes. It serves as a major energy source and is a precursor for the synthesis of other fatty acids, as well as certain hormones and signaling molecules. Fatty acid esters are prolific producers of adenosine triphosphate (ATP), the main energy source in living cells; according to one account, one palmitate molecule generates 129 molecules of ATP.

4. Scientific Evidence by Area of Use

4.1 Vitamin A Deficiency

Vitamin A deficiency (VAD) is a leading cause of pediatric morbidity and mortality due to infectious diseases. From 1995 to 2005, the number of preschool-age children with vitamin A deficiency dropped from 251 million to 190 million globally; however, in 2019, over 3 million disability-adjusted life years (DALYs) were still lost due to VAD globally.

Clinical evidence — Equivalence with beta-carotene: A randomized blind equivalence trial set in a rural area in Senegal enrolled children aged 2–15 years suffering from vitamin A deficiency, who were randomly allocated treatment with retinyl palmitate (n=256) and beta-carotene (n=254). Seven weeks after the supplement was given, 51.2% of children taking retinyl palmitate and 50.0% of those taking beta-carotene reverted to normal eye cytology; according to equivalence testing procedure, the two treatments were statistically equivalent. This is a well-designed RCT but limited to a single geographic setting and short follow-up.

Clinical evidence — Fortification: A study from 2002 found that red palm oil groups experienced a greater increase in retinol and β-carotene levels compared to groups receiving groundnut oil fortified with retinyl palmitate. While the number of studies directly comparing the effects of retinyl palmitate and red palm oil on vitamin A status is limited, the existing studies demonstrate that red palm oil may be as effective as retinyl palmitate when added to the diet in a way that preserves the original contents of the oil.

4.2 Child Mortality and Infectious Disease

Numerous intervention studies, particularly in developing countries, have shown that vitamin A supplementation can significantly reduce morbidity and mortality from infectious diseases in children. The World Health Organization and UNICEF endorse vitamin A supplementation as a cost-effective strategy to improve child health outcomes.

Meta-analytic evidence: Pooled results for preventive vitamin A supplementation showed that it reduced all-cause mortality by 25% (RR 0.75; 95% CI 0.64–0.88) in children 6–59 months of age. Vitamin A supplementation also reduced diarrhea-specific mortality by 30% (RR 0.70; 95% CI 0.58–0.86) in children 6–59 months. Vitamin A supplementation had no statistically significant effect on measles (RR 0.71, 95% CI: 0.43–1.16), meningitis, or pneumonia specific mortality.

The majority of trials (42/47) administered large doses of vitamin A ranging from 50,000 IU to 200,000 IU, and retinol palmitate was most commonly used. Provision of vitamin A supplements every four to six months is an inexpensive, quick, and effective way to improve vitamin A status and reduce child morbidity and mortality in the long term.

4.3 Measles

Vitamin A deficiency is a recognized risk factor for severe measles infections. The World Health Organization (WHO) recommends administration of an oral dose of vitamin A (200,000 IU, or 100,000 IU in infants) each day for two days to children with measles when they live in areas where vitamin A deficiency may be present.

Vitamin A supplementation reduced the risk of new cases of measles by 50%. However, a Cochrane Review found that vitamin A supplementation did not affect the risk of death due to measles, based on the results from six clinical trials in a total of 1,088,261 children. In a systematic review of RCTs, stratifying the analysis by vitamin A treatment dose, at least two doses of 200,000 IU for children ≥1 year of age and 100,000 IU for infants was found to reduce measles mortality by 62% (RR 0.38; 95% CI 0.18–0.81). Evidence strength for measles incidence reduction is strong; the mortality reduction evidence is mixed and dose-dependent.

4.4 Tuberculosis

A randomized controlled trial of vitamin A supplementation enrolled 85 South African children with TB who were not co-infected with HIV. Children were given either 200,000 IU of retinyl palmitate or placebo on day 0 and day 1, then followed up during three months of conventional anti-TB therapy. Nearly two-thirds of the patients were vitamin A-deficient at the beginning of the study. Vitamin A status improved in both groups, but supplementation had no significant effect on treatment outcome. Evidence in this area remains limited and inconclusive.

4.5 Vision and Ocular Health

The role of retinyl palmitate in restoring and maintaining vision in deficient populations is well established. One of retinol's primary roles is in vision: retinol is oxidized to retinal, which is crucial for the formation of rhodopsin, a pigment in the retina responsible for low-light vision. In a clinical trial context, children with vitamin A deficiency defined by abnormal eye cytology reverted to normal eye cytology at rates of 51.2% (retinyl palmitate group) and 50.0% (beta-carotene group) seven weeks after supplementation.

An NIH clinical study has also investigated vitamin A palmitate supplementation in patients with reticular pseudodrusen (RPD) and delayed dark adaptation, examining whether it could improve scotopic (dark-adapted) visual function. This area remains actively under investigation; results from such trials are not yet fully reported in the published record.

4.6 Immune Function and Vaccination Response

Pre-clinical studies have revealed that vitamin A deficiency impairs mucosal IgA-producing antibody forming cell (AFC) responses toward a paramyxovirus vaccine in the upper respiratory tract, impeding a first line of defense at the pathogen's point of entry. In a mouse model, oral doses of either retinyl palmitate or retinoic acid administered on days 0, 3, and 7 relative to vaccination rescued IgA-producing AFC responses that were significantly reduced following vaccination in vitamin A-deficient animals. These findings are from animal studies; human clinical translation remains preliminary.

In a small human RCT at St. Jude Children's Research Hospital: researchers performed a study of healthy children 1–4 years of age. Participants received a booster pneumococcus vaccine and a hepatitis A vaccine with or without an oral supplement of 10,000 IU retinyl palmitate. There were 20 evaluable participants enrolled, limiting statistical power. This study was small and exploratory.

4.7 Skin and Anti-Aging (Topical Use)

Retinyl palmitate, a more stable esterified form of retinol, is considered as an alternative to retinol and is used as an active ingredient in pharmaceuticals and cosmetics as an effective anti-aging agent.

In vitro / preclinical evidence: In a study published in Frontiers in Pharmacology (2023): immunofluorescence assay demonstrates that retinyl palmitate can reduce collagen degradation in skin cells by UVB radiation and reduce apoptosis of skin cells. Cell migration assay reveals that it can increase cell migration rate, helping to repair skin damage and restore cell viability. Immunohistochemical assays indicate that it can significantly reduce the expression of IL-6, IL-1β, and TNF-α induced by UVB radiation. Metabolomics and transcriptomics results suggest that it regulates several metabolic pathways and gene expression, particularly in inflammatory signaling pathways, collagen synthesis, and apoptosis. These findings are from cell and tissue models, not clinical trials.

Clinical/human evidence: The clinical evidence base for retinyl palmitate in topical anti-aging specifically is less robust than for tretinoin (retinoic acid). Physiologically, it is credited with increasing epidermal thickness, stimulating the production of more epidermal protein, and increasing skin elasticity. Cosmetically, retinyl palmitate is used to reduce the number and depth of fine lines and wrinkles, and to prevent skin roughness resulting from UV exposure. These claims derive largely from extrapolation from retinoic acid studies and limited clinical trials. Overall, clinical evidence for retinyl palmitate as an anti-aging agent is considered weaker than for prescription-strength retinoids.

4.8 Cancer — Lung Cancer Risk in High-Risk Populations

One of the most consequential areas of clinical evidence concerns the CARET trial. The CARET trial showed that supplementation with a large amount of beta-carotene (30 mg/day) plus 7,500 mcg RAE (25,000 IU)/day retinyl palmitate for 4–8 years in current and former smokers as well as some men occupationally exposed to asbestos increased the risk of lung cancer and death from lung cancer. The study randomized participants to take supplements containing 30 mg beta-carotene plus 25,000 IU (7,500 mcg RAE) retinyl palmitate or a placebo daily for about 6 years to evaluate the potential effects on lung cancer risk. The trial was ended prematurely after a mean of 4 years, partly because the supplements were unexpectedly found to have increased risk.

The CARET and ATBC study results suggest that large supplemental doses of beta-carotene with or without retinyl palmitate have detrimental effects in current or former smokers and workers exposed to asbestos. However, other studies that used similar vitamin A doses but had smaller proportions of current or former smokers do not raise this concern. Among nonsmokers, beta-carotene and vitamin A supplements do not appear to affect the risk of cancer.

In contrast, vitamin A palmitate supplementation alone has not been associated with a higher risk of lung cancer in tobacco-based trials. The risk observed in CARET appears to be attributable to the combination of high-dose beta-carotene with retinyl palmitate in smokers, not to retinyl palmitate independently.

Studies in cell culture and animal models have documented the capacity for natural and synthetic retinoids to reduce carcinogenesis significantly in skin, breast, liver, colon, prostate, and other sites. However, the results of human studies examining the relationship between the consumption of preformed vitamin A and cancer do not currently suggest that consuming vitamin A at intakes greater than the RDA benefits cancer prevention.

4.9 Photocarcinogenicity Controversy (Topical Use in Sunscreens)

A study by the National Toxicology Program (NTP), known as the "Photocarcinogenesis study of retinoic acid and retinyl palmitate in SKH-1 mice," involved treating the skin of hairless mice with retinyl palmitate and exposing them to simulated sunlight. The findings indicated that mice treated with retinyl palmitate developed significantly more skin tumors compared to a control group exposed only to simulated sunlight without the ingredient.

Despite previous concerns about the cancer-causing potential of sunscreens containing retinyl palmitate, an independent analysis published in the Journal of the American Academy of Dermatology determined that there is no evidence that the inclusion of retinyl palmitate in sunscreens can cause cancer in humans. Although there are no published human studies on the potential of retinyl palmitate or other retinoids to cause cancer, observations from decades of clinical practice do not support the notion that retinyl palmitate in sunscreen causes or promotes skin cancer.

In vitro experiments show that retinyl palmitate breaks down with UV exposure to form reactive oxygen species. These can damage cellular structures like DNA, leading to oxidative stress, which is one of the ways skin cancer can form. However, regulatory bodies in Europe and the United States have reviewed this evidence. The European Commission's Scientific Committee on Consumer Safety (SCCS), in its 2022 report, again concluded that retinyl palmitate posed no safety concerns in sunscreens. The overall evidence on topical photocarcinogenicity in humans remains limited to animal and in vitro studies; no clinical human evidence of harm has been established.

5. Body Systems Associated with Palmitate

• Visual system: Retinol is oxidized to retinal, which is crucial for the formation of rhodopsin, a pigment in the retina responsible for low-light vision. Night blindness and xerophthalmia are the hallmark manifestations of vitamin A deficiency.
• Immune system: Vitamin A derivatives serve essential roles in maintenance of the immune system.
• Epithelial and skin tissues: Vitamin A derivatives are essential for protection of epithelial tissues.
• Reproductive system and embryogenesis: Vitamin A derivatives are essential for embryonic growth and development.
• Liver (storage): Because vitamin A is fat soluble, the body stores excess amounts primarily in the liver, and these levels can accumulate.
• Cell nucleus (gene regulation): Retinoic acid modulates gene expression by binding to nuclear receptors (RARs and RXRs), which regulate transcription of genes involved in cell proliferation, differentiation, and apoptosis.
• Cardiovascular system (palmitic acid component): It is well accepted in the medical community that palmitic acid from dietary sources raises low-density lipoprotein (LDL) and total cholesterol. The World Health Organization has stated there is convincing evidence that palmitic acid increases cardiovascular disease risk.

6. Dosage Forms and Dosages Reported in Studies

6.1 Oral Supplementation Dosages in Clinical Research

• Studies have shown that doses between 100,000–400,000 IU vitamin A are associated with significant protection from morbidity and mortality in children with measles.
• The WHO recommends an oral dose of vitamin A of 200,000 IU (or 100,000 IU in infants) each day for two days to children with measles in areas where vitamin A deficiency may be present.
• The majority of trials (42/47) in the Cochrane review administered large doses of vitamin A ranging from 50,000 IU to 200,000 IU, with retinol palmitate most commonly used.
• A South African pediatric TB trial administered 200,000 IU of retinyl palmitate on day 0 and day 1.
• A small RCT at St. Jude Children's Research Hospital used 10,000 IU retinyl palmitate as an oral supplement co-administered with vaccines in children aged 1–4 years.
• A study of pharmacokinetic metabolites over 20 days in adult men who received vitamin A at doses equivalent to 50,000 IU found these doses consumed over this length of time did not lead to hypervitaminosis A.
• The CARET trial used 25,000 IU (7,500 mcg RAE) retinyl palmitate daily (in combination with 30 mg beta-carotene) for approximately 6 years.

6.2 Topical Concentrations

• In the NTP photocarcinogenesis animal study, mice received topical applications of 0.1%, 0.5%, 1.0%, or 2.0% retinyl palmitate.
• Retinyl palmitate is used as a constituent of intraocular treatment for dry eyes at a concentration of 138 μg/g.

6.3 Established Dietary Reference Values

The recommended daily allowance (RDA) for vitamin A is measured in retinol activity equivalents (RAE) to account for the different bioactivities of retinol and provitamin A carotenoids. Notably, 1 RAE is equivalent to 1 mcg of retinol or 3 International Units (IU). The upper limits apply exclusively to preformed vitamin A (retinyl palmitate, retinyl acetate, retinol). Beta-carotene from food has no established Tolerable Upper Intake Level (UL) because the body regulates its conversion to retinol.

7. Safety Considerations and Interactions

7.1 Hypervitaminosis A and Acute Toxicity

The condition caused by vitamin A toxicity is called hypervitaminosis A. It is caused by overconsumption of preformed vitamin A, not carotenoids. Acute vitamin A toxicity, also referred to as hypervitaminosis A, occurs within days to weeks after someone ingests one or a few very high doses (typically more than 100 times the RDA). Retinyl palmitate is a pre-formed version of vitamin A; therefore, intake should not exceed the Recommended Dietary Allowance. Overdosing on preformed vitamin A forms, such as retinyl palmitate, leads to adverse physiological reactions (hypervitaminosis A).

Acute toxicity from a single dose has been documented at approximately 350,000 Units in infants and over 2 million Units in adults. Chronic toxicity occurs at approximately 4,000 Units/kg body weight for 6 to 15 months in infants.

The effects of chronic high-dose vitamin A toxicity may include hepatomegaly, elevated blood lipid levels, bone changes, and increased intracranial pressure.

7.2 Hypercalcemia with Prolonged High-Dose Use

A case series reviewed adult patients with ≥20% total body surface area burns who received vitamin A 25,000 units thrice weekly for more than 2 weeks. Of 25 included patients, 9 patients (36%) developed hypercalcemia. Patients with hypercalcemia had significantly longer courses of vitamin A (56 vs 27 days, p=0.03) as well as longer length of stay. All improved with cessation of vitamin A supplementation. This observation underscores that prolonged high-dose administration carries meaningful clinical risk.

7.3 Teratogenicity

The key role of retinoic acid in embryonic development mediates the high teratogenicity of retinoid pharmaceuticals. Oral megadoses of preformed vitamin A (retinyl palmitate) and retinoic acid itself also have teratogenic potential by this same mechanism. Studies show there may be a possible risk of teratogenicity in a fetus when a participant of childbearing potential consumes high doses (i.e., >10,000 IU/day) of preformed vitamin A palmitate. There have been reports of malformations in children when their mothers consumed high doses (>25,000 IU/day) of preformed vitamin A during pregnancy.

Retinyl palmitate is a known laboratory animal teratogen inducing abnormalities of the second visceral arch when administered on day 9 of gestation in the rat. However, there are significant problems when attempting to extrapolate this result to the human.

7.4 Injectable Route Risk

Anaphylactic shock and death have been reported using the intravenous route of vitamin A palmitate administration. Allergic reactions have been reported rarely with administration of Aquasol A Parenteral, including one case of an anaphylactoid type reaction.

7.5 Drug Interactions

Isotretinoin (Accutane) should never be combined with vitamin A supplements of any kind, as both are vitamin A derivatives and combined use causes additive toxicity. Orlistat (Xenical/Alli) blocks fat absorption, significantly reducing vitamin A uptake.

Certain dermatological medications, such as isotretinoin, contain analogs of vitamin A. Prolonged or excessive usage of these medications can lead to an accumulation of vitamin A stores, resulting in hypervitaminosis A, toxicity, and teratogenic effects.

7.6 Cardiovascular Risk of Dietary Palmitic Acid

The palmitate moiety, as the free fatty acid palmitic acid consumed from dietary sources, carries its own established cardiovascular risk profile. It is well accepted in the medical community that palmitic acid from dietary sources raises low-density lipoprotein (LDL) and total cholesterol. The World Health Organization has stated there is convincing evidence that palmitic acid increases cardiovascular disease risk. However, this risk profile applies to dietary palmitic acid consumed as a saturated fat in foods, not to the trace palmitate moiety present in retinyl palmitate supplements.

7.7 Smokers and High-Risk Populations

The CARET and ATBC study results suggest that large supplemental doses of beta-carotene with or without retinyl palmitate have detrimental effects in current or former smokers and workers exposed to asbestos. Current guidelines advise special caution in these populations when using high-dose preformed vitamin A supplements.

References

• NIH Office of Dietary Supplements — Vitamin A and Carotenoids: Health Professional Fact Sheet
• Wikipedia — Retinyl Palmitate
• Wikipedia — Palmitic Acid
• DrugBank — Vitamin A Palmitate (DBSALT000855)
• NIST WebBook — Vitamin A Palmitate (CAS 79-81-2)
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• PMC — Oral Retinyl Palmitate or Retinoic Acid Corrects Mucosal IgA Responses Toward an Intranasal Influenza Virus Vaccine in Vitamin A Deficient Mice
• PMC — Efficacy and Mechanism of Retinyl Palmitate Against UVB-Induced Skin Photoaging
• Frontiers in Pharmacology — Efficacy and Mechanism of Retinyl Palmitate Against UVB-Induced Skin Photoaging
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• Journal of the American Academy of Dermatology — Safety of Retinyl Palmitate in Sunscreens: A Critical Analysis
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• PMC — Cost-effectiveness of Vitamin A Supplementation Among Children in Sub-Saharan Africa
• PMC — Reevaluating Vitamin A for Measles Management in High-Income Settings