Carotenoid
Introduction
Section titled “Introduction”Carotenoids are a diverse group of naturally occurring pigments synthesized by plants, algae, and photosynthetic bacteria. Humans and animals cannot synthesize carotenoids de novo, thus they must obtain these essential compounds through their diet.[1]They are responsible for the vibrant red, orange, and yellow hues found in many fruits and vegetables. The six carotenoids most abundant in human serum include beta-carotene, alpha-carotene, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin.[1]
Biological Basis
Section titled “Biological Basis”Biologically, carotenoids serve crucial functions in the human body. Many carotenoids act as precursors to vitamin A, which is vital for vision, immune response, and cellular differentiation.[1]Additionally, they possess antioxidant properties, helping to protect cells from damage.[1] The body’s circulating levels of carotenoids are influenced by numerous factors beyond dietary intake, including absorption, digestion, transportation, storage, chemical transformation, and excretion.[1] Genetic variations can significantly affect these processes. For instance, the BCMO1(beta-carotene 15,15’-monooxygenase 1) gene plays a key role in catalyzing the first step of converting dietary provitamin carotenoids into vitamin A.[1] Studies have shown that common genetic polymorphisms near the BCMO1gene are associated with substantial and significant increases in antioxidant carotenoid plasma levels.[1]
Clinical Relevance
Section titled “Clinical Relevance”Understanding individual carotenoid levels is of significant clinical relevance. Observational studies have linked high circulating carotenoid concentrations to protection against age-related declines in muscle strength, physical and cognitive disability, and chronic morbidity.[1] Conversely, low plasma levels of carotenoids are associated with an increased risk of chronic diseases and disability.[1]Genetic variants affecting carotenoid levels can be utilized in Mendelian randomization studies to explore the causal relationships between carotenoid status and various health outcomes.[1] Methods such as High-Performance Liquid Chromatography (HPLC) are commonly used to simultaneously determine concentrations of various carotenoids, retinol, and tocopherols in plasma or serum.[2]
Social Importance
Section titled “Social Importance”The ability to accurately assess carotenoid levels and understand the genetic factors influencing them holds considerable social importance. It contributes to a deeper understanding of personalized nutrition, allowing for tailored dietary recommendations and supplementation strategies based on an individual’s genetic predisposition and metabolic efficiency. This knowledge can also inform public health initiatives aimed at preventing chronic diseases and promoting healthy aging, ultimately enhancing overall well-being across populations.
Methodological and Statistical Considerations
Section titled “Methodological and Statistical Considerations”The initial genome-wide association study (GWAS) relied on a discovery cohort of 1191 participants, which, while substantial, may limit the statistical power to detect all genetic associations, particularly those with smaller effect sizes.[1]This could lead to an underestimation of the full genetic architecture influencing carotenoid levels. Furthermore, the phenotype itself, circulating carotenoid levels, is subject to considerable inter-individual variability in response to standardized intake, reflecting complex physiological processes such as absorption, digestion, and metabolism.[1] While various data transformations were employed to ensure statistical assumptions were met.[1] the use of different assay methodologies across various cohorts could introduce potential variability that necessitates careful standardization during analysis.[3] For specific carotenoids like lutein and zeaxanthin, the inability to separate them in some baseline assays means that distinct genetic or environmental influences on each compound might be obscured in certain analyses, limiting the precision of findings.[1]
Generalizability and Population Specificity
Section titled “Generalizability and Population Specificity”A significant limitation stems from the demographic characteristics of the primary study population. The discovery cohort, InCHIANTI, comprised exclusively individuals of European ancestry from a specific region in Italy.[1]While replication efforts were made in other cohorts, the findings may not be broadly generalizable to populations of different ancestral backgrounds. Genetic variants and their functional consequences can vary considerably across diverse ethnic groups, implying that the identified associations with carotenoid levels might not be universally applicable.[1]This highlights the ongoing need for research in more diverse populations to fully characterize the genetic determinants of carotenoid levels worldwide.
Complex Biological and Environmental Influences
Section titled “Complex Biological and Environmental Influences”The regulation of circulating carotenoid levels is a complex biological process, influenced by numerous factors beyond genetics, including dietary intake, lifestyle, and a multitude of physiological mechanisms such as absorption, transport, storage, and excretion.[1] Although the analyses accounted for basic demographic covariates like age and sex.[1] the potential impact of unmeasured environmental or gene–environment confounders remains. These uncharacterized interactions could significantly influence the observed genetic associations and complicate the comprehensive interpretation of results.
Despite the identification of significant genetic associations, a substantial portion of the variability in carotenoid levels remains unexplained, pointing to a “missing heritability” component. This could be attributed to genetic factors with smaller individual effects, rare variants, complex epistatic interactions, or the predominant role of unmeasured environmental factors.[1]The current understanding of the complete genetic and environmental regulation of carotenoid metabolism is still evolving, and future studies, potentially employing advanced methods like Mendelian randomization, are crucial for elucidating the causal directions and broader biological implications of these genetic findings.[1] The absence of certain candidate genes in the top hits does not preclude their role, suggesting that current GWAS methodologies may not capture all genetic influences, especially those with subtle effects.[3]
Variants
Section titled “Variants”Genetic variations in genes involved in carotenoid metabolism and broader metabolic pathways can significantly influence circulating levels of various carotenoids. Among these, variants near theBCMO1 gene play a central role, while others, such as those associated with PKD1L2, RNU2-54P, and LINC01111, may exert their effects through related physiological processes like lipid transport or gene regulation. Understanding these genetic influences is crucial for interpreting individual differences in carotenoid and their potential health implications.
The BCMO1 (beta-carotene 15,15’-monooxygenase 1) gene encodes an enzyme that performs the critical first step in converting dietary provitamin A carotenoids, such as beta-carotene, into retinol (vitamin A).[1]The single nucleotide polymorphism (SNP)rs6564851 , located in a region on chromosome 16 that includes the PKD1L2 gene and is positioned upstream of BCMO1, is strongly associated with circulating carotenoid levels.[1] Specifically, the G allele of rs6564851 is linked to significantly higher plasma beta-carotene levels, along with increased alpha-carotene and lower levels of lutein, zeaxanthin, and lycopene.[1] This pattern suggests that this variant may reduce BCMO1enzymatic activity, leading to decreased conversion of these carotenoids into vitamin A and consequently higher concentrations of the unconverted forms in the bloodstream.[1] Other variants, such as rs9708919 and rs12926540 , are also located in genomic regions that may influence carotenoid levels, often through their impact on broader metabolic processes. While not directly detailed in the context, these SNPs can be associated with thePKD1L2 (Polycystic kidney disease 1-like 2) gene, which is situated near BCMO1.[1] PKD1L2 is involved in calcium signaling and mechanosensation, and variants within or near it could potentially affect gene regulation or be in linkage disequilibrium with other functional variants that impact lipid transport, absorption, or the overall bioavailability of fat-soluble compounds like carotenoids.[1] Such indirect mechanisms can modulate the efficiency with which the body handles dietary carotenoids, thereby influencing their plasma concentrations.
Furthermore, variants like rs75226183 are associated with non-coding RNA genes such as RNU2-54P (RNA, U2 small nuclear 54, pseudogene) and LINC01111 (Long intergenic non-coding RNA 01111). RNU2-54P is a pseudogene related to a crucial component of the spliceosome, while LINC01111 is a long non-coding RNA, both of which are known to play roles in regulating gene expression.[1] Variations in these non-coding regions, such as rs75226183 , might impact the expression or stability of these regulatory RNAs, which in turn could affect the transcription or translation of genes involved in nutrient metabolism, including those related to carotenoid absorption, transport, or storage.[1]These regulatory effects can contribute to individual variability in circulating carotenoid levels, highlighting the complex genetic architecture underlying these important micronutrient measurements.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs6564851 rs9708919 rs12926540 | PKD1L2 - BCO1 | carotenoid |
| rs75226183 | RNU2-54P - LINC01111 | carotenoid gut microbiome , environmental exposure |
Definition and Biological Significance of Carotenoids
Section titled “Definition and Biological Significance of Carotenoids”Carotenoids are a diverse group of naturally occurring pigments synthesized by plants, algae, and certain microorganisms, which are acquired by humans primarily through dietary intake.[4] These lipophilic compounds play crucial roles in human health, with some, such as beta-carotene, serving as provitamin A carotenoids. The beta-carotene 15,15’-monooxygenase 1 (BCMO1) gene encodes an enzyme that catalyzes the initial step in the conversion of dietary provitamin A carotenoids into retinol, or vitamin A.[1]Beyond their provitamin A activity, circulating carotenoid levels are recognized as valuable biomarkers of dietary intake and are associated with a spectrum of physiological functions.[4]Research highlights their potential significance in various health contexts, including associations with frailty, cognitive function, cardiovascular health, skeletal muscle strength, and offering protection against disability in older individuals.[1]
Classification and Nomenclature of Carotenoid Species
Section titled “Classification and Nomenclature of Carotenoid Species”The study of carotenoids involves the identification and quantification of numerous individual species present in human plasma, serum, or adipose tissue. Commonly measured carotenoids include alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein, zeaxanthin, and lycopene.[1], [2], [5]While not explicitly detailed as a formal classification system in all contexts, these carotenoids can be conceptually categorized based on their chemical structure (e.g., carotenes like beta-carotene, and xanthophylls like lutein) and their provitamin A activity. Due to their shared metabolic pathways and dietary origins, carotenoids are frequently assessed simultaneously with other fat-soluble vitamins, such as retinol (vitamin A) and alpha- and gamma-tocopherols (vitamin E), to provide a comprehensive understanding of an individual’s micronutrient status.[1], [2], [5]
Approaches and Operational Criteria
Section titled “Approaches and Operational Criteria”The established method for precisely quantifying circulating carotenoid levels in biological specimens, such as plasma or serum, is High-Performance Liquid Chromatography (HPLC).[1], [2], [5] This analytical technique is capable of simultaneously determining concentrations of multiple individual carotenoids, alongside retinol and tocopherols. Methodological variations exist, for instance, in the ability to separate and quantify closely related carotenoids like lutein and zeaxanthin.[1], [5]For statistical analyses, especially in large-scale studies, operational definitions often include data transformations for non-normally distributed measures; examples include inverse normal transformation for retinol and log-transformation for alpha-tocopherol.[1], [6] The reliability and precision of these analytical methods are typically documented through within-run and between-run coefficients of variation (CVs), which provide crucial quality control metrics for the accurate assessment of these vital compounds.[1]
Carotenoids: Essential Nutrients and Their Physiological Roles
Section titled “Carotenoids: Essential Nutrients and Their Physiological Roles”Carotenoids are a diverse group of lipid-soluble pigments vital for human health, serving as precursors for vitamin A and playing crucial roles in various biological functions. While plants are capable of synthesizing these compounds de novo, humans must obtain essential carotenoids, such as beta-carotene, alpha-carotene, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin, through their diet.[1] These compounds are integral to the immune response, vision, and cellular differentiation, contributing significantly to overall physiological homeostasis.[1]Beyond their foundational roles, high circulating levels of carotenoids have been associated with protective effects against age-related decline in muscle strength, physical and cognitive disability, and chronic morbidity.[1]Conversely, low plasma levels of carotenoids are linked to an increased risk of chronic diseases and disability, and can correlate with conditions like frailty, poor cognitive function, and a mild pro-inflammatory state often observed in older individuals.[1]This underscores their importance not just as dietary components, but as key modulators of health and disease progression, particularly in aging populations.
Metabolic Pathways and Key Biomolecules
Section titled “Metabolic Pathways and Key Biomolecules”The bioavailability and ultimate physiological impact of dietary carotenoids are governed by complex metabolic pathways involving numerous key biomolecules. Following dietary intake, carotenoids undergo digestion and absorption primarily in the intestine, a process that can vary significantly between individuals.[1]Once absorbed, some provitamin A carotenoids, such as beta-carotene, are cleaved by enzymes to form vitamin A (retinol), a critical process for vision and cellular health.[1] This conversion is predominantly catalyzed by the enzyme beta-carotene 15,15’-monooxygenase 1, encoded by the BCMO1gene, which represents the first committed step in vitamin A synthesis.[1] Beyond conversion, carotenoids are transported throughout the body, often in association with lipoproteins, and stored in various tissues. For instance, the enzyme BCMO1is crucial for maintaining appropriate levels of both carotenoids and vitamin A, as a loss-of-function mutation in this enzyme can lead to hypercarotenemia (high carotenoid levels) and hypovitaminosis A (low vitamin A levels).[7]Furthermore, other lipid-soluble antioxidants like alpha-tocopherol (vitamin E) are also transported in the circulation, with their plasma concentrations potentially influenced by genetic variations in genes such asAPOA5, which plays a role in lipid metabolism, including circulating triglycerides and chylomicrons.[1]
Genetic Regulation of Carotenoid and Vitamin Levels
Section titled “Genetic Regulation of Carotenoid and Vitamin Levels”Genetic mechanisms exert a significant influence on the circulating levels of carotenoids and other dietary antioxidants, explaining why dietary intake often correlates only moderately with plasma concentrations.[1] Genome-wide association studies (GWAS) have successfully identified specific genetic variants associated with these circulating levels. For example, common polymorphisms near the BCMO1gene have been strongly linked to substantial increases in plasma levels of several antioxidant carotenoids.[1] Specifically, the G allele of rs6564851 , located near BCMO1, is associated with significantly higher beta-carotene levels, and other single nucleotide polymorphisms (SNPs) in the same genomic region on chromosome 16 also affect carotenoid concentrations.[1] These genetic variations in BCMO1are likely to impact the efficiency of vitamin A synthesis from provitamin A carotenoids, thereby influencing the balance between circulating carotenoids and their converted products.[1] Similarly, genetic factors influence the levels of other essential lipid-soluble vitamins. A notable example is the SNP rs12272004 , which is highly correlated with the S19W variant in the APOA5gene and significantly affects plasma concentrations of alpha-tocopherol.[1]This genetic effect on alpha-tocopherol is thought to be mediated or confounded by its role in regulating circulating lipids, highlighting the intricate genetic architecture underlying nutrient metabolism and transport.[1]
Tissue Distribution and Systemic Health Consequences
Section titled “Tissue Distribution and Systemic Health Consequences”Carotenoids, once absorbed and metabolized, are distributed throughout various tissues and organs, contributing to systemic health and influencing a range of physiological processes. Plasma and serum are key compartments where these compounds circulate, with specific carotenoids such as beta-carotene, alpha-carotene, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin being the most abundant forms found in human serum.[1] The concentrations of these circulating carotenoids serve as important biomarkers of dietary intake and nutritional status.[4]Beyond their presence in the bloodstream, carotenoids accumulate in various tissues, including adipose tissue, where they can be stored. Their systemic impact is broad, extending to protection against age-related conditions, cardiovascular health, and cognitive performance.[8]For instance, low plasma carotenoid levels have been directly linked to a decline in skeletal muscle strength over time and are considered protective against disability in older persons.[9]Furthermore, adequate levels of carotenoids and alpha-tocopherol in serum have been studied for their potential role in reducing the risk of nonmelanoma skin cancer.[10]This widespread distribution and diverse functional roles underscore the critical importance of maintaining optimal carotenoid levels for long-term health and disease prevention.
Risk Assessment and Prognostic Indicators
Section titled “Risk Assessment and Prognostic Indicators”Measuring circulating carotenoid levels holds significant promise for risk assessment and predicting long-term health outcomes. These levels, particularly in plasma and adipose tissue, serve as objective biomarkers of dietary intake, offering a more stable reflection of an individual’s long-term nutritional status compared to self-reported dietary questionnaires.[4]Studies have indicated that low plasma carotenoid concentrations are associated with a decline in skeletal muscle strength over several years and an increased risk of disability in older populations.[9]highlighting their prognostic value for physical function and healthy aging. Furthermore, plasma carotenoids, including lycopene and beta-carotene, have been investigated for their association with cardiovascular disease risk in men.[11]and the risk of non-melanoma skin cancer.[10] suggesting their utility in identifying high-risk individuals for targeted prevention strategies.
Clinical Applications and Monitoring
Section titled “Clinical Applications and Monitoring”The clinical utility of carotenoid measurements extends to diagnostic applications and guiding personalized health interventions. As objective indicators, they can help identify individuals with suboptimal carotenoid intake, especially in populations where dietary assessment might be challenging or unreliable. While the direct selection of specific treatments based solely on carotenoid levels is still an evolving area, understanding an individual’s genetic profile, such as common polymorphisms near theBCMO1gene that influence circulating carotenoid levels, could enable personalized dietary recommendations.[1] The BCMO1gene, for example, plays a crucial role in converting provitamin carotenoids to vitamin A.[1]impacting overall vitamin A status. Monitoring circulating carotenoid concentrations over time can also assess the effectiveness of nutritional interventions, given that individual responses to carotenoid ingestion can vary considerably.[12]
Associations with Health Conditions and Comorbidities
Section titled “Associations with Health Conditions and Comorbidities”Carotenoid levels are intricately associated with a range of health conditions and comorbidities, emphasizing their broad clinical significance. Research has linked plasma carotenoid levels to cognitive performance in elderly populations.[13]suggesting their potential role in cognitive health. Additionally, low carotenoid status has been observed as a component of frailty.[14] and a protective factor against disability in older persons.[9]underscoring their importance in geriatric medicine. The conversion of provitamin carotenoids to vitamin A, influenced by genes likeBCMO1, is fundamental for preventing conditions such as xerophthalmia, a severe form of vitamin A deficiency.[15] While complex, the relationship between carotenoids and inflammatory states, often present in age-related conditions, is also an area of active investigation.[16] Dissecting the causal directions of these associations, particularly through methods like Mendelian randomization studies, remains a key focus for future research.[1]
Large-scale Cohorts and Longitudinal Investigations
Section titled “Large-scale Cohorts and Longitudinal Investigations”Population studies on carotenoid levels often leverage extensive cohort designs to understand their distribution and temporal patterns across diverse groups. The InCHIANTI study, for instance, was conducted on a representative population in the Tuscany Chianti area, Italy, utilizing a genome-wide association study (GWAS) to identify genetic factors influencing carotenoid and tocopherol levels.[1]This study involved longitudinal measurements, with carotenoid levels assessed at baseline and across 1-year, 3-year, and 6-year follow-up periods, providing insights into long-term stability and changes.[1]Similarly, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) was a large-scale, randomized, double-blind, placebo-controlled intervention trial involving male smokers aged 50–69 from southwestern Finland.[17]This cohort collected fasting blood samples at baseline and stored them for later analysis, allowing for comprehensive investigations into the effects of supplementation on various health outcomes, including cancer incidence.[17]Further longitudinal data comes from studies like the Women’s Health and Aging Study (WHAS), which focused on moderately to severely disabled older women and included carotenoid measurements at baseline and a 1-year follow-up.[7], [18]These large cohorts, often supported by public health initiatives, establish crucial biobanks of biological samples and genetic data, enabling extensive research into the complex interplay between genetic predispositions, environmental factors, and circulating carotenoid concentrations over time.[1]Such studies are foundational for understanding the natural history and determinants of carotenoid levels within populations, forming the basis for subsequent epidemiological and genetic research.
Genetic and Epidemiological Determinants
Section titled “Genetic and Epidemiological Determinants”Epidemiological research has consistently explored the prevalence patterns and incidence rates of various health conditions in relation to circulating carotenoid levels, alongside identifying demographic and genetic correlates. A significant GWAS identified common genetic variants near thebeta-carotene 15,15’-monooxygenase 1 (BCMO1) gene that are strongly associated with substantial increases in plasma levels of antioxidant carotenoids, specifically beta-carotene and lutein.[1] The BCMO1gene plays a critical role in the conversion of provitamin carotenoids, suggesting a genetic predisposition influences an individual’s circulating carotenoid concentrations.[1]Beyond genetics, studies have linked higher carotenoid levels to protective effects against disability in older persons, while higher alpha-tocopherol levels have been associated with protection against disability and frailty in this demographic.[1]Population-level intervention trials, such as the ATBC Study, have investigated the impact of alpha-tocopherol and beta-carotene supplementation on health outcomes like lung cancer incidence in male smokers, demonstrating the potential for both beneficial and adverse effects depending on the context.[17]Furthermore, observational studies have explored associations between serum carotenoids and alpha-tocopherol and the risk of nonmelanoma skin cancer.[10]These epidemiological investigations, often adjusting for demographic factors like age and sex, highlight the complex relationships between dietary intake, genetic background, circulating carotenoid levels, and long-term health outcomes, emphasizing the need for carefully designed studies to dissect causal directions.[1]
Cross-Population Variations and Methodological Approaches
Section titled “Cross-Population Variations and Methodological Approaches”The of carotenoids across different populations has unveiled variations influenced by geographic, ethnic, and demographic factors, while also highlighting the importance of robust methodologies. Studies have compared serum carotenoid and tocopherol levels across diverse groups, such as the representative population in Tuscany, Italy (InCHIANTI study), male smokers in southwestern Finland (ATBC study), and even urban and rural adolescents in Costa Rica for alpha-tocopherol intake.[1]These comparisons reveal how dietary habits and genetic backgrounds inherent to specific populations can lead to distinct circulating carotenoid profiles. For instance, the Jackson Heart Study validated food-frequency questionnaires (FFQs) by demonstrating associations between carotenoid intakes assessed by FFQs and serum carotenoid concentrations in its population.[19] a finding also observed in other elderly populations.[20] Methodologically, the accurate of carotenoids and other fat-soluble vitamins in population studies relies heavily on techniques like High-Performance Liquid Chromatography (HPLC) for serum analysis, which allows for the simultaneous determination of various carotenoids and tocopherols.[1] Researchers carefully address statistical considerations, such as transforming non-normally distributed data or applying inverse normal transformations for specific measures like retinol, to enable meta-analysis across studies using different units.[1]While dietary questionnaires provide valuable insights into intake, their correlation with plasma levels can be moderate for carotenoids and notably poor for alpha-tocopherol, underscoring the need for direct biomarker measurements.[1]The use of covariates such as age, sex, and BMI in statistical models helps to control for confounding factors in large sample sizes, contributing to the representativeness and generalizability of findings, although individual variability in response to carotenoid ingestion remains a known challenge.[1]
Frequently Asked Questions About Carotenoid
Section titled “Frequently Asked Questions About Carotenoid”These questions address the most important and specific aspects of carotenoid based on current genetic research.
1. Why do some people absorb more nutrients from veggies than me?
Section titled “1. Why do some people absorb more nutrients from veggies than me?”Your body’s ability to absorb and utilize carotenoids from food really does vary. Genes, like BCMO1, influence how efficiently you convert these pigments into useful compounds. So, even if you eat the same amount, your unique genetic makeup can lead to different circulating levels in your bloodstream.
2. I eat lots of carrots; why might my beta-carotene levels still be low?
Section titled “2. I eat lots of carrots; why might my beta-carotene levels still be low?”Eating carrots is great, but your body’s circulating carotenoid levels depend on more than just intake. Factors like how well you absorb them, your digestion, and genetic variations in enzymes likeBCMO1, which converts beta-carotene, all play a role. These can affect how much actually makes it into your bloodstream.
3. Can my family’s health history impact my carotenoid levels?
Section titled “3. Can my family’s health history impact my carotenoid levels?”Yes, absolutely. Your family history reflects shared genetics, and specific genetic variations can influence how your body handles carotenoids. For example, common differences near the BCMO1 gene can significantly affect your circulating levels, impacting your overall health risks.
4. Does my ethnic background change how my body uses carotenoids?
Section titled “4. Does my ethnic background change how my body uses carotenoids?”Yes, it can. Research shows that genetic variants influencing carotenoid levels can differ significantly across various ethnic groups. Studies often focus on specific populations, so what’s true for one group might not be universally applicable to your specific background.
5. Why do some people seem to age better, even with similar diets?
Section titled “5. Why do some people seem to age better, even with similar diets?”It’s not just diet; individual differences in carotenoid levels play a big part. People with naturally higher circulating carotenoid concentrations, often due to genetic factors or better absorption, tend to show more protection against age-related declines in physical and cognitive health.
6. Is getting my carotenoid levels tested actually useful for me?
Section titled “6. Is getting my carotenoid levels tested actually useful for me?”Yes, it can be very useful. Knowing your individual carotenoid levels can help guide personalized nutrition and supplementation strategies. It provides insight into your unique metabolic efficiency and genetic predisposition, allowing for more tailored advice to support your health.
7. Can a DNA test tell me if I need more carotenoids?
Section titled “7. Can a DNA test tell me if I need more carotenoids?”A DNA test can reveal genetic variations that influence how your body processes carotenoids, such as those near the BCMO1 gene. This information can indicate if you might be less efficient at converting or maintaining levels, helping to inform personalized dietary or supplementation choices.
8. Does stress affect how many carotenoids my body uses?
Section titled “8. Does stress affect how many carotenoids my body uses?”While the direct link isn’t fully clear, overall lifestyle factors, which include stress, can influence your body’s complex physiological processes like absorption and metabolism. These unmeasured environmental influences could subtly affect your circulating carotenoid levels and how efficiently your body uses them.
9. Why do some people seem to fight off illness better than me?
Section titled “9. Why do some people seem to fight off illness better than me?”Carotenoids are crucial for a strong immune system, partly because many are converted to Vitamin A. If your body’s circulating carotenoid levels are naturally lower, perhaps due to genetics or other factors, you might be at an increased risk of chronic diseases and have a less robust immune response.
10. If I eat healthy, can I overcome my family’s low carotenoid levels?
Section titled “10. If I eat healthy, can I overcome my family’s low carotenoid levels?”Eating healthy is extremely important and can definitely help optimize your carotenoid intake. While genetics do play a significant role in your baseline levels, lifestyle and diet are powerful influences. You can certainly improve your levels, even if you have a genetic predisposition for lower absorption or metabolism.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Ferrucci L, et al. “Common variation in the beta-carotene 15,15’-monooxygenase 1 gene affects circulating levels of carotenoids: a genome-wide association study.” Am J Hum Genet. 2009.
[2] Milne, D.B., and J. Botnen. “Retinol, alpha-tocopherol, lycopene, and alpha- and beta-carotene simultaneously determined in plasma by isocratic liquid chromatography.”Clin. Chem., vol. 32, 1986, pp. 874–876.
[3] Wang, TJ et al. “Common genetic determinants of vitamin D insufficiency: a genome-wide association study.”Lancet, vol. 376, no. 9736, 2010, pp. 181-9.
[4] El-Sohemy, A. et al. “Individual carotenoid concentrations in adipose tissue and plasma as biomarkers of dietary intake.”Am. J. Clin. Nutr., vol. 76, 2002.
[5] Steghens, J.P. et al. “Simultaneous of seven carotenoids, retinol and alpha-tocopherol in serum by high-performance liquid chromatography.”J. Chromatogr. B Biomed. Sci. Appl., vol. 694, 1997, pp. 71–81.
[6] Major, J.M. et al. “Genome-wide association study identifies three common variants associated with serologic response to vitamin E supplementation in men.”J Nutr, 2012.
[7] Lindqvist, A., et al. “Loss-of-function mutation in carotenoid 15,15’-monooxygenase identified in a patient with hypercarotenemia and hypovitaminosis A.”Journal of Nutrition, vol. 137, 2007, pp. 2346–2350.
[8] Voutilainen, S., et al. “Carotenoids and cardiovascular health.”Am J Clin Nutr, vol. 83, no. 5, 2006, pp. 1265-71.
[9] Lauretani, F., et al. “Carotenoids as protection against disability in older persons.” Rejuvenation Res, vol. 11, no. 3, 2008, pp. 557-63.
[10] Dorgan, J. F., et al. “Serum carotenoids and alpha-tocopherol and risk of nonmelanoma skin cancer.”Cancer Epidemiology, Biomarkers & Prevention, vol. 13, 2004, pp. 1276–1282.
[11] Sesso, H.D., et al. “Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in men.”Am J Clin Nutr, vol. 81, no. 5, 2005, pp. 990-7.
[12] Costantino, J.P., et al. “Serum level changes after administration of a pharmacologic dose of beta-carotene.” Am J Clin Nutr, vol. 48, no. 5, 1988, pp. 1277-83.
[13] Akbaraly, N. T., et al. “Plasma carotenoid levels and cognitive performance in an elderly population: Results of the EVA Study.”Journal of Gerontology: Series A, Biological Sciences and Medical Sciences, vol. 62, 2007, pp. 308–316.
[14] Ferrucci, L., et al. “Low nutrient intake is an essential component of frailty in older persons.”J Gerontol A Biol Sci Med Sci, vol. 61, no. 6, 2006, pp. 589-93.
[15] Sommer, A. “Xerophthalmia and vitamin A status.”Prog Retin Eye Res, vol. 17, no. 1, 1998, pp. 9-31.
[16] Di Iorio, A., et al. “Markers of inflammation, vitamin E and peripheral nervous system function: the InCHIANTI study.”Neurobiol Aging, vol. 27, no. 9, 2006, pp. 1280-8.
[17] The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. “The alpha-tocopherol, beta-carotene lung cancer prevention study: design, methods, participant characteristics, and compliance.”Ann. Epidemiol., vol. 4, 1994, pp. 1–10.
[18] Kasper, J.D., et al. “Designing a community study of moderately to severely disabled older women: The women’s health and aging study.”Ann. Epidemiol., vol. 9, 1999, pp. 498–507.
[19] Talegawkar, S.A., et al. “Carotenoid intakes, as-sessed by food-frequency questionnaires (FFQs), are associated with serum carotenoid concentrations in the Jackson heart study: Validation of the Jackson heart study delta NIRI adult FFQs.”Public Health Nutr., vol. 11, 2008, pp. 989–997.
[20] Tucker, K.L., et al. “Carotenoid intakes, assessed by dietary questionnaire, are associated with plasma carot-enoid concentrations in an elderly population.”J. Nutr., vol. 129, 1999, pp. 2118–2126.