Skip to main content
Download PDF
Download ePub

Dietary carotenoid intake and fracture risk based on NHANES 2013–2018 data: a propensity score matching

Journal of Health, Population and Nutrition volume 44, Article number: 119 (2025) Cite this article

Abstract

Introduction

Several epidemiological studies have reported inconsistent findings on the association between carotenoid intake and fracture risk. This study aimed to determine the association between individual carotenoid intake and fracture risk.

Methods

A cross-sectional study based on data from the National Health and Nutrition Examination Survey (NHANES), 2013–2018. This study identified elderly individuals with valid and complete data on carotenoid intake and fracture risk. The average dietary intakes of α-carotene, β-carotene, β-cryptoxanthin, lycopene, and lutein + zeaxanthin was taken based on the two 24-hour recall interviews. Matching was done based on age, sex, and body mass index (BMI). Logistic regression models were used to test the associations between carotenoids and fracture risk. All analyses were performed by using R (version 3.4.3; R Foundation for Statistical Computing, Vienna, Austria).

Results

A total of 5491 (1140 cases and 4351 control) subjects were included in this study. The average age of the subjects was 55.62 ± 14.84 years old. In the adjusted model, the risk of osteoporotic fracture was decreased by 6.2% (odd ratio (OR): 0.938; 95% confidence interval (CI): 0.699 to 0.989) and 1.4% (OR 0.986; 95% CI: 0.975 to 0.997) for dietary intake of beta-carotene and lycopene, respectively.

Conclusions

Dietary intakes of beta-carotene and lycopene have significantly reduced the risk of osteoporotic fracture among the elderly population in the United States of America.

Introduction

Osteoporosis and its related fractures cause increased morbidity, mortality, and reduced quality of life. Osteoporotic fracture is a major health problem in the aging population [1], which is recognized as the cause of morbidity and mortality in the elderly [2,3,4]. The incidence of osteoporosis and related fractures is expected to rise in the world due to the rapidly aging population; these adverse consequences also extend to the growing healthcare expenditures for treating the disease [5,6,7]. Although significant advances have been made in the management of osteoporosis, it is widely recognized that prevention of the disease and its related fractures is essential to reducing risk.

Nutrition is an important modifiable factor influencing bone health [8]. Dietary antioxidant carotenoids have been reported to promote bone formation in experimental studies [9, 10], and to protect against osteoporosis and related fractures in some but not all epidemiological studies [11,12,13,14,15]. Additionally, a dietary lycopene carotenoid was shown to inhibit osteoclast formation in rat bone marrow cultures [16] and was negatively related to bone resorption biomarkers and oxidative stress in postmenopausal women [16, 17]. This indicates that antioxidant carotenoids may counteract the adverse effect of reactive oxygen species in bone turnover, and therefore can potentially protect against osteoporotic fractures.

Numerous studies have been conducted on the association between dietary carotenoid intakes and fracture risk. Some of them found favorable evidence of associations between dietary carotenoid intakes with a low incidence of fractures [12, 18, 19]. In these studies, the findings were inconsistent, the reason may be due to the small number of study participants incorporated into their analysis. This study has several unique characteristics compared to previous studies [12, 18, 19], including the specific population studied, the methodology employed (e.g., propensity score matching), and refinements in our analysis that provide new insights or enhance the existing evidence base. This study aimed to investigate the robust estimates involving large sample size on the potential associations of dietary carotenoid intakes (α-carotene, β-carotene, β-cryptoxanthin, lutein + zeaxanthin, and lycopene) with the risk of osteoporotic fracture based on the National Health and Nutrition Examination Survey (NHANES) 2013–2018.

Method and material

Study setting and design

The National Health and Nutrition Examination Survey (NHANES) is an ongoing cross-sectional and population-based survey conducted to obtain health and nutritional status by the Centers for Disease Control and Prevention of the National Center for Health Statistics. The NHANES is a big dataset that is freely available at www.cdc.gov/nchs/nhanes. This survey is a community-based survey conducted every year. To download and access the survey questionnaires or variables, we used Statistical Analysis System (SAS) (Version 9.1, SAS Institute Inc., Cary, NC) software. The survey uses a complex, multistage, stratified, and clustered design and provides demographic, socio-economic, behavioral, and dietary data on a representative sample of the civilian, non-institutionalized US population (households). Demographic and health history information was collected through extensive household interviews, and standardized physical examinations, including anthropometric, blood pressure, and laboratory measurements, were conducted at mobile examination centers (MEC).

Inclusion and exclusion criteria

In this study, we included all participants with complete and valid data on osteoporotic fracture risk. Individuals were excluded from this study due to the following reasons: (a) Participants younger than 40 years old; (b) Participants with missing or invalid data on alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, and lutein + zeaxanthin; (c) participants with missing or invalid data on prior fracture. Finally, a total of 5491 study subjects were included in this study to investigate the association between carotenoid intake and fracture risk.

Fig. 1
figure 1

Flow chart of sample selection from the NHANES 2013–2018

Full size image

Study variables and covariates

The dependent variable in this study was any fracture risk. The self-reported information on any fracture on the whole body was collected through the method of questionnaires. Covariates included in this study were age, gender, body mass index, smoking status, prior history of hypertension, alcohol use, dietary intake (alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, zeaxanthin, calcium intake, and vitamin D intake), physical activity, and race. Race/ethnicity was categorized as non-Hispanic White (reference), Mexican American, non-Hispanic Black, Hispanic, and others. Physical activity was self-reported for three levels of activity intensity: walking (light intensity), moderate physical activity, and vigorous physical activity. We computed each physical activity as the metabolic equivalent of the task (MET) value per week. One MET is the amount of energy used while sitting quietly. The light intensity uses 1.6-3.0 METs, the moderate intensity uses 3.0–6.0 METs, and the vigorous intensity uses 6.0 + METs. For instance, reading may use about 1.3 METs, while running may use 8–9 METs. The physical activity for each type can be obtained as the product of the weekly time spent in each activity reported by the participant multiplied by the metabolic equivalent of the task (MET) value for that activity. The total MET scores were created by summing the weekly MET values for the three levels [20].

Statistical analysis

In descriptive statistics, continuous variables are presented as the mean ± standard deviation, while categorical variables are presented as the number and percentage of subjects. The logistic regression model was used to test the association between dietary carotenoid intake and fracture risk in the adjusted models. The outcomes considered in the models were the fracture cases.

The magnitude of the association between a risk factor and fracture risk was expressed as an odds ratio (OR) with a 95% CI. Covariates considered in the model were age, gender, body mass index, smoking status, prior history of hypertension, alcohol use, calcium intake, vitamin D intake, and physical activity.

Missing values are often found in data due to various reasons and can occur during the data extraction and data collection processes. Missing value treatment is required to be done on the data before it can be used for statistical analysis because missing values in the data can reduce the power of the model and can make us draw wrong inferences from the model, often leading to wrong predictions and classifications [21]. Therefore, we used generalized mean imputation methods to replace missing values for normally distributed data and the median for skewed datasets in our study for variables with 5% or less missingness [22]. Matching on these variables minimizes confounding and ensures balanced comparisons between groups, as age impacts health risks, sex influences biological and behavioral outcomes, and BMI is a critical risk factor for many health conditions. In this study, we used the generalized mean imputation method for variables such as calcium, weight, height, and age. For skewed variables, such as vitamin D, physical activity, alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, and lutein + zeaxanthin, we used the generalized median imputation method.

To reduce the risk of participant selection bias, we performed propensity score matching (PSM) to balance baseline differences and covariates. For each prior fracture case and non-prior fracture case, a propensity score was calculated to estimate the probability of a prior fracture case using a logistic regression model based on age, sex, and body mass index (BMI) covariates. Although individuals under 40 were excluded, the study was conducted in the USA, where the aging population is very high. Age may still vary significantly within the eligible sample (e.g., 40–80 + years). Including age in propensity score matching accounts for this variability, minimizes residual confounding, and ensures robust comparability between groups, as age often correlates with key health outcomes and risk factors. Propensity score matching was performed using a caliper width equal to 0.25 SD based on the logit model [23]. Age, sex, and body mass index (BMI) were chosen as matching variables because they are well-established factors that influence health outcomes. Age and sex are key demographic variables that affect disease risk, while BMI serves as an important indicator of nutritional status and overall health. Matching on these variables helps reduce potential confounding, ensuring a more accurate comparison between the groups in our study. Matching without replacement and nearest neighbor was used to match each prior fracture case with a non-prior fracture case in a 1:4 ratio (Suppl 1). All analyses were performed using R (version 3.4.3; R Foundation for Statistical Computing, Vienna, Austria).

Results

Characteristics of the study participants

Among the 19,429 participants in NHANES 2013–2018, we excluded 8,209 males and females younger than 40 years old. Individuals with missing or invalid data on alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, and lutein + zeaxanthin (n = 3161) and data on the prior fracture (n = 2568). Finally, 5491 participants were included in the analysis (Fig. 1).

After 1:4 propensity score matching, 1140 subjects with prior fracture cases and 4351 subjects without prior fracture were included in our study from NHANES 2013–2018 (Fig. 1). All baseline characteristics, were well-balanced between the two groups. There were no significant differences between the groups for all baseline characteristics including age, sex, and bone mass index (BMI).

Of the total included subjects, 2609 subjects were men, accounting for 47.51% of the total enrolled population, and 2881 subjects were women, accounting for 52.49%. The average age of the subjects was 55.62 years old. Over 75% of the study population is overweight, with an average body mass index (BMI) greater than 25 kg/m2. Only 21.60% of the study population weighed within the normal range. 44.64% of the study population suffered from hypertension. In the survey population, the majority of the population were never smokers, which accounts for 82.30%; only 17.70% were reported as smokers in this cross-sectional data. Out of the total population in this study, 84.87% were alcohol users, and 15.13% were non-users. The study population was mostly non-Hispanic white (2177 people) followed by non-Hispanic black (1317 people), accounting for 39.65% and 23.98% of the total study subjects respectively. The demographic characteristics of the research participants are shown in (Table 1).

Table 1 Demographic characteristics of the research population of NHANES
Full size table

Table 2 lists the daily calcium, vitamin D intake, and physical activity of the study subjects. The average intake of calcium in the study subjects is 0.89 mg/day/kcal, which is lower than the recommended dietary allowance (reference value) level as per United States guidelines. The median daily intake of vitamin D was 4.00 mg/day/kcal, which is within the reference value of 1 ~ 4. The median duration of physical activity performed was 1.67 h per day. It is within the clinically normal reference value range.

Table 2 Dietary calcium, vitamin D intake, and physical activity per day of the participants
Full size table

Carotenoid intakes among the study subject

In this study, lycopene had the highest average dietary intake among individual carotenoids, which accounts for a median of 2.170 mg/day/kcal. The median dietary intakes of α-carotene, β-carotene, β-cryptoxanthin, and Lutein + zeaxanthin were 0.085, 1.210, 0.041, and 0.885 mg/day/kcal, respectively (Table 3).

Table 3 A dietary carotenoid intake with bone mineral density and fracture risk of the study population
Full size table

Dietary carotenoids and fracture risk

In the multivariate logistic regression model, we included variables such as smoking status, alcohol use, and race. In this analysis, only alcohol use was statistically significant (p < 0.001). For a non-alcohol user, the odds ratio of fracture risk was 0.658 (95% CI: 0.401 to 0.942) compared with the alcohol users. Compared to Mexican Americans, the non-Hispanic white race was associated with a reduction in fracture risk but was not statistically significant.

The relationship between dietary individual carotenoid intake and the risk of fracture was determined using a multiple logistic regression model. The results of this analysis show that dietary beta-carotene and lycopene significantly reduce the risk of fracture. The risk of fracture was decreased by 6.2% (OR: 0.938; 95%CI: 0.699 to 0.989) and 1.4% (OR 0.986; 95%CI: 0.975 to 0.997) for dietary intake of beta-carotene and lycopene, respectively. Moreover, dietary intakes of alpha-carotene, beta-cryptoxanthin, and lutein + zeaxanthin were protective against the risk of fracture but not statistically significant (Table 4).

Table 4 Multivariate logistic regression analysis of osteoporotic fracture risk and related factors
Full size table

Discussion

In this study, we used the NHANES (2013–2018) database to explore whether there was an independent association between dietary carotenoid intake and fracture risk. Using the propensity score, a 1:4 matched cross-sectional study was included, with 1140 prior fracture cases and 4351 non-prior fracture cases. Dietary beta-carotene and lycopene intake decreased the risk of fracture by 6.2% and 1.4%, respectively. This indicates that dietary beta-carotene intake played a significant role in the protection of bone fracture risk, independent of bone mineral density.

Several studies have investigated the relationship between carotenoid intake and fracture risk [12, 19, 24,25,26,27,28,29], with varying results. While some research supports a protective role of carotenoids in bone health, others, particularly certain case-control [27,28,29] and cohort studies [12, 19], have not observed a significant association. Recent prospective studies have highlighted those dietary total carotenoids and specific carotenoid such as α-carotene, β-carotene, and lutein/zeaxanthin are associated with a reduced risk of hip fracture in men but not in women [18, 28]. For instance, men with the highest quartile (Q4) of carotenoid intake had a 26–39% lower risk of hip fracture compared to those in the lowest quartile (Q1) (HR range: 0.61–0.74, all p < 0.05). Additionally, Zhang et al. [28] found a dose-response relationship between β-carotene intake and a reduced risk of osteoporotic hip fracture, particularly among ever-smokers in the elderly Utah population. Our study aligns with these findings, as we observed an inverse association between β-carotene intake and fracture risk, independent of bone mineral density (BMD).

β-carotene intake has been linked to improved bone health markers. In postmenopausal women, dietary β-carotene was positively associated with femur neck BMD (β = 0.0012, p = 0.035), supporting the hypothesis that carotenoids contribute to bone strength. Chen et al. [30] further reported a favorable association between β-carotene (a primary source of dietary vitamin A) and BMD, which is consistent with multiple studies [11,12,13,14]. In the Framingham Osteoporosis Study [12], a higher intake of β-carotene (mean intake: 4.77 mg/day in females, 3.89 mg/day in males) was linked to reduced BMD loss (P-trend = 0.02). moreover, a systematic review also suggested that adequate vitamin A intake, whether from dietary sources or supplements, is essential for maintaining bone health [31], indirectly affecting fracture risk. These findings collectively indicate that β-carotene and other carotenoids play a role in reducing bone loss and potentially lowering fracture risk, though further studies are needed to confirm these associations across different populations and study designs.

Our study found an inverse association between dietary intake of lycopene and β-cryptoxanthin and the risk of fracture in both men and women. This finding aligns with previous research, particularly the study by Sahni et al. [12], which demonstrated that higher intakes of total carotenoids and lycopene were inversely related to the risk of hip fracture. However, Sahni et al. [12] reported that other specific carotenoids did not show a significant association with fracture risk, suggesting that the protective effects of carotenoids may vary depending on the type of carotenoid and its role in bone metabolism.

Our finding of an inverse association between the dietary intake of lycopene and the risk of fracture in men and women is consistent with the previously reported study [12]. Sahni et al. [12] demonstrated that intakes of total carotenoids and lycopene (but not other specific carotenoids) were inversely related to the risk of hip fracture. In contrast to our findings, recent in vitro and in vivo experimental studies suggest that dietary intakes of β-cryptoxanthin have a beneficial effect on bone metabolism [10, 32, 33], in which β-cryptoxanthin enhanced the calcium content and alkaline phosphatase activity in the femoral-diaphyseal and femoral-metaphyseal tissues of young rats at physiologically low concentrations in vitro [10]. Furthermore, they found a stimulatory effect on bone formation and an inhibitory effect on bone resorption in tissue culture [32]. The in vivo study found that the oral administration of β-cryptoxanthin caused a significant increase in the calcium content and alkaline phosphatase activity in the femoral-diaphyseal and femoral-metaphyseal tissues [33].

There are potential biological mechanisms that show an inverse association between dietary carotenoids and bone health. Some of the mechanisms are: dietary intakes of carotenoids may reduce oxidative stress levels in the body by scavenging singlet oxygen and peroxyl radicals. Antioxidants can suppress the expression of the receptor activator of NF-kB ligand (RANKL) and thus suppress osteoclastic differentiation [34], promote osteoblast mineralization [35], and stimulate the alkaline phosphatase activity of osteoblasts [36]. A sufficient intake of vitamin A including beta-carotene is essential for normal physiological activities [37] by affecting the growth hormone axis [38, 39]. In vitro and in vivo studies suggest that antioxidant intakes contribute to a body’s defense against reactive oxygen species [35]. In addition, antioxidant seem to be a reactive oxygen species that enhance osteoclast genesis and reduce osteoblast apoptosis by stabilizing the β-catenin signaling pathway, which leads to a decrease in bone resorption [40,41,42]. Another mechanism is that carotenoids may interfere with growth factor receptor signaling by regulating IGF-1/IGFBP3, which are associated with cognitive function [43], and impaired cognitive function is a known risk factor for falls and hip fractures [44]. Therefore, dietary carotenoids would have great benefits in protecting bone fragility and its consequent osteoporotic fractures.

Our analysis has several strengths. First, in this study, we used propensity score matching to balance between fracture cases and non-fracture cases to avoid any influence of the baseline characteristics of the included participants. Second, a wide range of potential confounders was adequately adjusted to ensure an independent association between dietary carotenoid intake and fracture risk. Also, a large sample size was used to represent the general US adult population.

This study has some limitations: Our cross-sectional design allows us to identify associations between dietary carotenoid intake and fracture risk, but it does not permit causal inferences. Future research employing longitudinal or experimental designs is recommended to better elucidate this relationship. In future studies, employing longitudinal or experimental designs could help better address potential confounders and establish more robust causal relationships. In the extracted data, a small number of hip and vertebral fracture cases were found. Therefore, we have not analyzed the effects of dietary carotenoid intakes on those fracture risks. Secondly, there were too many missing values for different covariates in the NHANES 2013–2018 database. Due to this. our analysis did not include lifestyle and other factors.

In conclusion: in this study, we found that dietary intakes of beta-carotene and lycopene have significantly reduced the risk of fracture among the elderly population in the United States of America.

Data availability

This study is based on publicly available data from the NHANES website: https://wwwn.cdc.gov/nchs/nhanes/.

References

  1. Danielson L, Zamulko A, Osteoporosis A, Review SD, Med. 2015. 68(11): pp. 503–5, 507–9.

  2. Cummings SR, Melton LJ. Epidemiology and outcomes of osteoporotic fractures. Lancet. 2002;359(9319):1761–7.

    Article  PubMed  Google Scholar 

  3. Bentler SE, et al. The aftermath of hip fracture: discharge placement, functional status change, and mortality. Am J Epidemiol. 2009;170(10):1290–9.

    Article  PubMed  PubMed Central  Google Scholar 

  4. Farahmand BY, et al. Survival after hip fracture. Osteoporos Int. 2005;16(12):1583–90.

    Article  PubMed  Google Scholar 

  5. Ioannidis G, Papaioannou A, Hopman WM, Akhtar-Danesh N, Anastassiades T, Pickard L, et al. Relation between fractures and mortality: results from the Canadian multicentre osteoporosis study. Can Med Assoc J. 2009;181(5):265–71.

    Article  Google Scholar 

  6. Tarride JE, Hopkins RB, Leslie WD, Morin S, Adachi JD, Papaioannou A, et al. Burd Illn Osteoporos Can Osteoporos Int. 2012;23(11):2591–600.

    Article  Google Scholar 

  7. Wiktorowicz ME, Goeree R, Papaioannou A, Adachi JD, Papadimitropoulos E. Economic implications of hip fracture: health service use, institutional care and cost in Canada. Osteoporos Int. 2001;12:271–8.

    Article  CAS  PubMed  Google Scholar 

  8. Mitchell PJ, et al. Life-course approach to nutrition. Osteoporos Int. 2015;26(12):2723–42.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Kim L, Rao RA. Lycopene II–effect on osteoblasts: the carotenoid lycopene stimulates cell proliferation and alkaline phosphatase activity of SaOS-2 cells. J Med Food. 2003;6:79–86.

    Article  CAS  PubMed  Google Scholar 

  10. Yamaguchi M. Effect of carotenoid on calcium content and alkaline phosphatase activity in rat femoral tissues in vitro: the unique anabolic effect of beta-cryptoxanthin. Biol Pharm Bull. 2003;26:1188–91.

    Article  CAS  PubMed  Google Scholar 

  11. Maggio D, et al. Low levels of carotenoids and retinol in involutional osteoporosis. Bone. 2006;38(2):244–8.

    Article  CAS  PubMed  Google Scholar 

  12. Sahni S, et al. Inverse association of carotenoid intakes with 4-y change in bone mineral density in elderly men and women: the Framingham osteoporosis study. Am J Clin Nutr. 2009;89(1):416–24.

    Article  CAS  PubMed  Google Scholar 

  13. Sugiura M, et al. Bone mineral density in post-menopausal female subjects is associated with serum antioxidant carotenoids. Osteoporos Int. 2008;19(2):211–9.

    Article  CAS  PubMed  Google Scholar 

  14. Sugiura M, et al. High serum carotenoids associated with lower risk for bone loss and osteoporosis in postmenopausal Japanese female subjects: prospective cohort study. PLoS ONE. 2012;7(12):e52643.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Yang Z, Penniston ZZ, Binkley KL, Tanumihardjo N. Serum carotenoid concentrations in postmenopausal women from the united States with and without osteoporosis. Int J Vitam Nutr Res. 2008;78:105–11.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Rao LG, Banasikowska KN, Rao K. Lycopene I–effect on osteoclasts: lycopene inhibits basal and parathyroid hormone-stimulated osteoclast formation and mineral resorption mediated by reactive oxygen species in rat bone marrow cultures. J Med Food. 2003;6:69–78.

    Article  CAS  PubMed  Google Scholar 

  17. Mackinnon ES, Josse RA, Rao RG. Supplementation with the antioxidant lycopene significantly decreases oxidative stress parameters and the bone resorption marker N-telopeptide of type I collagen in postmenopausal women. Osteoporos Int. 2011;22:1091–101.

    Article  CAS  PubMed  Google Scholar 

  18. Dai Z, Ang WR, Low LW, Yuan YL, Koh JM. Protective effects of dietary carotenoids on risk of hip fracture in men: the Singapore Chinese health study. J Bone Min Res. 2014;29:408–17.

    Article  CAS  Google Scholar 

  19. Ambrosini GL, et al. No dose-dependent increase in fracture risk after long-term exposure to high doses of retinol or beta-carotene. Osteoporos Int. 2013;24(4):1285–93.

    Article  CAS  PubMed  Google Scholar 

  20. F ATB. Development of the world health organization global physical activity questionnaire (GPAQ). J Public Health. 2006;14:66–70.

    Article  Google Scholar 

  21. Mundfrom DJaW. Imputing missing values: the effect on the accuracy of classification. Multiple Linear Regres Viewpoints. 1998;25(1):13–9.

    Google Scholar 

  22. Bramer M. Principles of Data Mining. England: London Limited, 2007.

  23. C AP. Optimal caliper widths for propensity score matching when estimating differences in means and differences in proportions in observational studies. Pharm Stat. 2011;10:150–61.

    Article  Google Scholar 

  24. Ambrosini GL, et al. Plasma retinol and total carotenes and fracture risk after long-term supplementation with high doses of retinol. Nutrition. 2014;30(5):551–6.

    Article  CAS  PubMed  Google Scholar 

  25. Feskanich D, et al. Vitamin A intake and hip fractures among postmenopausal women. JAMA. 2002;287(1):47–54.

    Article  CAS  PubMed  Google Scholar 

  26. Hayhoe RPG, Marleen AH, Lentjes., Angela A, Mulligan., Robert NL, Kay-Tee K, Ailsa A, Welch. Carotenoid dietary intakes and plasma concentrations are associated with heel bone ultrasound Attenuation and osteoporotic fracture risk in the European prospective investigation into cancer and nutrition (EPIC)-Norfolk cohort. Br J Nutr. 2017;117:1439.– 1453.

    Article  CAS  PubMed  Google Scholar 

  27. Sun LL, et al. Associations between the dietary intake of antioxidant nutrients and the risk of hip fracture in elderly Chinese: a case-control study. Br J Nutr. 2014;112(10):1706–14.

    Article  CAS  PubMed  Google Scholar 

  28. Zhang J, et al. Antioxidant intake and risk of osteoporotic hip fracture in Utah: an effect modified by smoking status. Am J Epidemiol. 2006;163(1):9–17.

    Article  PubMed  Google Scholar 

  29. Cao WT, et al. Higher dietary carotenoid intake associated with lower risk of hip fracture in middle-aged and elderly Chinese: A matched case-control study. Bone. 2018;111:116–22.

    Article  CAS  PubMed  Google Scholar 

  30. Chen GD, et al. Association of dietary consumption and serum levels of vitamin A and beta-carotene with bone mineral density in Chinese adults. Bone. 2015;79:110–5.

    Article  CAS  PubMed  Google Scholar 

  31. Yee MMF et al. Vitamin A and bone health: A review on current evidence. Molecules, 2021. 26(6).

  32. Yamaguchi M. Beta-Cryptoxanthin stimulates bone formation and inhibits bone resorption in tissue culture in vitro. Mol Cell Biochem. 2004;258:137–44.

    Article  CAS  PubMed  Google Scholar 

  33. Uchiyama S. Oral administration of Betacryptoxanthin induces anabolic effects on bone components in the femoral tissues of rats in vivo. Biol Pharm Bull. 2004;27:232–5.

    Article  CAS  PubMed  Google Scholar 

  34. Bliuc D, et al. Accelerated bone loss and increased post-fracture mortality in elderly women and men. Osteoporos Int. 2015;26(4):1331–9.

    Article  CAS  PubMed  Google Scholar 

  35. Stahl W, Sies H. Antioxidant activity of carotenoids. Mol Aspects Med. 2003;24(6):345–51.

    Article  CAS  PubMed  Google Scholar 

  36. Eimar H, et al. Association between sleep apnea and low bone mass in adults: a systematic review and meta-analysis. Osteoporos Int. 2017;28(6):1835–52.

    Article  CAS  PubMed  Google Scholar 

  37. Mellanby E. Vitamin A and bone growth: the reversibility of vitamin A-deficiency changes. J Physiol. 1947;105(4):382–99.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  38. Djakoure C, et al. Vitamin A and retinoic acid stimulate within minutes cAMP release and growth hormone secretion in human pituitary cells. J Clin Endocrinol Metab. 1996;81(8):3123–6.

    CAS  PubMed  Google Scholar 

  39. Raifen R, Altman Y, Zadik Z. Vitamin A levels and growth hormone axis. Horm Res. 1996;46(6):279–81.

    Article  CAS  PubMed  Google Scholar 

  40. Jilka RL, et al. Quantifying osteoblast and osteocyte apoptosis: challenges and rewards. J Bone Min Res. 2007;22(10):1492–501.

    Article  Google Scholar 

  41. Wang F, et al. beta-Carotene suppresses osteoclastogenesis and bone resorption by suppressing NF-kappaB signaling pathway. Life Sci. 2017;174:15–20.

    Article  CAS  PubMed  Google Scholar 

  42. Wattanapenpaiboon N, et al. Dietary carotenoid intake as a predictor of bone mineral density. Asia Pac J Clin Nutr. 2003;12(4):467–73.

    CAS  PubMed  Google Scholar 

  43. Kim Y, et al. The effects of combined antioxidant (beta-carotene, alpha-tocopherol and ascorbic acid) supplementation on antioxidant capacity, DNA single-strand breaks and levels of insulin-like growth factor-1/IGF-binding protein 3 in the ferret model of lung cancer. Int J Cancer. 2007;120(9):1847–54.

    Article  CAS  PubMed  Google Scholar 

  44. Landi F, et al. Free insulin-like growth factor-I and cognitive function in older persons living in community. Growth Horm IGF Res. 2007;17(1):58–66.

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

The authors like to acknowledge the government of the United States of America for providing free data. We also like to thank the research square for sharing our manuscript as a preprint under a CC BY 4.0 License. https://doiorg.publicaciones.saludcastillayleon.es/10.21203/rs.3.rs-3202228/v1.

Funding

This research received no specific grant from any funding agency, but it was performed as part of the employment of Dr. Tesfaye Getachew at Adama Hospital Medical College, Ethiopia. The Adama Hospital Medical College is not involved in the manuscript writing, editing approval, or decision to publish.

Author information

Authors and Affiliations

  1. Department of Public Health, Adama Hospital Medical College, Adama, Ethiopia

    Tesfaye Getachew Charkos & Hunde Lemi

  2. School of Public Health, Washington University, Seattle, USA

    Kemal Sherefa Oumer

Authors
  1. Tesfaye Getachew Charkos
    View author publications

    You can also search for this author inPubMed Google Scholar

  2. Hunde Lemi
    View author publications

    You can also search for this author inPubMed Google Scholar

  3. Kemal Sherefa Oumer
    View author publications

    You can also search for this author inPubMed Google Scholar

Contributions

Conceptualization, TGC; data curation, TGC, KSO; formal analysis, TGC, KSO, and HL; project administration, TGC; supervision, TGC; writing-original draft, HL and TGC; writing-review & editing, HL and TGC. All authors contributed to the article and approved the submitted version.

Corresponding author

Correspondence to Tesfaye Getachew Charkos.

Ethics declarations

Ethics approval and consent to participate

The National Center for Health Statistics Research Ethics Review Board reviewed and approved the survey protocols and written informed consent for data collection was obtained from all participants.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Supplementary Material 1

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Charkos, T.G., Lemi, H. & Oumer, K.S. Dietary carotenoid intake and fracture risk based on NHANES 2013–2018 data: a propensity score matching. J Health Popul Nutr 44, 119 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s41043-025-00858-7

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s41043-025-00858-7

Keywords

Journal of Health, Population and Nutrition

ISSN: 2072-1315

Contact us