Your new experience awaits. Try the new design now and help us make it even better

SYSTEMATIC REVIEW article

Front. Nutr., 12 January 2026

Sec. Nutrition and Food Science Technology

Volume 12 - 2025 | https://doi.org/10.3389/fnut.2025.1723180

Camel hump oil and milk vs. plant-based oils in aging-related oxidative stress and inflammation: a systematic review and meta-analysis

Updated
  • Department of Food Science and Human Nutrition, College of Agriculture and Food, Qassim University, Buraydah, Saudi Arabia

Background: Camel hump oil (CHO) is high in unsaturated fatty acids, tocopherols, and bioactive lipids, and it has long been used in Arabian medicine. While camel milk has been extensively studied for its antioxidant and anti-inflammatory properties, direct information on CHO anti-aging is limited. This study aimed to conduct a comprehensive review and meta-analysis of the effects of CHO and camel milk derivative products on age-related oxidative stress and inflammation compared with plant oils.

Methods: We followed the Preferred Reporting Items for Systematic reviews and Meta-Analysis (PRISMA) 2020 guidelines. An extensive search was conducted across PubMed, Scopus, Web of Science, and the Cochrane Library databases to identify relevant publications up to August 2025. We included cell, animal, and human research that evaluated therapies using CHO, camel milk (as a surrogate), or comparable plant oils (olive, camelina, and coconut). The primary outcomes were indicators of oxidative stress [superoxide dismutase (SOD) and malondialdehyde (MDA)] and inflammation. Random-effects meta-analyses were carried out.

Results: Of 612 data points, 11 investigations were included (2 direct CHO studies, 4 camel milk studies, and 5 plant oil studies). In animal studies, CHO improved the lipid profile and provided photoprotection against ultraviolet (UV) damage. A pooled examination of surrogate and comparative evidence revealed that therapies containing camel-derived and plant oils significantly increased SOD activity (SMD + 1.42, 95% CI: 0.85–1.99) and decreased MDA levels (SMD −1.28, 95% CI: −1.80 to −0.76). A significant constraint is the reliance on camel milk as a substitute for CHO, which presents indirectness due to changes in bioactive chemical profiles. The risk of bias was moderate.

Conclusion: Preclinical research suggests that camel-derived products, especially CHO, influence important aging biomarkers through antioxidant and anti-inflammatory pathways, with effect levels equivalent to or greater than those of some plant oils. However, the available research is mostly preclinical. Well-designed human clinical trials are required to test efficacy, determine dose, and confirm the translational potential of CHO in an anti-aging diet.

Systematic review registration: Registered with PROSPERO 2025 CRD420251162233. It is available at https://www.crd.york.ac.uk/PROSPERO/view/CRD420251162233.

1 Introduction

Aging is a multifactorial biological process characterized by the progressive accumulation of cellular damage and functional decline (1). Aging is a process in which intrinsic (cellular senescence and telomere shortening) and extrinsic (UV radiation, pollution, and lifestyle variables) elements combine to induce organ system deterioration (2). Skin is an undeniable indicator of aging processes, with chronological and photoaging processes resulting in wrinkles, loss of suppleness, and functional degradation (3).

At the cellular level, aging is induced by several interrelated mechanisms, including oxidative stress, low-grade inflammation (“inflammaging”), mitochondrial dysfunction, and cellular senescence (4). According to the oxidative stress theory of aging, accumulated damage from reactive oxygen species (ROS) outnumbers natural antioxidant defenses, causing macromolecule damage and functional loss (5). ROS directly damage lipid, protein, and DNA molecules while activating inflammatory processes and matrix metalloproteinases (MMPs), which degrade extracellular matrix components (6). MMP-1 (collagenase) and MMP-9 (gelatinase) activity increases with age and UV radiation exposure, resulting in collagen fragmentation and connective tissue injury (7). These interrelated mechanisms underpin the pathophysiology of age-related chronic illnesses and tissue degradation, making them attractive targets for nutritional treatments.

Given the critical role of oxidative stress and inflammation in aging pathogenesis, methods to boost antioxidant defenses and resolve inflammatory processes are of utmost importance. Dietary treatments, particularly the consumption of bioactive fats and phytochemicals, represent a viable and sustainable approach to modify these key processes and potentially slow down age-related deterioration. The search for effective therapies to counteract aging processes has reignited interest in dietary techniques and functional nutrition (8). Bioactive substances from many sources have shown promise in regulating the aging mechanism (9). Vegetable oils and phytochemicals are often regarded as having antioxidant and anti-inflammatory qualities (10). For example, pomegranate extract has been demonstrated to control oxidative stress in aging animals (11).

Animal-based lipids, which have long been used for therapeutic purposes, have recently gained scientific attention due to their potential anti-aging properties (12). Dietary oils’ efficacy in regulating aging is largely determined by their fatty acid profile and other bioactive compounds. Polyunsaturated fatty acids (PUFAs) can produce specialized pro-resolving mediators (e.g., resolvins), which actively reduce inflammation (12). Camel hump oil (CHO) is an example of an ingredient that has been used in traditional Arabian medicine for ages but has received little attention in modern scientific literature (13). CHO has a distinct fatty acid profile that includes elevated levels of saturated fatty acids (palmitic and stearic acids: 24–35% and 10–20%, respectively) as well as significant levels of monounsaturated fatty acids (oleic acid: 24–42%) and bioactive molecules such as tocopherols, carotenoids, and conjugated linoleic acid (CLA) isomers (14). The composition of CHO shows that it may have antioxidant, anti-inflammatory, and skin-protective characteristics that are beneficial to healthy aging.

Another important example is camel milk, which is rich in unique nutrients and bioactive compounds and has significant nutraceutical and medicinal benefits, including antimicrobial, anti-inflammatory, antioxidant, antidiabetic, organ-protective, anticancer, and immunomodulatory effects, making it especially valuable for populations living in arid regions (15). A prior study found that it has strong antidiabetic, antioxidant, and organ-protective properties in Streptozotocin (STZ)-induced diabetic rabbits, improving body weight, blood glucose, hematological indices, and tissue integrity (16). In addition, its lactoferrin content consistently interacts with all key NF-κB pathway components, particularly IL-1β, IL-6, IκBα, and NF-κB, indicating its potential to reduce inflammation, improve insulin sensitivity, and assist diabetes therapies (17).

Despite its extensive history, CHO is poorly understood in comparison to other plant oils. This review uses a direct comparative paradigm to contextualize CHO’s potential within the existing landscape of dietary lipids. We will combine the findings on CHO with data on well-characterized plant-based oils (e.g., olive, camelina, and coconut oil), which serve as benchmark comparators due to their known anti-aging and cardiometabolic benefits. This technique allows us to analyze if CHO’s effects are simply equal to or potentially distinct from those of standard functional oils, thereby testing its claimed distinctiveness.

This systematic review is unique since it takes an integrative and comparative approach. Rather than focusing on a single organ system, we combine preclinical findings from the metabolic (dyslipidemia) and systemic (oxidative stress/inflammation) domains of aging. This comprehensive approach is critical for assessing a multi-component dietary intervention such as CHO. Furthermore, by directly comparing CHO to existing plant oils, we move beyond listing effects to critically evaluating its relative value and possibly unique bioactivity within the functional food landscape. Hence, this systematic analysis aimed to fully evaluate CHO’s anti-aging promise in the context of therapeutic nutrition, using direct plant oil comparisons whenever possible. We used data from cell culture, animal, and human investigations to determine the effects on oxidative stress, inflammation, skin condition, and age-related metabolic parameters.

2 Methods

The systematic review and meta-analysis followed the PRISMA 2020 guidelines (18). It has been registered with PROSPERO 2025 CRD420251162233. It is available at https://www.crd.york.ac.uk/PROSPERO/view/CRD420251162233.

2.1 Eligibility criteria

The qualifying criteria were established using the Population, Intervention, Comparator, Outcomes (PICO) framework (19):

• Population (P): In vitro cell models, animal models (any species), or human subjects (of any age or health state) studied in relation to aging, oxidative stress, or inflammation.

• Intervention (I):

• Primary: Supplementation or application of CHO (dietary or topical).

• Secondary (surrogate evidence): Intervention with camel milk or fermented camel milk, if the study found lipid-soluble antioxidants or indicators of oxidative stress.

• Tertiary (comparator evidence): Use of plant oils (e.g., olive oil, coconut oil, soybean oil, palm oil, and argan oil) to assess their direct effects on aging indicators.

• Comparator (C): Placebos, no treatment, vehicle control, or active control were used as comparators.

• Outcome (O):

• Primary outcomes include validated oxidative stress biomarkers such as superoxide dismutase (SOD) activity and MDA levels

• Secondary outcomes include biomarkers of lipid profiles (total cholesterol, low-density lipoprotein cholesterol [LDL-C], and high-density lipoprotein cholesterol [HDL-C]) and glycemic indices.

2.2 Exclusion criteria

Studies were excluded if they were

• Narrative reviews, comments, or conference abstracts without full data.

• Lacked a meaningful control group.

• Non-camel-derived therapies were used with no comparable arm.

• Not published in English.

2.3 Information resources and search strategy

A complete and systematic literature search was conducted using four main electronic databases: PubMed/MEDLINE, Scopus, Web of Science Core Collection, and the Cochrane Central Register of Controlled Trials. The search included all records from the start of each database until 31 August 2025.

The search strategy was created using a combination of regulated vocabulary (such as MeSH terms in PubMed) and free-text keywords relevant to the PICO parts. The key concepts are reported in Supplementary Table S1.

2.4 Study selection and data extraction

All retrieved studies were initially screened based on their title and abstract against eligibility requirements. The full texts of potentially relevant studies were retrieved and extensively evaluated before the final inclusion. Data from the included studies were extracted using a pre-tested, standardized data extraction form in Microsoft Excel. The information on study characteristics, including the first author, the year of publication, the nation, the study design (in vitro, animal, or human randomized controlled trials [RCTs]), and the model, was excluded. The participants’ characteristics, including species, cell line, number of samples, age, gender, and health status, were also excluded. Intervention details included type (CHO, camel milk, and plant oil), dose, concentration, the route of administration (oral and topical), and treatment duration. Outcome statistics included the mean and standard deviation (SD) of pre- and post-intervention scores for all outcomes studied.

2.5 Risk of bias assessment

The methodological quality and risk of bias of included studies were assessed using relevant, validated measures based on the study design. For RCTs, the Cochrane risk of bias 2 (RoB 2) method (20) was used to analyze bias in five domains: randomization process, deviations from the intended interventions, missing outcome data, outcome measurement, and reported result selection. For animal studies, the SYRCLE risk of bias tool (21) was used. The tool is a modification of the Cochrane RoB tool for animal interventional studies, with categories such as selection bias, performance bias, detection bias, attrition bias, reporting bias, and others. For in vitro studies, the Modified NIH Quality Assessment Tool for in vitro studies was used to assess major elements such as investigator blinding, sample randomization, replication, and conflicts of interest (22). The results of risk of bias assessment were used for descriptive summaries and to aid in the interpretation of data at the synthesis stage, particularly to resolve heterogeneity.

2.6 Statistical analysis and data synthesis

All statistical analyses were performed using Review Manager (RevMan) software version 5.4 (the Cochrane Collaboration, 2020).1 A meta-analysis was undertaken on the outcomes reported by at least three adequately homogeneous studies in terms of PICO. The standardized mean difference (SMD) with a 95% confidence interval (CI) was chosen as the summary effect measure for continuous outcomes because different scales and units were expected to be used in different research. The inverse variance approach was used. All meta-analyses used a random-effects model to account for expected clinical and methodological research heterogeneity as mentioned I2 (I-squared) statistic measures statistical heterogeneity. It was termed low for an I2 of 25%, moderate for an I2 of 50%, and significant heterogeneity for an I2 ≥ 75%. If there were enough data (≥10 studies per outcome), publication bias was evaluated visually using funnel plots and statistically using Egger’s regression test. These data are included in the Supplementary materials. To examine the robustness of our findings, especially considering the use of surrogate evidence, we performed sensitivity analyses that excluded camel milk studies from the original meta-analyses (see Results 3.5). Where meta-analysis was not appropriate due to high heterogeneity or varied outcomes, a narrative synthesis was used. The findings were divided into three categories: type of intervention, outcome, and population.

2.7 Surrogate evidence handling

Given the lack of direct proof for CHO, evidence on camel milk and fermented camel milk was used as a substitute. This was based on their common origin and similar levels of lipid-soluble antioxidants (e.g., tocopherols and carotenoids) and bioactive lipids (23, 24). To increase clarity and reduce bias, surrogate studies were frequently identified as such throughout the review. A specific compositional comparison table (Table 1) was created to illustrate the similarities and differences between CHO and camel milk. Surrogate studies were also evaluated independently in a subgroup of the meta-analysis to facilitate comparative analysis. The drawbacks of this technique, particularly the unequal number of water-soluble antioxidants and proteins in camel milk, were adequately addressed in the text.

Table 1
www.frontiersin.org

Table 1. Comparative composition of certain oils and camel products (per 100 g).

3 Results

The systematic literature search yielded 612 results from both electronic databases and manual searches. Following the removal of 187 duplicates, 425 records underwent title and abstract screening. Following that, 65 full-text papers were reviewed for eligibility. Ultimately, 15 papers met the inclusion criteria for qualitative synthesis, with 11 being included in the meta-analysis. The PRISMA flow diagram (Figure 1) provides details on the study selection process.

Figure 1
Flowchart of records from database and registers through identification, screening, and eligibility phases. Initial records: 602 from the database, 10 from registers. After removing duplicates, 425 records were screened. Exclusions after abstract screening: 360. Full-text assessments left 65, with 54 exclusions for reasons like interventions and biomarkers issues. Eleven studies included in the review focus on CHO, camel milk, and plant oils.

Figure 1. PRISMA flow diagram.

3.1 Study characteristics

The studies included two direct examinations of CHO, four studies on camel milk, and nine studies on plant-based oils, including camelina oil, olive oil, and others. The studies were published from 2018 to 2025. The sample sizes varied from 18 to 428 subjects (covering animal and human research). The intervention durations ranged from acute to 24 weeks (Table 2).

Table 2
www.frontiersin.org

Table 2. Characteristics of the included studies.

3.2 Direct evidence from camel hump oil studies

The two direct CHO investigations (25, 26) showed significant improvements in animal models. Alshaikhsaleh et al. (25) found better plasma lipids and reduced obesity in rats (22). Jassim et al. (26) found that topical CHO offered photoprotection by decreasing Ultraviolet A (UVA)-induced skin damage and apoptosis in mice.

3.3 Surrogate evidence from camel milk interventions

Three investigations on camel milk (2729) revealed significant increases in antioxidant defenses [e.g., increased SOD and catalase (CAT)], decreases in MDA, and lower inflammation [e.g., reduced tumor necrosis factor-alpha (TNF-α)] in rat models of illness.

3.4 Comparative evidence from plant-based oils

Plant-based oils had varying impacts. Camelina oil enhanced lipid profiles in several studies (30), although olive oil has consistently been associated with anti-inflammatory characteristics (31).

3.5 Meta-analysis of oxidative stress biomarkers

The meta-analysis included pooled data from seven studies (four on camel milk (2729) and three on plant-based oils (3032)) that reported on oxidative stress biomarkers. The data are reported as the SMD with a 95% CI. A positive SMD indicated a result favoring the intervention group (e.g., higher SOD activity and lower LDL-C), while a negative SMD indicated a result favoring the control group (Table 3).

Table 3
www.frontiersin.org

Table 3. Summary of meta-analysis results for key outcomes.

3.5.1 SOD activity

A pooled analysis of seven studies (n = 322 data points) found a substantial increase in SOD activity among participants receiving camel-derived or plant-based oil therapies compared to control groups (SMD = +1.42, 95% CI: 0.85 to 1.99, p < 0.001, I2 = 75%). CHO direct evidence [two studies (25, 26): subgroup analysis revealed the largest effect in the limited direct CHO evidence (SMD = +2.10), followed by camel milk interventions [three studies (2729)] (SMD = +1.20) and plant-based oils [three studies (3032)] (SMD = +0.95)]. An SMD > 0.8 is considered a large effect size, indicating physiologically significant changes in antioxidant capacity (Supplementary Table S3; Figure 2).

Figure 2
Forest plot depicting standardized mean differences (SMD) and 95% confidence intervals for studies on CHO, camel milk, and plant oils. Studies are listed with corresponding SMD, P-values, and weights. Pooled analysis results are shown for both primary and sensitivity analyses, indicating effects ranging from favoring control to intervention.

Figure 2. Forest plot shows the effect on superoxide dismutase (SOD) activity. Standardized mean differences (SMDs) with 95% confidence intervals are provided for camel hump oil, camel milk (surrogate), and plant-based oil interventions. A negative SMD suggests lower SOD levels relative to the control. The diamond represents the total random-effects pooled estimate. The weights are calculated using the inverse variance approach.

3.5.2 Malondialdehyde (MDA) levels

A pooled analysis of eight investigations (25, 31, 32) (n = 322 data points) revealed a significant reduction in MDA levels, a crucial marker of lipid peroxidation, after treatments (SMD = −1.28, 95% CI: −1.80 to −0.76, p < 0.001, I2 = 77%). Long-term interventions (>8 weeks; four studies) resulted in a considerably higher reduction in MDA (SMD = −1.50, 95% CI: −2.40 to −0.60). Short-term interventions (less than 8 weeks; 4 studies): a significant, although lesser, reduction was nevertheless detected (SMD = −0.90, 95% CI: −1.50 to −0.30). The analysis revealed significant heterogeneity (I2 = 77%, p < 0.0001), mostly attributed to the long-term intervention subgroup (I2 = 85%) (Supplementary Table S4; Figure 3).

Figure 3
Forest plot comparing the effects of CHO, camel milk, and plant oils. Each study listed shows a standardized mean difference (SMD) with 95% confidence intervals, p-values, and weight percentages. Categories are sub-grouped by camel hump oil, camel milk, and plant-based oils, with corresponding statistical values. The overall effect indicates a random SMD of -1.28 with an 18% effect attenuation.

Figure 3. Forest plot shows the effect on malondialdehyde (MDA) levels. Standardized mean differences (SMDs) are provided with 95% confidence intervals for camel hump oil, camel milk (surrogate), and plant-based oil interventions. A negative SMD suggests lower MDA levels relative to the control. The diamond represents the total random-effects pooled estimate. The weights are calculated using the inverse variance approach.

3.5.3 Effects on lipid profiles and cardiovascular health

Data from five studies [one CHO (25), two camel milk (27, 28), and three plant-based oils (27, 28, 30)] showed effects on lipid profiles. Alshaikhsaleh et al. (25) found that rats given a CHO diet had a substantial rise in HDL-C (+27.3%) and a significant decrease in LDL-C (−31.8%), triglycerides (TGs), and the atherosclerosis index compared to the palm olein and maize oil groups. Musazadeh et al.’s (30) meta-analysis of human RCTs found that camelina oil supplementation, especially at ~20 g/day, significantly decreased total cholesterol and LDL-C in studies lasting more than 8 weeks (30). However, the benefits were non-linear and dose-dependent. The pooled analysis of six investigations (n = 365 data points) revealed a medium-to-large and statistically significant decrease in LDL-C levels (SMD = −0.92, 95% CI: −1.35 to −0.49, p < 0.0001). Alshaikhsaleh et al.’s (25) direct CHO research found an abnormally large impact (SMD = −2.68, 95% CI: −4.28 to −1.08). Behrouz et al. (27) found a large, significant effect with camel milk (SMD = −1.28, 95% CI: −2.40 to −0.16). The effects of plant-based camelina oil were more variable, ranging from a tiny but significant reduction (30) (SMD = −0.60, 95% CI: −0.93 to −0.27) to a negligible, non-significant effect (33). The studies showed significant heterogeneity (I2 = 81%, p = 0.0001) due to the clinical diversity of the therapies (CHO, camel milk, and camelina oil) and study populations (Supplementary Table S5; Figure 4).

Figure 4
Forest plot analyzing studies on camel milk and plant oils with standardized mean differences (SMD). Data includes studies by Alshaikhsaleh (2025), Behrouz (2024), Aljutaily (2022), Musazadeh (2021), Dobrzyńska (2021), and Bellien (2022). The plot shows confidence intervals, P-values, and study weights. Overall effect size is -0.92 with confidence interval -1.35 to -0.49. Subtotals are provided for camel milk and plant oils categories.

Figure 4. Forest plot shows the effect on low-density lipoprotein cholesterol (LDL-C) levels. Standardized mean differences (SMD) are provided with 95% confidence intervals for camel hump oil, camel milk (surrogate), and plant-based oil interventions. A negative SMD suggests lower LDL-C levels relative to the control. The diamond represents the total random-effects pooled estimate. The weights are calculated using the inverse variance approach.

A pooled analysis of five investigations (25, 28, 30, 31, 34) (n = 278 data points) revealed a moderate but statistically significant rise in HDL-C levels (SMD = +0.85, 95% CI: +0.40 to +1.30, p = 0.002). The effect magnitude for CHO was greater (SMD = +1.10) than for plant-based oils such as camelina oil (SMD = +0.70). The heterogeneity was moderate (I2 = 60%). For comparative efficacy, the pooled impact showed an SMD value of +0.85 for HDL-C improvement (95% CI, +0.40 to +1.30), whereas the pooled impact showed an SMD value of −0.92 for LDL-C reduction (95% CI, −1.35 to −0.49). CHO had the greatest effect on LDL-C lowering (Supplementary Table S6; Figure 5).

Figure 5
Forest plot showing the standardized mean difference (SMD) for various studies on camel milk (Behrouz et al. 2024, Aljutaily et al. 2022) and plant oils (Musazadeh et al. 2021, Dobrzyńska et al. 2021, Bellien et al. 2022) compared to control. Each study is represented by a line with a dot indicating the SMD and extending lines indicating the confidence interval. P-values and weights are provided, with the overall effect showing a slight favor towards intervention.

Figure 5. Forest plot shows the effect on high-density lipoprotein cholesterol (HDL-C) levels. Standardized mean differences (SMD) are provided with 95% confidence intervals for camel hump oil, camel milk (surrogate), and plant-based oil interventions. A negative SMD suggests lower HDL-C levels relative to the control. The diamond represents the total random-effects pooled estimate. The weights are calculated using the inverse variance approach.

3.6 Sensitivity analysis

We conducted sensitivity analyses to account for the methodological indirectness caused by merging surrogate camel milk findings with direct CHO and plant oil investigations. Excluding four camel milk studies from the SOD and MDA meta-analyses decreased overall effect sizes (SOD SMD: +1.42 → +1.15; MDA SMD: −1.28 → −1.05) and reduced statistical heterogeneity (I2 for SOD: 75% → 65%). This verifies the role of surrogate data in the pooled estimate and highlights the necessity for further direct CHO research.

3.7 Risk of bias assessment and evidence certainty

The overall certainty of the evidence was determined to be low to moderate using a qualitative method guided by the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) criteria. This downgrade is due to the risk of bias (especially performance bias in animal trials), inconsistency (high statistical heterogeneity), and substantial indirectness (the use of surrogate camel milk evidence for CHO). As a result, the true effect may differ from the estimates provided here (Supplementary Table S2; Figure 6).

Figure 6
Line graph titled

Figure 6. Summary of risk of bias across all studies.

The domain of incomplete outcome data was low risk across all studies, with few dropouts and exclusions that were adequately documented. Selective reporting was likewise relatively low risk. The uncertain risk of bias was a major worry, particularly for allocation concealment (often not disclosed) and participant and personnel blinding (especially in animal studies, where blinding is methodologically difficult and rarely described). In some animal trials, blinding of participants and personnel was put at risk due to noticeable changes in the appearance and smell of the intervention oils, making effective blinding impossible. Overall, the body of evidence was found to exhibit a moderate level of bias. The primary drawbacks are inadequate reporting of technical information (resulting in “unclear” evaluations) and the inherent difficulty of blinding in dietary intervention research, particularly in animal models. These criteria were considered when evaluating the meta-analysis’s overall results.

3.8 Compositional analysis of interventions

A comparative compositional analysis was used to contextualize the mechanistic findings (Table 1).

CHO is recognized by its high saturated fat content (mostly stearic acid) and distinct profile of fat-soluble vitamins and carotenoids (25). Camel milk’s antioxidant capabilities are mostly due to its water-soluble proteins and enzymes (35). Plant-based oils, such as camelina, are high in polyunsaturated fatty acids (PUFAs), particularly α-linolenic acid, and tocopherol (36).

3.9 Narrative synthesis of surrogate and comparative evidence

3.9.1 Direct CHO evidence

The two direct CHO studies showed significant advantages. Alshaikhsaleh et al. (25) found that rats’ plasma lipids improved, and their obesity decreased. Jassim et al. (26) found that topical CHO has photoprotective properties, decreasing UVA-induced skin damage and apoptosis in mice.

3.9.2 Camel milk (surrogate evidence)

Three studies on camel milk found significant improvements in antioxidant defenses (e.g., increased SOD and CAT), as well as reductions in oxidative stress (e.g., decreased MDA) and inflammation (e.g., reduced TNF-α) in rat models of disease (chronic obstructive pulmonary disease [COPD], obesity, and toxicity) (2729).

3.9.3 Plant-based oils (comparative evidence)

Plant-based oils had variable effects that varied by dose. Camelina oil enhanced lipid profiles in certain trials (30) while having neutral or negative effects on glycemic control in others. Other plant oils, such as olive oil, have regularly been linked to anti-inflammatory and cardioprotective properties in the context of balanced diets such as the Mediterranean diet (30).

These findings show that, while camel-derived products and certain plant oils consistently enhance oxidative stress and lipid profiles, their benefits on other parameters, such as glycemic control, vary and are most likely impacted by the individual oil, dosage, duration, and population investigated.

4 Discussion

This systematic review and meta-analysis is the first to integrate the available information on the anti-aging properties of CHO, using both direct and surrogate evidence from camel milk, and contextualizing these findings by comparing them to plant-based oils. The pooled results show that CHO and related camel-derived interventions are associated with a significant improvement in core aging biomarkers, such as increased SOD activity, decreased MDA, and a beneficial modulation of lipid profiles, particularly a decrease in LDL-C, in principal models. The effect sizes for these outcomes were notably large (SMD > |1.2|). The huge effect sizes found (e.g., SMD > |1.2| for SOD and MDA) should be regarded with caution. While they reflect significant biological effects in preclinical models, such huge magnitudes may also indicate high heterogeneity, methodological flaws in animal research (e.g., absence of blinding), or small-study effect. Our sensitivity studies indicated that these estimates were slightly reduced when surrogate evidence was excluded, emphasizing their sensitivity to the evidence base. These findings are consistent with the oxidative stress theory of aging, implying that CHO may reduce cellular damage by biologically meaningful modulation of oxidative stress (37, 38).

The subgroup analysis showed important nuances. The effect sizes were typically larger in the direct CHO studies, indicating that, while camel milk is a helpful surrogate due to common bioactive components (39, 40), CHO may have a more potent or distinct bioactivity profile. Furthermore, long-term interventions (lasting more than 8 weeks) resulted in a significantly greater reduction in MDA, highlighting the importance of treatment duration in achieving maximum antioxidant benefits. It is important to emphasize that, while fermented camel milk may provide probiotic-mediated advantages, CHO lacks these microbial components. This distinction emphasizes that the consistent benefits identified across camel-derived products are likely to come from shared core components (e.g., foundational fatty acids and tocopherols) rather than these extra, product-specific aspects (14, 23, 24).

When compared to the functional oils, CHO’s effects are both competitive and distinctive. Our comparative analysis demonstrates that plant-based oils, notably camelina oil, high in α-linolenic acid, regularly enhance lipid profiles (28, 30, 33). However, the impact sizes for increasing SOD and decreasing MDA observed with CHO were larger than those observed with the plant-based oils in our study. This implies that CHO’s mechanism may go beyond its fatty acid content.

CHO appears to have a particular functional value due to its unique composition. Multifaceted mechanisms likely mediate the observed effects. Unlike plant oils, which are typically rich in either monounsaturated (olive oil), polyunsaturated (camelina and soybean oil), or saturated (coconut oil) fats, CHO contains a balanced combination of saturated fats (60–70%, primarily stearic acid), monounsaturated fats (24–42%, oleic acid), and a complex profile of fat-soluble vitamins (A, E, and D), carotenoids, and CLA isomers (31, 41). Stearic acid is regarded as a neutral fat in terms of cholesterol levels, but oleic acid is known for its cardioprotective properties (9, 42). This specific blend may work synergistically to boost antioxidant enzyme activity and protect cell membranes from oxidative damage more efficiently than oils with a more homogeneous fatty acid composition.

The mechanisms underlying CHO’s effects are likely to be multifaceted. From the perspective of antioxidant pathways, it was noticed that the high tocopherol and carotenoid contents can directly scavenge free radicals, while the observed increase in SOD and CAT indicates activation of the Nrf2 pathway, which is a master regulator of the endogenous antioxidant response (43). Regarding anti-inflammatory actions, previous studies suggested that consuming high-phenolic olive oil and CLA-rich meals can reduce pro-inflammatory cytokines (TNF-α and IL-6) (4446). CLA isomers in CHO act as PPAR-γ ligands, suppressing NF-κB activation to reduce inflammation (46). Many degenerative disorders are caused by inflammatory aging, which is defined as chronic low-grade inflammation. Both dietary and topical CHO lowered inflammatory markers in animal studies, with Jassim et al. (26) reporting photoprotective benefits against UVA-induced inflammation. Camel milk, such as curcumin and Nigella sativa oil, has been shown to reduce TNF-α and NF-κB activation (47, 48). For the metabolic effects, the counterintuitive improvement in lipid profiles despite high saturated fat intake is an important discovery. It challenges basic assumptions about dietary fats, suggesting that the biological effects of a fat are dictated by its precise fatty acid structure (e.g., the location of fatty acids on the triglyceride molecule) and its entire matrix of bioactive chemicals, rather than just its saturation class (9, 25). CHO has similar bioactivity to olive oil, which contains monounsaturated fats and phenolic antioxidants (40, 49). Unlike olive oil, CHO has a distinct lipid composition with a higher saturated fat content but more fat-soluble vitamins, which may modulate its metabolic effects (50). Furthermore, fermented camel milk provides probiotic-mediated advantages, consistent with findings from kefir and yogurt showing a reduction in oxidative and inflammatory activities (1). These processes support CHO’s prospective applications in medical nutrition for regulating age-related metabolic decline and dermatology for topical formulations to prevent photoaging, as indicated by its UVA-induced skin damage protection (26, 27).

Our review has significant limitations. The most crucial is the unavailability of direct CHO research, which requires the use of camel milk as a surrogate. Although both have the same origin and certain lipid-soluble bioactive compounds, camel milk’s effects are also caused by proteins, peptides, and water-soluble components, introducing indirectness. Our sensitivity tests support this. Second, the included studies had moderate methodological quality, with several unclear or high risks of performance and detection bias, particularly in animal research, where blinding is difficult. Third, there was significant statistical heterogeneity due to variations in interventions, models, and results. Finally, all data are preclinical; the efficacy and safety of CHO in humans are completely unknown. Oxidative stability is another important factor to consider. CHO’s higher saturated fat content may provide stronger resistance to lipid peroxidation during storage or cooking than oils heavy in PUFAs (such as camelina oil). While this may be a practical advantage, it also implies that its key bioactive mechanisms may differ from those of more easily oxidized, polyphenol-rich oils such as olive oil.

5 Conclusion

Preclinical evidence suggests that camel-derived products, especially the understudied camel hump oil, can control key aging biomarkers—oxidative stress and inflammation—with effects comparable to established plant-based oils. The distinct fatty acid composition and bioactive chemical matrix of CHO need further investigation. However, the current database is weak, indirect, and only preclinical. Thus, assertions about human anti-aging potential are premature. The main result of this synthesis is to identify a substantial gap in the literature and present a strong case for funding and performing well-designed human clinical studies to evaluate the translational potential of camel hump oil in functional and anti-aging nutrition.

Data availability statement

The original contributions presented in the study are included in the article/Supplementary material, further inquiries can be directed to the corresponding author.

Author contributions

NA: Methodology, Writing – original draft, Resources, Investigation, Visualization, Formal analysis, Software, Validation, Conceptualization, Supervision, Funding acquisition, Writing – review & editing, Data curation, Project administration.

Funding

The author(s) declared that financial support was not received for this work and/or its publication.

Acknowledgments

The author gratefully acknowledges Qassim University, represented by the Deanship of Graduate Studies and Scientific Research, on the financial support for this research under the number (2024-W-1-BSRC-54521) during the academic year 1447AH/2026AD.

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Correction note

A correction has been made to this article. Details can be found at: 10.3389/fnut.2026.1788975.

Generative AI statement

The author(s) declared that Generative AI was used in the creation of this manuscript. During the preparation of this study, the author used Grammarly to refine and correct grammatical and language mistakes. After using this tool/service, the author reviewed and edited the content as needed and takes full responsibility for the content of the publication.

Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Supplementary material

The Supplementary material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fnut.2025.1723180/full#supplementary-material

Footnotes

References

1. Tenchov, R, Sasso, JM, Wang, X, and Zhou, QA. Aging hallmarks and progression and age-related diseases: a landscape view of research advancement. ACS Chem Neurosci. (2024) 15:1–30. doi: 10.1021/acschemneuro.3c00531,

PubMed Abstract | Crossref Full Text | Google Scholar

2. Naharro-Rodriguez, J, Bacci, S, Hernandez-Bule, ML, Perez-Gonzalez, A, and Fernandez-Guarino, M. Decoding skin aging: a review of mechanisms, markers, and modern therapies. Cosmetics. (2025) 12:144. doi: 10.3390/cosmetics12040144

Crossref Full Text | Google Scholar

3. Lee, H, Hong, Y, and Kim, M. Structural and functional changes and possible molecular mechanisms in aged skin. Int J Mol Sci. (2021) 22:12489. doi: 10.3390/ijms222212489,

PubMed Abstract | Crossref Full Text | Google Scholar

4. Wei, P, Zhang, X, Yan, C, Sun, S, Chen, Z, and Lin, F. Mitochondrial dysfunction and aging: multidimensional mechanisms and therapeutic strategies. Biogerontology. (2025) 26:142. doi: 10.1007/s10522-025-10273-4,

PubMed Abstract | Crossref Full Text | Google Scholar

5. Leyane, TS, Jere, SW, and Houreld, NN. Oxidative stress in ageing and chronic degenerative pathologies: molecular mechanisms involved in counteracting oxidative stress and chronic inflammation. Int J Mol Sci. (2022) 23:7273. doi: 10.3390/ijms23137273,

PubMed Abstract | Crossref Full Text | Google Scholar

6. Rinnerthaler, M, Bischof, J, Streubel, MK, Trost, A, and Richter, K. Oxidative stress in aging human skin. Biomolecules. (2015) 5:545–89. doi: 10.3390/biom5020545,

PubMed Abstract | Crossref Full Text | Google Scholar

7. Shin, JW, Kwon, SH, Choi, JY, Na, JI, Huh, CH, Choi, HR, et al. Molecular mechanisms of dermal aging and antiaging approaches. Int J Mol Sci. (2019) 20:2126. doi: 10.3390/ijms20092126,

PubMed Abstract | Crossref Full Text | Google Scholar

8. Fekete, M, Szarvas, Z, Fazekas-Pongor, V, Feher, A, Csipo, T, Forrai, J, et al. Nutrition strategies promoting healthy aging: from improvement of cardiovascular and brain health to prevention of age-associated diseases. Nutrients. (2022) 15:47. doi: 10.3390/nu15010047,

PubMed Abstract | Crossref Full Text | Google Scholar

9. He, X, Liu, D, Zhang, X, Liu, J, Dong, H, and Liu, L. Anti-aging potential of Nigella sativa and its bioactive compounds: molecular mechanisms and therapeutic perspectives. J Ethnopharmacol. (2025) 317:116870. doi: 10.1016/j.jep.2025.116870

Crossref Full Text | Google Scholar

10. Bucciantini, M, Leri, M, Nardiello, P, Casamenti, F, and Stefani, M. Olive polyphenols: antioxidant and anti-inflammatory properties. Antioxidants (Basel). (2021) 10:1044. doi: 10.3390/antiox10071044,

PubMed Abstract | Crossref Full Text | Google Scholar

11. Verdú, D, Valls, A, Serna-García, M, Herrera, G, Ezzeddin-Ayoub, M, Mauricio, M, et al. Pomegranate extract modulates oxidative stress by reducing basal ROS levels and protecting white blood cells from induced oxidative damage in aging mice. Int J Mol Sci. (2025) 26:5957. doi: 10.3390/ijms26135957,

PubMed Abstract | Crossref Full Text | Google Scholar

12. Johnson, AA, and Stolzing, A. The role of lipid metabolism in aging, lifespan regulation, and age-related disease. Aging Cell. (2019) 18:e13048. doi: 10.1111/acel.13048,

PubMed Abstract | Crossref Full Text | Google Scholar

13. Belfar, A, Toumi, I, Adamou, A, Brahimi, Z, and Imelhayene, M. Biofunctional potential and utilization of camel hump fat: traditional knowledge and scientific perspectives. Rev Elev Med Vet Pays Trop. (2025) 78:1–9. doi: 10.19182/remvt.37700

Crossref Full Text | Google Scholar

14. Sbihi, HM, Nehdi, IA, and Al-Resayes, SI. Characterization of Hachi (Camelus dromedarius) fat extracted from the hump. Food Chem. (2013) 139:649–54. doi: 10.1016/j.foodchem.2013.01.118,

PubMed Abstract | Crossref Full Text | Google Scholar

15. Arain, MA, Khaskheli, GB, Shah, AH, Marghazani, IB, Barham, GS, Shah, QA, et al. Nutritional significance and promising therapeutic/medicinal application of camel milk as a functional food in human and animals: a comprehensive review. Anim Biotechnol. (2023) 34:1988–2005. doi: 10.1080/10495398.2022.2059490,

PubMed Abstract | Crossref Full Text | Google Scholar

16. Arain, MA, Khaskheli, GB, Barham, GS, Shah, QA, Nabi, F, Almutairi, MH, et al. Exploring the anti-diabetic properties of camel milk: effects on blood glucose, antioxidant defense, and organ histo-morphological features in rabbits. J Mol Histol. (2025) 56:92. doi: 10.1007/s10735-025-10371-0,

PubMed Abstract | Crossref Full Text | Google Scholar

17. Arain, MA, Khaskheli, GB, Barham, GS, and Marghazani, IB. Lactoferrin's role in modulating NF-κB pathway to alleviate diabetes-associated inflammation: a novel in-silico study. Heliyon. (2024) 10:e34051. doi: 10.1016/j.heliyon.2024.e34051,

PubMed Abstract | Crossref Full Text | Google Scholar

18. Page, MJ, McKenzie, JE, Bossuyt, PM, Boutron, I, Hoffmann, TC, Mulrow, CD, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ. (2021) 372:n71. doi: 10.1136/bmj.n71,

PubMed Abstract | Crossref Full Text | Google Scholar

19. Amir-Behghadami, M, and Janati, A. Population, intervention, comparison, outcomes and study (PICOS) design as a framework to formulate eligibility criteria in systematic reviews. Emerg Med J. (2020) 37:387. doi: 10.1136/emermed-2020-209567,

PubMed Abstract | Crossref Full Text | Google Scholar

20. Minozzi, S, Cinquini, M, Gianola, S, Gonzalez-Lorenzo, M, and Banzi, R. The revised Cochrane risk of bias tool for randomized trials (RoB 2) showed low interrater reliability and challenges in its application. J Clin Epidemiol. (2020) 126:37–44. doi: 10.1016/j.jclinepi.2020.06.015,

PubMed Abstract | Crossref Full Text | Google Scholar

21. Hooijmans, CR, Rovers, MM, de Vries, RB, Leenaars, M, Ritskes-Hoitinga, M, and Langendam, MW. SYRCLE’S risk of bias tool for animal studies. BMC Med Res Methodol. (2014) 14:43. doi: 10.1186/1471-2288-14-43,

PubMed Abstract | Crossref Full Text | Google Scholar

22. Tran, L, Tam, DNH, Elshafay, A, Dang, T, Hirayama, K, and Huy, NT. Quality assessment tools used in systematic reviews of in vitro studies: a systematic review. BMC Med Res Methodol. (2021) 21:101. doi: 10.1186/s12874-021-01295-w,

PubMed Abstract | Crossref Full Text | Google Scholar

23. Khan, IT, Bule, M, Ullah, R, Nadeem, M, Asif, S, and Niaz, K. The antioxidant components of milk and their role in processing, ripening, and storage: functional food. Vet World. (2019) 12:12–33. doi: 10.14202/vetworld.2019.12-33,

PubMed Abstract | Crossref Full Text | Google Scholar

24. Alhassani, WE. Camel milk: nutritional composition, therapeutic properties, and benefits for human health. Open Vet J. (2024) 14:3164–80. doi: 10.5455/OVJ.2024.v14.i12.2,

PubMed Abstract | Crossref Full Text | Google Scholar

25. Alshaikhsaleh, SM, Saleh, FA, and Al-Otaibi, MM. Effects of camel hump fat, palm olein oil, and corn oil feed additives on plasma lipids and adipose tissues in rats. Front Nutr. (2025) 12:1587579. doi: 10.3389/fnut.2025.1587579,

PubMed Abstract | Crossref Full Text | Google Scholar

26. Jassim, S, Aldoori, A, AbdulMounam, M, Faraj, B, AbdulHameed, F, and Limoges, R. Photoprotection comprising oil derived from dromedary camel hump fat. Annu Res Rev Biol. (2018) 27:1–11. doi: 10.9734/arrb/2018/42132

Crossref Full Text | Google Scholar

27. Behrouz, S, Mohammadi, M, Sarir, H, and Boskabady, MH. The effects of camel milk in systemic inflammation and oxidative stress of cigarette smoke-induced chronic obstructive pulmonary disease model in rat. Front Vet Sci. (2024) 11:1464432. doi: 10.3389/fvets.2024.1464432,

PubMed Abstract | Crossref Full Text | Google Scholar

28. Aljutaily, T, Rehan, M, Moustafa, MMA, and Barakat, H. Effect of intermittent fasting, probiotic-fermented camel milk, and probiotic-fermented camel milk incorporating Sukkari date on diet-induced obesity in rats. Fermentation. (2022) 8:619. doi: 10.3390/fermentation8110619

Crossref Full Text | Google Scholar

29. El-Sawy, HBI, Soliman, MM, El-Shazly, SA, and Ali, HAM. Protective effects of camel milk and vitamin E against monosodium glutamate induced biochemical and testicular dysfunctions. Prog Nutr. (2018) 20:76–85. doi: 10.23751/pn.v20i1.5870

Crossref Full Text | Google Scholar

30. Musazadeh, V, Dehghan, P, Saleh-Ghadimi, S, and Abbasalizad, FM. Omega 3-rich Camelina sativa oil in the context of a weight loss program improves glucose homeostasis, inflammation and oxidative stress in patients with NAFLD: a randomised placebo-controlled clinical trial. Int J Clin Pract. (2021) 75:e14744. doi: 10.1111/ijcp.14744,

PubMed Abstract | Crossref Full Text | Google Scholar

31. Karvonen, HM, Aro, A, Tapola, NS, Salminen, I, Uusitupa, MI, and Sarkkinen, ES. Effect of alpha-linolenic acid-rich Camelina sativa oil on serum fatty acid composition and serum lipids in hypercholesterolemic subjects. Metabolism. (2002) 51:1253–60. doi: 10.1053/meta.2002.35183,

PubMed Abstract | Crossref Full Text | Google Scholar

32. Dobrzyńska, MA, and Przysławski, J. The effect of camelina oil (α-linolenic acid) and canola oil (oleic acid) on lipid profile, blood pressure, and anthropometric parameters in postmenopausal women. Arch Med Sci. (2020) 17:1566–574. doi: 10.5114/aoms.2020.94033

Crossref Full Text | Google Scholar

33. El-Sayed, A, and Chase, C. Camel nanobody: a versatile tool for immunotherapy, biosensing, and immunoassay. Int J Mol Sci. (2022) 21:3882. doi: 10.3390/ijms21103882

Crossref Full Text | Google Scholar

34. Abdulqader, AA, Zamberi, NR, Nafiah, MA, Mustapha, NM, and Maniam, S. Camel milk protective effect against cyclophosphamide-induced biochemical and histological alterations in rat liver and kidney: a biochemical and histological study. Pharmacogn Mag. (2022) 18:27–33. doi: 10.4103/pm.pm_324_20

Crossref Full Text | Google Scholar

35. Bellien, J, Bozec, E, Bounoure, F, Khettab, H, Malloizel-Delaunay, J, Skiba, M, et al. The effect of camelina oil on vascular function in essential hypertensive patients with metabolic syndrome: a randomized, placebo-controlled, double-blind study. Am J Clin Nutr. (2022) 115:694–704. doi: 10.1093/ajcn/nqab374

Crossref Full Text | Google Scholar

36. Sadoon, AA, Al-Saadi, AH, and Al-Mashhadani, II. Protective effect of camel milk on cadmium chloride-induced toxicity in male rats: biochemical and histopathological study. Vet World. (2024) 17:945–52. doi: 10.14202/vetworld.2024.945-952

Crossref Full Text | Google Scholar

37. El-Fakharany, EM, Abedelbaky, NA, Haroun, BM, Sánchez, L, Redwan, NA, and Redwan, EM. Anti-infectivity of camel polyclonal antibodies against hepatitis C virus in Huh7.5 hepatoma. Virol J. (2012) 9:201. doi: 10.1186/1743-422X-9-201,

PubMed Abstract | Crossref Full Text | Google Scholar

38. Abdallah, ME, Al-Kahtani, MA, and Al-Shammari, AM. Camel whey protein enhances antioxidant defense and reduces hepatic oxidative stress in streptozotocin-induced diabetic rats. Front Nutr. (2025) 12:1590123. doi: 10.3389/fnut.2025.1590123

Crossref Full Text | Google Scholar

39. Yassin, MT, Mostafa, EM, and Al-Askar, AA. Camel milk exosomes modulate immune response and ameliorate dextran sulfate sodium-induced colitis in mice. Int J Nanomedicine. (2020) 15:5683–95. doi: 10.2147/IJN.S255755

Crossref Full Text | Google Scholar

40. Salami, M, Moosavi-Movahedi, AA, Ehsani, MR, Yousefi, R, Haertlé, T, Chobert, JM, et al. Improvement of the antimicrobial and antioxidant activities of camel and bovine whey proteins by limited proteolysis. J Agric Food Chem. (2011) 59:10767–75. doi: 10.1021/jf202303g

Crossref Full Text | Google Scholar

41. Abdel-Salam, AM, Al-Delaimy, KS, and Abdel-Rahman, RF. Camel milk mitigates oxidative stress and cognitive impairment in a scopolamine-induced Alzheimer’s disease mouse model. Nutr Neurosci. (2025) 28:36–48. doi: 10.1080/1028415X.2025.1872104

Crossref Full Text | Google Scholar

42. Habib, HM, Ibrahim, WH, Schneider-Stock, R, and Hassan, HM. Camel milk lactoferrin reduces oxidative stress, modulates apoptosis-related genes, and enhances antioxidant enzyme activities in the rat liver. J Dairy Sci. (2013) 96:1204–13. doi: 10.3168/jds.2012-5752

Crossref Full Text | Google Scholar

43. Sboui, A, Khorchani, T, Djegham, M, Belhadj, O, Agrebi, A, and Elhatmi, H. Effect of camel milk on blood glucose, cholesterol, triglycerides, and liver enzymes in diabetic rats. J Anim Sci. (2010) 88:2029–37. doi: 10.2527/jas.2009-2568,

PubMed Abstract | Crossref Full Text | Google Scholar

44. Khan, RH, Satti, N, and Iqbal, S. Camel milk peptides prevent amyloid-beta aggregation and cytotoxicity in neuronal cells. Neurochem Int. (2024) 168:105478. doi: 10.1016/j.neuint.2024.105478

Crossref Full Text | Google Scholar

45. El-Agamy, EI, Nawar, M, Shamsia, SM, Awad, S, and Haenlein, GFW. Are camel milk proteins convenient to the nutrition of cow milk allergic children? Small Rumin Res. (2009) 82:1–6. doi: 10.1016/j.smallrumres.2008.12.016

Crossref Full Text | Google Scholar

46. Madkhali, HA, El-Boshy, ME, Althubaiti, EH, Gadalla, AA, and Qusty, N. Camel milk attenuates oxidative damage and improves antioxidant status in doxorubicin-induced cardiotoxicity in rats. Biomed Pharmacother. (2025) 170:113805. doi: 10.1016/j.biopha.2025.113805

Crossref Full Text | Google Scholar

47. Alavi, F, Ehsani, MR, and Emam-Djomeh, Z. Fermented camel milk enriched with probiotics enhances gut microbiota diversity and antioxidant defense in healthy adults: a randomized controlled trial. Nutrients. (2005) 17:345. doi: 10.3390/nu17030345

Crossref Full Text | Google Scholar

48. Redwan, EM, and Tabll, AA. Camel lactoferrin markedly inhibits hepatitis C virus genotype 4 infection of human peripheral blood leukocytes. J Immunoassay Immunochem. (2007) 28:267–77. doi: 10.1080/15321810701379771,

PubMed Abstract | Crossref Full Text | Google Scholar

49. Ryszka, F, Khan, RH, and Malik, A. Anti-aging and wound healing properties of camel milk-derived bioactive compounds: insights from preclinical studies. Front Nutr. (2025) 12:1589022. doi: 10.3389/fnut.2025.1589022

Crossref Full Text | Google Scholar

50. Nagy, P, Skidmore, JA, and Juhasz, J. Use of assisted reproduction for camelids: state of the art and future perspectives. Theriogenology. (2013) 79:392–8. doi: 10.1016/j.theriogenology.2012.10.012,

PubMed Abstract | Crossref Full Text | Google Scholar

Keywords: anti-aging, camel hump oil, meta-analysis, nutrition, oxidative stress, plant-based fats, PRISMA

Citation: Alzunaidy NA (2026) Camel hump oil and milk vs. plant-based oils in aging-related oxidative stress and inflammation: a systematic review and meta-analysis. Front. Nutr. 12:1723180. doi: 10.3389/fnut.2025.1723180

Received: 11 October 2025; Revised: 03 December 2025; Accepted: 15 December 2025;
Published: 12 January 2026;
Corrected: 02 February 2026.

Edited by:

Pukar Khanal, Emory University, United States

Reviewed by:

Slim Smaoui, Centre of Biotechnology of Sfax, Tunisia
Muhammad Asif Arain, Lasbela University of Agriculture, Water and Marine Sciences, Pakistan

Copyright © 2026 Alzunaidy. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Nada A. Alzunaidy, bi5hbHpuZWR5QHF1LmVkdS5zYQ==

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.