Abstract
Background
Tea, known for its high content of antioxidants and anti-inflammatory compounds such as catechins, is believed to support liver health. This study aimed to explore the relationship between tea consumption and hepatic steatosis and fibrosis.
Methods
This longitudinal study involved 2,537 participants from the Ravanser Non-Communicable Disease (RaNCD) cohort, conducted from 2015 to 2023. Dietary intake was evaluated using a 118-item food frequency questionnaire (FFQ). The Fibrosis-4 (FIB-4) index and the Hepatic Steatosis Index (HSI) were utilized as predictive indicators for hepatic fibrosis and steatosis, respectively.
Results
After adjusting for potential confounding factors, our findings indicated that tea consumption was not significantly associated with an increased risk of worsening hepatic steatosis or fibrosis (P-value > 0.05). However, participants who consumed more than 2.88 cups of tea per day had a 27% lower likelihood of experiencing improvement in hepatic steatosis compared to those who consumed less than 1.92 cups per day (Relative Risk: 0.73; 95% CI: 0.53–0.99; P-value: 0.046).
Conclusion
Our study suggests that higher tea consumption is not significantly linked to an elevated risk of worsening hepatic steatosis or fibrosis. However, it is noteworthy that individuals who consumed more tea were less likely to see improvements in hepatic steatosis. This finding highlights the need for further research to better understand the potential effects of tea on liver health.
Keywords: Hepatic fibrosis, Hepatic steatosis, NAFLD, Liver, Tea
Introduction
Non-alcoholic fatty liver disease (NAFLD) is a significant public health concern due to its rising global prevalence and potentially severe health consequences. NAFLD represents the liver manifestation of metabolic syndrome and serves as a risk factor for conditions such as type 2 diabetes, dyslipidemia, and hypertension. It encompasses a spectrum of liver conditions, ranging from simple fat accumulation (steatosis) to more advanced non-alcoholic steatohepatitis (NASH), which can progress to hepatic fibrosis and hepatocellular carcinoma [1]. NASH, the more advanced stage of the disease, is characterized by steatosis, inflammation, and ballooning of liver cells, often accompanied by varying degrees of fibrosis [2].
Tea is a widely consumed beverage with a history spanning thousands of years. Certain components in tea, such as catechins and polyphenols, possess pharmacological properties and are commonly used as health supplements [3, 4]. In recent years, interest in the potential health benefits of tea consumption, particularly in relation to liver health, has grown. Tea is thought to have protective effects on the liver because of its high content of antioxidants and anti-inflammatory properties. Several studies have reported an inverse relationship between tea consumption and the risk of developing liver diseases, including hepatic steatosis and fibrosis [5–8]. However, the evidence remains controversial and inconclusive, and further research is necessary to establish a clear connection between tea consumption and liver health.
Most research has focused on cross-sectional analyses, which limit the ability to establish causality and the temporal relationship between tea consumption and liver health outcomes. Additionally, longitudinal studies that comprehensively examine the impact of varying levels of tea intake on the progression of hepatic steatosis and fibrosis over time are lacking. On the other hand, the effect of tea consumption on improving hepatic steatosis in NAFLD patients remains unclear. Therefore, we aim to investigate the associations between tea intake and improving or worsening hepatic steatosis and fibrosis in a population-based longitudinal cohort study.
Methods
Study design and participants
This study utilized a longitudinal design, drawing data from the Ravanser Non-Communicable Disease (RaNCD) cohort initiated in 2014. The project aims to investigate noncommunicable diseases among 10,047 Kurds aged 35–65 years residing in the Ravansar district of Kermanshah Province, Western Iran. The exclusion criteria were based on factors such as unreliable energy intake reports (less than 800 Kcal/day and more than 4200 Kcal/day), regular alcohol consumption, viral hepatitis (types B and C), liver failure or cirrhosis, and missing laboratory test results. The study followed the principles outlined in the Helsinki Declaration. Informed consent was obtained from all participants before data collection.
Data collection
Data collection involved face-to-face interviews conducted by trained personnel at the Ravansar cohort center. Participants completed baseline questionnaires that gathered comprehensive information on demographics, physical activity, smoking habits, socioeconomic status (SES), alcohol consumption, medical history, dietary habits, and food frequency questionnaires (FFQs). SES was assessed using 18 items analyzed through principal component analysis, which categorized individuals into five socioeconomic strata. Physical activity was measured using a standardized 22-item PERSIAN Cohort questionnaire, which reported physical activity levels based on metabolic equivalent (MET-min/day).
Tea consumption within the RaNCD cohort was assessed using the Iranian Food Frequency Questionnaire (FFQ). This tool monitors participants’ consumption of various foods and beverages over the previous year. Specifically designed for the Iranian diet, the questionnaire consists of 118 items, including local foods and drinks, collecting information on consumption frequency, cooking techniques, and use of herbal beverages. Participants with energy intakes exceeding 4200 Kcal/day were excluded following standard nutritional epidemiology practices, aimed at identifying and reducing the influence of extreme or potentially inaccurate dietary reports [9]. Tea consumption was reported in cups per day. Each cup was equivalent to 240 ml.
Anthropometric measurements
Anthropometric data were collected via the InBody 770 device (Inbody Co., Seoul, Korea) to measure weight, with participants weighing in light clothing and without shoes. Height was measured via an automated stadiometer (BSM 370, Biospace Co., Seoul, Korea). Waist circumference (WC) was measured three times via flexible tape, and the average was recorded for analysis.
Assessment of hepatic steatosis and fibrosis
The Hepatic Steatosis Index (HSI) is a reliable and non-invasive method for predicting simple steatosis in individuals with NAFLD. An HSI score below 30 indicates the absence of simple hepatic steatosis, while a score above 36 confirms its presence [10]. HSI is calculated using the formula: 8 × (Alanine aminotransferase/Aspartate aminotransferase) + BMI + 2 for females + 2 for those with diabetes mellitus.
The Fibrosis-4 index (FIB-4) is another non-invasive diagnostic tool that uses serum biomarkers to assess the likelihood of hepatic fibrosis. FIB-4 values are calculated using the following formula:
 |
The FIB-4 index has been extensively validated across various racial and ethnic groups, consistently yielding reliable results [10]. Scores below 1.30 for individuals under 65 years and below 2.0 for those aged 65 or older suggest the absence of hepatic fibrosis, while scores above 2.67 indicate the presence of hepatic fibrosis [11, 12].
Statistical analysis
Statistical analyses were performed using SPSS version 21. The participants were categorized based on tea consumption tertiles. Continuous variables are expressed as the means ± standard deviations and median [interquartile ranges], whereas categorical variables are expressed as numberers (frequencies). The Kolmogorov-Smirnov test was employed to assess the normality of the variables. Differences in baseline characteristics across tea consumption tertiles were evaluated using one-way ANOVA for normally distributed variables, Kruskal–Wallis tests for non-normally distributed variables, and the chi-squared and Fisher’s exact tests for nominal variables.
Participants were also categorized into three groups based on their liver indices: “liver disease unlikely”, “indeterminate”, and “liver disease likely”. Improvement in liver indices was identified when participants moved from “liver disease likely” at baseline to other categories at reassessment, or from “indeterminate” to “liver disease unlikely”. Conversely, worsening was noted if participants transitioned from “liver disease unlikely” at baseline to other categories at reassessment, or from “indeterminate” to “liver disease likely” [11]. The relative risks (RRs) of improving and worsening liver indices across tea consumption tertiles were estimated using the Poisson regression test in crude and adjusted models. These adjusted models included covariates such as energy, age, physical activity, SES, education, smoking, sleep duration, drug usage, and dietary supplements. A significance level of P-value < 0.05 was set for all analyses.
Results
Table 1 presents the baseline characteristics of the study participants stratified by tertiles of tea consumption. A total of 2,537 participants were included, with 708 in Tertile 1 (T1), 1,008 in Tertile 2 (T2), and 821 in Tertile 3 (T3). The mean age of participants differed significantly across the tertiles, with T1 averaging 46.90 years (± 7.94), T2 at 47.84 years (± 8.06), and T3 at 47.80 years (± 7.75) (P = 0.028). The distribution of sex also varied significantly across tertiles; T1 comprised 67.34% females (n = 477), T2 consisted of 53.37% females (n = 538), and T3 included 44.33% females (n = 364), indicating a statistically significant trend (P < 0.001). Weight and waist circumference (WC) measurements were significantly different among the tertiles. The average weight for T1 was 71.12 kg (± 12.40), that for T2 was 73.84 kg (± 12.23), and that for T3 was 74.70 kg (± 13.90) (P < 0.001). Similarly, the WC values were 96.80 cm (± 10.20) for T1, 98.24 cm (± 10.18) for T2, and 97.93 cm (± 10.68) for T3 (P = 0.033). Other variables, including body mass index (BMI), sleep duration, socioeconomic status (SES), and the use of antidiabetic and antilipidemic medications, did not significantly differ across tertiles (P > 0.05).
Table 1.
Baseline characteristics of participants according to tertiles of tea consumption
| Variables | Tea consumption Tertiles | P-value | ||
|---|---|---|---|---|
| T1 1.92 > cups |
T2 | T3 2.88 < cups |
||
| Number | 708 | 1008 | 821 | - |
| Age, years | 46.90 ± 7.94 | 47.84 ± 8.06 | 47.80 ± 7.75 | 0.028 |
| Female, n% | 477(67.34) | 538(53.37) | 364(44.33) | < 0.001 |
| Weight, Kg | 71.12 ± 12.40 | 73.84 ± 12.23 | 74.70 ± 13.90 | < 0.001 |
| BMI; kg/m2 | 27.58 ± 4.30 | 27.93 ± 4.44 | 27.68 ± 4.72 | 0.693 |
| WC, cm | 96.80 ± 10.20 | 98.24 ± 10.18 | 97.93 ± 10.68 | 0.033 |
| Sleep Duration, h/day | 7.12 ± 1.20 | 7.06 ± 1.21 | 7.09 ± 1.19 | 0.684 |
| Physical activity, MET-min/day | 39.63 ± 6.35 | 40.05 ± 7.33 | 42.16 ± 9.12 | < 0.001 |
| Socioeconomic status; rank | 3.03 ± 1.32 | 3.16 ± 1.33 | 3.08 ± 1.34 | 0.442 |
| Anti-diabetic agents, n% | 45(6.35) | 63(6.25) | 44(5.36) | 0.648 |
| Anti-lipidemic agents, n% | 41(5.79) | 43(4.27) | 31(3.77) | 0.146 |
| Dietary supplements, n% | 195(27.54) | 247(24.50) | 201(24.48) | 0.286 |
| Smoking status, n% | < 0.001 | |||
| Non-smoker | 359(50.84) | 472(46.82) | 317(38.61) | |
| Passive smoker | 291(41.11) | 401(39.78) | 305(37.15) | |
| Former smoker | 29(4.10) | 66(6.55) | 87(10.59) | |
| Current smoker | 28(3.95) | 69(6.85) | 112(13.65) | |
| Education, n% | 0.115 | |||
| Illiterate | 339(47.88) | 461(45.73) | 368(44.82) | |
| Elementary school | 192(27.12) | 256(25.37) | 235(28.62) | |
| Middle school | 75(10.59) | 100(9.92) | 76(9.26) | |
| High school | 54(7.63) | 95(9.44) | 87(10.60) | |
| Academic degree | 48(6.78) | 96(9.54) | 55(6.70) | |
| HSI category; n% | 0.051 | |||
| Steatosis unlikely | 49 (6.9%) | 77 (7.6%) | 77 (9.4%) | |
| Indeterminate | 272 (38.4%) | 424 (42.1%) | 355 (43.2%) | |
| Steatosis likely | 387 (54.7%) | 507 (50.3%) | 389 (47.4%) | |
| FIB-4 category; n% | 0.569 | |||
| Fibrosis unlikely | 631 (89.1%) | 892 (88.5%) | 713 (86.8%) | |
| Indeterminate | 73 (10.3%) | 113 (11.2%) | 104 (12.7%) | |
| Fibrosis likely | 4 (0.6%) | 3 (0.3%) | 4 (0.5%) | |
Abbreviations. BMI: body mass index, WC: waist circumference, MET: metabolic equivalent, HSI: hepatic steatosis index, FIB-4: fibrosis-4 index
Data are expressed as the means ± standard deviations and numberers (frequencies).
P-values were derived using the one-way ANOVA for quantitative variables and the Chi-squared test.
Each cup was equivalent to 240 ml
Table 2 summarizes the relative risks associated with worsening hepatic steatosis resulting from tea consumption. The crude model indicated no significant association between tea consumption and worsening hepatic steatosis, with T1 as the reference group (RR for T2: 1.10, 95% CI: 0.86–1.41; T3: 1.15, 95% CI: 0.91–1.46; P-trend = 0.234). Subsequent models (Model 1 to Model 3), which were adjusted for various confounders, such as energy intake and physical activity, revealed no significant changes in risk across tertiles, indicating that higher tea consumption was not associated with an increased risk of worsening hepatic steatosis. Table 3 highlights the relative risk for improvement in hepatic steatosis. The crude model indicated a significant reduction in risk for both T2 (RR: 0.64, 95% CI: 0.48–0.86) and T3 (RR: 0.69, 95% CI: 0.51–0.94) patients compared with T1 patients, with a P-trend of 0.016. These findings suggest that greater tea consumption may be associated with a lower likelihood of improvement in hepatic steatosis. The trend persisted in the adjusted models, notably in Model 3 (RR for T2: 0.67, 95% CI: 0.50–0.91; T3: 0.73, 95% CI: 0.53–0.99; P-trend = 0.046), reinforcing the unfavorable effect of tea consumption.
Table 2.
The relative risk for worsening hepatic steatosis
| Model | Tea consumption Tertiles | P-trend | ||
|---|---|---|---|---|
| T1 1.92 > cups |
T2 | T3 2.88 < cups |
||
| Model crude | 1 | 1.10 (0.86–1.41) | 1.15 (0.91–1.46) | 0.234 |
| Adjusted Model 1 | 1 | 1.04 (0.81–1.34) | 1.04 (0.81–1.32) | 0.754 |
| Adjusted Model 2 | 1 | 1.04 (0.81–1.33) | 1.01 (0.79–1.29) | 0.914 |
| Adjusted Model 3 | 1 | 1.03 (0.80–1.33) | 0.95 (0.75–1.22) | 0.724 |
Data are shown as means (95% confidence interval) and obtained from Poisson regression models.
Model 1: Adjusted for energy
Model 2. Adjusted for energy and physical activity
Model 3. Adjusted for energy, physical activity, SES, education, smoking, sleep duration, drug usage, and dietary supplements
Table 3.
The relative risk for improvement of hepatic steatosis
| Model | Tea consumption Tertiles | P-trend | ||
|---|---|---|---|---|
| T1 1.92 > cups |
T2 | T3 2.88 < cups |
||
| Model crude | 1 | 0.64 (0.48–0.86) | 0.69 (0.51–0.94) | 0.016 |
| Adjusted Model 1 | 1 | 0.67 (0.50–0.90) | 0.74 (0.54–1.02) | 0.059 |
| Adjusted Model 2 | 1 | 0.67 (0.50–0.90) | 0.75 (0.54–1.02) | 0.060 |
| Adjusted Model 3 | 1 | 0.67 (0.50–0.91) | 0.73 (0.53–0.99) | 0.046 |
Data are shown as means (95% confidence interval) and obtained from Poisson regression models.
Model 1: Adjusted for energy
Model 2. Adjusted for energy and physical activity
Model 3. Adjusted for energy, physical activity, SES, education, smoking, sleep duration, drug usage, and dietary supplements
Table 4 shows the relative risk factors for worsening hepatic fibrosis. The crude model revealed no significant differences across tertiles (P-trend = 0.549). Subsequent adjusted models (Models 1–4) also failed to demonstrate significant associations, indicating that tea consumption does not significantly influence the risk of worsening hepatic fibrosis. As shown in Table 5, the analysis of improvement in hepatic fibrosis revealed no significant differences across tertiles, with the P-trend ranging from 0.239 to 0.568 in various models. These findings suggest that tea consumption does not significantly affect the likelihood of improvement in hepatic fibrosis.
Table 4.
The relative risk for worsening of hepatic fibrosis
| Model | Tea consumption Tertiles | P-trend | ||
|---|---|---|---|---|
| T1 1.92 > cups |
T2 | T3 2.88 < cups |
||
| Model crude | 1 | 1.06 (0.81–1.40) | 0.92 (0.68–1.23) | 0.549 |
| Adjusted Model 1 | 1 | 1.00(0.76–1.32) | 0.83(0.61–1.12 | 0.220 |
| Adjusted Model 2 | 1 | 1.02(0.77–1.34) | 0.86(0.63–1.16) | 0.309 |
| Adjusted Model 3 | 1 | 1.02(0.77–1.35) | 0.86(0.63–1.16) | 0.310 |
| Adjusted Model 4 | 1 | 1.01 (0.76–1.33) | 0.83 (0.61–1.13) | 0.226 |
Data are shown as means (95% confidence interval) and obtained from Poisson regression models.
Model 1: Adjusted for gender
Model 2: Adjusted for gender and energy
Model 3. Adjusted for gender, energy, and physical activity
Model 4. Adjusted for gender, energy, physical activity, SES, education, smoking, sleep duration, drug usage, and dietary supplements
Table 5.
The relative risk for improvement of hepatic fibrosis
| Model | Tea consumption Tertiles | P-trend | ||
|---|---|---|---|---|
| T1 1.92 > cups |
T2 | T3 2.88 < cups |
||
| Model crude | 1 | 1.28 (0.84–1.96) | 1.29 (0.83–2.00) | 0.281 |
| Adjusted Model 1 | 1 | 1.20 (0.78–1.84) | 1.15 (0.74–1.81) | 0.568 |
| Adjusted Model 2 | 1 | 1.30 (0.84–2.00) | 1.33 (0.84–2.10) | 0.239 |
| Adjusted Model 3 | 1 | 1.30 (0.85–2.01) | 1.32 (0.83–2.08) | 0.259 |
| Adjusted Model 4 | 1 | 1.23 (0.80–1.90) | 1.17 (0.74–1.86) | 0.545 |
Data are shown as means (95% confidence interval) and obtained from Poisson regression models.
Model 1: Adjusted for gender
Model 2: Adjusted for gender and energy
Model 3. Adjusted for gender, energy, and physical activity
Model 4. Adjusted for gender, energy, physical activity, SES, education, smoking, sleep duration, drug usage, and dietary supplements
As shown in Fig. 1, a significant correlation was observed between tea consumption and sugar intake (Pearson correlation coefficient: 0.551; P-value:0.001). When we also adjusted the intake of sugar, the association between tea consumption and improvement of hepatic steatosis became statistically non-significant [T2 (RR: 0.71, 95% CI: 0.52–0.96); T3 (RR: 0.83, 95% CI: 0.58–0.1.18); P-trend: 0.239].
Fig. 1.
Association between sugar intake and tea consumption
Discussion
Tea is one of the most popular beverages worldwide and is known for its health benefits. However, the effects of its active compounds on NAFLD have not been extensively studied. Tea is rich in bioactive compounds that may influence NAFLD, including catechins, flavonoids, theanine, tea pigments, and polysaccharides [13]. In this study, we investigated the relationship between tea consumption and liver health by evaluating hepatic steatosis and liver fibrosis in the adult population of the Ravansar cohort. Our findings suggest that increased tea consumption is not significantly associated with a greater risk of worsening hepatic steatosis or fibrosis. Interestingly, we observed a lower likelihood of improvement in hepatic steatosis among those with higher tea intake. We recorded various factors, including age, BMI, socioeconomic status, education, smoking status, energy intake, physical activity, drugs, and dietary supplements. These confounding factors were adjusted in Poisson regression to explore the associations between daily tea consumption and liver health. People often add sugar to their tea to enhance its flavor, which may influence the relationship between tea consumption and liver health [14]. However, the extent of this collinearity can vary based on individual preferences, cultural practices, and dietary habits.
Our findings suggest that the observed association between tea consumption and the lack of improvement in hepatic steatosis may be influenced by the concomitant intake of sugar commonly consumed with tea in Iranian culture. Tea is traditionally accompanied by sugar cubes or other sweeteners, which may contribute to higher sugar intake and subsequently affect liver health. After adjusting for sugar intake, the association between tea consumption and improvement in hepatic steatosis became statistically non-significant, further highlighting the potential mediating role of sugar. In a meta-analysis conducted by Hongwei Chen et al., it was demonstrated that consumers of sugar-sweetened beverages (SSBs) are at a significantly increased risk of developing non-alcoholic fatty liver disease (NAFLD). These results align with our study’s observations [15].
Supporting our findings, Yang et al.‘s study revealed no significant associations between the daily consumption of green, oolong, black, or jasmine tea and the prevalence of newly diagnosed NAFLD in Chinese adults [16]. Previous research has primarily focused on the effects of green tea extracts on NAFLD. The protective effects of green tea against NAFLD are largely attributed to the catechins it contains. Green tea is rich in polyphenolic catechins, which have hypolipidemic, thermogenic, antioxidant, and anti-inflammatory properties that might help reduce the onset and progression of NAFLD [8].
Evidence from in vitro and in vivo studies suggests that green tea can reduce dietary lipid absorption [17], decrease lipid buildup in the liver and adipose tissue [18], enhance insulin sensitivity [19], and provide antioxidant benefits [20]. A previous meta-analysis of four clinical trials indicated that green tea extract supplementation positively impacts risk factors related to NAFLD, significantly modifying blood levels of alanine and aspartate aminotransferases. Additionally, supplementation with green tea extract has beneficial effects on BMI, triacylglycerol, total cholesterol, and low-density lipoprotein cholesterol [21].
In contrast, Shuyu Liu et al. reported that tea consumption lowers the incidence of NAFLD and improves the severity of hepatic fibrosis in individuals already affected by this condition. Their research suggested that increased black tea intake is linked to a reduction in the severity of hepatic fibrosis, highlighting its protective effects against NAFLD [22]. This may be due to the superior effectiveness of black tea polyphenols compared to green tea in facilitating weight loss and addressing obesity, a key factor in treating NAFLD [23]. Epigallocatechin gallate, a tea polyphenol, has been shown to help protect rats from nonalcoholic fatty liver disease and related endotoxemia by regulating gut microbiota imbalances, improving intestinal barrier function, and reducing associated inflammation. Additionally, Gaolong Zuo et al. reported similar findings regarding the protective effects of epigallocatechin gallate against NAFLD and endotoxemia [24].
Despite the longitudinal design of this study, the extended follow-up duration, and the thorough adjustment for covariates—factors that enhance our findings regarding the causal relationship between tea consumption and liver health outcomes—we acknowledge certain limitations. One limitation is that the food frequency questionnaire (FFQ) did not differentiate between green and black tea consumption, which may have affected the interpretation of our results concerning tea’s association with liver conditions. Additionally, since the questionnaire relied on self-reported data, there is a potential for recall bias, which could lead to inaccuracies in the reported amount of tea consumed. While we accounted for a wide range of covariates, it remains possible that unmeasured factors may influence the observed associations. Moreover, previous studies examining the relationship between tea and NAFLD have typically reported effects at doses exceeding 500 mg of catechins per day, roughly equivalent to nine cups of green tea. It is plausible that the lack of a significant association in our study is due to the low percentage of participants in the general population who consume sufficient amounts of tea daily.
Conclusion
Overall, our findings underscore the complexity of the role of tea in liver health. While tea consumption was not associated with an increased risk of hepatic steatosis or fibrosis progression, the observed association with reduced improvement in hepatic steatosis highlights the need for further investigation. Understanding the potential adverse and beneficial effects of different tea types and doses may lead to more tailored recommendations for tea consumption in populations at risk for hepatic conditions.
Acknowledgements
The authors thank the PERSIAN cohort Study collaborators and of Kermanshah University of Medical Sciences.
Author contributions
J.M, Y.P conceived the idea of the study, developed the statistical analysis plan and conducted the statistical analyses D.S contributed to the interpretation of the results, and SH.Q. and N.SH. drafted the original manuscript. All authors reviewed the manuscript draft and revised it critically on intellectual content. All authors approved the final version of the manuscript to be published.
Funding
None.
Data availability
The data analyzed in the study are available from the corresponding author upon reasonable request.
Declarations
Ethics approval and consent to participate
The study was approved by the ethics committee of Kermanshah University of Medical Sciences (IR.KUMS.REC.1403.038). All methods were carried out in accordance with relevant guidelines and regulations. All the participants provided oral and written informed consent. All methods were carried out in accordance with the relevant guidelines and regulations. This study was conducted in accordance with the Declaration of Helsinki.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
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Data Availability Statement
The data analyzed in the study are available from the corresponding author upon reasonable request.