Dietary fiber has a significant impact on health and aging. Numerous studies show that individuals who consume high levels of fiber live longer and experience less disease than their counterparts [1
]. The benefits are consistently inverse, dose–response, and apply to both men and women. As fiber intake increases, risk of disease and premature death decreases. In short, fiber consumption is an important part of healthy aging.
Among the key recommendations of the recent Dietary Guidelines for Americans (2015–2020), individuals are encouraged to consume foods that are nutrient dense and “retain naturally occurring components, such as dietary fiber” [3
]. The Guidelines define fiber as nondigestible carbohydrates and lignin that are intact in plants and present naturally in foods. According to the Guidelines, fiber can also be extracted from natural sources or synthetically manufactured and added to foods. The Guidelines recommend the intake of at least 14 g of fiber per 1000 kcal [3
]. However, in the United States, intake is only about one-half that amount (see Table 1
Fiber consumption is inversely related to a number of age-related killers. At least five prospective cohort studies have focused on fiber intake and total mortality, showing that as fiber consumption increases, mortality decreases [4
]. Meta-analysis results indicate that for every 10 g increase in fiber consumption, risk of death decreases by 11% [2
]. Moreover, in the same meta-analysis, when adults with high fiber intake were compared to those with low intake, mortality was 23% lower among those with high consumption [2
Besides total mortality, diseases common to advancing age, such as heart disease, stroke, type 2 diabetes, breast cancer, and others are also less common among those with high fiber intake [9
]. For example, in a 2015 meta-analysis by Wu et al. that analyzed 18 prospective cohort studies, coronary heart disease mortality was 17% lower in those with the highest fiber consumption compared to those with the lowest [15
]. In a meta-analysis by Threapleton et al., risk of stroke was 7% lower for each 7 g of fiber eaten per day [14
]. Moreover, Schulze et al. reported in a meta-analysis summarizing nine prospective cohort investigations that risk of developing type 2 diabetes was 33% lower in adults with high cereal fiber intake compared to those with low consumption [16
]. A meta-analysis by Dong et al. that included 10 prospective cohort investigations indicated that breast cancer for the highest compared to the lowest fiber consumption was 11% lower [17
]. Similarly, dose–response analysis showed that for every 10 g per day increment in dietary fiber intake there was a 7% reduction in breast cancer risk [17
There are several pathways by which fiber consumption could decrease risk of disease and premature mortality. One is telomeres. Telomeres are nucleoprotein caps positioned at both ends of chromosomes, analogous to the caps that protect the ends of shoe laces. Each time mitotic cells divide, telomeres shorten and part of the telemetric DNA fails to replicate. Over time, cells undergo a limited number of divisions. Hence, the shortening of telomeres is a mechanism of biologic aging and a measure of the senescence of cells [18
The length of telomeres is highly related to chronological age [20
]. In fact, telomeres are sometimes called the molecular clock of cells [22
]. As age increases, telomeres become shorter by about 15 base pairs per year [24
]. Telomere length is also a key factor in the pathobiology of disease and premature mortality [18
]. Individuals with shorter telomeres tend to have higher rates of cancer [26
], heart disease [28
], diabetes [31
], osteoporosis [33
], and other chronic conditions [18
], including total mortality [34
Factors other than chronological age also affect telomere length and, therefore, biologic aging. For example, adults who engage in high levels of physical activity have longer telomeres than their counterparts [21
]. Obese individuals have shorter telomeres than normal weight persons [35
], and smokers have shorter telomeres than nonsmokers [36
]. Low sleep quality and quantity are also significant predictors of telomere length [37
], as is low socioeconomic level [25
Diet also seems to affect telomere length. Some foods and nutrients contribute to longer telomeres and therefore reduce biologic aging, whereas others account for shorter telomeres. For example, individuals who consume high levels of nuts and seeds tend to have longer telomeres than those with lower intakes [38
], whereas in the Multi-Ethnic Study of Atherosclerosis (MESA), processed meat intake was inversely related to telomere length, signifying increased aging [39
]. Using a case-control design, Hou et al. [40
] found that fruit intake was positively related to telomere length in a study conducted in Poland, but in a large sample of U.S. adults, Tucker found that as caffeine consumption increased, telomeres decreased in length [24
]. In multiple investigations, intake of fats and oils has also been associated with shorter telomeres [41
]. Similarly, persons with higher intakes of gamma-tocopherol tend to have shorter telomeres than their counterparts [43
]. Conversely, Marcon et al. showed that individuals with higher vegetable consumption have longer telomeres than others [44
To date, few investigations have studied the effect of fiber consumption on biologic aging. Results from the Nurses’ Health Study, which investigated white women primarily and no men, indicated that among a variety of dietary factors, fiber intake was directly related to telomere length [45
]. Furthermore, as shown in a 2017 review by Rafie et al., a number of other studies have examined the relationship between various foods, food groups, and eating patterns and telomere length [46
]. Results have been mixed. Some of the foods and food groups have been good sources of fiber, such as whole grains, cereals, nuts, legumes, fruits, and vegetables. However, fiber intake specifically has rarely been associated with biologic aging [46
Numerous investigations indicate that dietary fiber reduces risk of disease and premature death. Some of the health benefits associated with dietary fiber could be a result of the preservation of telomeres, or, in other words, reduced cell aging. To date, the relationship between fiber consumption and telomere length has received minimal attention, and the association has never been evaluated in a large sample representing men and women of the United States. Hence, the purpose of the present study was to determine the extent to which fiber intake accounts for differences in telomere length in 5674 randomly selected adults from the National Health and Nutrition Examination Study (NHANES). A secondary objective was to ascertain the effects of several potential confounding factors, including age, gender, race, housing status, misreported energy intake, smoking, physical activity, alcohol use, and body mass index, on the fiber and telomere relationship.
Individual sample weights were utilized so that the results are generalizable to the civilian adult population of the United States. Average (±SE) age of the sample was 46.5 ± 0.5 years, mean fiber consumption was 15.6 ± 0.3 g per day, and average fiber intake per 1000 kcal was 7.5 ± 0.1 g per day. Using estimated energy intake instead of self-reported, average fiber intake per 1000 kcal was 6.7 ± 0.1 g per day. Mean telomere length was 5826 ± 39 base pairs. Additional descriptive information for the sample is displayed in Table 1
Linear regression showed that age was predictive of leukocyte telomere length (F = 598, p < 0.0001). The Pearson correlation was −0.44 (p < 0.0001). For each additional year of age, telomere length was 15.5 base pairs shorter, on average.
Descriptive information about each categorical variable is displayed in Table 2
. For each subgroup, the number of subjects (N
) is given in unweighted form, along with the percentage and the standard error of the percentage. The percentages displayed in Table 2
represent the weighted distribution of the sample. Attention should be focused more on the weighted percentages because they are generalizable to the civilian, noninstitutionalized adults in the United States.
With both fiber intake (grams per 1000 kcal) and telomere length treated as continuous variables, regression analysis showed that the relationship between the two variables was linear. After adjusting for differences in age, gender, race, housing status, and misreported energy intake, the association between fiber consumption (per 1000 kcal) and telomere length was significant (F = 9.5, p = 0.0045), with 29 degrees of freedom (df) in the denominator. Specifically, for each increase of 1 gram of fiber per 1000 kcal, telomeres were 8.3 base pairs longer, on average. After adjusting for all of the covariates simultaneously (age, gender, race, housing status, BMI, smoking pack years, physical activity, alcohol use, and misreported energy intake), the relationship remained linear and significant. For each increase of 1 g of fiber per 1000 kcal, telomeres were 6.7 base pairs longer, on average (F = 7.6, p = 0.0101).
shows mean differences in telomere length after adjusting for age, gender, race, housing status, and misreported energy intake (Model 1). Model 2 displays mean differences in telomeres across fiber intake categories after adjusting for differences in all the potential confounding factors, including age, gender, race, housing status, misreported energy intake, BMI, smoking, physical activity, and alcohol use. The difference between those with Moderate fiber intake and those with Low intake was not significant. However, adults with High fiber consumption had significantly longer telomeres than those with Moderate or Low fiber levels (F
= 3.8, p
= 0.0357). On average, there were 75 base pairs separating those in the High compared with the Low fiber intake categories, with all of the potential confounders controlled.
Effect modification was tested with subjects stratified according to BMI levels. Focusing on individuals with BMI levels below 25 kg/m2, the relationship between fiber intake per 1000 kcal and telomere length was evaluated. After adjusting for differences in age, gender, race, housing status and misreported energy intake, for each 1 g increment in fiber consumption, telomere length showed a tendency to be longer by 10.0 base pairs (F = 3.95, p = 0.0563). With the sample delimited to overweight and obesity individuals, a BMI of 25 kg/m2 or higher, the fiber–telomere association was linear and significant (F = 4.89, p = 0.0350). Specifically, for each 1 g increase in fiber consumption per 1000 kcal, telomeres were 6.4 base pairs longer, on average, with age, gender, race, housing status, and misreported energy intake controlled. After adjusting for all the covariates, for each 1 g increase or decrease in fiber intake, telomeres remained 6.4 base pairs longer or shorter, respectively (F = 4.76, p = 0.0374). Similarly, with BMI delimited to obese adults—BMI > 30 kg/m2—the association between fiber intake and telomere length was linear and significant (F = 5.92, p = 0.0213), with age, gender, race, housing status, and misreported energy intake controlled. Specifically, among the obese, telomere length was 10.8 base pairs longer for each increment in fiber consumption per 1000 kcal. Likewise, after adjusting for all the covariates, the relationship remained linear and significant (F = 6.66, p = 0.0152), and telomeres were 11.9 base pairs longer for each 1 g increase in fiber consumption per 1000 kcal.
The main objective of the present investigation was to evaluate the association between dietary fiber intake (per 1000 kcal) and leukocyte telomere length in a randomly selected NHANES (1999–2002) sample of 5674 adults, representative of the U.S. population. A secondary purpose was to determine the extent to which a number of demographic and lifestyle factors influence the relationship between fiber consumption and telomere length.
Results showed that total fiber intake was low, signifying that U.S. adults typically consume inadequate amounts of fiber. As shown in Table 1
, median total fiber consumption was 13.6 g per day. The Dietary Guidelines for Americans (2015–2020) recommend that individuals consume at least 14 g per 1000 kcal [3
]. When taking into account energy intake, the median intake in this U.S. sample was only 6.6 g per 1000 kcal—less than one-half the amount recommended by the Guidelines. Even adults reaching the 90th percentile in the present sample (12.8 g per 1000 kcal) fell short of the recommended standard. With self-reported energy intake replaced with estimated energy consumption, the median intake was even less at 5.7 g per 1000 kcal.
In the present study, women had to consume about 10 g of dietary fiber per 1000 kcal or more and men had to eat at least 8.7 g per 1000 kcal to be assigned to the High fiber category—the upper sex-specific quartile. Given the significant advantage participants had when they achieved these levels of fiber consumption and attained the highest quartile, it appears that adults may not have to reach the Guideline recommendation of 14 g per 1000 kcal to receive some cellular aging benefits.
Despite the overall low fiber intake, there was a significant linear relationship between fiber consumption and telomere length. The more fiber subjects consumed, the longer their telomeres tended to be. Specifically, for each 1 g increment of fiber intake per 1000 kcal, telomeres were 6.7 base pairs longer, on average, after adjusting for all the covariates. Given each additional year of chronological age was associated with telomeres that were 15.5 base pairs shorter, on average, it appears that a 10 g increase in fiber per 1000 kcal would be associated with telomeres that are 67 base pairs longer. On average, this would equate to 4.3 fewer years of biologic aging (67 base pairs ÷ 15.5).
Treating fiber intake as a categorical variable, quartiles were used to separate participants. Given there was a difference of 93 base pairs between the lowest and highest quartiles of fiber intake, with age, gender, race, housing status, and misreported energy intake controlled, the findings indicate that adults with High fiber consumption have a cell aging advantage of about 6.0 years over those with low intakes (93 ÷ 15.5). Adjusting for differences in all the potential confounders simultaneously (age, sex, race, housing status, misreported energy intake, smoking pack years, BMI, energy intake, alcohol use, and physical activity) attenuated the biologic aging benefit some. Specifically, after controlling for all the covariates, the telomere length difference was 75 base pairs. Hence, the cellular aging difference was approximately 4.8 years (75 base pairs ÷ 15.5)—a significant and meaningful spread.
Calculating the biologic aging advantages or disadvantages of other lifestyle factors can add perspective to the fiber intake and telomere relationship. For example, research shows that for each 100 mg of caffeine consumed per day, adults have about 2.3 years of increased cell aging [24
]. Conversely, consumption of nuts and seeds has been shown to predict less biologic aging. Specifically, for each 200 kcal of nuts and seeds consumed per day, adults have 1.7 years less biological aging [38
]. Furthermore, consumption of sugar-sweetened soda appears to increase cell aging by 1.8 years for each 8 ounce serving per day [62
]. Clearly, comparing fiber consumption to caffeine use, nut and seed consumption, and sugar-sweetened soda intake suggests that fiber intake plays a meaningful role in biologic aging differences.
Adjusting for differences in the lifestyle variables in addition to the demographic factors weakened the relationship between fiber intake and telomere length by about 15%. However, the association remained significant and meaningful. Apparently, only a small portion of the differences in telomere length across the fiber intake groups can be attributed to differences in smoking, BMI, alcohol use, and physical activity.
In the present investigation, fiber intake was linearly related to telomere length. Higher levels of fiber consumption were correlated with longer telomeres, suggesting that a high-fiber diet may account for reduced biologic aging. Nevertheless, consumption of specific nutrients rarely occurs in isolation. In the present study, it is likely that individuals who consumed large amounts of fiber also ate significant quantities of fruits, vegetables, and whole grains [3
]. Fiber intake is strongly linked to decreased risk of disease and premature death [2
]. Likewise, consumption of fruits, vegetables, and whole grains is related to reduced disease and mortality [3
]. Some of the health benefits associated with consumption of fruits, vegetables, and whole grains may be due to high levels of fiber intake. Similarly, some of the biologic aging advantages ascribed to high fiber intake may be a result of high intake of fruits, vegetables, and whole grains. Diets high in fiber and diets with significant amounts of fruits, vegetables, and whole grains go hand in hand. In the present study, part of the association between fiber intake and biologic aging could be a function of differences in fruit, vegetable, and whole grain consumption.
To date, only one other large investigation has focused on the relationship between fiber intake and telomere length [45
]. Telomere data were gathered via blood samples collected in 1989 and 1990. Using 2284 primarily white women and no men from the Nurses’ Health Study, Cassidy et al. determined that fiber consumption is directly related to telomere length. As expected, chronological age was inversely related to telomere length (r
= −0.11, p
< 0.0001), but the association was substantially weaker than the relationship between age and telomere length found in the present study (r
= −0.44, p
In an investigation that used rats as subjects, the effect of dietary fiber on telomere length was studied indirectly [65
]. The rats were fed cooked meat at 15%, 25%, and 35% of their diets. Colonocyte telomere length was the outcome measure. After a month-long intervention, results showed that the telomere shortening effect of the high-meat diet was attenuated by resistant starch (insoluble fiber) intake. In short, dietary fiber reduced the unfavorable effects of the high-meat diet on the colon [65
In 2017, Rafie et al. published a review of dietary variables as they relate to differences in telomere length [46
]. A total of 17 studies were included in the review. Three of the studies indicated that the Mediterranean dietary pattern is associated with less cell aging. Similarly, five investigations showed that fruits and vegetables are favorably related to telomere length. Except for the Mediterranean diet pattern and fruit and vegetable consumption, findings were inconsistent. The majority of studies included in the review indicated no relationship between diet and telomere length. Only the Nurses’ Health Study by Cassidy focused on fiber intake specifically and telomere length [45
A favorable relationship between telomere length and health outcomes is not automatic. Some investigations have revealed no relationship between markers of risk or disease and telomere length. For example, Njajou et al. studied 3075 men and women aged 70–79 years old and found no association between telomere length and overall mortality [66
]. Additionally, mortality due to cancer and cardiovascular disease was not higher among those with shorter telomeres [66
]. Similarly, Bischoff et al. uncovered no relationship between telomere length and survival in 812 adults, ages 73–101 [67
]. Moreover, in a study conducted by the Telomeres Mendelian Randomization Collaboration et al., longer telomeres were actually related to increased risk of developing some cancers [68
]. Consequently, the association between telomere length, disease, and mortality is still debated.
In the present study, fiber intake accounted for significant and meaningful differences in telomere length. Why? Although the specific mechanism is not known, it is well established that telomere length and biological aging are strongly linked to inflammation and oxidative stress [69
]. It is likely that the benefits of a high-fiber diet stem partly from this relationship.
Diet can contribute positively or negatively to inflammation and oxidative stress, as shown by Zhou et al. [73
]. Of the many dietary factors affecting inflammation and oxidative stress, fiber is significant. Numerous investigations show that as fiber intake increases, markers of inflammation and oxidative stress tend to decrease [10
]. For example, in an investigation by Ma et al., which studied 524 individuals, both cross-sectional and prospective analyses indicated that fiber consumption protects against elevated C-reactive protein (CRP) levels [81
]. Similarly, in a study of almost 5000 NHANES participants, King et al. showed that those with above-average levels of fiber consumption had significantly lower concentrations of CRP, even after adjustments for a host of demographic and lifestyle factors [82
]. Additionally, in a sample of approximately 3500 older men, dietary fiber was inversely related to the inflammatory markers CRP and interleukin-6 [83
]. It is likely that some, if not most, of the favorable association between fiber and biologic aging in the present study was a function of reduced inflammation and oxidative stress resulting from high levels of fiber consumption.
An additional mechanism that could explain some of the shared variance between fiber intake and telomere length is blood glucose levels. As blood glucose concentrations increase, levels of inflammation and oxidative stress increase [84
]. Fiber consumption slows the absorption of sugars, lowering blood glucose levels, insulin resistance, and risk of diabetes significantly [83
]. Therefore, it is logical that high fiber intake could slow biologic aging and protect telomeres by reducing inflammation and oxidative stress caused by elevated blood sugar concentrations.
The present investigation had multiple limitations. First, NHANES data are cross-sectional. Consequently, causal conclusions are unwarranted. Second, participants who reported high levels of fiber intake could represent unique individuals who have lifestyles that are healthier than others. Because of this threat, a number of potential confounding factors were controlled statistically, including age, gender, race, housing status, misreported energy intake, smoking pack years, BMI, alcohol use, and physical activity. These variables had little effect on the fiber–telomere association. However, other unmeasured factors could account for some of the association uncovered in this study. Third, the survey provided data about total fiber intake, but not insoluble or soluble fiber consumption. Information about fiber types would have strengthened the present study, but insoluble and soluble fiber data were not available and therefore could not be used in the present study. Finally, leukocyte telomere length can be altered by different diseases, particularly some cancers. Associations tend to be stronger for rarer cancers and at tissue locations with lower rates of stem cell division. The current study did not control for the presence of cancer or other disorders and, therefore, the results could be influenced by these diseases.
The present study also had several strengths. First, the sample was multiracial, large, and randomly selected using a multistage, probability sampling design. Hence, the findings are representative of the civilian, noninstitutionalized adult population of the United States. Second, a number of demographic and lifestyle variables were controlled statistically, minimizing their effect on the relationship. Results showed that the fiber–telomere relationship was independent of these factors. Third, a reputable laboratory was employed to measure leukocyte telomeres. Well-accepted methods were used to produce the telomere data, and chronological age was strongly related to telomere length, as it should be.