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. Author manuscript; available in PMC: 2025 Aug 5.
Published in final edited form as: Eur J Epidemiol. 2024 Nov 6;39(10):1183–1197. doi: 10.1007/s10654-024-01165-x

Influence of consuming coffee and other beverages in adolescence on risk of type 2 diabetes in adulthood

Derrick Johnston Alperet 1,2,3,†, Xiaowen Wang 1,†, Lu Zhu 1, Klodian Dhana 4, Jorge E Chavarro 1,5,6,7, Jess Haines 8, Frank B Hu 1,6,7, Walter C Willett 1,6,7, Qi Sun 1,6,7,9
PMCID: PMC12324064  NIHMSID: NIHMS2099253  PMID: 39503925

Abstract

Background:

Dietary strategies for type 2 diabetes (T2DM) prevention have mainly focused on solid foods and nutrients. Emanating evidence suggests that beverage consumption in adulthood may also influence T2DM development, whereas the role of beverages during adolescence remains unknow.

Objective:

To examine adolescent beverages consumption, and their changes from adolescence to adulthood in relation to T2DM risk in adulthood.

Methods:

This prospective cohort study, conducted within the Nurses’ Health Study II (NHS II), enrolled 41,317 women who completed a food-frequency questionnaire (FFQ) regarding their diet in high school and had no diabetes, cardiovascular disease, or cancer at baseline (1997). Beverage consumption including coffee, tea, regular or diet soda, fruit juice or milk, was assessed using the FFQ. Cox proportional hazards models were utilized to estimate hazard ratios (HRs) for the association between beverage consumption in adolescence and risk of incident type 2 diabetes (T2DM) in adulthood, adjusting for potential confounders.

Results:

During 725,650 person-years of follow-up, 2,844 participants developed T2DM. After adjustment for demographic, lifestyle and dietary risk factors, comparing ≥1 serving/day with non-consumers, adolescent coffee [HR, 0.86 (95% confidence interval: 0.75 to 0.98); P-trend = 0.02)] and orange juice [HR, 0.83 (0.71 to 0.96); P-trend = 0.0008)] consumption was associated with lower T2DM risk, whereas, regular soda [HR, 1.37 (1.20 to 1.57); P-trend < 0.0001)] and iced tea [HR, 1.41 (1.21 to 1.65); P-trend < 0.0001)] intake was associated with higher T2DM risk. Increased coffee intake from adolescence to adulthood in 1991 was associated with a lower T2DM risk [HR, 0.70 (0.61 to 0.80); P-trend < 0.0001), comparing ≥+3 servings/day with no change], whereas the opposite was observed for increased regular soda [HR, 1.20 (1.06 to 1.35); P-trend = 0.004), comparing ≥+1 or more servings/week with no change)] and diet soda consumption [HR, 1.59 (1.41 to 1.80); P-trend = 0.0002), comparing ≥+2 servings/day with no change].

Conclusion:

Adolescent consumption of coffee or orange juice intake was associated with a lower risk of T2DM, whereas the opposite was observed for intake of regular soda or iced tea. In addition, increased coffee intake was associated with a lower diabetes risk, whereas the opposite was observed for regular or diet soda intake. These data highlight a potentially important role of beverage intake at early life in the etiology of diabetes during adulthood.

Keywords: Coffee, tea, fruit juice, soda, regular soda, diet soda, milk, adolescent, adulthood, metabolic health, type 2 diabetes mellitus, non-insulin dependent diabetes mellitus, humans

1. INTRODUCTION

Owing to heterogeneity in sugar, fiber, vitamins and phytochemical content, different beverages are likely to differentially influence the development of T2DM. Indeed, numerous prospective studies have shown that a higher consumption of regular soda(1), diet soda(1, 2) or fruit juice(2) in adulthood is associated with a higher risk of T2DM, whereas, a higher intake of coffee(3) or tea(4) is associated with a lower risk of T2DM later in life. In contrast to the abundant evidence often focusing on the effects of middle-aged intake on T2DM risk, few studies have examined early-life intake of beverages in relation to T2DM risk in adulthood. Since the landmark trio of studies(5–7) by Barker and colleagues, evidence on the influence of environmental factors, such as nutrition, during early development on risk of disease in adult life has been mounting in support of the “Developmental Origins of Health and Disease” (DOHaD) framework (8). While research testing DOHaD hypotheses has primarily focused on early life periods, late developmental phases, such as adolescence, with significant physiological plasticity (e.g. puberty, spiked growth) when life-long health-related dietary and lifestyle habits are established, receive little attention (9).

In this regard, it is not well understood if intake of different beverages in adolescence influences risk of T2DM in adulthood differentially. To address this gap in knowledge, we conceived the current study to investigate whether consumption of commonly-consumed beverages in adolescence influences the risk of T2DM in adulthood. Moreover, potential changes in beverage intake during the transition from adolescence to adulthood could have a lasting impact on metabolic health. In light of this, we also evaluated changes of beverage intake from adolescence to early adulthood in relation to T2DM risk later in life.

2. METHODS

2.1. Design and study population

At its inception in 1989, 116,671 registered female nurses (25 to 42 years old) from the U.S. were enrolled into the Nurses’ Health Study II (NHSII). Follow-up is conducted biennially with the use of self-administered questionnaires assessing lifestyle, diet and medical history (10). A total of 45,948 participants completed a food-frequency questionnaire (FFQ) in 1997 to assess diet in high school (HS). Women who did not complete the HS-FFQ were not substantially different with respect to age, physical activity, alcohol, beverage intake, but were less likely to be Caucasians and more likely to have a higher body mass index (BMI) and smoke, as compared to women who returned the HS-FFQ (Supplementary Table 1).

At baseline in 1997 when HS diet was assessed, we excluded women with missing date of birth (n=83), implausible (<500 or ≥3,500 kcal/day) adulthood energy intake values (n=1,364), missing HS/adulthood beverage intake (n=2), and, reported cardiovascular disease (n=896), cancer (n=1,367) or diabetes (n=805) diagnosis. Additionally, we excluded those who were lost to follow-up (n=114), resulting in a total of 41,317 women for the current study (Supplementary Figure 1). Study protocol was approved by the institutional review boards of the Brigham and Women’s Hospital and the Harvard T.H. Chan School of Public Health. Return of the completed questionnaire was considered to imply consent.

2.2. Assessment of beverage intake in high school and adulthood

The HS-FFQ inquired intake frequencies of caffeinated coffee, iced tea, hot tea, regular soda with caffeine, regular soda without caffeine, diet soda with caffeine, diet soda without caffeine, orange juice, apple juice, other juices and milk. Reproducibility (11, 12) and validity (12, 13) of the HS-FFQ have been demonstrated previously (Supplementary Method).

Adulthood diet has been assessed quadrennially since 1991 using a 130-item semi-quantitative FFQ in the NHSII. For the current study, reported intakes in the 1991 and 1995 cycles were averaged to measure adulthood beverage consumption. Adulthood beverage intake was examined with nine response categories similar to that of those used in HS-FFQ. The FFQs in NHSII have been validated, as described previously (14).

2.3. Assessment of covariates

Body mass index in adolescence (at age 18) was ascertained from the 1989 NHSII questionnaire. Weight in adolescence was validated (r = 0.87) with measured weight from physical examination records (15). Data on other potential risk factors such as physical activity, smoking, and alcohol intake during adolescence were obtained from the 1989 NHSII questionnaire. High school diet quality was assessed by deriving the adolescent Alternative Healthy Eating Index (16).

2.4. Assessment of type 2 diabetes incidence

Self-reported diabetes diagnosis was confirmed with the use of a supplementary questionnaire assessing details on symptoms, medication use, and glucose/HbA1c information. In previous validation studies, 98% questionnaire-confirmed T2DM cases in the Nurses’ Health Study(17) were re-confirmed by blinded-physician medical record reviews. Prior to 1998, T2DM diagnosis was based on the National Diabetes Data Group criterion [1) fasting glucose of ≥140 mg/dL (7.8 mmol/L) or non-fasting glucose of ≥200 mg/dL (11.1 mmol/L); 2) elevated fasting glucose on ≥2 occasions or an abnormal oral glucose tolerance test; 3) present consumption of oral hypoglycemic agents or insulin for diabetes treatment]. In 1998, the criterion was amended to include individuals with fasting glucose of ≥126 mg/dL (7.0 mmol/L) in line with recommendations by the American Diabetes Association (18).

2.5. Statistical analysis

Person-years for each participant were computed from baseline (1997) to June 2017, while censoring at date of T2DM diagnosis, death, or last questionnaire return date (if lost to follow-up), whichever came first. Associations between adolescent and adulthood beverage intakes were assessed using Spearman’s correlation coefficients. Hazard ratios (HRs) and 95% confidence intervals (95%CIs) of T2DM risk were estimated with the use of Cox proportional hazards regression models. Of note, we collapsed some intake levels for the beverages to ensure an adequate sample size for each category.

For investigation of adolescent beverage intake in relation to T2DM risk in adulthood, multivariable models were adjusted for age, family history of diabetes, BMI at age 18, total energy intake, cigarette smoking, physical activity, alcohol intake, and Alternate Healthy Eating Index (without sugar-sweetened beverage and alcohol) in adolescence. We further mutually adjusted for individual elements of adolescent beverage intake, which aids in isolating the independent effect of different types of beverages on T2DM risk. In a secondary analysis, to assess the impact of adulthood beverage consumption on associations between adolescent beverage intake and T2DM risk, we further adjusted for adulthood covariates (Supplementary Method). Tests for trend across intake categories were conducted by modeling the median value from each category as a continuous variable.

For investigation of change in beverage intake from adolescence to adulthood in relation to T2DM risk, multivariable models were adjusted for the same set of covariates as well as changes from adolescence to adulthood (Supplementary Method). We additionally adjusted for BMI at age 18, and change in weight from adolescence to adulthood in a separate model to assess potential mediation-association.

In secondary analyses, the analyses were stratified by adolescent weight status [lean (<25kg/m2); overweight or obese (≥25kg/m2)], adolescent physical activity level [less active (<54 Met-hours/wk); more active (≥54 Mets/wk)], or family history of diabetes (yes vs. no).

To illustrate potential joint effects, we jointly-categorized study participants into nine categories by tertiles of adolescence and adulthood intake levels. To address potential reverse causation in the relationship between changes in beverage intake from adolescence to adulthood and T2DM risk, we performed 2-, 4- and 8-year lagged analyses. Specifically, cases occurring within 2, 4, and 8 years after baseline were excluded from the respective analyses. Moreover, we used only the 1991 NHSII FFQ to measure adulthood beverage consumption, to minimize the impact of recent lifestyle changes made among higher-risk individuals.

Statistical analyses were performed with the use of SAS version 9 for UNIX (SAS Institute Inc, Cary, NC), STATA version 13.1 (StataCorp LP, College Station, TX), and R version 3.5.2. All statistical tests were 2-sided, and significance was defined as P < 0.05.

3. RESULTS

During 725,650 person-years of follow-up from 1997 to 2017, we ascertained and confirmed 2,844 cases of incident T2DM. Characteristics of the study population in high school were shown by extreme categories of high school beverage intake (Table 1). Beverage intake levels in high school were modestly correlated with those in adulthood: Spearman correlation coefficients were 0.33 for regular soda, 0.37 for coffee and diet soda, 0.44 for fruit juices and milk, and 0.45 for tea (Supplementary Figure 2).

Table 1.

Age-adjusted characteristics of women in the Nurses’ Health Study II during high school by extreme categories of adolescent beverage intake.

Caffeinated Coffee Tea Regular Soda Diet Soda Fruit Juice Milk
All Never ≥1/day Never ≥2/day Never ≥1/day Never ≥1/day Never ≥1/day Never ≥2/day
N 41,317 31,082 3,439 13,097 3,237 8,864 5,426 24,139 4,787 3,055 13,118 4,115 17,114
Caucasian, % 97.6 97.5 97.8 97.6 97.7 97.8 97.5 96.8 99.0 96.0 98.0 95.5 98.6
Weight in high school, Kg 57.4 (9.2) 57.3 (9.2) 58.1 (9.6) 57.4 (9.0) 58.1 (10.4) 59.0 (9.8) 56.6 (9.6) 55.6 (8.3) 61.5 (11.0) 58.0 (10.0) 56.9 (8.7) 56.7 (9.6) 57.4 (8.8)
BMI at age 18 years, kg/m2 21.1 (3.1) 21.0 (3.1) 21.4 (3.2) 21.1 (3.0) 21.4 (3.6) 21.7 (3.3) 20.9 (3.3) 20.5 (2.8) 22.6 (3.7) 21.4 (3.3) 20.8 (2.9) 21.1 (3.3) 21.0 (3.0)
Physical activity in high school, METs/wk 54.1 (17.2) 54.1 (17.3) 53.8 (17.6) 53.4 (17.5) 54.6 (17.4) 52.7 (17.4) 55.0 (17.6) 54.5 (17.3) 52.9 (17.6) 51.6 (18.1) 55.5 (17.1) 52.4 (17.7) 55.1 (17.1)
Alcohol intake in high school, grams/day 0.3 (1.9) 0.3 (1.8) 0.5 (2.5) 0.3 (2.1) 0.3 (1.8) 0.3 (2.0) 0.5 (2.6) 0.3 (1.8) 0.5 (2.6) 0.3 (1.8) 0.3 (1.6) 0.4 (2.2) 0.2 (1.8)
High school cigarette smoking, % 22.9 19.1 39.2 21.1 23.1 21.8 30.3 21.1 31.9 23.8 21.2 24.5 20.0
Family history of diabetes, % 16.1 15.5 18.9 15.3 18.3 16.6 17.6 15.4 18.3 18.7 15.0 17.8 14.9
Family history of myocardial infarction, % 31.6 31.0 35.9 30.7 34.2 30.6 34.9 31.1 34.6 34.2 29.9 34.1 30.1
Family history of hypertension, % 53.2 52.5 55.7 51.6 54.3 52.3 55.7 52.2 56.1 53.0 52.3 55.0 51.7
Total energy intake in high school, kcal/day 2739.5 (788.0) 2735.4 (781.1) 2789.2 (817.4) 2645.4 (771.6) 2999.2 (805.0) 2514.3 (759.4) 3171.3 (786.1) 2748.0 (786.0) 2811.2 (818.8) 2345.2 (783.2) 3017.8 (769.5) 2450.5 (806.3) 2969.1 (732.3)
High school caffeinated coffee intake, cups/week 1.3 (3.8) 0.0 (0.0) 11.4 (6.9) 0.9 (3.2) 1.9 (4.9) 1.7 (4.5) 1.3 (3.9) 1.0 (3.3) 2.4 (5.4) 1.9 (4.9) 1.1 (3.4) 1.9 (4.8) 0.9 (3.1)
Tea intake in high school, cups/week 3.6 (6.0) 3.5 (6.0) 5.0 (6.9) 0.0 (0.0) 20.8 (7.2) 3.5 (6.4) 4.8 (6.9) 3.6 (5.9) 4.6 (7.2) 4.6 (7.6) 3.4 (5.6) 5.1 (7.6) 2.6 (4.9)
Regular soda intake in high school, cups/week 3.2 (4.7) 3.3 (4.8) 3.3 (5.0) 3.0 (4.7) 4.1 (5.8) 0.0 (0.0) 12.5 (6.8) 4.1 (5.4) 1.9 (4.0) 3.1 (5.5) 3.0 (4.2) 4.1 (6.3) 2.7 (3.9)
Diet soda intake in high school, cups/week 2.4 (5.2) 2.1 (5.0) 4.1 (6.9) 2.2 (5.2) 3.3 (6.7) 5.3 (7.8) 1.3 (4.2) 0.0 (0.0) 13.9 (8.0) 2.8 (6.2) 2.1 (4.8) 3.4 (6.7) 1.7 (4.2)
Fruit juice intake in high school, cups/week 4.9 (4.6) 5.0 (4.7) 4.5 (4.6) 4.8 (4.7) 4.4 (4.5) 4.6 (4.7) 4.5 (4.3) 5.0 (4.8) 4.5 (4.4) 0.0 (0.0) 9.9 (4.7) 4.0 (4.6) 5.6 (4.9)
Milk intake in high school, cups/week 10.2 (8.4) 10.8 (8.5) 7.9 (7.6) 11.9 (8.9) 7.5 (7.5) 10.1 (8.7) 8.4 (7.8) 10.9 (8.7) 7.7 (7.4) 8.1 (8.5) 11.9 (8.4) 0.0 (0.0) 19.1 (4.7)
Alternate healthy eating index score in high school 34.1 (7.9) 33.9 (7.9) 34.5 (7.9) 33.6 (8.4) 33.8 (7.8) 36.0 (8.5) 30.9 (7.2) 33.7 (8.0) 33.9 (7.8) 32.3 (8.4) 36.0 (8.1) 33.9 (8.5) 33.8 (7.7)
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Values are means(SD) for continuous variables; percentages for categorical variables.

Adolescent intake of caffeinated coffee was significantly associated with a 14% lower T2DM risk [HR=0.86 (95% CI: 0.75, 0.98)] in adulthood among women who consumed ≥1 serving/day compared with non-consumers (Table 2). A similar inverse association was observed for orange juice intake [HR=0.83 (0.71, 0.96)]. In contrast, intake of regular soda and iced tea in adolescence was associated with higher T2DM risk [HR=1.37 (1.20, 1.57)], comparing ≥1 serving/day; 1.41 (1.21, 1.65), comparing ≥2 servings/day with non-drinkers, respectively]. Intake of other beverages in adolescence, including apple and other juices, diet soda, and milk, were not associated with T2DM risk later in life (Table 2). Only iced tea intake remained associated with higher T2DM risk [HR=1.25 (1.07, 1.47), comparing ≥2 servings/day with non-drinkers] after additional adjustment for adulthood consumption of the same beverage and covariates (Table 2).

Table 2.

Association between adolescent beverage intake and risk of type 2 diabetes in the Nurses’ Health Study II.

Median intake (servings/wk) Cases / Person-years Hazard Ratio (95% Confidence Interval)
Model 1a Model 2b Model 3c Model 4d
Caffeinated coffee
 Never 0.0 2,131 / 545,874 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 <1/wk 0.5 269 / 67,207 1.00 (0.88, 1.14) 0.97 (0.86, 1.10) 0.97 (0.85, 1.10) 1.11 (0.98, 1.27)
 1/wk to <1/day 3.0 205 / 52,516 0.96 (0.83, 1.11) 0.92 (0.80, 1.06) 0.90 (0.78, 1.05) 1.07 (0.92, 1.24)
 ≥1/day 7.0 239 / 60,053 0.98 (0.86, 1.12) 0.89 (0.78, 1.02) 0.86 (0.75, 0.98) 1.05 (0.91, 1.22)
P-trend - - 0.69 0.06 0.02 0.48
Tea
 Never 0.0 843 / 229,778 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 <1/wk 0.5 583 / 172,731 0.93 (0.83, 1.03) 0.93 (0.83, 1.03) 0.93 (0.83, 1.03) 0.95 (0.85, 1.06)
 1/wk to <4/wk 3.0 506 / 135,422 1.03 (0.92, 1.15) 1.01 (0.90, 1.13) 1.01 (0.90, 1.13) 1.04 (0.92, 1.17)
 4/wk to <1/day 6.0 281 / 57,928 1.34 (1.17, 1.53) 1.30 (1.13, 1.49) 1.28 (1.12, 1.47) 1.27 (1.10, 1.47)
 1/day to <2/day 7.5 341 / 73,729 1.29 (1.13, 1.46) 1.22 (1.08, 1.39) 1.18 (1.04, 1.34) 1.16 (1.01, 1.33)
 ≥2/day 17.5 290 / 56,062 1.47 (1.29, 1.68) 1.32 (1.15, 1.51) 1.27 (1.11, 1.46) 1.22 (1.05, 1.42)
P-trend - - < 0.0001 < 0.0001 < 0.0001 0.0003
 Iced Tea
  Never 0.0 1,110 / 305,721 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
  <1/wk 0.5 709 / 204,443 0.97 (0.88, 1.07) 0.95 (0.87, 1.05) 0.96 (0.87, 1.06) 0.98 (0.88, 1.08)
  1/wk to <4/wk 3.0 389 / 94,719 1.16 (1.03, 1.30) 1.11 (0.99, 1.25) 1.10 (0.98, 1.24) 1.07 (0.95, 1.21)
  4/wk to <1/day 5.5 217 / 41,227 1.50 (1.30, 1.74) 1.42 (1.23, 1.65) 1.40 (1.21, 1.63) 1.28 (1.10, 1.49)
  1/day to <2/day 7.0 206 / 42,588 1.39 (1.19, 1.61) 1.31 (1.13, 1.52) 1.25 (1.07, 1.46) 1.16 (0.99, 1.36)
  ≥2/day 17.5 213 / 36,916 1.70 (1.47, 1.98) 1.47 (1.27, 1.71) 1.41 (1.21, 1.65) 1.25 (1.07, 1.47)
P-trend - - < 0.0001 < 0.0001 < 0.0001 0.0003
 Hot Tea
  Never 0.0 1,643 / 421,339 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
  <1/wk 0.5 670 / 175,719 0.98 (0.89, 1.07) 0.97 (0.88, 1.06) 0.97 (0.88, 1.06) 0.97 (0.88, 1.07)
  1/wk to <1/day 3.0 327 / 79,142 1.04 (0.93, 1.17) 1.03 (0.91, 1.16) 1.01 (0.89, 1.15) 1.07 (0.94, 1.21)
  ≥1/day 7.0 204 / 49,414 1.05 (0.91, 1.22) 1.01 (0.87, 1.17) 0.96 (0.83, 1.12) 1.02 (0.87, 1.18)
P-trend - - 0.34 0.71 0.82 0.5
Regular soda
 Never 0.0 561 / 155,471 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 <1/wk 1.0 743 / 206,578 0.95 (0.85, 1.06) 1.02 (0.91, 1.13) 1.03 (0.92, 1.16) 0.95 (0.85, 1.07)
 1/wk to <4/wk 3.0 764 / 198,234 1.04 (0.93, 1.16) 1.10 (0.99, 1.23) 1.09 (0.97, 1.23) 0.94 (0.83, 1.05)
 4/wk to <1/day 6.0 287 / 72,054 1.08 (0.93, 1.24) 1.12 (0.97, 1.30) 1.10 (0.94, 1.28) 0.93 (0.80, 1.09)
 ≥1/day 8.5 489 / 93,315 1.47 (1.30, 1.65) 1.44 (1.27, 1.64) 1.37 (1.20, 1.57) 1.03 (0.89, 1.19)
P-trend - - < 0.0001 < 0.0001 < 0.0001 0.52
Diet soda
 Never 0.0 1,620 / 423,749 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 <1/wk 1.0 364 / 93,670 1.05 (0.94, 1.18) 0.96 (0.86, 1.08) 1.01 (0.90, 1.13) 0.99 (0.88, 1.12)
 1/wk to <4/wk 3.0 348 / 87,119 1.11 (0.99, 1.25) 0.95 (0.84, 1.06) 0.99 (0.88, 1.12) 1.01 (0.90, 1.15)
 4/wk to <1/day 6.0 149 / 38,024 1.12 (0.95, 1.33) 0.90 (0.76, 1.06) 0.95 (0.80, 1.12) 0.95 (0.79, 1.13)
 ≥1/day 11.1 363 / 83,089 1.29 (1.15, 1.45) 0.98 (0.87, 1.11) 1.03 (0.91, 1.17) 0.95 (0.83, 1.08)
P-trend - - < 0.0001 0.59 0.77 0.41
Fruit juice
 Never 0.0 235 / 52,312 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 <1/wk 1.0 511 / 121,486 0.94 (0.81, 1.10) 0.95 (0.82, 1.11) 0.95 (0.81, 1.11) 0.96 (0.82, 1.13)
 1/wk to <4/wk 3.0 918 / 211,804 0.98 (0.85, 1.13) 1.02 (0.88, 1.18) 1.02 (0.88, 1.18) 1.04 (0.90, 1.21)
 4/wk to <1/day 6.0 397 / 106,771 0.84 (0.72, 0.99) 0.89 (0.75, 1.05) 0.90 (0.76, 1.06) 0.97 (0.82, 1.16)
 ≥1/day 8.0 783 / 233,278 0.76 (0.65, 0.88) 0.82 (0.70, 0.95) 0.85 (0.73, 0.99) 0.98 (0.84, 1.16)
P-trend - - < 0.0001 0.0001 0.002 0.77
 Orange juice
  Never 0.0 322 / 73,145 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
  <1/wk 1.0 922 / 214,546 0.98 (0.86, 1.11) 0.99 (0.87, 1.12) 0.97 (0.85, 1.11) 0.99 (0.86, 1.13)
  1/wk to <4/wk 3.0 780 / 195,400 0.92 (0.81, 1.05) 0.93 (0.82, 1.07) 0.93 (0.81, 1.06) 0.99 (0.86, 1.14)
  4/wk to <1/day 5.5 305 / 87,254 0.80 (0.68, 0.93) 0.83 (0.71, 0.97) 0.84 (0.71, 0.99) 0.93 (0.79, 1.10)
  ≥1/day 7.0 515 / 155,269 0.75 (0.66, 0.87) 0.81 (0.70, 0.93) 0.83 (0.71, 0.96) 0.96 (0.83, 1.12)
P-trend - - < 0.0001 < 0.0001 0.0008 0.47
 Apple juice
  Never 0.0 1,558 / 398,406 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
  <1/wk 0.5 1,012 / 251,621 1.03 (0.95, 1.12) 1.04 (0.96, 1.13) 1.09 (0.99, 1.19) 1.06 (0.97, 1.16)
  ≥1/wk 3.0 274 / 75,587 0.96 (0.84, 1.09) 1.01 (0.88, 1.15) 1.09 (0.94, 1.26) 1.12 (0.97, 1.30)
P-trend - - 0.52 0.89 0.28 0.12
 Other fruit juices
  Never 0.0 1,230 / 301,189 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
  <1/wk 0.5 1,204 / 308,773 0.95 (0.88, 1.03) 0.98 (0.90, 1.06) 0.96 (0.88, 1.05) 0.97 (0.89, 1.07)
  1/wk to <4/wk 3.0 302 / 81,892 0.91 (0.80, 1.03) 0.96 (0.84, 1.09) 0.96 (0.83, 1.10) 0.99 (0.86, 1.14)
  ≥4/wk 7.0 108 / 33,760 0.82 (0.67, 0.99) 0.87 (0.71, 1.06) 0.90 (0.73, 1.11) 0.99 (0.80, 1.22)
P-trend - - 0.03 0.16 0.35 0.99
Milk
 Never 0.0 311 / 71,200 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 <1/wk 0.5 215 / 56,658 0.89 (0.75, 1.06) 0.89 (0.75, 1.06) 0.87 (0.73, 1.04) 0.90 (0.75, 1.07)
 1/wk to <4/wk 3.0 371 / 89,220 0.97 (0.84, 1.13) 0.97 (0.83, 1.13) 0.97 (0.83, 1.13) 0.98 (0.84, 1.14)
 4/wk to <1/day 5.5 292 / 69,294 0.97 (0.83, 1.14) 0.95 (0.81, 1.12) 0.96 (0.82, 1.13) 0.98 (0.83, 1.16)
 1/day to <2/day 7.0 563 / 135,955 0.96 (0.83, 1.10) 0.94 (0.82, 1.08) 0.96 (0.83, 1.11) 0.98 (0.85, 1.13)
 ≥2/day 17.5 1,092 / 303,323 0.81 (0.72, 0.92) 0.81 (0.71, 0.93) 0.88 (0.77, 1.01) 0.93 (0.80, 1.07)
P-trend - - < 0.0001 0.0001 0.07 0.35
Open in a new tab
a

Model 1 was adjusted for age.

b

Model 2 was additionally adjusted for family history of diabetes (yes, no), BMI at age 18 (<18.5, 18.5 to <22.5, 22.5 to <25.0, 25.0 to <30.0, or ≥30.0 kg/m2), adolescent total energy intake (quintiles, kcal/day), adolescent cigarette smoking (none, 1 to 4, 5 to 14, or ≥15 cigarettes/day), adolescent physical activity [quintiles, metabolic equivalents (Mets)/week], adolescent alcohol intake (grams/day), and, adolescent alternate healthy eating index without sugar-sweetened beverage and alcohol (quintiles).

c

Model 3 was additionally mutually adjusted for adolescent beverage intake: coffee intake (never, <1/wk, 1/wk to <1/day, or ≥1/day), tea intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day 1/day to <2/day, or ≥2/day), iced tea intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day 1/day to <2/day, or ≥2/day), hot tea intake (never, <1/wk, 1/wk to <1/day, or ≥1/day), regular soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), diet soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), fruit juice intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), orange juice intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), apple juice intake (never, <1/wk, ≥1/wk), other fruit juice intake (never, <1/wk, 1/wk to <4/wk, ≥4/wk), milk intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, or ≥2/day).

d

Model 4 was additionally adjusted for adulthood lifestyle covariates: cigarette smoking (never smoker, past smoker, current smoker: 1–14 cigarettes/day, or current smoker: ≥15 cigarettes/day), physical activity (quintiles, Mets/week), oral contraceptive use (never, past, or current), postmenopausal hormone use (never, past, or current), history of hypertension (yes, no), history of hypercholesterolemia (yes, no), and, aspirin use (yes, no); adulthood dietary covariates: total energy intake (quintiles, kcal/day), alcohol intake (0, 0.1 to 4.9, 5.0 to 14.9, 15.0 to 29.9, or ≥30 grams/day), and, alternate healthy eating index without sugar-sweetened beverage and alcohol (quintiles); adulthood beverages: total coffee intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, 2/day to <3/day, 3/day to <4/day, or ≥4/day), tea intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, or ≥2/day), regular soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), diet soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, 2/day to <3/day, or ≥3/day), fruit juice intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), milk intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, or ≥2/day), and punch intake (never, <1/wk, 1/wk to <4/wk, or ≥4/wk).

For the analyses of changes in beverage intake and T2DM risk, Supplementary Table 2 shows the characteristics of participants at baseline in 1997 by changes of beverage intake from adolescence to adulthood. After multivariate adjustments, increased caffeinated or total coffee intake from adolescence to adulthood was associated with 15% [HR=0.85 (0.73, 0.99)] or 24% [HR=0.76 (0.66, 0.87)] lower T2DM risk, respectively, comparing an increment of ≥3 servings/day with no change (Table 3). In contrast, among women who increased regular soda intake from adolescence to adulthood, a significant 20% higher risk [HR=1.20 (1.06, 1.35)] of T2DM was observed (Table 3). Additional adjustment for high school BMI and change in weight from adolescence to adulthood attenuated this association for increased regular soda intake. An increase in diet soda intake was significantly associated with a 26% higher risk [HR=1.26 (1.11, 1.42)] of developing T2DM even after adjustment of weight changes from adolescence to adulthood (Table 3). Exclusion of T2DM cases diagnosed within two, four or eight years of 1997 FFQ administration, or the utility of only the 1991 NHSII FFQ for the assessment of adulthood intakes did not materially change our observations (Supplementary Table 3).

Table 3.

Association between change in beverage intake from adolescence to adulthood and risk of type 2 diabetes in the Nurses’ Health Study II.

Median intake (servings/wk) Cases / Person-years Hazard Ratio (95% Confidence Interval)
Model 1a Model 2b Model 3c
Caffeinated coffee
 −1/wk or less −5.3 116 / 25,198 0.98 (0.81, 1.19) 1.03 (0.82, 1.29) 1.05 (0.83, 1.31)
 No change (>−1/wk to <+1/wk) 0.0 1,206 / 274,571 1.00 (reference) 1.00 (reference) 1.00 (reference)
 +1/wk to <+1/day +3.5 456 / 112,913 0.90 (0.81, 1.01) 0.97 (0.87, 1.09) 0.99 (0.88, 1.11)
 +1/day to <+2/day +10.3 449 / 136,651 0.71 (0.64, 0.80) 0.84 (0.75, 0.94) 0.91 (0.81, 1.02)
 +2/day to <+3/day +17.5 372 / 113,593 0.69 (0.61, 0.77) 0.82 (0.73, 0.93) 0.89 (0.78, 1.00)
 ≥+3/day +26.0 245 / 62,725 0.79 (0.69, 0.91) 0.82 (0.71, 0.95) 0.85 (0.73, 0.99)
P-trend - - < 0.0001 < 0.0001 0.004
Total coffee
 −1/wk or less −5.0 59 / 12,726 0.96 (0.74, 1.24) 0.94 (0.71, 1.25) 0.90 (0.67, 1.20)
 No change (>−1/wk to <+1/wk) 0.0 1,056 / 230,007 1.00 (reference) 1.00 (reference) 1.00 (reference)
 +1/wk to <+1/day +3.7 454 / 108,414 0.89 (0.80, 0.99) 0.97 (0.87, 1.09) 1.00 (0.89, 1.12)
 +1/day to <+2/day +10.5 473 / 138,488 0.70 (0.63, 0.78) 0.82 (0.73, 0.92) 0.92 (0.82, 1.03)
 +2/day to <+3/day +17.5 457 / 135,441 0.66 (0.59, 0.74) 0.80 (0.71, 0.91) 0.90 (0.80, 1.02)
 ≥+3/day +26.7 345 / 100,575 0.64 (0.57, 0.73) 0.70 (0.61, 0.80) 0.76 (0.66, 0.87)
P-trend - - < 0.0001 < 0.0001 < 0.0001
Tea
 −4/wk or less −7.0 399 / 78,617 1.43 (1.27, 1.61) 1.15 (0.98, 1.34) 1.11 (0.94, 1.30)
 >−4/wk to −1/wk −2.5 313 / 76,845 1.14 (1.00, 1.29) 1.05 (0.91, 1.22) 0.99 (0.85, 1.15)
 No change (>−1/wk to <+1/wk) 0.0 996 / 275,864 1.00 (reference) 1.00 (reference) 1.00 (reference)
 +1/wk to <+4/wk +2.3 452 / 125,852 0.99 (0.89, 1.11) 0.98 (0.88, 1.10) 0.97 (0.87, 1.09)
 +4/wk to <+2/day +7.2 484 / 120,871 1.08 (0.97, 1.21) 1.00 (0.89, 1.12) 1.01 (0.90, 1.13)
 ≥+2/day +17.5 200 / 47,601 1.09 (0.94, 1.27) 0.96 (0.82, 1.12) 0.96 (0.82, 1.13)
P-trend - - 0.02 0.11 0.32
Regular soda
 −4/wk or less −6.8 533 / 116,720 1.32 (1.19, 1.46) 0.89 (0.74, 1.07) 0.96 (0.80, 1.16)
 >−4/wk to −1/wk −2.8 619 / 152,206 1.16 (1.05, 1.27) 1.14 (0.98, 1.33) 1.12 (0.96, 1.30)
 No change (>−1/wk to <+1/wk) 0.0 1,221 / 352,874 1.00 (reference) 1.00 (reference) 1.00 (reference)
 ≥+1 or more/wk +3.3 471 / 103,850 1.33 (1.19, 1.48) 1.20 (1.06, 1.35) 1.13 (0.99, 1.27)
P-trend - - 0.04 0.004 0.13
Diet soda
 −1/wk or less −4.0 254 / 75,713 1.23 (1.06, 1.41) 1.11 (0.93, 1.31) 1.09 (0.92, 1.29)
 No change (>−1/wk to <+1/wk) 0.0 798 / 270,752 1.00 (reference) 1.00 (reference) 1.00 (reference)
 +1/wk to <+4/wk +2.5 440 / 119,372 1.24 (1.10, 1.39) 1.24 (1.10, 1.40) 1.15 (1.02, 1.29)
 +4/wk to <+1/day +5.5 326 / 76,256 1.42 (1.25, 1.61) 1.34 (1.17, 1.53) 1.24 (1.09, 1.42)
 +1/day to <+2/day +9.5 522 / 100,606 1.75 (1.56, 1.95) 1.54 (1.37, 1.73) 1.31 (1.16, 1.47)
 ≥+2/day +19.3 504 / 82,953 2.05 (1.83, 2.29) 1.59 (1.41, 1.80) 1.26 (1.11, 1.42)
P-trend - - < 0.0001 < 0.0001 0.0002
Fruit juice
 −4/wk or less −6.0 474 / 124,529 0.92 (0.83, 1.03) 1.09 (0.95, 1.25) 0.99 (0.86, 1.14)
 >−4/wk to −1/wk −2.3 669 / 161,246 1.02 (0.92, 1.13) 1.08 (0.96, 1.21) 1.01 (0.90, 1.13)
 No change (>−1/wk to <+1/wk) 0.0 864 / 211,485 1.00 (reference) 1.00 (reference) 1.00 (reference)
 +1/wk to <+4/wk +2.2 513 / 130,633 0.97 (0.87, 1.08) 1.00 (0.90, 1.12) 1.00 (0.90, 1.12)
 ≥+4/wk +6.5 324 / 97,757 0.82 (0.73, 0.94) 0.90 (0.79, 1.03) 0.92 (0.81, 1.05)
P-trend - - 0.13 0.01 0.37
 Orange juice
  −4/wk or less −5.5 357 / 98,517 0.89 (0.79, 1.00) 1.03 (0.89, 1.19) 0.95 (0.82, 1.10)
  >−4/wk to −1/wk −2.5 834 / 212,197 0.98 (0.90, 1.07) 1.06 (0.95, 1.17) 0.99 (0.89, 1.10)
  No change (>−1/wk to <+1/wk) 0.0 1,169 / 289,839 1.00 (reference) 1.00 (reference) 1.00 (reference)
  +1/wk to <+4/wk +2.0 380 / 91,092 1.03 (0.92, 1.15) 1.03 (0.91, 1.16) 1.00 (0.89, 1.13)
  ≥+4/wk +6.0 104 / 33,970 0.74 (0.61, 0.90) 0.81 (0.66, 0.99) 0.82 (0.67, 1.00)
P-trend - - 0.96 0.08 0.46
 Apple juice
  −1/wk or less −2.5 236 / 64,022 0.94 (0.82, 1.07) 1.10 (0.95, 1.27) 1.09 (0.94, 1.27)
  No change (>−1/wk to <+1/wk) 0.0 2,355 / 586,057 1.00 (reference) 1.00 (reference) 1.00 (reference)
  ≥+1/wk +2.0 253 / 75,535 0.89 (0.78, 1.01) 0.96 (0.84, 1.10) 0.96 (0.83, 1.10)
P-trend - - 0.61 0.17 0.17
 Other fruit juice
  −1/wk or less −2.7 274 / 74,030 0.91 (0.80, 1.03) 1.00 (0.87, 1.15) 0.99 (0.86, 1.15)
  No change (>−1/wk to <+1/wk) 0.0 1,842 / 444,160 1.00 (reference) 1.00 (reference) 1.00 (reference)
  +1/wk to <+4/wk +2.0 571 / 151,832 0.93 (0.85, 1.02) 1.01 (0.91, 1.11) 1.04 (0.94, 1.15)
  ≥+4/wk +6.3 157 / 55,591 0.70 (0.60, 0.83) 0.85 (0.72, 1.01) 0.94 (0.80, 1.12)
P-trend - - 0.001 0.14 0.84
Milk
 −2/day or less −16.5 272 / 77,296 0.78 (0.68, 0.90) 0.85 (0.72, 1.01) 0.88 (0.74, 1.04)
 >−2/day to −1/day −10.5 426 / 111,710 0.88 (0.78, 1.00) 0.98 (0.85, 1.14) 0.98 (0.84, 1.14)
 >−1/day to −4/wk −5.3 287 / 78,310 0.87 (0.76, 1.00) 0.88 (0.76, 1.02) 0.89 (0.76, 1.03)
 >−4/wk to −1/wk −2.5 386 / 95,310 0.96 (0.85, 1.09) 0.92 (0.80, 1.05) 0.90 (0.78, 1.03)
 No change (>−1/wk to <+1/wk) 0.0 670 / 162,616 1.00 (reference) 1.00 (reference) 1.00 (reference)
 +1/wk to <+4/wk +2.2 378 / 90,495 1.03 (0.91, 1.17) 1.00 (0.87, 1.14) 0.98 (0.86, 1.12)
 ≥+4/wk +7.0 425 / 109,914 0.98 (0.86, 1.10) 0.95 (0.84, 1.07) 0.94 (0.83, 1.07)
P-trend - - 0.0001 0.25 0.39
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a

Model 1 was adjusted for age.

b

Model 2 was additionally adjusted for family history of diabetes (yes, no), change in smoking status (neither adolescent nor current smoker, adolescent smoker but not current smoker, current smoker but not adolescent smoker, adolescent and current smoker), adolescent physical activity [quintiles, metabolic equivalents (Mets)/week], change in physical activity from adolescence to adulthood (quintiles, Mets/week), adolescent alcohol intake (grams/day), change in alcohol intake from adolescence to adulthood (quintiles, grams/day), oral contraceptive use (never, past, or current), postmenopausal hormone use (never, past, or current), history of hypertension (yes, no), history of hypercholesterolemia (yes, no), aspirin use (yes, no), adolescent total energy intake (quintiles, kcal/day), change in total energy intake from adolescence to adulthood (quintiles, kcal/day), adolescent alternate healthy eating index without sugar-sweetened beverage and alcohol (quintiles), change in alternate healthy eating index without sugar-sweetened beverage and alcohol from adolescence to adulthood (quintiles), adolescent total/caffeinated coffee intake (never, <1/wk, 1/wk to <1/day, or ≥1/day), change in total/caffeinated coffee intake from adolescence to adulthood [−1/wk or less, no change (>−1/wk to <+1/wk), +1/wk to <+1/day, +1/day to <+2/day, +2/day to <+3/day, or ≥+3/day], adolescent tea intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day 1/day to <2/day, or ≥2/day), change in tea intake from adolescence to adulthood [−4/wk or less, >−4/wk to −1/wk, no change (>−1/wk to <+1/wk), +1/wk to <+4/wk, +4/wk to <+2/day, or ≥+2/day], adolescent regular soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), change in regular soda intake from adolescence to adulthood [−4/wk or less, >−4/wk to −1/wk, no change (>−1/wk to <+1/wk), or ≥+1/wk], adolescent diet soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), change in diet soda intake from adolescence to adulthood [−1/wk or less, no change (>−1/wk to <+1/wk), +1/wk to <+4/wk, +4/wk to <+1/day, +1/day to <+2/day, or ≥+2/day], adolescent fruit juice intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), adolescent orange juice intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), adolescent apple juice intake (never, <1/wk, ≥1/wk), adolescent other fruit juice intake (never, <1/wk, 1/wk to <4/wk, ≥4/wk), change in fruit juice intake from adolescence to adulthood [−4/wk or less, >−4/wk to −1/wk, no change (>−1/wk to <+1/wk), +1/wk to <+4/wk, or ≥+4/wk], change in orange juice intake from adolescence to adulthood [−4/wk or less, >−4/wk to −1/wk, no change (>−1/wk to <+1/wk), +1/wk to <+4/wk, or ≥+4/wk], change in apple juice intake from adolescence to adulthood [−1/wk or less, no change (>−1/wk to <+1/wk), or ≥+1/wk], change in other fruit juice intake from adolescence to adulthood [−1/wk or less, no change (>−1/wk to <+1/wk), +1/wk to <+4/wk, or ≥+4/wk], adolescent milk intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, or ≥2/day), or, change in milk intake from adoescence to adulthood [−2/day or less, >−2/day to −1/day, >−1/day to −4/wk, >−4/wk to −1/wk, no change (>−1/wk to <+1/wk), +1/wk to <+4/wk, or ≥+4/wk].

c

Model 3 was additionally adjusted for BMI at age 18 (<18.5, 18.5 to <22.5, 22.5 to <25.0, 25.0 to <30.0, or ≥30.0 kg/m2), and, change in weight from adolescence to adulthood (kilograms).

In stratified analyses, the associations for increases in caffeinated/total coffee or diet soda intakes were more apparent among women who were lean or more physically active, but less so among their counterparts in adolescence, although tests for interaction were not significant (Supplementary Tables 4 and 5). We nonetheless observed a significantly lower T2DM risk among active adolescents who reduced regular soda intake, whereas among less active adolescents this association was significantly positive (P-interaction=0.04). Similar results were obtained among women with and without family history of diabetes (Supplementary Table 6).

As shown in Figure 1, women with higher intake of coffee in adulthood had lower T2DM risk regardless of whether they were coffee consumers in adolescence. Women who consumed at least 3 servings of coffee daily in adulthood had 31% or 26% lower T2DM risk if they were non-consumers or if they consumed at least 1 serving weekly in adolescence, respectively (Figure 1). Women with higher intake of diet soda in adulthood had higher T2DM risk regardless of whether they were diet soda consumers in adolescence. Women who consumed at least 2 servings of diet soda daily in adulthood had 38% or 28% higher T2DM risk if they were non-consumers or if they consumed at least 4 servings weekly in adolescence, respectively (Figure 1). We otherwise did not observe a clear pattern of joint associations for other beverages.

Figure 1. Joint analysis between adolescent and adulthood beverage intake in relation to type 2 diabetes (T2D) risk.

Figure 1.

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Low, medium and high intakes of beverage in adolescence and adulthood were cross-classified into a single categorical variable and evaluated for risk of T2D with low intake in adolescence and adulthood used as the reference category in a multivariable model. The multi variable model was adjusted for age, family history of diabetes (yes, no), adolescent covariates: BMI at age 18 (<18.5, 18.5 to <22.5, 22.5 to <25.0, 25.0 to <30.0, or ≥30.0 kg/m2), total energy intake (quintiles, kcal/day), cigarette smoking (none, 1 to 4, 5 to 14, or ≥15 cigarettes/day), physical activity [quintiles, metabolic equivalents (Mets)/week], alcohol intake (continuous, grams/day), alternate healthy eating index without sugar-sweetened beverage and alcohol (quintiles), and mutually adjusted for coffee intake (never, <1/wk, 1/wk to <1/day, or ≥1/day), tea intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day 1/day to <2/day, or ≥2/day), regular soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), diet soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), fruit juice intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), milk intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, or ≥2/day), and, adulthood covariates: total energy intake (quintiles, kcal/day), cigarette smoking (never smoker, past smoker, current smoker: 1–14 cigarettes/day, or current smoker: ≥15 cigarettes/day), physical activity (quintiles, Mets/week), oral contraceptive use (never, past, or current), postmenopausal hormone use (never, past, or current), history of hypertension (yes, no), history of hypercholesterolemia (yes, no), aspirin use (yes, no), alcohol intake (0, 0.1 to 4.9, 5.0 to 14.9, 15.0 to 29.9, or ≥30 grams/day), alternate healthy eating index without sugar-sweetened beverage and alcohol (quintiles), and mutually adjusted for total coffee intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, 2/day to <3/day, 3/day to <4/day, or ≥4/day), tea intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, or ≥2/day), regular soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), diet soda intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, 2/day to <3/day, or ≥3/day), fruit juice intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, or ≥1/day), milk intake (never, <1/wk, 1/wk to <4/wk, 4/wk to <1/day, 1/day to <2/day, or ≥2/day), and punch intake (never, <1/wk, 1/wk to <4/wk, or ≥4/wk). Median adolescent beverage intake (servings/wk): coffee (low: 0.0, medium: 0.5, high: 7.0); tea (low: 0.0, medium: 1.0, high: 7.5); regular soda (low: 0.5, medium: 3.0, high: 7.0); diet soda (low: 0.0, medium: 1.0, high: 7.5); fruit juice (low: 0.5, medium: 3.5, high: 8.0); and, milk (low: 0.0, medium: 3.0, high: 17.5). Median adulthood beverage intake (servings/wk): coffee (low: 1.5, medium: 17.5, high: 27.8); tea (low: 0.2, medium: 3.3, high: 12.3); regular soda (low: 0.0, medium: 1.0, high: 7.2); diet soda (low: 0.2, medium: 7.5, high: 19.7); fruit juice (low: 0.5, medium: 2.5, high: 7.3); and, milk (low: 0.5, medium: 3.7, high: 12.3). P-interaction was assessed by multiplying median values of low, medium and high adolescent and adulthood intake categories. Ref: reference.

4. DISCUSSION

In this analysis among US women, higher intake of caffeinated coffee or orange juice in adolescence was associated with lower risk of T2DM, whereas higher intake of regular soda or iced tea was associated with higher risk of T2DM in adulthood. In addition, increasing coffee consumption from adolescence to adulthood was associated with a lower T2DM risk, while the opposite was observed for increased regular or diet soda intake. Joint investigations of adolescent and adulthood beverage intakes revealed that, with the exception of adolescent iced tea consumption, beverage intake in adulthood may play a more important role in the associations of certain beverages with T2DM risk.

There is relatively abundant evidence that collectively suggests beneficial effects of coffee intake on lowering diabetes risk. For example, a meta-analysis of cohort studies among adults described an inverse dose-response relationship (6% lower T2DM risk for every 1 cup/day increment) between higher coffee intakes and risk of T2DM (3). Increases in adulthood coffee and caffeine intakes were associated with less weight gain in adults (19, 20). Evidence from trials that focused on intermediate metabolic outcomes among adults has been somewhat inconclusive (21–24) (25). In a 12-week trial, significant increases in adiponectin were observed only among individuals with higher levels of insulin resistance (26). In a recent 24-week trial (24), caffeinated coffee intake did not influence insulin sensitivity but was associated with fat loss in the absence of lifestyle changes, which was in agreement with a caffeine supplementation trial (27). In addition, accumulating evidence suggests that other beverages may also influence diabetes risk in adults. Meta-analyses of studies among adults described a 7% higher T2DM risk with every 1 serving/day increase in fruit juice (2), and the intake of both regular and diet soda was associated with higher T2DM among adults (2, 28–34), whereas, daily tea intake was associated with lower T2DM risk among adults (4).

Evidence for the association between beverage consumption in adolescence and T2DM risk later in adulthood was unknow. Nonetheless, previous studies among adolescents focused on body weight. For example, coffee or diet soda intakes were not associated with BMI or weight gain (35, 36), whereas fruit juice had a positive association before energy adjustment (36). Of note, in the current study, while orange juice intake was inversely associated with T2DM risk independent of BMI at age 18, changes in intake between adolescence and adulthood were not associated with T2DM risk after adjusting for weight changes. In addition, sugar-sweetened beverage consumption has been shown to promote weight gain in adolescents (37, 38). High sugar content in these beverages may lead to excess calories intake with limited nutritional value, promoting weight gain and metabolic disturbances such as insulin resistance and dyslipidemia. To our knowledge, our study provides the first evidence examining adolescent beverage intake, as well as changes between adolescence and adulthood, in relation to later-life T2DM risk. Further focused research on these beverages is needed to corroborate our observations and to provide more data that may help form specific dietary recommendations for adolescents.

Our findings are biologically plausible. Polyphenol constituents in coffee such as chlorogenic acids (39) have been shown to improve insulin sensitivity and/or postprandial glucose tolerance, as demonstrated in in vitro and animal model studies (40, 41). In addition, orange juice flavanones, such as hesperidin and naringin, may improve glucose homeostasis in liver and fat tissues (42, 43). Other mechanisms such as caffeine-mediated thermogenesis resulting in increased energy expenditure (44) and mitigating gut microbial changes associated with obesity, total body and liver fat (45) have also been proposed for coffee. Declining nutrient quality of fruits from the 1970s, as a result of pursuing high yields, better appearance, storability and transportability, could explain the discrepancy in findings between adolescent and adulthood fruit juice intakes (46). Contrasting findings between iced and hot tea intake in adolescence could be attributed to higher added sugar (47) and lower antioxidant content of iced tea as compared to hot tea (48, 49). Added sugar from iced tea can contribute to increased caloric intake and higher risks of developing obesity and related metabolic disorders such as T2DM (47). Furthermore, the process of making iced tea, including longer storage and dilution, may reduce the levels of beneficial antioxidants such as catechins. Antioxidants play a crucial role in protecting cells from damage and reducing inflammation, which are important for metabolic health (50). Hot tea, on the other hand, is generally freshly brewed and contains higher concentrations of these health-promoting compounds(48, 49). Enhanced bioavailability of liquid sugars from regular soda may result in uncontrolled glycemic spikes (51), chronic stress on β-cells, and long-term hyperinsulinemic state (52). Moreover, decreased insulin sensitivity during puberty coupled with sugar-mediated elevated postprandial glycemic environment, imposes particular strain on β-cell function (53), possibly explaining the stronger association for adolescent intake as opposed to adulthood consumption. Unfavorable changes in adiposity as a result of chronic fuel surfeit by regular soda intake could further explain our finding (54). Diet sodas do not contain substantial amount of simple sugars, although artificial sweeteners have been shown to impair glucose tolerance through functional and compositional alterations of the gut microbiome (55). Lack of caloric contribution and hence, absence of satiation is likely to result in food-seeking behavior due to failure in activating the food reward pathway (56). In our study, discrepancy in T2DM risk between high school intake and changes in consumption between adolescence and adulthood could be explained by contrasting magnitudes of intake (median intakes of highest categories: 11.1 servings/wk vs. an addition of 19.3 servings/wk, respectively), possibly due to greater ubiquity and accessibility of diet soda as a result of FDA approval(57) of several artificial sweeteners during adulthood period.

Several limitations need to be acknowledged. We cannot exclude the possibility that the recall of high school diet may be influenced by the current dietary habits, although the modest correlations observed between adolescent and adulthood intakes suggested that such a probability was low. Recall bias due to that women with overly healthy lifestyle differentially recalling adolescent diet compared to others is possible but likely to be minimal given the prospective design of the study compared with cross-sectional design. Confounding due to unmeasured or imperfectly measured covariates is a possibility. Our findings for diet soda could be influenced by reverse causation (higher-risk individuals are likely to switch from regular to diet soda to control weight) and surveillance (high-risk participants are more likely to be regularly screened for T2DM) (2, 29, 58) biases. Meanwhile, we observed positive associations for increased diet soda intake primarily among active and lean women at adolescence, suggesting that reverse causation may not fully explain our findings. Further, we cannot exclude the possibility of the aforementioned biases given the retrospective assessment of adolescent diet in our study. We did also not consider the specific duration between adolescence and adulthood, as the variations in the transition periods among participants could potentially influence their beverage consumption patterns. Moreover, adjusting for adulthood covariates (adulthood beverage intake and risk factors) may introduce collider-stratification bias. Future research utilizing advanced causal inference methods may provide a clearer understanding of these relationships. Lastly, our findings emanate from predominantly Caucasian females, and thus, may not be generalizable to racially diverse populations or men.

In conclusion, our findings suggest that earlier-life beverage consumption habits are associated with later-life risk of T2DM. Higher intake of coffee and orange juice, in adolescence, was associated with lower T2DM risk, whereas higher adolescent intake of regular soda or iced tea was associated with higher later-life T2DM risk. In addition, changes of beverage intake, including coffee and regular and diet soda, from adolescence and adulthood were associated with risk of T2DM. Our findings support current recommendations to limit soda intake and include daily coffee consumption as part of an overall healthy diet and to establish healthy beverage consumption patterns early in life.

Supplementary Material

Supplementary materials

ACKNOWLEDGEMENTS

The authors would like to thank the participants and staff of the Nurses’ Health Study II for their valuable contributions to the cohort over many years since its inception in 1991.

FUNDING

The current study was funded by the National Institutes of Health grants, U01 CA176726, R01 CA67262, R01 DK112940, R01 ES022981, R01 DK126698, R01 HL035464, and R01 DK120870. In addition, Derrick Johnston Alperet was supported by the Agency for Science Technology and Research (A*STAR) International Fellowship award. The funders had no role in the study design; in the collection, analysis, and interpretation of data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. All authors confirm the independence of researchers from funders.

Footnotes

COMPETING INTERESTS

We have no conflict of interest to declare.

ETHICS APPROVAL

Study protocol was approved by the institutional review boards of the Brigham and Women’s Hospital and the Harvard T.H. Chan School of Public Health.

CONSENT TO PARTICIPATE

Return of the completed questionnaire was considered to imply consent.

CONSENT TO PUBLISH

We confirm that consent to publish has been received from all participants.

Data Share Statement:

Data described in the manuscript, codebook, and analytic code will be made available upon request.

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Supplementary Materials

Supplementary materials
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Data Availability Statement

Data described in the manuscript, codebook, and analytic code will be made available upon request.

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