Abstract
Background
We prospectively examined the associations of total fat and fatty acid intake with type 2 diabetes (T2D) among Japanese adults.
Methods
This study was conducted using data from the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC). A validated food frequency questionnaire evaluated the intake of total fat and fatty acids. Diabetes was assessed using self-reported data. Multivariable logistic regression analysis was performed to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) of incident T2D across quintiles of total fat and fatty acid intake after adjusting for potential confounders.
Results
A total of 19,088 non-diabetic participants (age range, 40–79 years) enrolled in the JACC between 1988 and 1990 were included in this study. During the 5-year study period, 494 the participants developed T2D. The OR of T2D for the highest versus lowest quintiles was 0.58 (95% CI, 0.37–0.90) for total fat, 0.78 (95% CI, 0.51–1.20) for saturated fatty acid (SFA), 0.55 (95% CI, 0.35–0.86) for monounsaturated fatty acids (MUFA), 0.61 (95% CI, 0.39–0.96) for polyunsaturated fatty acids (PUFA), 0.64 (95% CI, 0.42–0.99) for n-3 PUFA, and 0.70 (95% CI, 0.45–1.09) for n-6 PUFA. Total fat and fatty acid (except SFA and n-6 PUFA) intake were inversely associated with T2D in men. Total fat and fatty acid intake were not associated with T2D in women.
Conclusion
Higher intakes of total fats, MUFA, PUFA, and n-3 PUFA were inversely associated with T2D among Japanese men.
Key words: fatty acid, Asia, diabetes, Japanese, epidemiology
INTRODUCTION
Type 2 diabetes (T2D) is a metabolic disorder caused by increased blood glucose concentrations due to insufficient insulin secretion and enhanced insulin resistance and increases mortality and morbidity.1 The estimated global healthcare cost of diabetes is 673 billion United States dollars.1 It is estimated that by 2040, the number of people with diabetes will rise by approximately 55%.1 A healthy diet is essential for the prevention of T2D.2 In an umbrella review of meta-analyses, various dietary factors, such as total fat and fatty acids, were reported for the prevention of T2D.3 For people aged 20 years and older in Japan, the energy intake from total fat is increasing (men 24.3% in 1995, 27.4% in 2019; women 25.9%, 29.2%, respectively). In addition, the intakes of fatty acids other than n-3 PUFA are also increasing (SFA: men 7.2% in 1995, 8.0% in 2019; women 7.9% in 1995, 8.8% in 2019; MUFA: men 7.9% in 2002, 10.4% in 2019; women 8.4% in 2002, 10.8% in 2019; n-6 PUFA: men 4.4% in 2005, 4.9% in 2019; women 4.6% in 2005, 5.2% in 2019; n-3 PUFA: men 1.2% in 2005, 1.1% in 2019; women 1.2% in 2005, 1.2% in 2019).4 For people over 20 and over in the United States, the energy intake from total fat, SFA in women, MUFA in women, and PUFA are increasing, and SFA in men and MUFA in men are decreasing (Total fat: men 35.0% in 1989–91 and 36.0% in 2017–2020, women 33.9% in 1989–91 and 37.0% in 2017–2020, SFA: men 12.2% in 1989–91 and 12.0% in 2017–2020, women 11.7% in 1989–91 and 12.0% in 2017–2020, MUFA: men 13.2% in 1989–91 and 12.0% in 2017–2020, women 12.4% in 1989–91 and 13.0% in 2017–2020, PUFA: men 6.9% in 1989–91 and 8.0% in 2017–2020, women 7.1% in 1989–91 and 9.0% in 2017–2020).5 Corresponding to increasing intakes of fat and some fatty acids, the number of diabetes cases is rising in both Japan and United States. In Japan, according to the National Health and Nutrition Survey reported by the Ministry of Health, Labour and Welfare, in 2009 and 2019, 15.9% and 19.7% in men and 9.4% and 10.8% in women, respectively, were suspected to have diabetes.4 In United States, the age-adjusted prevalence of diagnosed and undiagnosed diabetes was 9.5% in 1999–2002 and 12.0% in 2013–2016.6
Previously, some meta-analyses7–11 examined the association of the intake of total fat and some fatty acids with T2D. A recent meta-analysis11 study reported that 11 studies were conducted in the United States, 7 studies in Europe, but only 4 studies in Asia, where fat intake is low. The amount of total fat and fatty acids and their sources vary by subject region, which may lead to different results. For example, in Asian populations, the intake of n-3 PUFA was linked to a significant reduction in the incidence of T2D, while in United States populations, it was linked to a significant increase. Thus, more research is needed, especially in Asian countries, such as Japan.
Therefore, the aim of this study was to clarify the associations of total fat and fatty acid intake with the risk of T2D in the Japanese population. We hypothesize that among Japanese, 1) higher n-3 PUFA intakes are associated with lower risk of T2D; 2) higher total fat and fatty acids other than n-3 PUFA intakes are associated with higher risk of T2D.
METHODS
Study design and participants
This research was conducted using JACC study data. The protocol for the JACC study has previously been reported.12 In brief, the JACC was conducted from 1988 through 1990 and was a multicenter collaborative study in which 24 institutions participated. In 36 of the 45 study areas covered in the JACC, informed consent was obtained from each participant before enrollment into the study. Consent was obtained from the leader of each remaining area as a group. The study protocol followed the guidelines of the Declaration of Helsinki and received approval from the Ethics Committee of Hokkaido University’s Faculty of Medicine (approval number 14-044).
Assessment of dietary intake
Assessment of dietary intakes, such as total fat and fatty acids, was conducted using a 40-item food frequency questionnaire (FFQ). Participants were asked to report their customary food and drink intake over the past year. The items in the FFQ had for five possible responses to questions on the frequency of consumption: rarely, 1–2 times/month, 1–2 times/week, 3–4 times/week, and almost daily.13 As energy intake is strongly correlated with nutrient intake, energy-adjusted dietary intake of nutrients was calculated using the residual method.14 A validation study to evaluate dietary intake over a 1-year period using four 3-day weighted dietary records of 85 participants (eight men and 77 women) was used as a reference to estimate size of each meal portion and obtain data on the validity of the FFQ-estimated intakes.13 Previously reported, the FFQ-estimated energy-adjusted total fat and fatty acids intakes showed moderate correlation with the ones estimated from dietary records in the validation study. The Spearman rank correlation coefficients were: 0.46 for total fat, 0.50 for SFA, 0.36 for MUFA, 0.15 for PUFA, 0.21 for n-3 PUFA, and 0.16 for n-6 PUFA.13 Intake of energy and nutrients, such as total fat and fatty acids, were computed using the Standard Tables of Food Composition in Japan, 5th Revised and Enlarged Edition.15
Assessment of diabetic status
The 5-year cumulative incidence of diabetes was used for analysis because the exact dates of the diabetes diagnoses of the participants were unknown. Therefore, an individual with incident diabetes was a participant who did not have diabetes at baseline but reported physician-diagnosed diabetes by the fifth follow-up year. In a sample 1,230 men and 1,837 women, the diagnosis of diabetes that was self-reported has been confirmed by comparing it with therapy data and laboratory findings.16 The sensitivity and specificity were found to be 70% and 95% for men and 75% and 98% for women, respectively. Information on the criteria used to diagnose diabetes has been previously explained.16
Assessment of other factors
The baseline self-administered questionnaire included items on lifestyle factors, including current smoking and drinking habits, hours of exercise, hours spent walking; medical history of diabetes, cancer, or myocardial infarction; family history of diabetes and hypertension; and height and weight. To calculate the body mass index (BMI), self-reported weight in kilograms was divided by the square of self-reported body height in meters.
Statistical analysis
Statistical analyses were performed using SAS software (version 9.4; SAS Institute Inc., Cary, NC, USA). Intake of six nutrients were examined (total fat, SFA, MUFA, PUFA, n-3 PUFA, and n-6 PUFA). Men and women were analyzed separately because the Japanese dietary intake differs according to sex (men: 2,118 kcal; total fat 66.4 g; women: 1,709 kcal; total fat 56.7 g).4
To analyze the relationship between the intake of total fat and fatty acids and various factors, we categorized the intake into five groups. We used the Mantel-Haenszel chi-squared test for categorical variables and linear regression analysis for continuous variables, with the median intake in each quintile category of total fat and fatty acid intake. Multivariable logistic regression was performed to evaluate the association between fat intake and the risk of T2D. The lowest quintile of fat intake was used as the reference group for the analysis. Model 1 was adjusted for age and stratified jointly according to area of residence (Hokkaido, Tohoku, Kanto, Chubu, Kinki, Chugoku, and Kyushu). Model 2 was additionally adjusted for family history of diabetes (yes or no), family history of hypertension (yes or no), smoking status (never, former smoker, or current smoker), BMI (<18.5, 18.5–24.9, 25.0–30.0, or >30.0 kg/m2), hours of walking (almost none, daily 0.5, 0.6–0.9, or ≥1.0 h), hours of exercise (almost none, weekly 1–2, 3–4, or ≥5 h), alcohol consumption (never, former drinker, or current drinker), energy intake (kcal, continuous), and carbohydrate (g/day, continuous). An indicator variable for missing data was created for each covariate. In addition, stratified analyses by age (<65 and ≥65 years) among both men and women were conducted. Further stratified analyses according to other factors, such as BMI, were considered but were not performed owing to the low incidence of diabetes among the participants. To calculate the P value for linear trend, we used a continuous variable of total fat and fatty acid intake assigning the median values in each quartile. P (two-tailed) <0.05 was considered statistically significant.
RESULTS
In the JACC study, 110,585 participants completed the questionnaire. We excluded those who were from areas not investigated on total fat and fatty acid intake (n = 24,184); those with missing dietary data (n = 24,614); those who reported extreme energy intakes (<500 kcal or >3,500 kcal) (n = 159); those with a medical history of diabetes, cancer, or myocardial infarction at baseline (n = 9,335); those living in areas not investigated for the development of diabetes after 5 years of follow-up (n = 5,044); and those who did not provide data on diabetes at the fifth year follow-up survey (n = 28,161). Thus, a total of 19,088 participants (7,044 men and 12,044 women) were included in the present study (Figure 1).
Figure 1. Flow diagram of participant inclusion.
A total of 494 (2.6%) participants (men, n = 247 [3.5%]; women, n = 247 [2.0%]) developed T2D during the study period. The baseline characteristics of the study population stratified according to quintiles of energy-adjusted total fat and fatty acid intake are presented in Table 1 and Table 2. For men, participants with higher total fat and fatty acid intake were older, exercised for longer, and had a lower proportion of current drinkers than those with lower total fat and fatty acid intake. For both sexes, participants with higher total fat and fatty acid intake had higher total protein intake, lower carbohydrate intake, and lower proportion of current smokers than those with lower total fat and fatty acid intake.
Table 1. Baseline characteristics of participants according to quintiles of energy-adjusteda total fat and fatty acid intake among men.
| Total fat | SFA | MUFA | |||||||
|
|
|
|
|||||||
| Q1 (low) | Q3 | Q5 (high) | Q1 (low) | Q3 | Q5 (high) | Q1 (low) | Q3 | Q5 (high) | |
| Age, years | 54.8 (9.2) | 55.7 (9.4) | 56.9 (9.5)** | 55.1 (9.3) | 55.8 (9.5) | 56.5 (9.7)** | 54.9 (9.3) | 55.6 (9.5) | 56.8 (9.4)** |
| Family history of diabetes, % | 7.9 | 12.5 | 10.4** | 8.4 | 11.3 | 11.1 | 8.3 | 12.6 | 10.2** |
| Family history of hypertension, % | 35.1 | 36.6 | 34.1 | 35.4 | 36.4 | 34.4 | 35.7 | 37.0 | 34.0 |
| Current smoker, % | 57.4 | 50.3 | 47.8** | 56.5 | 47.3 | 51.6** | 57.1 | 52.2 | 48.8** |
| Current drinker, % | 85.4 | 82.9 | 70.3** | 84.9 | 76.2 | 70.0** | 84.7 | 76.9 | 72.0** |
| BMI, kg/m2 | 22.7 (2.6) | 22.8 (4.4) | 22.6 (2.6) | 22.7 (2.6) | 22.8 (4.4) | 22.5 (2.6) | 22.7 (2.6) | 22.6 (2.7) | 22.5 (2.7) |
| BMI ≥25 kg/m2, % | 18.2 | 18.6 | 16.3 | 17.1 | 18.6 | 15.8 | 17.5 | 16.6 | 16.7 |
| Exercise ≥5 h/week, % | 6.2 | 7.3 | 9.7 | 7.0 | 7.1 | 8.9 | 6.3 | 6.7 | 9.9** |
| Walking ≥0.5 h/week, % | 86.7 | 86.4 | 89.0 | 86.1 | 87.6 | 89.5 | 86.7 | 87.0 | 89.4* |
| Energy intake, kcal/day | 1,920 (516) | 1,737 (491) | 1,899 (516) | 1,883 (526) | 1,757 (500) | 1,855 (497) | 1,929 (516) | 1,739 (500) | 1,906 (522) |
| Carbohydrate, % energy | 61.3 (11.5) | 57.7 (9.5) | 53.4 (8.0)** | 60.5 (11.6) | 57.9 (9.6) | 54.2 (8.4)** | 61.4 (11.4) | 57.5 (9.5) | 53.3 (8.2)** |
| Total protein, % energy | 9.6 (1.3) | 12.7 (1.5) | 15.0 (2.0)** | 10.0 (1.6) | 12.7 (1.9) | 14.4 (2.3)** | 9.8 (1.4) | 12.6 (1.7) | 14.9 (2.1)** |
| Total fat, % energy | 10.4 (1.8) | 16.7 (1.9) | 22.9 (3.6)** | 10.8 (2.2) | 16.7 (2.6) | 22.5 (3.9)** | 10.6 (1.9) | 16.7 (2.1) | 22.8 (3.7)** |
| SFA, % energy | 3.0 (0.7) | 5.1 (1.0) | 7.2 (1.6)** | 2.9 (0.5) | 5.0 (0.7) | 7.6 (1.5)** | 3.0 (0.7) | 5.1 (1.1) | 7.2 (1.6)** |
| MUFA, % energy | 3.2 (0.6) | 5.3 (0.8) | 7.5 (1.4)** | 3.3 (0.8) | 5.3 (1.0) | 7.3 (1.4)** | 3.2 (0.6) | 5.3 (0.7) | 7.5 (1.3)** |
| PUFA, % energy | 2.8 (0.7) | 4.1 (0.8) | 5.2 (1.0)** | 3.1 (0.8) | 4.1 (1.0) | 4.7 (1.2)** | 2.9 (0.8) | 4.0 (0.9) | 5.1 (1.0)** |
| n-3 PUFA, % energy | 0.5 (0.2) | 0.8 (0.2) | 1.0 (0.3)** | 0.6 (0.2) | 0.8 (0.3) | 0.9 (0.3)** | 0.5 (0.2) | 0.8 (0.2) | 1.0 (0.3)** |
| n-6 PUFA, % energy | 2.3 (0.6) | 3.2 (0.7) | 4.1 (0.8)** | 2.5 (0.7) | 3.3 (0.8) | 3.8 (0.9)** | 2.4 (0.7) | 3.2 (0.7) | 4.1 (0.8)** |
|
| |||||||||
|
| |||||||||
| PUFA | n-3 PUFA | n-6 PUFA | |||||||
|
|
|
|
|||||||
| Q1 (low) | Q3 | Q5 (high) | Q1 (low) | Q3 | Q5 (high) | Q1 (low) | Q3 | Q5 (high) | |
|
| |||||||||
| Age, years | 54.7 (9.2) | 55.9 (9.4) | 57.2 (9.4)** | 54.3 (9.4) | 55.9 (10.0) | 57.3 (9.1)** | 55.0 (9.2) | 55.8 (9.6) | 57.4 (9.5)** |
| Family history of diabetes, % | 8.5 | 12.3 | 9.2** | 8.8 | 10.1 | 9.9 | 8.4 | 11.4 | 8.9 |
| Family history of hypertension, % | 34.5 | 36.1 | 33.1 | 35.7 | 35.9 | 33.5 | 34.0 | 36.7 | 33.4 |
| Current smoker, % | 57.0 | 51.1 | 43.9** | 56.2 | 51.5 | 47.3** | 57.3 | 51.1 | 43.9** |
| Current drinker, % | 84.3 | 79.6 | 70.8** | 81.3 | 77.6 | 76.1** | 84.7 | 77.9 | 69.7** |
| BMI, kg/m2 | 22.6 (2.6) | 22.7 (4.3) | 22.7 (2.7) | 22.6 (2.6) | 22.6 (2.6) | 22.8 (4.4) | 22.6 (2.6) | 22.7 (4.4) | 22.6 (2.7) |
| BMI ≥25 kg/m2, % | 17.9 | 16 | 18.3 | 18 | 16.3 | 18.5 | 17.4 | 16.6 | 17.8 |
| Exercise ≥5 h/week, % | 7.2 | 7.0 | 10.3** | 6.4 | 6.8 | 9.5** | 7.3 | 7.3 | 10.4** |
| Walking ≥0.5 h/week, % | 86.6 | 87.6 | 88.4** | 87.1 | 85.9 | 87.9** | 86.4 | 87.1 | 88.4** |
| Energy intake, kcal/day | 1,922 (491) | 1,739 (494) | 1,904 (552) | 1,905 (477) | 1,738 (508) | 1,890 (520) | 1,925 (490) | 1,735 (495) | 1,895 (547) |
| Carbohydrate, % energy | 60.6 (11.5) | 57.3 (9.6) | 54.8 (8.3)** | 61.8 (10.9) | 57.5 (9.1) | 53.4 (8.6)** | 60.0 (11.6) | 57.6 (9.7) | 55.3 (8.3)** |
| Total protein, % energy | 9.8 (1.5) | 12.6 (1.5) | 15.1 (2.0)** | 9.7 (1.4) | 12.6 (1.4) | 15.2 (2.0)** | 10.0 (1.7) | 12.6 (1.7) | 14.9 (2.1)** |
| Total fat, % energy | 11.8 (3.3) | 16.8 (3.5) | 21.5 (4.2)** | 12.4 (3.8) | 17.0 (4.0) | 20.6 (4.4)** | 12.0 (3.4) | 16.7 (3.5) | 21.5 (4.3)** |
| SFA, % energy | 3.9 (1.6) | 5.2 (1.7) | 6.2 (1.7)** | 4.1 (1.8) | 5.2 (1.8) | 5.9 (1.7)** | 3.9 (1.6) | 5.1 (1.7) | 6.2 (1.7)** |
| MUFA, % energy | 3.7 (1.2) | 5.3 (1.3) | 6.9 (1.6)** | 3.9 (1.3) | 5.4 (1.5) | 6.6 (1.6)** | 3.8 (1.2) | 5.3 (1.3) | 6.9 (1.6)** |
| PUFA, % energy | 2.5 (0.4) | 4.0 (0.3) | 5.6 (0.8)** | 2.8 (0.6) | 4.1 (0.7) | 5.2 (1.0)** | 2.6 (0.5) | 4.0 (0.3) | 5.6 (0.8)** |
| n-3 PUFA, % energy | 0.5 (0.2) | 0.8 (0.2) | 1.1 (0.2)** | 0.4 (0.1) | 0.8 (0.1) | 1.2 (0.2)** | 0.5 (0.2) | 0.8 (0.2) | 1.0 (0.2)** |
| n-6 PUFA, % energy | 2.0 (0.4) | 3.2 (0.3) | 4.5 (0.7)** | 2.3 (0.6) | 3.3 (0.7) | 4.0 (0.9)** | 2.0 (0.4) | 3.2 (0.2) | 4.5 (0.6)** |
BMI, body mass index; MUFA, monounsaturated fatty acid; PUFA, polyunsaturated fatty acid; SD, standard deviation; SFA, saturated fatty acid.
All values are mean (SD) or percentages.
aTotal fat and fatty acid levels were adjusted for energy intake using the nutrient residual model.
P-trend was calculated using the Mantel-Haenszel chi-squared test for categorical variables and linear regression analysis for continuous variables, with the median intake in each quintile category of total fat and fatty acid intake.
*<0.05, **<0.01.
Participants with missing information were excluded (BMI: n = 206; smoking status: n = 117; drinking status: n = 0; sports information: n = 134; walking information: n = 181).
Table 2. Baseline characteristics of participants according to quintiles of energy-adjusteda total fat and fatty acid intake among women.
| Total fat | SFA | MUFA | |||||||
|
|
|
|
|||||||
| Q1 (low) | Q3 | Q5 (high) | Q1 (low) | Q3 | Q5 (high) | Q1 (low) | Q3 | Q5 (high) | |
| Age, years | 57.0 (9.6) | 55.1 (9.3) | 54.6 (9.2)** | 57.5 (9.4) | 55.6 (9.3) | 54.3 (9.3)** | 57.3 (9.5) | 55.2 (9.3) | 54.4 (9.2)** |
| Family history of diabetes, % | 9.7 | 11.0 | 11.0 | 9.5 | 11.0 | 12.1* | 10.3 | 10.8 | 11.0 |
| Family history of hypertension, % | 33.1 | 36.3 | 36.6** | 32.8 | 37.2 | 37.2** | 33.1 | 37.7 | 36.4** |
| Current smoker, % | 5.6 | 3.0 | 2.8** | 4.8 | 2.7 | 3.5** | 5.1 | 2.9 | 2.8** |
| Current drinker, % | 25.2 | 24.5 | 25.7 | 23.2 | 23.6 | 28.9** | 24.5 | 23.5 | 26.4 |
| BMI, kg/m2 | 23.0 (6.4) | 22.9 (2.9) | 22.6 (2.8) | 23.1 (6.4) | 22.9 (2.9) | 22.5 (2.7)** | 22.9 (3.1) | 22.9 (6.2) | 22.6 (2.8)** |
| BMI ≥25 kg/m2, % | 22.6 | 20.9 | 18.1 | 23.5 | 21.1 | 16.0 | 21.7 | 20.5 | 17.7 |
| Exercise ≥5 h/week, % | 4.6 | 3.3 | 5.5** | 5.2 | 3.8 | 4.8 | 4.9 | 3.7 | 5.1* |
| Walking ≥0.5 h/week, % | 87.4 | 86.1 | 87.8** | 87.5 | 87.4 | 89.2** | 87.7 | 86.6 | 88.0** |
| Energy intake, kcal/day | 1,544 (422) | 1,378 (323) | 1,546 (368) | 1,526 (412) | 1,401 (341) | 1,520 (357) | 1,544 (414) | 1,383 (332) | 1,542 (371) |
| Carbohydrate, % energy | 71.2 (6.1) | 62.5 (3.7) | 54.8 (4.4)** | 70.4 (6.2) | 62.5 (4.5) | 56.0 (5.0)** | 71.1 (6.0) | 62.5 (3.9) | 55.0 (4.5)** |
| Total protein, % energy | 11.9 (1.5) | 15.0 (1.5) | 17.0 (1.9)** | 12.5 (1.9) | 15.0 (1.9) | 16.3 (2.1)** | 12.1 (1.7) | 15.0 (1.7) | 16.8 (2.0)** |
| Total fat, % energy | 13.7 (2.4) | 20.7 (1.1) | 27.0 (2.8)** | 14.2 (2.9) | 20.7 (2.4) | 26.3 (3.2)** | 13.9 (2.6) | 20.7 (1.5) | 26.8 (2.9)** |
| SFA, % energy | 4.0 (0.9) | 6.4 (0.9) | 8.6 (1.4)** | 3.8 (0.7) | 6.4 (0.4) | 8.9 (1.2)** | 4.1 (1.0) | 6.4 (1.0) | 8.5 (1.5)** |
| MUFA, % energy | 4.2 (0.9) | 6.6 (0.6) | 8.9 (1.1)** | 4.4 (1.0) | 6.6 (1.0) | 8.6 (1.3)** | 4.2 (0.8) | 6.6 (0.4) | 9.0 (1.1)** |
| PUFA, % energy | 3.5 (0.8) | 4.8 (0.8) | 5.8 (1.0)** | 3.9 (1.1) | 4.8 (1.1) | 5.2 (1.1)** | 3.6 (0.9) | 4.8 (0.9) | 5.8 (1.0)** |
| n-3 PUFA, % energy | 0.7 (0.2) | 1.0 (0.3) | 1.2 (0.3)** | 0.8 (0.3) | 1.0 (0.3) | 1.0 (0.3)** | 0.7 (0.2) | 1.0 (0.3) | 1.1 (0.3)** |
| n-6 PUFA, % energy | 2.8 (0.7) | 3.8 (0.7) | 4.7 (0.8)** | 3.1 (0.9) | 3.9 (0.9) | 4.2 (0.9)** | 2.9 (0.8) | 3.8 (0.7) | 4.6 (0.8)** |
|
| |||||||||
|
| |||||||||
| PUFA | n-3 PUFA | n-6 PUFA | |||||||
|
|
|
|
|||||||
| Q1 (low) | Q3 | Q5 (high) | Q1 (low) | Q3 | Q5 (high) | Q1 (low) | Q3 | Q5 (high) | |
|
| |||||||||
| Age, years | 56.3 (9.7) | 55.0 (9.4) | 55.9 (9.1) | 55.6 (9.8) | 55.0 (9.4) | 56.4 (8.9)* | 56.5 (9.6) | 55.0 (9.4) | 55.9 (9.1)* |
| Family history of diabetes, % | 11.2 | 11.9 | 9.3** | 12.0 | 11.8 | 9.2 | 11.0 | 12.1 | 10.1** |
| Family history of hypertension, % | 33.9 | 36.9 | 36.5* | 34.8 | 37.8 | 37.0 | 34.7 | 36.7 | 36.8 |
| Current smoker, % | 6.5 | 3.5 | 1.7** | 5.7 | 3.9 | 1.9** | 6.4 | 3.3 | 1.8** |
| Current drinker, % | 29.5 | 24.6 | 20.8** | 30.4 | 23.4 | 22.4** | 30.0 | 24.7 | 21.0** |
| BMI, kg/m2 | 22.9 (6.3) | 22.8 (2.9) | 22.9 (2.9) | 22.7 (3.0) | 22.8 (2.9) | 23.0 (3.0)** | 22.9 (6.3) | 22.7 (2.9) | 22.9 (2.9) |
| BMI ≥25 kg/m2, % | 21.4 | 19.0 | 22.2 | 19.7 | 20.5 | 23.0 | 21.9 | 18.9 | 21.9 |
| Exercise ≥5 h/week, % | 4.6 | 3.5 | 5.1** | 3.8 | 4.0 | 5.7** | 4.8 | 3.5 | 5.2** |
| Walking ≥0.5 h/week, % | 89.2 | 86.9 | 86.2** | 88.1 | 88.4 | 85.6** | 89.3 | 87.2 | 86.7** |
| Energy intake, kcal/day | 1,529 (396) | 1,385 (333) | 1,547 (384)** | 1,533 (383) | 1,393 (347) | 1,521 (375)** | 1,525 (396) | 1,384 (331) | 1,544 (385)** |
| Carbohydrate, % energy | 69.5 (7.1) | 62.6 (5.2) | 56.7 (5.3)** | 68.7 (7.0) | 62.7 (5.6) | 57.0 (5.6)** | 69.0 (7.5) | 62.5 (5.4) | 57.1 (5.5)** |
| Total protein, % energy | 12.0 (1.6) | 14.9 (1.4) | 17.2 (1.9)** | 12.0 (1.5) | 14.8 (1.2) | 17.5 (1.8)** | 12.3 (1.9) | 14.9 (1.7) | 16.8 (1.9)** |
| Total fat, % energy | 15.2 (3.8) | 20.8 (3.6) | 25.0 (3.7)** | 16.5 (4.7) | 20.7 (4.0) | 24.1 (4.0)** | 15.4 (4.0) | 20.9 (3.6) | 24.9 (3.8)** |
| SFA, % energy | 5.1 (1.8) | 6.5 (1.8) | 7.2 (1.6)** | 5.6 (2.1) | 6.5 (1.8) | 6.9 (1.6)** | 5.1 (1.8) | 6.6 (1.8) | 7.2 (1.6)** |
| MUFA, % energy | 4.9 (1.4) | 6.7 (1.4) | 8.1 (1.5)** | 5.3 (1.7) | 6.7 (1.5) | 7.8 (1.6)** | 4.9 (1.4) | 6.7 (1.4) | 8.1 (1.5)** |
| PUFA, % energy | 3.2 (0.5) | 4.7 (0.2) | 6.3 (0.7)** | 3.5 (0.8) | 4.8 (0.8) | 6.0 (0.9)** | 3.2 (0.6) | 4.7 (0.3) | 6.3 (0.7)** |
| n-3 PUFA, % energy | 0.6 (0.2) | 0.9 (0.2) | 1.3 (0.3)** | 0.6 (0.1) | 0.9 (0.1) | 1.4 (0.2)** | 0.7 (0.3) | 0.9 (0.3) | 1.2 (0.3)** |
| n-6 PUFA, % energy | 2.5 (0.5) | 3.8 (0.3) | 5.1 (0.6)** | 2.9 (0.7) | 3.9 (0.7) | 4.5 (0.9)** | 2.5 (0.4) | 3.8 (0.2) | 5.1 (0.6)** |
BMI, body mass index; MUFA, monounsaturated fatty acid; PUFA, polyunsaturated fatty acid; SD, standard deviation; SFA, saturated fatty acid.
All values are mean (SD) or percentages.
aTotal fat and fatty acid levels were adjusted for energy intake using the nutrient residual model.
P-trend was calculated using the Mantel-Haenszel chi-squared test for categorical variables and linear regression analysis for continuous variables, with the median intake in each quintile category of total fat and fatty acid intake.
*<0.05, **<0.01.
Participants with missing information were excluded (BMI: n = 408; smoking status: n = 928; drinking status: n = 462; sports information: n = 338; walking information: n = 430).
The odds ratios (ORs) and 95% confidence intervals (CIs) of T2D stratified according to the energy-adjusted total fat and fatty acid intake in men and women are shown in Table 3 and Table 4. For men, the multivariable-adjusted OR of incident T2D for the highest versus lowest quintiles was 0.58 (95% CI, 0.37–0.90; P-trend = 0.037) for total fat, 0.78 (95% CI, 0.51–1.21; P-trend = 0.120) for SFA, 0.55 (95% CI, 0.35–0.86; P-trend = 0.019) for MUFA, 0.61 (95% CI, 0.39–0.96; P-trend = 0.059) for PUFA, 0.64 (95% CI, 0.42–0.99; P-trend = 0.111) for n-3 PUFA, and 0.70 (95% CI, 0.45–1.09; P-trend = 0.115) for n-6 PUFA, indicating that total fat, MUFA, PUFA, and n-3 PUFA were inversely associated with T2D. For women, total fat and fatty acid intake were not significantly associated with T2D.
Table 3. Odds ratios and 95% confidence intervals of type 2 diabetes according to quintiles of energy-adjusteda total fat and fatty acid intake among men.
| Q1 (low) | Q2 | Q3 | Q4 | Q5 (high) | P for trendb | |
| Total fat, g/day | <25.34 | 25.34–30.31 | 30.32–34.45 | 34.46–40.05 | >40.05 | |
| Number of participants | 1,408 | 1,409 | 1,409 | 1,409 | 1,409 | |
| Number of cases | 61 | 44 | 50 | 51 | 41 | |
| Model 1 | 1.00 (reference) | 0.72 (0.48–1.07) | 0.82 (0.56–1.21) | 0.81 (0.55–1.20) | 0.66 (0.43–0.995) | 0.102 |
| Model 2 | 1.00 (reference) | 0.72 (0.48–1.08) | 0.78 (0.52–1.17) | 0.79 (0.53–1.19) | 0.58 (0.37–0.90) | 0.037 |
| SFA, g/day | <7.12 | 7.12–8.90 | 8.91–10.50 | 10.51–12.57 | >12.57 | |
| Number of participants | 1,408 | 1,409 | 1,409 | 1,409 | 1,409 | |
| Number of cases | 52 | 51 | 57 | 39 | 48 | |
| Model 1 | 1.00 (reference) | 1.00 (0.67–1.49) | 1.11 (0.75–1.63) | 0.73 (0.48–1.13) | 0.88 (0.59–1.33) | 0.289 |
| Model 2 | 1.00 (reference) | 0.98 (0.66–1.47) | 1.07 (0.72–1.59) | 0.70 (0.45–1.08) | 0.78 (0.51–1.21) | 0.120 |
| MUFA, g/day | <7.79 | 7.79–9.42 | 9.43–10.94 | 10.95–12.89 | >12.89 | |
| Number of participants | 1,408 | 1,409 | 1,409 | 1,409 | 1,409 | |
| Number of cases | 58 | 50 | 45 | 55 | 39 | |
| Model 1 | 1.00 (reference) | 0.86 (0.58–1.27) | 0.77 (0.52–1.15) | 0.92 (0.63–1.36) | 0.65 (0.43–0.99) | 0.084 |
| Model 2 | 1.00 (reference) | 0.83 (0.56–1.24) | 0.74 (0.49–1.11) | 0.86 (0.58–1.28) | 0.55 (0.35–0.86) | 0.019 |
| PUFA, g/day | <6.19 | 6.19–7.40 | 7.41–8.45 | 8.46–9.73 | >9.73 | |
| Number of participants | 1,408 | 1,409 | 1,409 | 1,409 | 1,409 | |
| Number of cases | 66 | 47 | 44 | 50 | 40 | |
| Model 1 | 1.00 (reference) | 0.71 (0.48–1.05) | 0.66 (0.44–0.99) | 0.78 (0.52–1.16) | 0.62 (0.40–0.96) | 0.061 |
| Model 2 | 1.00 (reference) | 0.72 (0.48–1.07) | 0.66 (0.44–1.00) | 0.77 (0.51–1.16) | 0.61 (0.39–0.96) | 0.059 |
| n-3 PUFA, g/day | <1.13 | 1.13–1.38 | 1.39–1.65 | 1.66–1.99 | >1.99 | |
| Number of participants | 1,408 | 1,409 | 1,409 | 1,409 | 1,409 | |
| Number of cases | 63 | 38 | 55 | 46 | 45 | |
| Model 1 | 1.00 (reference) | 0.60 (0.40–0.91) | 0.88 (0.60–1.29) | 0.74 (0.50–1.10) | 0.73 (0.49–1.10) | 0.282 |
| Model 2 | 1.00 (reference) | 0.59 (0.39–0.90) | 0.87 (0.59–1.28) | 0.70 (0.46–1.06) | 0.64 (0.42–0.99) | 0.111 |
| n-6 PUFA, g/day | <4.95 | 4.95–5.94 | 5.95–6.80 | 6.81–7.84 | >7.84 | |
| Number of participants | 1,408 | 1,409 | 1,409 | 1,409 | 1,409 | |
| Number of cases | 49 | 45 | 52 | 47 | 54 | |
| Model 1 | 1.00 (reference) | 0.64 (0.43–0.95) | 0.79 (0.54–1.17) | 0.59 (0.39–0.91) | 0.69 (0.45–1.05) | 0.088 |
| Model 2 | 1.00 (reference) | 0.65 (0.43–0.98) | 0.80 (0.54–1.20) | 0.60 (0.38–0.92) | 0.70 (0.45–1.09) | 0.115 |
BMI, body mass index; MUFA, monounsaturated fatty acid; PUFA, polyunsaturated fatty acid, Q, quintile; SFA, saturated fatty acid.
Bold P values are statistically significant (P < 0.05).
The lowest quintiles of total fat and fatty acid intake were used as the reference group in the analysis. Model 1 was adjusted for age and stratified jointly according to areas (Hokkaido, Tohoku, Kanto, Chubu, Kinki, Chugoku, and Kyusyu). Model 2 was additionally adjusted for family history of diabetes (yes, no); family history of hypertension (yes, no); smoking status (never, former smoker, current smoker); body mass index (<18.5, 18.5–24.9, 25.0–30.0, >30.0 kg/m2); walking hours (almost none, daily 0.5, 0.6–0.9, and ≥1.0 h); hours of exercise (almost none, weekly 1–2, 3–4, and ≥5 h); alcohol consumption habit (never, former drinker, current drinker); energy intake (kcal, continuous); and carbohydrate (g/day; continuous).
aTotal fat and fatty acid intake were adjusted for energy intake using the nutrient residual model.
bThe P value for linear trend was calculated using a continuous variable of total fat and fatty acid intake assigning the median values in each quartile.
Table 4. Odds ratios and 95% confidence intervals of type 2 diabetes according to quintile categories of energy-adjusteda total fat and fatty acid intake among women.
| Women | Q1 (low) | Q2 | Q3 | Q4 | Q5 (high) | P for trendb |
| Total fat, g/day | <26.75 | 26.75–31.06 | 31.07–34.78 | 34.79–39.25 | >39.25 | |
| Number of participants | 2,408 | 2,409 | 2,409 | 2,409 | 2,409 | |
| Number of cases | 61 | 47 | 47 | 41 | 46 | |
| Model 1 | 1.00 (reference) | 0.76 (0.51–1.12) | 0.77 (0.52–1.14) | 0.67 (0.44–1.01) | 0.76 (0.51–1.14) | 0.144 |
| Model 2 | 1.00 (reference) | 0.72 (0.47–1.11) | 0.76 (0.48–1.21) | 0.70 (0.41–1.18) | 0.80 (0.43–1.51) | 0.455 |
| SFA, g/day | <7.68 | 7.68–9.36 | 9.37–10.83 | 10.84–12.53 | >12.53 | |
| Number of participants | 2,408 | 2,409 | 2,409 | 2,409 | 2,409 | |
| Number of cases | 53 | 58 | 43 | 44 | 44 | |
| Model 1 | 1.00 (reference) | 1.11 (0.76–1.62) | 0.82 (0.54–1.24) | 0.85 (0.56–1.29) | 0.82 (0.54–1.25) | 0.182 |
| Model 2 | 1.00 (reference) | 1.12 (0.75–1.69) | 0.85 (0.53–1.34) | 0.93 (0.57–1.54) | 0.93 (0.53–1.65) | 0.643 |
| MUFA, g/day | <8.34 | 8.34–9.85 | 9.86–11.19 | 11.20–12.82 | >12.82 | |
| Number of participants | 2,408 | 2,409 | 2,409 | 2,409 | 2,409 | |
| Number of cases | 59 | 55 | 40 | 46 | 42 | |
| Model 1 | 1.00 (reference) | 0.95 (0.65–1.38) | 0.68 (0.45–1.03) | 0.78 (0.53–1.17) | 0.73 (0.49–1.11) | 0.084 |
| Model 2 | 1.00 (reference) | 0.86 (0.57–1.30) | 0.65 (0.40–1.04) | 0.73 (0.45–1.21) | 0.68 (0.37–1.25) | 0.181 |
| PUFA, g/day | <6.16 | 6.16–7.17 | 7.18–8.06 | 8.07–9.15 | >9.15 | |
| Number of participants | 2,408 | 2,409 | 2,409 | 2,409 | 2,409 | |
| Number of cases | 54 | 46 | 47 | 54 | 41 | |
| Model 1 | 1.00 (reference) | 0.85 (0.57–1.28) | 0.90 (0.60–1.36) | 1.05 (0.70–1.57) | 0.80 (0.51–1.25) | 0.585 |
| Model 2 | 1.00 (reference) | 0.87 (0.57–1.34) | 0.96 (0.62–1.51) | 1.16 (0.72–1.85) | 0.91 (0.51–1.60) | 0.899 |
| n-3 PUFA, g/day | <1.11 | 1.11–1.35 | 1.36–1.60 | 1.61–1.91 | >1.91 | |
| Number of participants | 2,408 | 2,409 | 2,409 | 2,409 | 2,409 | |
| Number of cases | 55 | 44 | 48 | 54 | 41 | |
| Model 1 | 1.00 (reference) | 0.81 (0.54–1.22) | 0.93 (0.62–1.38) | 1.05 (0.71–1.55) | 0.78 (0.51–1.20) | 0.557 |
| Model 2 | 1.00 (reference) | 0.80 (0.52–1.22) | 0.88 (0.58–1.36) | 1.05 (0.67–1.63) | 0.75 (0.45–1.28) | 0.608 |
| n-6 PUFA, g/day | <4.90 | 4.90–5.74 | 5.75–6.46 | 6.47–7.32 | >7.32 | |
| Number of participants | 2,408 | 2,409 | 2,409 | 2,409 | 2,409 | |
| Number of cases | 57 | 47 | 43 | 47 | 48 | |
| Model 1 | 1.00 (reference) | 0.83 (0.55–1.23) | 0.77 (0.51–1.17) | 0.85 (0.56–1.29) | 0.88 (0.57–1.35) | 0.617 |
| Model 2 | 1.00 (reference) | 0.86 (0.57–1.31) | 0.83 (0.53–1.29) | 0.95 (0.60–1.51) | 1.01 (0.60–1.70) | 0.889 |
BMI, body mass index; MUFA, monounsaturated fatty acid; PUFA, polyunsaturated fatty acid, Q, quintile; SFA, saturated fatty acid.
Bold P values are statistically significant (P < 0.05).
The lowest quartiles of total fat and fatty acid intake were used as the reference group in the analysis. Model 1 was adjusted for age and stratified jointly according to areas (Hokkaido, Tohoku, Kanto, Chubu, Kinki, Chugoku, and Kyusyu). Model 2 was additionally adjusted for family history of diabetes (yes, no); family history of hypertension (yes, no); smoking status (never, former smoker, current smoker); body mass index (<18.5, 18.5–24.9, 25.0–30.0, >30.0 kg/m2); walking hours (almost none, daily 0.5, 0.6–0.9, and ≥1.0 h); hours of exercise (almost none, weekly 1–2, 3–4, and ≥5 h); alcohol consumption habit (never, former drinker, current drinker); energy intake (kcal, continuous); and carbohydrate (g/day; continuous).
aTotal fat and fatty acid intake were adjusted for energy intake using the nutrient residual model.
bThe P value for linear trend was calculated using a continuous variable of total fat and fatty acid intake assigning the median values in each quartile.
eTable 1 and eTable 2 show results of stratified analyses by age (<65 and ≥65 years) among both men and women. In men, higher MUFA and n-3 PUFA intake were inversely associated with T2D among those aged <65 years, while the association was not significant among those aged ≥65 years. Among those aged ≥65 years, consumption of more PUFA in men and consumption of more n-6 PUFA in women were inversely associated with T2D. However, this association was not observed among those aged <65 years.
DISCUSSION
In this study, we analyzed the associations of total fat and fatty acid intake with the risk of T2D in Japanese adults. The results of this study indicated that total fat, MUFA, PUFA, and n-3 PUFA intakes were inversely associated with T2D in Japanese men but not in women. SFA and n-6 PUFA intake were not associated with T2D in either sex. In women, total fat and fatty acid intake were not significantly associated with T2D. Given the large difference in ORs for the associations of total fat, MUFA, PUFA, and n-3 PUFA with T2D in the Q1 and Q2–5 group of men and the fact that OR of Q1–Q5 is not clearly linear, we think that the lowest total fat, MUFA, PUFA, and n-3 PUFA intake in men may be at a risk of T2D, but higher intake itself is not associated with a reduced risk.
In Japan, the number of diabetes cases is rising, and intakes of total fat and fatty acids other than n-3 PUFA are also increasing. However, our result reported higher intakes of total fat and all fatty acids were not associated with higher risk of T2D. Thus, total fat and fatty acids intake may not be a significant contributor to the incidence of T2D in Japan.
The results of the present study regarding total fat, PUFA, and n-3 PUFA intakes in men are inconsistent with those of previous meta-analyses.7–11 However, most of the studies included in those meta-analyses were not conducted in Asia. In contrast, the results of two studies conducted in Asia,17,18 which were included in the abovementioned meta-analyses,7,8 are consistent with the results of the present study. This discrepancy may be attributed to the fact that Asians have a lower fat intake19 and a higher intake of fish rich in n-3 PUFA and n-3 PUFA than non-Asians20 (fish intake in 2013: Japan, 48.60 kg/capita/year; United States, 21.51 kg/capita/year; United Kingdom, 20.76 kg/capita/year; n-3 PUFA: Japan, 1.3% energy in men, 1.4% energy in women; United States, 0.7% energy in men, 0.7% energy in women; United Kingdom, 0.7% energy in men, 0.8% energy in women). Although it is believed that n-3 PUFA may reduce the risk of developing diabetes by modulating insulin sensitivity in phospholipid membranes,20 the detailed reason for the discrepancy of association of n-3 PUFA and T2D between Asia and non-Asia is unknown.
A previous cross-sectional study demonstrated a favorable relationship between MUFA and β-cell insulin secretion.21 In addition, a cohort study indicated that increased intake of MUFA is associated with better β-cell function.22 This is because intake of MUFA preserves or even enhances β-cell proliferation and has as an anti-apoptotic effect.23 The results of the present study indicated that MUFA intake is associated with a reduced risk of T2D in men, a finding that is in line with those of the abovementioned previous studies.21–23 In contrast, a previous meta-analysis11 indicated that MUFA intake is not associated with the risk of T2D. The reason for the discrepancy between the results of the present study and those of this previous meta-analysis11 are unknown. Therefore, further research is needed clarify the relationship between MUFA intake and the risk of T2D.
The results of the present study for both sexes indicated that n-6 PUFA and SFA intake were not associated with the risk of T2D, a finding that is consistent with those of a previous meta-analysis.11 Experimental evidence suggests that n-6 PUFA is associated with favorable insulin sensitivity and protection against the development of T2D.24 In contrast, in vitro experimental data have demonstrated that SFA induces insulin resistance.25 Thus, although n-6 PUFA and SFA have mechanisms associated with the reduction or increase in the risk of developing diabetes, they may not affect the risk of diabetes in the amounts habitually consumed by humans.
The results of the present study indicate that there are sex-specific differences in the associations of total fat intake and intake of most fatty acids with the risk of T2D. Total fat, MUFA, PUFA, and n-3 PUFA intakes were associated with a lower risk of T2D in men but not in women. These sex-specific differences may be attributed to the fact that women tend to follow a healthier lifestyle in general, and the intake of fat and fatty acids they consumed may not have had a significant impact on their likelihood of developing diabetes.26
The present study has several limitations. First, some misclassification of the diagnosis of T2D was unavoidable because all diagnoses were self-reported. However, the self-reported T2D diagnoses were validated, and the results showed moderate sensitivity (70% for men and 75% for women) and specificity (95% for men and 98% for women).16 Second, it is worth noting that dietary intakes were only measured once, which means the data may not have fully captured long-term intake. Unfortunately, this could have resulted in an underestimation of the association between dietary intake and the risk of T2D, due to non-differential misclassifications. Third, even though the present study had a prospective design, there is a concern about reverse causation due to the short follow-up period of 5 years. Some participants may have already had prediabetes at the beginning of the study and altered their diet accordingly. Furthermore, we were unable to exclude participants who had undiagnosed diabetes or prediabetes because we did not gather information on their blood glucose levels at the start of the study. Thus, the incidence of T2D in our study may be substituted for prevalence. Fourth, result of this study in the late 1980s may not be applicable to the Japanese population in 2023 because mean ratio of energy intake from total fat are increasing for people 20 and over in Japan (men 24.3% in 1995, 27.4% in 2019; women 25.9% in 1995, 29.2% in 2019).4 Fifth, the validation study showed low Spearman rank correlation coefficients of 0.15 for PUFA, 0.21 for n-3 PUFA, and 0.16 for n-6 PUFA, indicating the possibility of misclassification. Sixth, data was only collected from one-third of the eligible participants due to limitations in the 5-year follow-up survey, which was conducted in specific baseline study areas and not all of them. However, there were no significant difference in the characteristics of the participants, including age, BMI, and other factors, between those who responded to the 5-year survey and those who did not.27 Finally, our study cannot rule out the possibility of residual confounding factors.
Conclusion
Higher intakes of total fats, MUFA, PUFA, and n-3 PUFA were inversely associated with T2D among Japanese men. In women, total fat and fatty acid were not significantly associated with T2D.
ACKNOWLEDGMENTS
The authors thank all staff members who were involved in this study for their valuable help in conducting the baseline survey and follow-up.
Author contributions: Formal analysis, A.Y. and T.K.; supervision, A.T.; writing – original draft, A.Y.; writing – review and editing, A.Y, T.K, K.W, H.I, and A.T; A.Y. and A.T. had primary responsibility for the final content. All the authors read and approved the final manuscript.
Funding: This study was supported by the Grants-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture of Japan (grant nos.: 61010076, 62010074, 63010074, 1010068, 2151065, 3151064, 4151063, 5151069, 6279102, and 11181101).
Institutional Review Board statement: The study was approved by the Institutional Review Committee for Ethical Issues of the Faculty of Medicine, Hokkaido University.
Informed consent statement: In most regions, informed consent was obtained individually and directly from members of the cohort. In other areas, informed consent was obtained at the community level after the purpose of the study and confidentiality of the data were explained to community leaders and mayors.
Data availability statement: The data presented in this study are not publicly available because of privacy and ethical restrictions.
Ethics statement: This study was approved by Ethics Committee of the Faculty of Medicine, Hokkaido University (approval no.: 14-044), and performed in accordance with the principles of the Declaration of Helsinki.
Conflicts of interest: None declared.
SUPPLEMENTARY MATERIAL
The following is the supplementary data related to this article:
eTable 1. Odds ratios and 95% confidence intervals of type 2 diabetes according to quintiles of energy-adjusteda total fat and fatty acid intake by the age (<65 and ≥65 years) among men
eTable 2. Odds ratios and 95% confidence intervals of type 2 diabetes according to quintiles of energy-adjusteda total fat and fatty acid intake by the age (<65 and ≥65 years) among women
REFERENCES
- 1.Ogurtsova K, da Rocha Fernandes JD, Huang Y, et al. IDF diabetes atlas: Global estimates for the prevalence of diabetes for 2015 and 2040. Diabetes Res Clin Pract. 2017;128:40–50. 10.1016/j.diabres.2017.03.024 [DOI] [PubMed] [Google Scholar]
- 2.Evert AB, Boucher JL, Cypress M, et al. ; American Diabetes Association . Nutrition therapy recommendations for the management of adults with diabetes. Diabetes Care. 2013;36:3821–3842. 10.2337/dc13-2042 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Neuenschwander M, Ballon A, Weber KS, et al. Role of diet in type 2 diabetes incidence: Umbrella review of meta-analyses of prospective observational studies. BMJ. 2019;366:l2368. 10.1136/bmj.l2368 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Ministry of Health, Labour and Wealth of Japan. The National Health and Nutrition Survey in Japan, https://www.mhlw.go.jp/bunya/kenkou/kenkou_eiyou_chousa.html; Accessed on 20 June 2023 (in Japanese).
- 5.National Health and Nutrition Examination Survey, https://www.ars.usda.gov/northeast-area/beltsville-md-bhnrc/beltsville-human-nutrition-research-center/food-surveys-research-group/docs/wweia-data-tables/; Accessed on 20 June 2023.
- 6.National Diabetes Statistics Report, 2020, https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf; Accessed on 20 June 2023.
- 7.de Souza RJ, Mente A, Maroleanu A, et al. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: Systematic review and meta-analysis of observational studies. BMJ. 2015;351:h3978. 10.1136/bmj.h3978 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Alhazmi A, Stojanovski E, McEvoy M, Garg ML. Macronutrient intakes and development of type 2 diabetes: a systematic review and meta-analysis of cohort studies. J Am Coll Nutr. 2012;31:243–258. 10.1080/07315724.2012.10720425 [DOI] [PubMed] [Google Scholar]
- 9.Zhou Y, Tian C, Jia C. Association of fish and n-3 fatty acid intake with the risk of type 2 diabetes: A meta-analysis of prospective studies. Br J Nutr. 2012;108:408–417. 10.1017/S0007114512002036 [DOI] [PubMed] [Google Scholar]
- 10.Wu JH, Micha R, Imamura F, et al. Omega-3 fatty acids and incident type 2 diabetes: A systematic review and meta-analysis. Br J Nutr. 2012;107(Suppl 2):S214–S227. 10.1017/S0007114512001602 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Neuenschwander M, Barbaresko J, Pischke CR, et al. Intake of dietary fats and fatty acids and the incidence of type 2 diabetes: A systematic review and dose-response meta-analysis of prospective observational studies. PLoS Med. 2020;17:e1003347. 10.1371/journal.pmed.1003347 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Tamakoshi A, Ozasa K, Fujino Y, et al. ; JACC Study Group . Cohort profile of the Japan Collaborative Cohort Study at final follow-up. J Epidemiol. 2013;23:227–232. 10.2188/jea.JE20120161 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Date C, Fukui M, Yamamoto A, et al. ; JACC Study Group . Reproducibility and validity of a self-administered food frequency questionnaire used in the JACC study. J Epidemiol. 2005;15(Suppl 1):S9–S23. 10.2188/jea.15.S9 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Willett W, Stampfer MJ. Total energy intake: Implications for epidemiologic analyses. Am J Epidemiol. 1986;124:17–27. 10.1093/oxfordjournals.aje.a114366 [DOI] [PubMed] [Google Scholar]
- 15.The Council for Science and Technology, Ministry of Education Culture, Sports, Science and Technology, Japan. Standard Tables of Food Composition in Japan. 5th revised and enlarged edition. Tokyo: National Printing Bureau; 2005. [Google Scholar]
- 16.Iso H, Date C, Wakai K, Fukui M, Tamakoshi A; JACC Study Group . The relationship between green tea and total caffeine intake and risk for self-reported type 2 diabetes among Japanese adults. Ann Intern Med. 2006;144:554–562. 10.7326/0003-4819-144-8-200604180-00005 [DOI] [PubMed] [Google Scholar]
- 17.Brostow DP, Odegaard AO, Koh WP, et al. Omega-3 fatty acids and incident type 2 diabetes: The Singapore Chinese Health Study. Am J Clin Nutr. 2011;94:520–526. 10.3945/ajcn.110.009357 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Ha K, Joung H, Song Y. Inadequate fat or carbohydrate intake was associated with an increased incidence of type 2 diabetes mellitus in Korean adults: A 12-year community-based prospective cohort study. Diabetes Res Clin Pract. 2019;148:254–261. 10.1016/j.diabres.2019.01.024 [DOI] [PubMed] [Google Scholar]
- 19.Zhou BF, Stamler J, Dennis B, et al. ; INTERMAP Research Group . Nutrient intakes of middle-aged men and women in China, Japan, United Kingdom, and United States in the late 1990s: the INTERMAP study. J Hum Hypertens. 2003;17:623–630. 10.1038/sj.jhh.1001605 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Tsugane S. Why has Japan become the world’s most long-lived country: insights from a food and nutrition perspective. Eur J Clin Nutr. 2021;75:921–928. 10.1038/s41430-020-0677-5 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Rojo-Martínez G, Esteva I, Ruiz de Adana MS, et al. Dietary fatty acids and insulin secretion: a population-based study. Eur J Clin Nutr. 2006;60:1195–1200. 10.1038/sj.ejcn.1602437 [DOI] [PubMed] [Google Scholar]
- 22.den Biggelaar LJCJ, Eussen SJPM, Sep SJS, et al. Prospective associations of dietary carbohydrate, fat, and protein intake with β-cell function in the CODAM study. Eur J Nutr. 2019;58:597–608. 10.1007/s00394-018-1644-y [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Morgan NG, Dhayal S, Diakogiannaki E, Welters HJ. The cytoprotective actions of long-chain mono-unsaturated fatty acids in pancreatic beta-cells. Biochem Soc Trans. 2008;36(Pt 5):905–908. 10.1042/BST0360905 [DOI] [PubMed] [Google Scholar]
- 24.Maki KC, Eren F, Cassens ME, Dicklin MR, Davidson MH. ω-6 Polyunsaturated fatty acids and cardiometabolic health: Current evidence, controversies, and research gaps. Adv Nutr. 2018;9:688–700. 10.1093/advances/nmy038 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Boden G. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes. 1997;46:3–10. 10.2337/diab.46.1.3 [DOI] [PubMed] [Google Scholar]
- 26.Ide R, Mizoue T, Fujino Y, et al. ; JACC Study Group . Cigarette smoking, alcohol drinking, and oral and pharyngeal cancer mortality in Japan. Oral Dis. 2008;14:314–319. 10.1111/j.1601-0825.2007.01378.x [DOI] [PubMed] [Google Scholar]
- 27.Eshak ES, Iso H, Muraki I, Tamakoshi A. Among the water-soluble vitamins, dietary intakes of vitamins C, B2 and folate are associated with the reduced risk of diabetes in Japanese women but not men. Br J Nutr. 2019;121:1357–1364. 10.1017/S000711451900062X [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.