Author: Damisha Henderson Florida A&M University, College of Pharmacy and Pharmaceutical Sciences, Fourth Year PharmD Candidate
Eating fruit sustains insulin sensitivity and lessens the risk of type 2 diabetes, but fruit juices do not convey the same benefit.
Type 2 diabetes mellitus (T2DM) is a combination of impaired insulin secretion (β-cell dysfunction) and insulin resistance. It is the 7th leading cause of disability worldwide and causes >2 million deaths each year. 451 million people are living with diabetes, expected to exceed 693 million in 2045. Evidence-based strategies support promoting a healthy diet and regular physical activity to decrease the risk of T2DM. An inverse association between fruit intake and T2DM has been reported. Australian Dietary Guidelines recommendation of two servings [150 g] of fruit per day was associated with a 32% lower risk of T2DM over 12 years in the Australian Diabetes, Obesity and Lifestyle Study. Adherence to these recommendations could have prevented 23% of T2DM cases (attributable population fraction: 23.3 [7.3- 38.2]). Higher consumptions of blueberries, grapes, apples, bananas, and grapefruit were associated with a lower risk of T2DM in 3 prospective cohorts. The study examined total intake of fruit, fruits commonly consumed, and fruit juice, on one: the association with insulin resistance and β-cell dysfunction; and two: incident diabetes at 5- and 12-years’ follow-up, in a cohort of Australian men and women.
Participants were men and women aged 25 years or older recruited to the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The methods and response rates of the AusDiab cohort have been described previously. In 1999 and 2000 (n = 11247), with follow-up in 2004 to 2005 (n = 6400) and 2011 to 2012 (n = 4614). Participants who did not complete a food frequency questionnaire (FFQ) at baseline (n = 204), energy intake < 2500 kJ/day or > 14500 kJ/day for women and < 3300 kJ/day or > 17500 kJ/day for men; n = 342, were pregnant n = 45, had diabetes at baseline (n = 968), had missing data for important covariates (n = 642), and who had missing outcome data at baseline (n = 1371) were excluded. 7675 participants remained for analyses. Follow-up data were available for 4674 participants at five years and 3518 participants at 12 years. The dietary intake of participants was assessed with the semiquantitative FFQ. Participants were asked their food items intake over the previous 12 months from a list of 74 food items. Food items included fruit juice and ten different types of fruit. The portion size was calculated using scaled portions of different food types. Using the NUTTAB95 nutrient database, intake calculations were analyzed by Cancer Council Victoria. Only fruit to contribute greater than 10% were investigated to prevent a type 1 error.
Primary outcomes included fasting plasma glucose (FPG), 2-hour post-load plasma glucose (PLG), updated homeostasis model assessment of β-cell function (HOMA2- %β), HOMA2 of insulin sensitivity (HOMA2-%S), and fasting insulin levels. FPG and PLG were determined using a spectrophotometric-hexokinase method, and serum insulin was measured using an automated chemiluminescence immunoassay. The HOMA2 computer model was used to estimate insulin sensitivity (HOMA2-%S) and β-cell function (HOMA2-%B) from fasting insulin and glucose concentrations. The secondary outcome was incident T2DM at 5- and 12-years follow-up. T2DM was classified as FPG >7.0 mmol/L, 2-hour PLG >11.1 mmol/L, or current treatment with insulin or oral hypoglycemic agents. Baseline demographic data were collected using questionnaires. They included: age, sex (male/ female), education level (never to some high school/ completed university or equivalent), physical activity (sedentary = 0 min/week; insufficient < 150 min/week; and sufficient ≥ 150 min/week), smoking status (current/ former/never), income, and parental history of diabetes (yes/no).
Australian Bureau of Statistics reports from the Socioeconomic Indexes for Areas (SEIFA) calculated body mass index, height to the nearest 0.5 cm using a stadiometer. Weight was measured to the nearest 0.1 kg using a mechanical beam balance. Linear models with a γ distribution were used to examine associations with continuous exposures. P values were obtained using likelihood ratio tests to compare models. Ratios of means and 95% CIs were obtained from the model with the exposure fitted as a continuous variable. Logistic regression models describe baseline fruit intake and the incident diabetes at 5 and 12 years. Three models of adjustment were used. Model 1 adjusted for age and sex; model 2 adjusted for age, sex, physical activity levels, level of education, SEIFA, income, body mass index (calculated as kg/m2), smoking status, self-reported prevalence of cardiovascular disease, and parental history of diabetes; model 3 adjusted for all covariates in model 2 plus energy intake, and intake of alcohol, vegetables, red meat, and processed meat.
Of 7674 Australians (45% male), the mean age was 54 years at baseline, and the median (interquartile range) total fruit intake was 162 g/day (95-283 g/day). Those with the highest total fruit intakes were mostly female, older, physically active, nonsmokers, and had a higher education degree. They also had a higher total energy intake, eating more vegetables and less red and processed meat. Apples contribute 23% to total fruit intake, bananas (~ 20%), oranges and other citrus fruits ~ 18%. Other fruits contributed less than 8% each and were not assessed. Total fruit intake was inversely associated with serum insulin and HOMA2-%β and significantly positively associated with HOMA2-%S (false discovery rate corrected P ≤ .05) for all. Total fruit intake was not associated with PLG or FPG. Participants in the highest intake quartile had a 3% lower PLG (0.97 [0.96-0.99]), a 5% lower serum insulin (0.95 [0.93-0.98]), a 2% lower HOMA2-%β (0.98 [0.96-1.00]), and a 6% higher HOMA2-%S (1.06 [1.03-1.09]). Apple intake was significantly inversely associated with serum insulin (P = .035) and nonlinearly inversely associated with PLG (P < .001; P nonlinearity < .001. These associations did not reach statistical significance. At five years, 179 participants of 4674 had diabetes. The association was inversely nonlinear at follow-up. Participants with moderate total fruit intake had 36% lower odds of having diabetes at five years (OR, 0.64; 95% CI, 0.44-0.92). Of the 3518 participants with follow-up at 12 years, 247 participants had diabetes. ORs indicated less prevalence of diabetes for moderate to high intakes of whole fruit, apples, oranges, and other citrus fruits and bananas.
In this cohort, higher total fruit intake was associated with better glucose tolerance and insulin sensitivity measures. In addition, moderate to high total fruit intake at five years of follow-up was associated with a lower incidence of diabetes. Insulin resistance, β-cell dysfunction, and obesity comprise the pathophysiology of T2DM. HOMA2 assesses β-cell function and insulin resistance using fasting glucose and insulin levels. Higher total fruit intake was associated with greater insulin sensitivity and lower β-cell function in a dose-response manner. In addition, a higher intake of fruit caused a slight decrease in PLG.
The risk of T2DM was 26% lower for blueberries, 12% lower for grapes and raisins, 7% lower for apples and pears, 5% lower for bananas, 5% lower for grapefruit, and 10% higher for cantaloupe based on three servings per week. Most fruits lowly contribute to energy intake, have a low glycemic load, are rich in fiber, vitamins, minerals, and phytochemicals. Insoluble and soluble fiber are both reported to improve glycemic control. Furthermore, fruits, including apples, contain flavonoids. This class of phytochemicals enhances insulin sensitivity, the mechanism of decreasing apoptosis and promoting the proliferation of pancreatic β cells, and reducing muscle inflammation and oxidative stress. Moreover, fruit intake managed adiposity.
Fruit juice consumption and insulin resistance, and β-cell dysfunction or incident diabetes, show no association. Future studies are to include investigation in other populations, primarily those lost to follow-up. The study population was a weakness of the study because there was an added advantage for women and higher education levels.
Practice Pearls:
- β-cell dysfunction and insulin resistance are crucial in developing T2DM.
- Promoting a healthy diet and lifestyle, including consuming whole fruits such as apples, bananas, and oranges, may lower T2DM incidence.
- Fruit juices have reduced beneficial fibers compared with whole fruit.
Bondonno, N., Davey, R., Murray, K., et al. (2021). Associations Between Fruit Intake and Risk of Diabetes in the AusDiab Cohort. The Journal Of Clinical Endocrinology & Metabolism.
Damisha Henderson Florida A&M University, College of Pharmacy and Pharmaceutical Sciences, Fourth Year PharmD Candidate
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Fruit Consumption and Incidence of Type 2 Diabetes - Diabetes In Control - Diabetes In Control
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