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Original Investigation
December 16, 2019

Ultraprocessed Food Consumption and Risk of Type 2 Diabetes Among Participants of the NutriNet-Santé Prospective Cohort

Author Affiliations
  • 1Paris 13 University, Inserm, Inra, Cnam, Nutritional Epidemiology Research Team (EREN), Epidemiology and Statistics Research Center–University of Paris (CRESS), 93017 Bobigny, France
  • 2Public Health Department, Avicenne Hospital, AP-HP, Bobigny, France
  • 3Department of Nutrition, School of Public Health, University of São Paulo, Av. Dr Arnaldo 715, São Paulo 01246-904, Brazil
JAMA Intern Med. Published online December 16, 2019. doi:10.1001/jamainternmed.2019.5942
Key Points

Question  Is consumption of ultraprocessed foods associated with the risk of developing type 2 diabetes (T2D)?

Findings  This observational prospective study of 104 707 participants found that a higher proportion of ultraprocessed foods in the diet was associated with a higher risk of T2D.

Meaning  Ultraprocessed food intake is a modifiable factor that may play a role in T2D etiology. Public health authorities in several countries recently started to recommend privileging unprocessed/minimally processed foods and limiting ultraprocessed food consumption.

Abstract

Importance  Ultraprocessed foods (UPF) are widespread in Western diets. Their consumption has been associated in recent prospective studies with increased risks of all-cause mortality and chronic diseases such as cancer, cardiovascular diseases, hypertension, and dyslipidemia; however, data regarding diabetes is lacking.

Objective  To assess the associations between consumption of UPF and risk of type 2 diabetes (T2D).

Design, Setting, and Participants  In this population-based prospective cohort study, 104 707 participants aged 18 years or older from the French NutriNet-Santé cohort (2009-2019) were included. Dietary intake data were collected using repeated 24-hour dietary records (5.7 per participant on average), designed to register participants' usual consumption for more than 3500 different food items. These were categorized according to their degree of processing by the NOVA classification system.

Main Outcomes and Measures  Associations between UPF consumption and risk of T2D were assessed using cause-specific multivariable Cox proportional hazard models adjusted for known risk factors (sociodemographic, anthropometric, lifestyle, medical history, and nutritional factors).

Results  A total of 104 707 participants (21 800 [20.8%] men and 82 907 [79.2%] women) were included. Mean (SD) baseline age of participants was 42.7 (14.5) years. Absolute T2D rates in the lowest and highest UPF consumers were 113 and 166 per 100 000 person-years, respectively. Consumption of UPF was associated with a higher risk of T2D (multi-adjusted hazard ratio [HR] for an absolute increment of 10 in the percentage of UPF in the diet, 1.15; 95% CI, 1.06-1.25; median follow-up, 6.0 years; 582 252 person-years; 821 incident cases). These results remained statistically significant after adjustment for several markers of the nutritional quality of the diet, for other metabolic comorbidities (HR, 1.13; 95% CI, 1.03-1.23), and for weight change (HR, 1.13; 95% CI, 1.01-1.27). The absolute amount of UPF consumption (grams per day) was consistently associated with T2D risk, even when adjusting for unprocessed or minimally processed food intake (HR for a 100 g/d increase, 1.05; 95% CI, 1.02-1.08).

Conclusions and Relevance  In this large observational prospective study, a higher proportion of UPF in the diet was associated with a higher risk of T2D. Even though these results need to be confirmed in other populations and settings, they provide evidence to support efforts by public health authorities to recommend limiting UPF consumption.

Trial Registration  ClinicalTrials.gov Identifier: NCT03335644

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    1 Comment for this article
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    A Plausible Mechanism Explains this Study’s Results
    Charles Fred, Electrical Engineering | Retired
    A plausible mechanism explains this study’s results.

    Human evolution expects glucose to be released little by little from the liver, just as needed. Then, blood glucose never rises very much or very fast and our beta cells are never overtaxed. But, dietary carbs, especially modern quick-digesting carbs, cause blood glucose to rise massively and quickly, requiring massive and quick insulin secretion. This threatens the very survival of our beta cells.

    The main trigger of apoptosis is failure of a cell to perform its function; so requiring beta cells to massively and quickly secrete insulin tempts
    them into failure and triggers apoptosis. When most of the pancreas’ beta cells have suffered apoptosis, you have diabetes.

    If, eight hours after eating, the pancreas is unable to supply enough insulin to push fasting blood glucose below 90, there must be few surviving beta cells - and each of those few survivors now are asked to secrete even more insulin. Thus an avalanche effect, fewer beta cells, more asked from each cell, faster apoptosis - worsening diabetes.

    Continued dietary carbs will continue to overtax and kill the remaining beta cells, while a very low carb diet may allow the survival of the remaining beta cells.
    CONFLICT OF INTEREST: None Reported
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