Factors Contributing to the Increase in Diabetes — A Narrative Review
Description
Abstract
The global prevalence of diabetes—primarily type 2 diabetes mellitus (T2DM)—has risen sharply over the last three decades. This narrative review synthesizes evidence about the major biological, behavioural, socioeconomic, and environmental drivers behind this increase. Key proximal drivers include overweight/obesity, physical inactivity, unhealthy diets (notably sugar-sweetened beverage consumption), population ageing, and genetic predisposition. Important distal and interacting drivers are urbanization, socioeconomic transition, prenatal and early-life influences, gestational diabetes, psychosocial stress, and environmental pollutants such as fine particulate matter (PM2.5). Health-system factors (screening gaps, delayed diagnosis, and unequal access to prevention and care) and social determinants (education, income inequality, food environments) amplify the epidemic, particularly in low- and middle-income countries. We present a conceptual model integrating these drivers and summarize evidence strength and public-health implications. Priority actions include population-level prevention (policy to reduce obesogenic environments and sugary-drink consumption), targeted screening for high-risk groups, maternal and early-life interventions, and air-quality improvements. Integrated policy responses are required to slow and reverse the global diabetes trend. PubMed+3Diabetes Atlas+3World Health Organization+3
Keywords
Type 2 diabetes, risk factors, obesity, physical inactivity, diet, air pollution, urbanization, gestational diabetes
1. Introduction
Diabetes mellitus is a chronic metabolic disease characterized by hyperglycaemia resulting from defects in insulin secretion, insulin action, or both. Type 2 diabetes (T2DM) accounts for the vast majority of cases globally and is responsible for substantial morbidity, mortality, and health-system costs. Over recent decades, prevalence has increased in almost every region of the world, driven by complex interactions between biological susceptibility and rapidly changing environmental and lifestyle exposures. According to the International Diabetes Federation (IDF), hundreds of millions of adults are living with diabetes, with projections indicating further large increases without effective prevention and policy responses. Diabetes Atlas+1
This review summarizes major factors that have contributed to the observed increase in diabetes prevalence and incidence, discusses mechanisms where evidence is available, and highlights population-level interventions that address primary drivers.
2. Methods (Narrative review approach)
This is a narrative, evidence-synthesis review. We searched authoritative international sources and recent high-quality reviews and cohort studies to identify major drivers of the diabetes epidemic (World Health Organization, International Diabetes Federation, Centers for Disease Control and Prevention, National Institute of Diabetes and Digestive and Kidney Diseases, Global Burden of Disease analyses, and selected peer-reviewed studies). Search emphasis was placed on publicly available epidemiological reports and systematic analyses to compile high-level evidence and quantify relative contributions where possible. (Search examples: IDF Diabetes Atlas, WHO diabetes fact sheet, CDC diabetes risk pages, GBD/Lancet analyses, and studies relating air pollution and sugary drinks to diabetes burden). The Lancet+3Diabetes Atlas+3World Health Organization+3
3. Major proximal drivers
3.1 Overweight and obesity
Obesity is the single strongest modifiable risk factor for T2DM. Excess adiposity—especially visceral fat—induces insulin resistance through multiple mechanisms including lipotoxicity, chronic low-grade inflammation, adipokine dysregulation, and ectopic fat deposition in liver and muscle. Population-level rises in mean body mass index (BMI) parallel the rise in diabetes prevalence. IDF and national estimates attribute a large fraction of new T2DM cases to increasing overweight and obesity prevalence. Diabetes Atlas+1
3.2 Physical inactivity and sedentary behaviour
Inactivity reduces insulin sensitivity and has independent metabolic harms beyond BMI. Modern economies have substituted physical jobs and active transport with sedentary occupations and motorized transport; leisure-time physical inactivity is common across many regions. Regular moderate-to-vigorous physical activity reduces the risk of progression from prediabetes to diabetes and is central in prevention programs. CDC+1
3.3 Unhealthy diets — energy-dense and sugar-sweetened beverages
Diets high in saturated fats, refined carbohydrates, and free sugars—particularly sugar-sweetened beverages (SSBs)—promote weight gain and have direct metabolic effects (hepatic de novo lipogenesis, ectopic fat). Recent analyses attribute millions of new diabetes cases globally to SSB consumption, with disproportionate impacts in Latin America, the Caribbean, and parts of Africa. Policy interventions such as taxation, marketing restrictions, and front-of-pack labelling are effective population strategies to reduce consumption. The Guardian+1
3.4 Ageing population
Age is a non-modifiable risk factor: insulin resistance and pancreatic β-cell dysfunction accumulate with age, and T2DM prevalence increases markedly after middle age. Global demographic transition—an increasing proportion of older adults—thus amplifies diabetes prevalence even when age-specific incidence is stable. World Health Organization
3.5 Genetic predisposition and family history
Genetic susceptibility—polygenic in T2DM—interacts with environmental exposures. Family history remains a practical clinical indicator of higher risk. While genes alone cannot explain the rapid global rise, genetic predisposition determines population and individual vulnerability to obesogenic environments. CDC
4. Distal, contextual, and interacting drivers
4.1 Urbanization and the built environment
Urbanization changes food systems (greater access to processed foods), reduces active transport, and increases exposure to obesogenic marketing. Urban design lacking safe walking/cycling infrastructure and neighbourhoods dominated by fast-food outlets contribute to unhealthy lifestyles. IDF and WHO note urbanization as a leading contextual factor linked with rising diabetes. International Diabetes Federation+1
4.2 Socioeconomic transition and inequality
Rapid economic growth—combined with persisting poverty—produces dual burdens: availability of cheap, high-calorie foods and limited access to healthy options for low-income groups. Education, income, and occupation shape health literacy, diet quality, and healthcare access. Diabetes prevalence is frequently higher in socioeconomically disadvantaged groups within countries. Diabetes Atlas+1
4.3 Early-life exposures, developmental origins, and intergenerational effects
Low birth weight, maternal malnutrition, maternal obesity, and gestational diabetes increase offspring susceptibility to insulin resistance and T2DM later in life. The ‘developmental origins of health and disease’ (DOHaD) paradigm explains how prenatal and early-life environments program metabolic pathways. Increasing rates of gestational diabetes thus create intergenerational amplification of diabetes risk. NIDDK
4.4 Gestational diabetes mellitus (GDM)
GDM incidence has been rising alongside obesity and older maternal age. Women with GDM have high lifetime risk of developing T2DM, and their children are at higher risk of obesity and glucose intolerance—creating a transgenerational loop. Screening and postpartum follow-up are essential prevention opportunities. NIDDK
4.5 Psychosocial stress, sleep disturbance and mental health
Chronic stress, shift work, and poor sleep quantity/quality alter glucose metabolism and appetite regulation (e.g., through cortisol, sympathetic activation) and are associated with higher diabetes risk. Shift-work and modern work patterns have been implicated in increased cardiometabolic risk. CDC
4.6 Environmental pollutants — air pollution and endocrine disruptors
Emerging evidence implicates environmental pollutants in T2DM risk. Ambient fine particulate matter (PM2.5) exposure was estimated to contribute substantially to the global burden of T2DM in recent GBD analyses, possibly via systemic inflammation, oxidative stress, and effects on insulin sensitivity. Other pollutants (persistent organic pollutants, endocrine-disrupting chemicals) have been associated with insulin resistance in observational studies. Environmental exposures may therefore account for a non-trivial fraction of population-level diabetes risk, especially in regions with poor air quality. PubMed+1
5. Health-system and measurement drivers
5.1 Improved detection, diagnosis, and survival
Part of the observed increase in prevalence derives from better case detection, diagnostic capacity, and longer survival of people with diabetes due to improved treatment of acute complications. However, a large fraction remains due to true increases in incidence. Substantial proportions of people with diabetes remain undiagnosed—especially in low- and middle-income countries—highlighting simultaneous under-detection and true epidemiologic growth. EatingWell+1
5.2 Screening gaps and delayed preventive action
Inadequate screening of high-risk groups, late-stage diagnosis, and insufficient uptake of lifestyle prevention programmes allow progression from prediabetes to diabetes at high rates. Strengthening primary-care screening and community-based prevention can reduce incidence. CDC
6. Quantifying contribution: what do global estimates show?
Global epidemiological resources indicate both rising prevalence and the relative importance of different drivers:
- IDF and GBD analyses report a steep increase in adult diabetes prevalence over the past decades; IDF estimates hundreds of millions of adults living with diabetes and projects substantial future increases if trends persist. Diabetes Atlas+1
- Analyses have attributed substantial fractions of population-level T2DM burden to overweight/obesity and physical inactivity. In addition, recent studies estimate that ambient PM2.5 exposure accounted for approximately 10–20% of diabetes burden in some analyses, showing that environmental factors are important contributors beyond traditional lifestyle risks. PubMed+1
7. Table — Major drivers of diabetes and evidence level
Major driver |
Mechanism summary |
Strength of evidence |
Population-level contribution (qualitative) |
Overweight/obesity |
Insulin resistance via lipotoxicity, inflammation, ectopic fat |
Very strong (multiple cohort/RCTs) |
High |
Physical inactivity |
Reduces insulin sensitivity; promotes weight gain |
Strong (cohort & intervention data) |
High |
Unhealthy diet / SSBs |
Promotes weight gain; direct hepatic metabolic effects |
Strong (epidemiology, modelling) |
High–moderate |
Ageing |
β-cell decline, insulin resistance |
Very strong (demographic data) |
Moderate–high |
Genetics / family history |
Polygenic susceptibility interacts with environment |
Strong (GWAS) |
Moderate (non-modifiable) |
Gestational diabetes & maternal factors |
Fetal programming, maternal hyperglycaemia |
Growing evidence (cohort studies) |
Moderate |
Urbanization / socioeconomic factors |
Food systems, activity patterns, stress |
Strong (ecological & cohort) |
Moderate–high |
Air pollution (PM2.5) |
Inflammation, oxidative stress, insulin resistance |
Emerging/strengthening (GBD analyses) |
Small–moderate but significant |
Psychosocial stress & sleep |
Neuroendocrine pathways, behaviour change |
Moderate |
Small–moderate |
Health-system factors (screening, access) |
Detection delays; missed prevention opportunities |
Strong (health services research) |
Indirect but important |
(Evidence sources: WHO, IDF, CDC, NIDDK, GBD/Lancet analyses, selected epidemiological studies).) PubMed+3World Health Organization+3Diabetes Atlas+3
8. Figure — Conceptual model (textual schematic)
[Macro drivers]
↓
[Urbanization] ←→ [Socioeconomic transition] ←→ [Food system shifts]
↓
[Individual exposures] —> Overweight/Obesity —> Insulin resistance → T2DM
↑ ↘
| Physical inactivity, Unhealthy diet (SSBs), Stress, Sleep
|
[Environmental exposures: PM2.5, EDCs] ——→ ↑
|
[Maternal & early-life factors] —> Developmental programming —> ↑ lifetime risk
|
[Health system factors] —> Screening & treatment gaps —> Higher undiagnosed burden
(Schematic integrates distal and proximal drivers producing higher population-level incidence and prevalence of diabetes.)
9. Discussion
9.1 Interconnected drivers and syndemic thinking
Diabetes rise cannot be ascribed to a single cause; it reflects a syndemic of metabolic risk factors interacting with social and environmental conditions. Overweight/obesity, unhealthy diets, and inactivity are proximate causes. These are in turn driven by urbanization, globalized food systems, socioeconomic inequality, and environmental factors (including air pollution). Maternal health and early-life programming create a transgenerational momentum. Recognizing these interactions is important for designing integrated interventions rather than isolated clinical approaches. International Diabetes Federation+1
9.2 Geographic and demographic heterogeneity
Although prevalence rises globally, the pace and pattern differ by region and socioeconomic status. Low- and middle-income countries now carry the majority of the global diabetes burden (over 80% of adults with diabetes live in LMICs), reflecting rapid urbanization, dietary shifts, and weaker health systems for prevention and chronic disease management. Age structure (younger populations) and under-detection can mask true public-health impacts in some regions. Diabetes Atlas+1
9.3 Environmental exposures represent a growing, underappreciated contributor
Recent GBD and cohort analyses point to air pollution and household pollution as contributors to T2DM burden; PM2.5 accounted for a measurable share of diabetes-related mortality and DALYs in some studies. Recognizing environmental determinants expands prevention options (e.g., air-quality policy, reduction of household pollution) beyond conventional lifestyle interventions. PubMed
9.4 Policy and intervention implications
Prevention strategies must be multi-level:
- Population-level regulation: taxation of sugar-sweetened beverages, restrictions on junk food marketing to children, reformulation incentives, improved food labeling. Evidence shows SSB taxes reduce purchases and can lower projected diabetes cases. The Guardian+1
- Urban design and active transport: create walkable neighbourhoods, safe cycling lanes, and public transport to increase daily physical activity. World Health Organization
- Maternal and early-life interventions: preconception care, optimal gestational diabetes screening and management, breastfeeding promotion, and early-childhood nutrition. NIDDK
- Air-quality improvements: reduce ambient PM2.5 via energy policy, clean household fuels, and transport emission controls—policies that bring co-benefits for cardiometabolic and respiratory health. PubMed
- Health system strengthening: targeted screening of high-risk groups, expanded primary-care prevention programs (lifestyle counselling, referral), and improved care cascades to prevent complications. CDC
9.5 Research gaps and priorities
Key gaps include causal mechanisms linking air pollution and metabolic disease, quantification of relative contributions across regions, and effective scalable interventions for early-life programming. Implementation research to adapt proven policies (taxation, labelling, urban planning) to low-resource settings is a priority.
10. Limitations of this review
This is a narrative (non-systematic) review drawing on authoritative reports and selected studies; it does not follow formal systematic-review methodology and therefore may not capture every primary study. Quantitative attributions (e.g., percent of cases due to a given factor) vary by study and context and were not meta-analysed here. Nevertheless, the review integrates widely accepted drivers and recent high-quality global analyses to provide a roadmap for policymakers and researchers.
11. Conclusions
The increase in diabetes prevalence is a multifactorial phenomenon driven principally by rising overweight/obesity, physical inactivity, and unhealthy diets, amplified by demographic ageing, urbanization, socioeconomic transition, and environmental exposures such as air pollution. Interventions must move beyond individual clinical counselling to population-level policies that reshape food environments, improve urban design, protect air quality, and prioritize maternal-child health. Strengthening health systems for early detection and prevention remains crucial. Urgent, integrated action can bend the curve of the diabetes epidemic.
12. Tables and Figures (embedded)
Table 1. Summary of major drivers and suggested policy responses
Driver |
Key policy/health actions |
Obesity & unhealthy diets |
SSB taxes; marketing restrictions; public procurement standards; nutrition labeling |
Physical inactivity |
Urban planning for active transport; workplace wellness; school physical education |
Ageing population |
Age-appropriate screening; community-based prevention for older adults |
Gestational diabetes & maternal factors |
Universal GDM screening; postpartum follow-up; maternal nutrition programs |
Air pollution |
Emission controls; clean household fuels; green transport policies |
Socioeconomic inequality |
Social protection, access to healthy foods, health literacy programs |
Health system gaps |
Strengthen primary care, implement risk stratification and screening |
(Adapted from international policy recommendations and epidemiologic synthesis).) Diabetes Atlas+1
13. References
- International Diabetes Federation. IDF Diabetes Atlas (data and facts). IDF. (Accessed 2024/2025). Diabetes Atlas+1
- World Health Organization. Diabetes fact sheet; Diabetes — key facts. WHO. (2024). World Health Organization
- Centers for Disease Control and Prevention. Type 2 Diabetes — Risk Factors & Diabetes Risk. CDC. (2023–2024). CDC+1
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Risk factors for Type 2 diabetes. (2025). NIDDK
- GBD / The Lancet. Global, regional, and national burden of diabetes and trends. (Relevant GBD/Lancet analyses; 2019–2023). The Lancet+1
- Li et al. (2024–2025) and related analyses: contribution of PM2.5 to global T2DM burden (Global Burden of Disease-derived analyses). PubMed
- The Guardian summary of a Nature Medicine analysis on sugar-sweetened beverages and diabetes (2025) — demonstrates SSB-related diabetes burden in several regions. The Guardian
- IDF Annual Report 2023 (PDF). International Diabetes Federation. International Diabetes Federation
- National Diabetes Statistics Report (CDC). Data, prevalence, and care cascades. CDC
Acknowledgements
This review used publicly available reports and peer-reviewed evidence from international agencies and large epidemiologic studies. No funding declared.
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References
- International Diabetes Federation. IDF Diabetes Atlas (data and facts). IDF. (Accessed 2024/2025). Diabetes Atlas+1 World Health Organization. Diabetes fact sheet; Diabetes — key facts. WHO. (2024). World Health Organization Centers for Disease Control and Prevention. Type 2 Diabetes — Risk Factors & Diabetes Risk. CDC. (2023–2024). CDC+1 National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Risk factors for Type 2 diabetes. (2025). NIDDK GBD / The Lancet. Global, regional, and national burden of diabetes and trends. (Relevant GBD/Lancet analyses; 2019–2023). The Lancet+1 Li et al. (2024–2025) and related analyses: contribution of PM2.5 to global T2DM burden (Global Burden of Disease-derived analyses). PubMed The Guardian summary of a Nature Medicine analysis on sugar-sweetened beverages and diabetes (2025) — demonstrates SSB-related diabetes burden in several regions. The Guardian IDF Annual Report 2023 (PDF). International Diabetes Federation. International Diabetes Federation National Diabetes Statistics Report (CDC). Data, prevalence, and care cascades. CDC