The accelerator hypothesis: a review of the evidence for insulin resistance as the basis for type I as well as type II diabetes
Abstract
Although some 40 years have passed since type I diabetes was first defined, its cause remains unknown. The autoimmunity paradigm of immune dysregulation has not offered an explanation for its rising incidence, nor means of preventing it, and there is arguably good reason to consider alternatives. The accelerator hypothesis is a singular, unifying concept that argues that type I and type II diabetes are the same disorder of insulin resistance, set against different genetic backgrounds. The hypothesis does not deny the role of autoimmuniy, only its primacy in the process. It distinguishes type I and type II diabetes only by tempo, the faster tempo reflecting the more susceptible genotype and (inevitably) earlier presentation. Insulin resistance is closely related to the rise in overweight and obesity, a trend that the hypothesis deems central to the rising incidence of all diabetes in the developed and developing world. Rather than overlap between the two types of diabetes, the accelerator hypothesis envisages overlay-each a subset of the general population differing from each other only by genotype. Indeed, it views type I and type II diabetes as a continuum, where the infinitely variable interaction between insulin resistance and genetic response determines the age at which beta-cell loss becomes critical. Adult diabetes is not viewed as an entity, but rather as diabetes presenting in adulthood. Childhood diabetes, similarly, is diabetes presenting in childhood. The increasin…
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Other factors that complicate diagnosis of type 1 diabetes include the growing problem of obesity, difficulties in health-care provider recognition of disease, and increasingly diverse genetic admixtures due to migration and social changes.
“Other factors that complicate diagnosis of type 1 diabetes include the growing problem of obesity (both childhood and adult), difficulties in health-care provider recognition of disease, and increasingly diverse genetic admixtures due to migration and social changes.45–47”
From Type 1 diabetes (2014) · cites this paper as [45]
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- Authors
- Wilkin, T. J.
- Affiliations
- Peninsula College of Medicine and Dentistry (GB)
- Corresponding author
- Wilkin, T J
- Venue
- International Journal of Obesity
- Published
- 2009-06-09
- Volume
- 33
- Issue
- 7
- Pages
- 716-726
- ISSN
- 0307-0565 (ISSN-L)
- 1476-5497
- OpenAlex
- W1969025116
- Cited by
- 158
- References
- 9
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 8 · 2023: 7 · 2022: 6 · 2021: 15 · 2020: 7 · 2019: 13 · 2018: 4 · 2017: 4 · 2016: 10 · 2015: 12 · 2014: 15 · 2013: 16 · 2012: 13
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- International Journal of Obesity (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- insulin resistance, type 1 diabetes, type 2 diabetes, autoimmunity, beta cell destruction, obesity, overweight, genetic susceptibility, diabetes incidence, lifestyle modification, pediatric diabetes
- MeSH terms
- Body Weight, Child, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Female, Humans, Insulin Resistance, Male, Obesity, Risk Factors, Incidence, Evidence-Based Medicine
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