August 2025
August 2025
INTRODUCTION —
Type 1 diabetes mellitus results from autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans, leading to dysregulated glucose metabolism with hyperglycemia and need for exogenous insulin [1]. Genetic markers associated with type 1 diabetes have been defined in many populations, and type 1 diabetes progresses in stages on a background of genetic risk (table 1 and figure 1) [2]. The first two stages of type 1 diabetes are preclinical stages of disease progression. Stage 1 is defined as the presence of two or more autoantibodies directed against beta cell antigens in the absence of symptoms or detectable glucose intolerance [3]. Stage 2 evolves after the loss of beta cell function leads to glucose intolerance, but symptoms remain absent. Stage 3 occurs when hyperglycemia meets the criteria for a clinical diagnosis of diabetes, and symptoms are often present.
The pathogenesis of type 1 diabetes differs from that of type 2 diabetes mellitus, in which both decreased insulin secretion and insulin resistance play important contributory roles. Consistent with this differential pathogenesis, genome-wide association studies have identified genetic loci in type 1 and type 2 diabetes that are predominantly, though not entirely, distinct. (See "Pathogenesis of type 2 diabetes mellitus".)
The pathogenesis of type 1 diabetes mellitus will be reviewed here. The diagnosis and management of type 1 diabetes are discussed separately.
●(See "Epidemiology, presentation, and diagnosis of type 1 diabetes mellitus in children and adolescents".)
●(See "Type 1 diabetes mellitus: Prevention and disease-modifying therapy".)
●(See "Associated autoimmune diseases in children and adolescents with type 1 diabetes mellitus".)
●(See "Overview of the management of type 1 diabetes mellitus in children and adolescents".)
FACETS OF PATHOPHYSIOLOGY —
Type 1 diabetes results from both beta cell and immune system dysfunction, which arise from a combination of genetic and environmental factors.
Autoimmunity — Immune system dysfunction plays a central role in type 1 diabetes pathogenesis [4]. Islet-directed autoantibodies have been identified in the vast majority of patients with newly diagnosed type 1 diabetes and in people at preclinical stages of disease, and are routinely used to classify type 1 diabetes and identify those at risk (table 1). (See "Type 1 diabetes mellitus: Disease prediction and screening", section on 'Stages of type 1 diabetes'.)
Autoantibody-negative type 1 diabetes occurs but is rare. Research efforts are focused on identifying biomarkers beyond autoantibodies that may help better predict diabetes risk and lend insight into the underlying pathophysiology. (See "Classification of diabetes mellitus and genetic diabetic syndromes", section on 'Type 1 diabetes'.)
Most autoantibody-focused research has been dedicated to identifying the specific antigens targeted by diabetes-associated autoantibodies and determining which autoantibodies are consistently associated with diabetes development. Whether autoantibodies play a role in disease pathogenesis is an unresolved question. While autoantibodies tend to decline over time and may become undetectable, this appears to occur decades after diagnosis, but uncommonly near the time of disease onset. The diagnostic utility of diabetes-related autoantibodies and the approach to antibody measurement are discussed separately. (See "Type 1 diabetes mellitus: Disease prediction and screening", section on 'How to screen'.)
Target autoantigens — Several antigens within pancreatic beta cells are consistently targeted by islet autoantibodies and T cells in people with and at risk for type 1 diabetes (table 2) [1,5-9]. Positive autoantibody tests to two or more of the autoantigens below strongly predict eventual clinical diagnosis. (See "Type 1 diabetes mellitus: Disease prediction and screening", section on 'How to screen'.)
●Insulin – Studies in the nonobese diabetic (NOD) mouse model of autoimmune diabetes suggest that proinsulin/insulin itself may be a primary autoantibody target [10,11], with subsequent extension of the immune response to other autoantigens [11]. In some children in birth cohort studies, insulin autoantibodies appear at very young ages and have been associated with early disease onset [12,13]. CD4+ and CD8+ T cells targeting insulin and/or proinsulin have been recognized in both NOD mice and humans with and at risk for type 1 diabetes [10,14,15]. (See "Type 1 diabetes mellitus: Prevention and disease-modifying therapy", section on 'Insulin antigen therapy'.)
Of note, most individuals develop insulin antibodies in response to exogenous, subcutaneous insulin administration; thus, after approximately two weeks of insulin injections, insulin autoantibody measurements cannot be used as a marker of type 1 diabetes [13].
●Glutamic acid decarboxylase (GAD) – Another important autoantigen against which antibodies are consistently detected is the enzyme GAD (a 65-kD protein), which is present in pancreatic islets as well as in the central nervous system and testes [6]. Antibodies to GAD (anti-GAD65 autoantibodies) are found in approximately 70 percent of patients with type 1 diabetes at the time of diagnosis.
GAD autoantibodies are not uncommon in type 2 diabetes [16]. GAD autoantibodies are also frequently detectable in the central nervous system in the context of the neurologic condition Stiff-person syndrome. As for type 1 diabetes, pathogenic roles for GAD autoantibodies in type 2 diabetes and Stiff-person syndrome have not been clearly established [17]. The presence of GAD autoantibodies in these other conditions underscores the importance of measuring at least two autoantibodies in the diagnostic evaluation of type 1 diabetes. (See "Type 1 diabetes mellitus: Disease prediction and screening", section on 'How to screen'.)
●Islet antigen 2 (IA-2) – Another autoantigen implicated in type 1 diabetes, IA-2, is a protein tyrosine phosphatase (PTP)-related protein found in neuroendocrine cells [7,8]. Autoantibodies to IA-2 usually appear later than autoantibodies to insulin and GAD, and they are highly associated with the expression of multiple anti-islet autoantibodies and thus progression to clinical (stage 3) type 1 diabetes [18].
●Zinc transporter 8 (ZnT8) – The cation efflux transporter ZnT8 has also been identified as a type 1 diabetes autoantigen [9]. In children followed from birth to the development of diabetes, ZnT8 autoantibodies appeared later than insulin autoantibodies [9]. ZnT8 is less often measured clinically but may be useful to recategorize individuals considered to be "antibody negative" at clinical diagnosis, and it is frequently utilized in studies that screen individuals for risk of type 1 diabetes. (See "Type 1 diabetes mellitus: Disease prediction and screening", section on 'How to screen'.)
●Other type 1 diabetes-related autoantigens – Progression of type 1 diabetes is often marked by an increase in the number of islet autoantigens targeted by T cells and autoantibodies. Several additional type 1 diabetes-related autoantigens have been identified in the context of research studies; in particular, T cell responses to the islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) and chromogranin A (ChgA) have been repeatedly observed [19,20]. However, autoantibodies against IGRP or ChgA have not been consistently detected, and thus, response to these antigens is not measured clinically.
Protein modifications — Both clinical and preclinical studies are investigating post-translationally modified versions of type 1 diabetes antigens. These "neoantigens" may shed light on how immune tolerance is initially broken in type 1 diabetes. Post-translational modification has also been identified as a key factor in the autoimmune response associated with rheumatoid arthritis. Protein modifications under investigation include changes to amino acids (eg, citrullination) [21], defective ribosomal products [22], and hybrid peptides combining elements of two autoantigens [23].
Pancreatic islet pathology — Type 1 diabetes is a disease of the beta cell as well as the immune system [4]. Beta cell stress occurs in people with and at risk for type 1 and type 2 diabetes [24]. It is often quantified by the increased release of prohormones such as proinsulin, rather than appropriately processed insulin. Considerable research efforts are dedicated to characterizing the causes and consequences of beta cell stress and its interactions with the immune system [25].
Understanding of islet pathology has grown. The presence of immune cell infiltrates around islets, referred to as insulitis, and the specific loss of beta cells in islets, have been repeatedly observed in human pancreatic specimens since the first clear detection of insulitis in 1965 [26,27]. Additional work has expanded and deepened our understanding of beta cell loss and immune infiltration; much of this effort has been supported by a pancreatic organ donation program called Network for Pancreatic Organ Donors with Diabetes (nPOD). Studies of pancreas specimens have indicated that insulin-producing cells may be more rapidly lost in children diagnosed early in life and have provided greater insight into the types of cells present in immune infiltrates; these include not only T cells but also neutrophils and B cells [28].
GENETIC DRIVERS
Genetic risk — Type 1 diabetes is multigenic, with individual genes contributing risks known to affect both beta cell and immune system function [29].
●Magnitude of genetic risk – The lifetime risk of type 1 diabetes is markedly increased in close relatives of individuals with type 1 diabetes, averaging approximately 6 percent in offspring, 5 percent in siblings, and 50 percent in identical twins (versus 0.4 percent in individuals with no family history) [1,30,31]. A monozygotic twin of a proband with type 1 diabetes has a higher risk of diabetes than a dizygotic twin, and the risk in a dizygotic twin sibling is similar to that in non-twin siblings [30]. Importantly, not all monozygotic twins of probands with type 1 diabetes develop diabetes, although the cumulative prevalence increases with long-term follow-up [30-32]. Approximately 15 percent of people diagnosed with type 1 diabetes have a family member with the disease, whereas approximately 85 percent have no family history of type 1 diabetes.
The National Institute of Diabetes and Digestive and Kidney Diseases has supported a program called Diabetes TrialNet, with the mission to prevent type 1 diabetes and stop disease progression by preserving insulin production before and after diagnosis. Relatives of patients with type 1 diabetes can be screened for diabetes-related autoantibodies, and clinical trial enrollment is available in multiple centers throughout the United States and the world. (See "Type 1 diabetes mellitus: Disease prediction and screening", section on 'How to screen'.)
●Risk alleles – Genetic risk for type 1 diabetes is predominantly carried in specific human leukocyte antigen (HLA) alleles. These genes code for major histocompatibility complex (MHC) class II molecules expressed on the cell surface of antigen-presenting cells. The mechanisms underlying genetic risk are imperfectly understood, but many genes (including HLA) have been tied to T cell function and activity. Similarly, roles for many other risk alleles have been identified in immune function. For example, a polymorphism of the protein tyrosine phosphatase (PTP) gene PTPN22 influences T cell receptor signaling, and the same polymorphism is a major risk factor for multiple autoimmune disorders [33]. (See "Human leukocyte antigens (HLA): A roadmap", section on 'Class II region'.)
In the context of HLA risk alleles, many studies have identified islet peptides presented by antigen-presenting cells and recognized by CD4+ T cells [34], linking HLA to autoimmune activity. Conversely, one HLA allele is highly protective against type 1 diabetes development; the mechanisms underlying this protective effect have not been fully delineated. The substantial contribution of HLA to genetic risk has enabled birth cohort studies enrolling participants based on the presence of high-risk HLA genes [35,36]. Other, non-HLA genes also contribute to risk and have helped increase understanding of disease pathogenesis.
●Genetic risk scores – While the individual contribution of any given gene to predicting risk beyond HLA is not marked, combining the additive risk of multiple genes can help refine risk prediction [37]. The background frequency of risk-conferring HLA alleles varies by population. In White Americans, the background frequency of risk HLA alleles varies from 2 to 10 percent, depending on the study, and among these individuals, only an estimated 3 percent will develop type 1 diabetes [38,39]. In addition, the prevalence of HLA risk alleles may differ in other racial and ethnic backgrounds [40]. For these reasons, HLA testing is not typically used in clinical practice to identify people at elevated risk for type 1 diabetes. (See "Type 1 diabetes mellitus: Disease prediction and screening", section on 'Whom to screen'.)
Understanding of type 1 diabetes genetics has enabled the development and validation of genetic risk scores (GRS) that differ in populations with type 1 versus type 2 diabetes [41,42]. These are also not perfectly predictive for the same reasons as above: much of the risk is HLA driven, and HLA risk alleles are relatively common depending on the population studied. GRS have been proposed as a strategy for filtering to identify individuals who should be screened for type 1 diabetes autoantibodies on a population basis. Further work is required to validate GRS in additional cohorts and to generate data needed to extend GRS to broad racial and ethnic backgrounds [43,44]; consequently, GRS remain a research tool and are not available for clinical use.
Shared susceptibility genetic variants — Rare genetic syndromes associated with type 1 diabetes have shed important light on pathogenesis. The immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is associated with neonatal type 1 diabetes. These infants usually die of overwhelming autoimmunity, often specifically from severe enteritis. They have a pathogenic variant in the FOXP3 gene, a "master-switch" for the development of regulatory T cells. Clinical and preclinical studies of IPEX syndrome have demonstrated that regulatory T cells (Tregs, formerly termed suppressor T cells) play a major physiologic role in suppressing autoimmunity.
Polyglandular autoimmune syndrome type 1 is caused by pathogenic variants in the AIRE gene, which encodes an autoimmune regulator protein. This protein regulates the expression of certain peripheral tissue antigens in the thymus, including insulin. Thus, through its influence on central T cell tolerance, this protein is believed to provide protection from autoimmune disorders, including type 1 diabetes [45].
Pathogenic variants in STAT3 have also been identified as a monogenic cause of autoimmunity, including type 1 diabetes [46]. De novo germline activating STAT3 variants are associated with a spectrum of early-onset autoimmune diseases, including type 1 diabetes, autoimmune thyroid dysfunction, and autoimmune enteropathy. In contrast, germline inactivating STAT3 variants result in hyperimmunoglobulin E (IgE) syndrome. (See "Autosomal dominant hyperimmunoglobulin E syndrome".)
ENVIRONMENTAL AND MODIFIABLE FACTORS
Role of nongenetic factors — Genetic influences only partially account for type 1 diabetes risk, indicating that other factors contribute to immune activation leading to autoantibody development. Environmental influences may have key roles in the development of type 1 diabetes. The best evidence for environmental influence on type 1 diabetes risk is the rapid increase over several decades in the incidence of type 1 diabetes in multiple populations worldwide at a rate that exceeds what can be expected due to genetic changes [47,48]. The etiology of this increase is unknown. Considerable efforts have been made to pinpoint dietary, viral, or modifiable factors that can influence risk of developing type 1 diabetes. Available evidence is not sufficient to support risk-modifying roles for specific dietary or nutrient factors. Viral infections have also been studied as potential pathogenic triggers.
Perinatal factors — Modestly greater risk of type 1 diabetes has been consistently observed for children born to fathers with type 1 diabetes compared with those born to mothers with type 1 diabetes [49]. The basis of this "relative protection" for children with affected mothers is unknown.
Early environmental exposures — Children in Russian Karelia have a sixfold lower risk of type 1 diabetes compared with children across the border in Finland, even among those with similar genetic backgrounds. In one cohort study, Finnish children tended to have a higher prevalence of autoantibodies against islet antigen 2 (IA-2) compared with Karelian children [50]. One hypothesis for this differential type 1 diabetes risk, termed the hygiene hypothesis, proposes that reduced early-life bacterial and viral exposures increase risk of immune-mediated disorders [51]. However, substantive differences in socioeconomic status and lifestyle exist between the two countries and likely confer a wide variety of effects on environmental exposures, microbial/viral exposures, and access to medical care. Differences between these groups have also been found in the evolution of their early-life microbiome [52]. Therefore, any single environmental factor is difficult to pinpoint as a driver of the differential risk.
Viral infections — Viral infections are a potential trigger for the immune activation that drives seroconversion to autoantibody positivity or the onset of clinical disease. Identifying temporal relationships between infection and diabetes onset can be challenging, particularly given the long, asymptomatic prodrome of type 1 diabetes and the frequency of upper respiratory and enteroviral infections, especially in children [53,54]. However, natural history studies have identified connections between infection and type 1 diabetes seroconversion or onset of clinical disease [55-57]. In addition, mechanistic data suggest that, for at least some individuals, infection may precede seroconversion or disease onset [58]. Further, in a trial in 96 children and adolescents with newly diagnosed type 1 diabetes, antiviral therapy for six months led to greater preservation of insulin secretion at 12 months compared with placebo [59].
Coxsackie B — Based on preclinical and clinical data implicating Coxsackie virus B in type 1 diabetes development [60], research efforts in Scandinavia are dedicated to developing a vaccine against coxsackievirus B for use as a preventive therapy [61].
COVID-19 — Some studies have reported an increase in type 1 diabetes incidence or autoantibody seroconversion during the coronavirus 2019 (COVID-19) pandemic [62-67], whereas other reports have not found these associations [68-71]. Such findings must be interpreted carefully; retrospective analyses may be limited by recall and selection bias and potential misclassification of diabetes type.
Childhood immunizations — Concern exists that childhood vaccination may be associated with subsequent development of chronic diseases, including type 1 diabetes. However, in genetically predisposed infants who have siblings with type 1 diabetes, immunization with viral and bacterial antigens has consistently not been associated with an increased risk of developing type 1 diabetes [72-74]. No increase in type 1 diabetes after immunization was observed in children in the general population [75] or in adult members of the United States military [76]. (See "Autism spectrum disorder and chronic disease: No evidence for vaccines or thimerosal as a contributing factor", section on 'Type 1 diabetes mellitus'.)
Early nutritional exposures — The possible role of several dietary factors in the development of type 1 diabetes has been studied. These include the timing of cow's milk introduction, vitamin D sufficiency, and timing and type of cereal consumption. Although observational studies have identified variable links between these nutritional factors and prevention or risk of type 1 diabetes, clinical trials have not yet verified any relationships between early-life nutritional exposures and type 1 diabetes risk. Accordingly, guidance for nutrition during infancy does not include specific dietary measures for people at risk for type 1 diabetes. (See "Introducing solid foods and vitamin and mineral supplementation during infancy".)
Cow's milk — Most epidemiologic data indicate that early exposure to, or high consumption of, cow's milk is not associated with increased risk of islet autoantibody development or type 1 diabetes [77]. In a phase 3 trial in 2159 at-risk infants, the incidence of type 1 diabetes during childhood did not differ for infants weaned to hydrolyzed casein compared with those weaned to a conventional cow's milk-based formula [78].
Vitamin D — Some early life epidemiological studies have found that low vitamin D levels may be associated with type 1 diabetes risk, while a similar number of studies have found no association [77]. In two trials in participants with new-onset type 1 diabetes, vitamin D supplementation did not improve insulin secretion compared with placebo [79,80].
Solid food introduction — Birth cohort studies in the United States, Germany, and Scandinavia have found inconsistent relationships between the timing of introduction of a variety of solid foods and risk of developing islet autoantibodies or clinical type 1 diabetes. The specific foods studied include any cereal, gluten, egg, and root vegetables [77]. For example, in a trial testing early versus later gluten exposure in the first year of life, the timing of gluten introduction did not affect the risk of developing islet autoantibodies or clinical type 1 diabetes [81]. (See "Introducing solid foods and vitamin and mineral supplementation during infancy", section on 'Optimal timing'.)
Immune checkpoint inhibitor therapy — Immune checkpoint inhibitors (ICIs) are monoclonal antibodies that block immune regulatory "checkpoint" proteins. These include the receptors cytotoxic T-lymphocyte associated protein 4 (CTLA-4) and programmed cell death 1 (PD-1) and the PD-1 ligand PD-L1. ICIs have durable benefit in the treatment of a variety of cancers, but immune checkpoint inhibition is also associated with a unique spectrum of side effects termed immune-related adverse events (irAEs). These adverse consequences of ICI therapy provide a further example of how acquired or induced changes in immune system function can lead to type 1 diabetes. (See "Overview of toxicities associated with immune checkpoint inhibitors".)
Autoimmune endocrine diseases and rheumatic diseases occur in approximately 50 percent of patients treated with antibodies to CTLA-4 and/or PD-1/PD-L1 [82-84]. These irAEs can be serious or even life-threatening, including autoimmune type 1 diabetes presenting with diabetic ketoacidosis (DKA), primary adrenal insufficiency caused by autoimmune adrenalitis, or myocarditis [85]. In one report, 50 percent of patients with ICI-related diabetes presented with DKA [85]. (See "Overview of toxicities associated with immune checkpoint inhibitors", section on 'Endocrinopathies'.)
SUBTYPES AND ETIOLOGIC HETEROGENEITY OF DISEASE —
Type 1 diabetes endotypes have been described as "a subtype of type 1 diabetes that can be defined by a distinct functional or pathobiological mechanism (that is also tractable therapeutically)" [86]. This definition is based on the endotype concept developed in allergy and asthma research, which demonstrated that subgroups of clinical trial participants responded differently to therapy based on their specific disease etiology. Proposed endotypes in type 1 diabetes include a "B cell endotype," which is mainly present in children diagnosed at age <7 years who have high levels of B cells in the islets [28]. Another proposed endotype is based on a frequently observed association between the early development of insulin autoantibodies and the specific human leukocyte antigen (HLA) risk allele HLA DR4 [87]. In clinical studies, heterogeneity among participants is consistently noted in the rate of disease progression, response to therapy, and immune markers. However, whether type 1 diabetes endotypes can be reliably detected and/or warrant specific treatment strategies remains uncertain.
LINKS TO OTHER AUTOIMMUNE CONDITIONS —
People with type 1 diabetes are at increased risk for developing other autoimmune diseases, most commonly autoimmune thyroiditis and celiac disease. This association is reviewed briefly below and in more detail separately. (See "Associated autoimmune diseases in children and adolescents with type 1 diabetes mellitus".)
●Thyroid autoimmunity is particularly common among people with type 1 diabetes, with anti-thyroid antibodies prevalent in more than one-fourth of individuals. In long-term observational studies of people with type 1 diabetes, the incidence of autoimmune thyroid disease is approximately 10 to 25 percent, with a higher rate in women than in men [88-90]. (See "Associated autoimmune diseases in children and adolescents with type 1 diabetes mellitus", section on 'Thyroid surveillance'.)
●Transglutaminase autoantibodies are present in approximately 10 percent of people with type 1 diabetes; of these individuals, approximately one-half will have high autoantibody levels and celiac disease on biopsy [91,92]. Certain alleles (eg, PTPN2, CTLA4, RGS1) confer genetic susceptibility to both type 1 diabetes and celiac disease, suggesting a shared biologic pathway [93]. (See "Associated autoimmune diseases in children and adolescents with type 1 diabetes mellitus", section on 'Celiac surveillance' and "Epidemiology, pathogenesis, and clinical manifestations of celiac disease in adults", section on 'Genetic factors'.)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Type 1 diabetes in adults (The Basics)")
●Beyond the Basics topics (see "Patient education: Type 1 diabetes: Overview (Beyond the Basics)")
SUMMARY
●Overview – Type 1 diabetes mellitus results from autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans, leading to dysregulated glucose homeostasis and need for exogenous insulin. Type 1 diabetes progresses in stages on a background of genetic risk (figure 1 and table 1). (See 'Introduction' above.)
●Facets of pathophysiology – Type 1 diabetes results from both beta cell and immune system dysfunction, which arise from a combination of genetic and environmental factors.
•Autoimmunity – Islet-directed autoantibodies have been identified in the vast majority of patients with newly diagnosed type 1 diabetes and in people at preclinical stages of disease (table 1). Several antigens within pancreatic beta cells are consistently targeted by islet autoantibodies and T cells in people with and at risk for type 1 diabetes (table 2). (See 'Autoimmunity' above and "Type 1 diabetes mellitus: Disease prediction and screening", section on 'Stages of type 1 diabetes'.)
•Pancreatic beta cells – Beta cell stress occurs in people with and at risk for type 1 and type 2 diabetes [24]. It is often quantified by the increased release of prohormones such as proinsulin, rather than appropriately processed insulin. (See 'Pancreatic islet pathology' above.)
●Genetic drivers – Type 1 diabetes is multigenic, with individual genes contributing risks known to affect both immune system and beta cell function. The lifetime risk of type 1 diabetes is markedly increased in close relatives of individuals with type 1 diabetes, and genetic risk is predominantly carried in specific human leukocyte antigen (HLA) alleles. These genes code for major histocompatibility complex (MHC) class II molecules expressed on the cell surface of antigen-presenting cells. (See 'Genetic drivers' above.)
●Environmental factors – Viral infections are a potential trigger for the immune activation that drives seroconversion to autoantibody positivity or the onset of clinical disease. Clinical trials have not yet verified any relationships between early-life nutritional exposures and type 1 diabetes risk. Accordingly, guidance for nutrition during infancy does not include specific dietary measures for people at risk for type 1 diabetes. (See 'Environmental and modifiable factors' above and "Introducing solid foods and vitamin and mineral supplementation during infancy".)
ACKNOWLEDGMENT —
The UpToDate editorial staff acknowledges Massimo Pietropaolo, MD, who contributed to earlier versions of this topic review.
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