<h2>Because pancreatic beta cell reserve determines the course of the T1D journey1-7</h2>

<h3>Autoimmune type 1 diabetes (T1D) is driven by the progressive and irreversible loss of beta cells.8-11</h3>
While exogenous insulin therapy is effective, it cannot fully replicate the full spectrum of functions beta cells perform in maintaining glucose homeostasis.12-14
The profound implications of this are clearly demonstrated:
<ul>
 <li>Patients with more vs less residual beta cell function, as indicated by C-peptide, are at lower risk of severe hypoglycaemia, diabetic ketoacidosis (DKA) and long-term complications.1-6,15-17,19</li>
 <li>While more betas are better, even limited residual activity can still positively impact the patient experience of T1D.1-7&nbsp;</li>
</ul>
As such, it is the pancreatic beta cell reserve that determines the course of the autoimmune T1D journey.1-7

<h3>It's time to recognise the role of beta cells beyond insulin. It’s time to recognise the value of every single beta cell.</h3>

<h2>Mechanisms of disease in autoimmune T1D</h2>
The progressive, irreversible decline of functional beta cell mass in autoimmune T1D can be detected up to 6 years before symptoms arise.8-11,19,20&nbsp;Autoantibody screening in this critical window of opportunity can help identify individuals at risk of progression to Stage 3 T1D, enabling a smoother transition to life with the condition.21-27

<h3>T1D is an autoimmune condition characterised by the progressive and irreversible loss of beta cells8-11</h3>
This loss drives8,10,28:
<ul>
 <li>metabolic failure</li>
 <li>vascular complications</li>
 <li>and life-long dependence on replacement insulin therapy</li>
</ul>
The condition manifests in four distinct stages as functional beta cell mass progressively declines.23,29,30&nbsp;Stages are defined by the presence of autoantibodies, level of glycaemic control, symptoms, insulin dependence and duration of diabetes.21,23,30

<h4>The four stages of autoimmune T1D21,23,29,30</h4>

Adapted from Breakthrough T1D. The stages of type 1 diabetes. Accessed September, 2025. https://jdrf.org.au/stages-of-type-1-diabetes/&nbsp;
*Reversion to single autoantibody or negative status can occur in some people with previously confirmed multiple autoantibody positivity.21

<figure class="table">
 <table>
 <tbody>
 <tr>
 <td style="background-color:#DAFAF9;border-color:hsl(0, 0%, 100%);">
 <h3>Pathogenesis is driven by autoreactive T cells – primarily CD8+ T cells, supported by CD4+ T cells11,31-34</h3></td>
 </tr>
 </tbody>
 </table>
</figure>

<figure class="table" style="width:57.66%;">
 <table class="ck-table-resized" style="background-color:#FEEAFD;">
 <colgroup>
 <col style="width:100%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#FEEAFD;border-color:hsl(0, 0%, 100%);">
 <h3>By the time symptoms appear, ~60–90% of beta cells may have already been destroyed*26,35-37</h3></td>
 </tr>
 </tbody>
 </table>
</figure>

*Beta cell mass is highly heterogeneous among patients with autoimmune T1D and may not correspond with severity of clinical presentation.38
Beta cell dysfunction can be detected up to 6 years before symptom onset, accompanying islet autoantibody seroconversion.19,20
<h3>Screening for T1D autoantibodies allows detection of beta cell dysfunction&nbsp;before symptoms appear21,22</h3>
Screening allows individuals and their families to get ahead of autoimmune T1D, helping21-28:
<ul>
 <li>prevent diabetic ketoacidosis</li>
 <li>avoid misdiagnosis</li>
 <li>reduce stress at diagnosis</li>
 <li>minimise the risk of long-term complications</li>
</ul>

<h4>Diabetic ketoacidosis</h4>
Up to 70% of patients present with DKA at diagnosis.*21,39

A life-threatening medical emergency,39&nbsp;&nbsp;DKA is associated with:
<ul>
 <li>approximately half of all hospitalisations in people with autoimmune T1D40,41</li>
 <li>a sustained negative effect on glycaemic control over time, increasing morbidity and mortality42</li>
 <li>beta cell loss, compounding damage already caused by autoimmunity18,42,43</li>
</ul>
Screening and monitoring programmes have lowered the rate of DKA at diagnosis by as much as 90%.†25,44,45

*Frequencies of DKA range from approximately 15% to 70% across Europe and North America.39&nbsp;
†In a public health screening programme that screened 90,632 children for autoimmune T1D islet autoantibodies in Bavaria, Germany, of the 62 children with presymptomatic autoimmune T1D who developed Stage 3 T1D, two (3.2%) were diagnosed with mild or moderate DKA without clinical symptoms, while 60 (96.8%) did not have DKA. The previously reported prevalence of DKA in unscreened children is over 20% in Germany.44

Browse the Resources below and make sure you’re aware of the risk factors associated with autoimmune T1D development.

Do you know who to screen for autoimmune T1D?

black

<h2>Beta cells: going beyond insulin</h2>
Modern treatment regimens have dramatically improved symptom management, but it is difficult to precisely mimic the complex, multifaceted role beta cells play in tissue health and glycaemic control.12,13,46,47,48
<h3>Despite significant advances, achieving glycaemic control remains challenging12,13,49,50</h3>
Technological advances have undoubtedly improved the way we manage autoimmune T1D:&nbsp;
<ul>
 <li>new continuous glucose monitoring (CGM) devices provide patients with glucose readings, trends and alerts in real time13</li>
 <li>automated insulin delivery (AID) systems automatically adjust insulin delivery based on a patient’s glucose readings.50 However, not all patients have access to this technology,51 and a high proportion of patients who do have access still do not achieve their glycaemic targets and continue to experience severe hypoglycaemic episodes.*52</li>
</ul>

*Retrospective, observational study of 2,074 adults (≥18 years) enrolled from the US T1D Exchange Registry/online community. Participants completed a one-time survey on HbA1c, severe hypoglycaemic episodes and impaired awareness of hypoglycaemia. The majority of participants (91.7%) were using a CGM plus MDI, AID systems or pump. Severe hypoglycaemia was defined as a hypoglycaemic event in the past 12 months where the patient experienced low blood glucose levels that they were unable to treat themselves and needed help from others.50

<figure class="table">
 <table>
 <tbody>
 <tr>
 <td style="background-color:#DAFAF9;border-color:hsl(0, 0%, 100%);">
 <h3>Conventional exogenous insulin regimens act as a hormone replacement therapy for patients with autoimmune T1D and while they address metabolic symptoms, they do not tackle the underlying autoimmune aetiology of T1D.53,54</h3></td>
 </tr>
 </tbody>
 </table>
</figure>
<figure class="table">
 <table style="background-color:#FB76F1;">
 <tbody>
 <tr>
 <td style="background-color:#FEEAFD;border-color:hsl(0, 0%, 100%);">
 <h3>The next era of T1D management will shift focus from solely symptom control to addressing the underlying immune-mediated cause of the disease11,53-55</h3></td>
 </tr>
 </tbody>
 </table>
</figure>

<h3>Beta cells are not only the exclusive producers of insulin46-48</h3>
The pancreatic islet is a complex ‘mini organ’ composed of different cell types that work together to integrate systemic and local signals and tightly control blood glucose levels.48,56
As such, beta cells do not exist in isolation, and, beyond insulin, release other hormones, peptides, neurotransmitters and metabolites vital to the complex cellular crosstalk&nbsp;that upholds the overall health and function of the pancreas.47,48,56-59&nbsp;
Beyond insulin, signalling molecules released by beta cells include:
<figure class="table" style="width:60%;">
 <table class="ck-table-resized">
 <colgroup>
 <col style="width:42.23%;">
 <col style="width:14.39%;">
 <col style="width:14.46%;">
 <col style="width:14.54%;">
 <col style="width:14.38%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#FB76F1;">
 Urocortin 3 
 Peptide hormone48,58</td>
 <td style="background-color:#06ded8;">
 GABA 
 Neurotransmitter 48,58</td>
 <td style="background-color:#440288;">
 Amylin&nbsp; Neuroendocrine hormone 60</td>
 <td style="background-color:#00a4b6;">
 Serotonin 
 Neurotransmitter 48,6</td>
 <td style="background-color:#fbea0c;">
 VEGF 
 Growth factor 47,58</td>
 </tr>
 <tr>
 <td colspan="2">
 Promote somatostatin release, which in turn regulates both beta and alpha cell activity</td>
 <td>
 Suppresses glucagon release, delays the rate of gastric emptying, promotes satiety</td>
 <td>
 Increases beta cell mass during metabolic challenge; suppresses glucagon release</td>
 <td>
 Stimulates blood vessel growth</td>
 </tr>
 </tbody>
 </table>
</figure>

Beta cells also display remarkable functional heterogeneity, differing in their insulin secretion capacity and responsiveness to glucose and other stimuli, and allowing for precise, adaptable and robust&nbsp;glucose regulation.46,57
<figure class="table">
 <table>
 <tbody>
 <tr>
 <td style="background-color:#DAFAF9;border-color:hsl(0, 0%, 100%);">
 <h3>The issue in autoimmune T1D isn’t just the loss of insulin – it’s the loss of beta cells and islet ability to sense and respond dynamically to the body’s needs.14,62-64&nbsp;</h3></td>
 </tr>
 </tbody>
 </table>
</figure>

The pancreatic beta cell reserve determines the course of the autoimmune T1D journey.1-7&nbsp;

Understanding autoimmune T1D means recognising the value of every single beta cell

<h2>C-peptide: a measure of beta cell function</h2>
<h3>Produced in a 1:1 molecular ratio with insulin, C-peptide is a direct, quantitative and reliable measure of beta cell function.6,16,19,65</h3>
C-peptide is a more reliable measure of beta cell function than endogenous insulin because it19,65:
<ol>
 <li>has a slower rate of degradation</li>
 <li>has a less variable rate of clearance</li>
 <li>is not impacted by exogenous insulin</li>
</ol>
 C-peptide is being increasingly recognised for its utility across clinical and research settings. In clinical practice, it can be used to differentiate between types of diabetes, and growing evidence suggests it may also help predict future level of glycaemic control and risk of complications.65-67 In research settings, C-peptide is serving as a valuable biomarker for assessing response to immunomodulatory treatment.6,68

Are you aware of the benefits associated with residual beta cell function?

A higher C-peptide level indicates greater residual beta cell function

<h2>The impact of residual beta cell function</h2>
The link between beta cell activity and clinical outcomes offers a strong, practical rationale for valuing and monitoring beta cell function in the management of autoimmune T1D.1-6,12-17,19
<h3>Greater residual beta cell activity is linked to improved outcomes1-6,12-17,19</h3>
The pancreatic beta cell reserve determines the course of the autoimmune T1D journey1-7&nbsp;with higher versus lower residual beta cell activity, as indicated by C-peptide, associated with:
<h4>1. Improved glycaemic control</h4>
Significantly improved parameters of daily glycaemic control have been observed in individuals with higher versus lower&nbsp;residual beta cell activity, as indicated by level of C-peptide.&nbsp;
Specifically, greater residual beta cell function correlates with*15:

longer time in range

lower HbA1c

lower total daily insulin dose

<h4 style="text-align:center;">Time in range by level of&nbsp;​C-peptide*15</h4>

Adapted from Snethlage CMF, et al.&nbsp;Diabetes Care. 2024;47:1114-1121.&nbsp;
*Cross-sectional cohort study of 489 Dutch adults with autoimmune T1D (median duration 15 years) assessing associations between residual beta cell function (measured by UCPCR), alpha cell function (glucagon/glucose ratio) and CGM metrics, including time in range, variability and hypoglycaemia. A higher UCPCR correlated with a longer time in range (r=0.330, p&lt;0.05), and correlated negatively with both HbA1c levels (r= –0.183, p&lt;0.05) and total daily insulin dose (r= –0.183, p&lt;0.05).&nbsp;UCPCR values: undetectable: &lt;0.01 nmol/mmol; low: 0.01–0.2 nmol/mmol; intermediate: 0.2–0.6 nmol/mmol; high: &gt;0.6 nmol/mmol.15

<h4>2. Reduced incidence of severe hypoglycaemia</h4>
Incidence of severe hypoglycaemia is significantly associated with level of residual beta cell function, as indicated by level of C-peptide.4†
<h4 style="text-align:center;">Proportion of patients with a history of severe&nbsp;hypoglycaemia†‡4</h4>

Adapted from Gubitosi-Klug RA, et al.&nbsp;J Clin Invest. 2021;131(3):e143011.
†Observational study of the DCCT/EDIC cohort (mean duration of T1D ~35 years). Serum C-peptide was measured during a 4-hour MMT. Associations with metabolic outcomes and complications were explored among non-responders (all C-peptide values after meal &lt;3 pmol/L) and three categories of responders.4&nbsp;‡Hypoglycaemia requiring assistance.4 §Based on Cochran-Armitage trend test.4

<h4>3. Reduced likelihood of DKA</h4>
Patients with higher versus lower residual beta cell activity are significantly less likely to experience DKA both at the time of diagnosis and 12 months after diagnosis.II18
<h4 style="text-align:center;">Longitudinal C-peptide levels according to DKA status at time of diagnosisII18</h4>

Adapted from Mortensen HB, et al.&nbsp;Pediatr Diabetes. 2010;11(4):218-226.
IIProspective, observational cohort study of 275 children with newly diagnosed T1D conducted across 18 centres in Europe and Japan, assessing predictors of residual beta cell function and glycaemic control over the first 12 months post-diagnosis using serial mixed-meal C-peptide tests, autoantibody levels, HLA typing, and HbA1c measurements. DKA with standard bicarbonate &lt;15 mmol/L was associated with significantly poorer residual beta cell function 1 (p=0.004) and 12 months (p=0.0003) after diagnosis.18

<h4>4. Reduced risk of microvascular complications</h4>
Patients with higher versus lower residual beta cell activity are at lower risk of long-term microvascular complications such as:

retinopathy5,6,16

nephropathy5

<h3>Even relatively low residual beta cell activity correlates with an increased likelihood of achieving recommended HbA1c targets and a reduced prevalence of severe hypoglycaemia2,4</h3>
Those with low residual beta cell function are still&nbsp;2x more likely to achieve HbA1c &lt;7.5% compared to patients with no residual beta cell function.¶2
<h4 style="text-align:center;">Patients with a HbA1c &lt;7.5%&nbsp;​by level of C-peptide¶​</h4>

¶Cross-sectional study of 342 Danish children (aged 4.8–18.9 years) with autoimmune T1D (duration 3–6 years) assessing residual beta cell function via meal- stimulated C-peptide and evaluating associations with hypoglycaemia, HbA1c and insulin needs. C-peptide levels: none: &lt;40 pmol/L; low: 40–200 pmol/L; high: ≥200 pmol/L.2​&nbsp;#Logistic regression analysis adjusted for sex, age, pubertal status, diabetes duration, and insulin administration technique.2
Relatively low residual beta cell activity is also associated with a protective effect against hypoglycaemia. In the DCCT, C-peptide levels above the detection threshold of 30 pmol/L were significantly associated with a lower prevalence of severe hypoglycaemia throughout the entire study period.4

<h2>Summary</h2>
<h3>The more beta cells the better, and even limited residual activity can still positively impact the patient journey1-6,15-17,19</h3>
<ul>
 <li>In symptomatic autoimmune T1D, clinically meaningful beta cell function is indicated by a C-peptide level over 0.2 pmol/mL7</li>
 <li>But improved outcomes are still observed with any level above 0.03 pmol/mL (detection threshold)2,4-7</li>
</ul>

Abbreviations
AID, automated insulin delivery system; CGM, continuous glucose monitor; DanDiabKids, Danish Study Group for Childhood Diabetes; DKA, diabetic ketoacidosis; DCCT, Diabetes Control and Complications Trial; EDIC, Epidemiology of Diabetes Interventions and Complications; GABA, gamma-aminobutyric acid; HbA1c, haemoglobin A1c; MDI, multiple daily injections; MMTT, mixed meal tolerance test; SDRNT1BIO, Scottish Diabetes Research Network Type 1 Bioresource Study; T1D, type 1 diabetes; UCPCR, urinary C-peptide-to-creatine ratio; US, United States; VEGF, vascular endothelial growth factor.

Because pancreatic beta cell reserve determines the course of the T1D journey.

There's a Beta Way to look at type 1 diabetes

AUTOIMMUNER-TYP-1-DIABETES

DIABETES

The heterogeneous pathogenesis of autoimmune T1D is characterised by factors related to a person's genetics and their environment. Whilst key autoantigens have been identified, the initial triggers of the autoimmune T1D immune response remain uncertain.3

<h3>Autoimmunity and beta-cell destruction</h3>

The pathogenesis of autoimmune T1D begins when autoreactive T cells recognize and destroy pancreatic beta cells. This leads to a critical decline in insulin levels, which in turn causes ineffective control of blood glucose levels. Eventually, the remaining beta cells become insufficient to maintain normal blood glucose, reducing insulin secretion and leading to autoimmune T1D.4

<h3>Autoantigens and immune response</h3>

Autoimmune T1D patient´s immune system erroneously identifies specific beta cell components as autoantigens and attacks them.5 These T1D autoantigens can include6
<ul>
 <li>insulin B chain peptide (11-23)</li>
 <li>other beta-cell components such as GAD65, an enzyme associated with secretory vesicles</li>
 <li>protein phosphatase like IA-2</li>
</ul>
The presence of autoantibodies against these antigens serves as an important biomarker for disease progression, which is exponentially increased by any additional autoantibodies.6 Early detection of presymptomatic stages through screening for autoantibodies provides us with an opportunity to intervene, delay, and potentially prevent the symptomatic manifestation of autoimmune T1D.2

A potential mechanism for triggering autoimmune response4&nbsp;

When it comes to genetic factors, autoimmune T1D is strongly associated with specific HLA class II chain alleles which confer a higher risk for autoimmune T1D development.6
It is noteworthy that people living with other associated autoimmune diseases, such as celiac disease and autoimmune thyroid disease, are at an increased risk of developing autoimmune T1D than the general population.7
Does your patient have an existing autoimmune condition? Learn more about <a href="${link:{uuid:{bb90e1f3-ac46-45f4-8892-4883f3ac2ccc},repository:{articles},path:{/Global/indications/t1d/check-for-autoimmune-type-1-diabetes}}}">genetic risk factors linked to autoimmune T1D</a>.

<h3>Metabolic consequences of insulin deficiency</h3>

The destruction of pancreatic beta-cells due to autoimmune T1D results in insulin deficiency. Insulin deficiency, coupled with increased counterregulatory hormones, triggers the release of free fatty acids from adipose tissue. These fatty acids are then oxidized in the liver to form ketone bodies, leading to diabetic ketoacidosis (DKA), which ultimately causes worsening of hyperglycemia.8 DKA is a life-threatening condition often associated with high mortality, morbidity, and healthcare expenditure.9 <a href="${link:{uuid:{8ba6793a-69c0-4421-8153-21249585cfee},repository:{articles},path:{/Global/indications/t1d/early-detection-of-autoimmune-type-1-diabetes-could-reduce-the-risk-of-diabetic-ketoacidosis}}}">Early screening and detection of autoimmune T1D is therefore crucial for preventing DKA</a>.

<h2>Stages of autoimmune T1D progression</h2>

There is a trigger event that initiates the pathogenesis of autoimmune T1D before it progresses through four stages and eventually results in symptomatic autoimmune T1D. An initial immune response occurs during this trigger event with the development of a single autoantibody. As soon as additional autoantigens are detected, the number of beta cells is already shrinking. However, the pace at which autoimmune T1D progresses from the first autoimmune reaction to symptomatic disease varies from individual to individual and can take anywhere from a few months to decades.2,9

<h3>Stage 1. Early autoimmunity and beta-cell decline</h3>

The first stage of a beginning autoimmunity is characterized by the presence of two or more autoantibodies against the pancreatic islets in the peripheral circulation. In this stage the functional impairment and reduction of beta-cells is already in progress, but the number is still sufficient to maintain normoglycemia. That is why no symptoms are apparent yet.2

<h3>Stage 2. Progressive beta-cell dysfunction</h3>

In stage 2, the destruction of the beta-cells progressively increases, resulting in the decrease of insulin production. Glycaemic control can no longer be maintained, which eventually leads to dysglycemia. Although still pre-symptomatic, the autoantibodies remain detectable in the peripheral circulation at this stage as a biomarker for autoimmunity.2

<h3>Stage 3. Clinical symptoms and insulin dependence</h3>

At this stage, the destruction of the beta-cells has reached a degree at which insulin production is no longer sufficient to keep the blood sugar stable. Patients at this stage now show the typical clinical symptoms of autoimmune T1D, such as polyuria, polydipsia, weight loss, fatigue, and diabetic ketoacidosis (DKA). Hyperglycemia also occurs at this point, which makes an insulin medication unavoidable.2

<h3>Stage 4. Long-standing autoimmune T1D</h3>

At stage 4, patient has long-standing autoimmune T1D after living with the condition for several years and is insulin dependent.10-11 Long-term health complications are common, and two or more autoantibodies may or may not be detected in the blood at stage 4 autoimmune T1D.11

<h2>Early detection and progression of autoimmune T1D</h2>

Due to the latest research evidence on pathophysiological mechanisms in the development of autoimmune T1D, it is now possible to screen patients in the presymptomatic stages (1 and 2) for suspicious autoantibodies. This provides the opportunity to intervene, delay and ultimately prevent the natural progression of autoimmune T1D, preserving beta cell function.2,12

<h3>Early identification of autoimmune T1D</h3>

Currently, first- or second-degree relatives of individuals with autoimmune T1D or pediatric population are being screened for increased risk of developing autoimmune T1D in the research setting.2 The improved understanding of the development and progression of autoimmune T1D enables early detection, utilising autoantibody screenings as a primary tool. It opens a variety of possibilities for patients and their relatives as well as for HCPs in their care.13
<h2>Learn more about <a href="${link:{uuid:{efa3fba3-4d30-4f15-bc79-a5c9cac2ba1d},repository:{articles},path:{/Global/indications/t1d/test-for-autoantibodies}}}">how autoantibodies can be used to screen for T1D</a></h2>

Autoimmune type 1 diabetes (autoimmune T1D) is a progressive autoimmune disorder that causes the destruction of insulin-producing beta cells in the pancreas, leading to an inability to regulate blood glucose levels.1 Understanding the pathophysiology of autoimmune T1D can help identify potential at-risk patients and facilitate early intervention.2

The pathophysiology of autoimmune type 1 diabetes

TYPE-1-DIABETES

The incidence of autoimmune T1D is growing worldwide,1 making the disease an increasingly important topic for HCPs. Patients can develop comorbidities and severe complications, such as life-threatening diabetic ketoacidosis, which can significantly diminish their quality of life.1
Learn more about these impacts from <a href="${link:{uuid:{df323a59-7a2d-4bf2-ba62-4751c29e540b},repository:{articles},path:{/Global/indications/t1d/real-life-stories-from-people-living-with-autoimmune-t1d}}}">real-life stories of people living with autoimmune T1D</a>.
Autoimmune T1D manifests in children and adolescents.1,4 However, an estimated 50% of new cases emerge in adults.5 Autoimmune T1D is often misdiagnosed as type 2 diabetes, complicating estimations of incidence rates.4,5

It is a progressive autoimmune disease characterized by the destruction of insulin-producing pancreatic beta cells. Early identification can help monitor disease progression and implement preventive measures before <a href="${link:{uuid:{efa3fba3-4d30-4f15-bc79-a5c9cac2ba1d},repository:{articles},path:{/Global/indications/t1d/test-for-autoantibodies}}}" target="_self">autoimmune</a> T1D onset.1,4,11 B cells produce autoantibodies against islet cells and activate T cells that target pancreatic cells.1,4 However, the exact causes of autoimmune T1D are not yet clearly identified.12
Learn more about the complex pathogenesis and pathophysiology of autoimmune T1D.

A mix of genetic and environmental risk factors likely trigger islet autoimmunity and development of autoimmune T1D and may also vary with age of disease onset. For example, increased inflammation detected in those who develop autoimmune T1D at a younger age might be one factor contributing to the heterogeneity of the disease.13

<h3>Genetic risk factors for autoimmune type 1 diabetes</h3>

Having a relative with autoimmune T1D is a risk factor. The risk of developing autoimmune T1D is between 1 in 300 to 1 in 250.* This risk increases to 1 in 40 to 1 in 35 for those with parents who have the disease. However, the majority of patients do not have a family history of the disease.14
Shared genetic risk factors are potentially implicated both in polyautoimmunity (occurrence of ≥2 autoimmune diseases in a single patient) and family autoimmunity (presence of ≥2 autoimmune diseases in members of a nuclear family) among individuals with autoimmune T1D.15
Human leukocyte antigen (HLA) plays a role in fighting pathogens. HLA genes encoding DR and DQ are also associated with a high risk of autoimmune T1D and therefore considered genetic risk factors for autoimmune T1D.16 The genotypes are detected in 90% of pediatric autoimmune T1D patients.17 Dysregulation of other genes such as cytotoxic T cell-associated protein 4 (CTLA-4) and protein tyrosine phosphatase, nonreceptor type 22 (PTPN22) might also contribute to the onset of autoimmune T1D.18
*based on a US population

<h3>Environmental risk factors for autoimmune T1D</h3>

Some studies suggest a link between infections and autoimmune T1D.1,14 For example, recent research suggests that SARS-CoV-2 increases the risk of autoimmune T1D and accelerates the progression of the disease.12 Enteroviruses and bacterial infections have also been implicated in other studies. However, further validation is required to confirm a causal relationship.12
Other risk factors for autoimmune T1D have been proposed, including exposure to toxins and maternal diet.19,20 However, the evidence presented in these studies is often weak and/or inconclusive. 19,20

<h3>Autoimmune conditions as risk factors for autoimmune T1D</h3>

Autoimmune T1D shows a genetic overlap with several autoimmune conditions. For instance, Addison's disease is associated with a higher risk of autoimmune T1D.21 Furthermore, patients with celiac and autoimmune thyroid disease have an estimated 4-9% and 15–30% increased risk, respectively, of developing autoimmune T1D.22
There is also a familial link between autoimmune T1D and autoimmune disease.2 &nbsp;First-degree relatives of individuals with other autoimmune diseases including celiac and thyroid diseases may also be more likely to develop &nbsp;autoimmune T1D.2
Learn more about the link between <a href="${link:{uuid:{bb90e1f3-ac46-45f4-8892-4883f3ac2ccc},repository:{articles},path:{/Global/indications/t1d/check-for-autoimmune-type-1-diabetes}}}" target="_self">autoimmune T1D and autoimmune disease</a>.

<h3>Obesity and diet as risk factors for autoimmune T1D</h3>

Obesity and autoimmune T1D are correlated. Obesity possibly contributes to the disease by increasing insulin resistance and causing systemic inflammation.23
The intake of certain nutrients has also been associated with a higher risk for the development of autoimmune T1D. For instance, research suggests that high sugar consumption can promote the progression of autoimmune T1D.24
Other potential nutritional risk factors for autoimmune T1D, such as gluten, have also been investigated. However, the studies are inconsistent with contradictory results.14

<h3>Psychological stress as a risk factor for autoimmune T1D</h3>

There may be a link between stress and the risk of autoimmune T1D.
For instance, mothers encountering a significant life event during pregnancy may increase the risk of their child developing autoimmune T1D.25,26
Additionally, some studies suggest that children who are exposed to excessive psychological stress, such as the divorce of their parents or experience of violence, have an increased risk of autoimmune T1D.14
Modifiable factors like nutritional intake and stress may contribute to the development of autoimmune T1D, potentially providing strategies to delay or prevent onset of the disease. However, in many cases, additional robust evidence is required before evidence-based recommendations can be made.14,24
In conclusion, early identification of individuals with islet autoantibodies before the clinical onset of T1D allows for the timely implementation of preventive measures and treatments that could prevent the natural progression of autoimmune T1D and preserve beta cell function.11

<h2>Learn more about how autoimmune type 1 diabetes can be detected years before symptom onset</h2>

The causes and risk factors of autoimmune type 1 diabetes (autoimmune T1D) are multifactorial. A combination of genetic susceptibility and other risk factors, like a family history of autoimmune disease, increase the risk of developing the pathology.1,2 Identifying these risk factors can help HCPs proactively screen high-risk patients and help avoid serious complications through targeted interventions.3

Etiology and risk factors for autoimmune type 1 diabetes

The progression of autoimmune type 1 diabetes (T1D) is gradual, often detectable months or even years before symptoms arise.1–3 Through proactive screening, we can identify the condition well in advance.3 Meet our ambassadors living with autoimmune T1D and discover the risk factors to look out for when considering who to screen.

Real-life stories from people living with autoimmune T1D 

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