The offspring of mothers who have autoimmune diseases during pregnancy are at increased risk for later development of type 1 diabetes (T1D), new research suggested.

In a Swedish nationwide cohort study of over 1 million children, maternal autoimmune diseases during pregnancy were associated with a 57% higher risk for T1D in their offspring. Both maternal and paternal autoimmune diseases showed similar associations, with some disease-specific differences.

“These findings suggest that shared familial susceptibility contributes to the intergenerational transmission of T1D risk, while some autoimmune diseases may involve additional parent-specific influences,” first author Huan Zhang, PhD, of the Department of Global Public Health, Karolinksa Institute, Stockholm, Sweden, and colleagues said in their JAMA Pediatrics report, published online on October 26, 2026.

A recent international consensus report called for general population screening for early-stage T1D and included “relatives of people with symptomatic type 1 diabetes or other autoimmune diseases” among those to be considered for prioritization. The paper also cites a 2025 study that found associations between parental autoimmune thyroid disease, celiac disease, rheumatoid arthritis, pernicious anemia, sarcoidosis, mixed connective tissue disease, or Sjögren disease and increased risk for clinical T1D in offspring.

However, a coauthor of the new study, Xingbo Mo, PhD, professor in the School of Public Health, Nanjing Medical University, Nanjing, China, cautioned about translating the data directly into routine screening recommendations. “Our study was observational and was not designed to evaluate the benefits, harms, or cost-effectiveness of screening for islet autoantibodies. Although offspring of parents with autoimmune diseases had an increased relative risk of type 1 diabetes, the absolute risk remained low for most children. Therefore, our findings alone do not support routine screening of all offspring of people with autoimmune diseases, nor do they establish which specific groups should be screened.”

Nevertheless, Mo added, the findings may “help inform future research into risk stratification and screening strategies. Decisions about screening should also consider existing clinical guidance, local resources, and whether appropriate confirmatory testing, counseling, and follow-up are available.”

Strong Links Found Between Parental Autoimmunity and Offspring T1D

The study population came from a total of 1,455,645 live-born singleton children recorded in the Swedish Medical Birth Register from 2001 to 2014. Of those, 6.1% (88,368) were exposed to maternal autoimmune disease during pregnancy. Those infants were more likely to be born preterm (9.1% vs 5.7%) and large for gestational age (14.9% vs 10.6%).

During a median 15.3 years’ follow-up, 10,273 total offspring (4.6 per 10,000 person-years) developed T1D. After adjustment for multiple variables including calendar year of birth, maternal parity, and other maternal conditions including cardiovascular disease, maternal autoimmune disease was associated with a significant 57% increased risk for T1D in offspring (hazard ratio [HR], 1.57). After further adjustment for maternal T1D, the association was still significant (HR, 4.51).

Both maternal and paternal T1D were associated with highly significantly increased risk in the offspring, with HRs of 4.51 and 5.79, respectively. Paternal autoimmune disease also elevated the risk by 51% (HR, 1.51).

In a separate analysis comparing offspring whose mothers had autoimmune disease with their cousins whose mothers did not have the corresponding disease, maternal autoimmune disease remained associated with an increased risk for T1D in offspring (HR, 1.27).

“Cousins share some genetic background and family environment, so this approach helps account for familial factors that may confound the association. The association was attenuated but remained present in the cousin analysis, compared with the main analysis. This suggests that shared familial factors may explain part, but not necessarily all, of the observed association. Cousin comparisons cannot fully control for genetic or environmental differences and do not, by themselves, establish a causal intrauterine effect,” Mo told Medscape Medical News.

Specific parental autoimmune conditions associated with a significantly increased risk for T1D in offspring included rheumatoid arthritis of roughly equal magnitude in both mothers (HR, 1.83) and fathers (HR, 1.79). The association with autoimmune thyroiditis was stronger for fathers (HR, 2.28) than mothers (HR, 1.45), but significant for both.

Significant associations were seen only for mothers with ankylosing spondylitis (HR, 2.00), Henoch-Schönlein purpura/immunoglobulin A vasculitis (HR, 1.54), vitiligo (HR, 1.91), and celiac disease (HR, 1.70). And for fathers only, sarcoidosis was also significantly associated with offspring T1D (HR, 1.64).

Offsprings’ risk for T1D also increased progressively with increasing parental autoimmunity, with the highest risk in those exposed from both parents, and particularly when both parents had T1D. The associations were also stronger for T1D diagnosed at younger ages in the offspring, and for mothers diagnosed prior to pregnancy rather than after delivery.

“The similar overall associations observed for maternal and paternal autoimmune diseases, together with the cousin analyses, suggest that shared familial susceptibility may explain part of the association. They do not exclude intrauterine influences, nor can they establish whether maternal immune effects are harmful or protective,” Mo said.

‘We Cannot Easily Explain All of the Findings’

Asked to comment, pediatric endocrinologist and T1D autoimmunity researcher William A. Hagopian, MD, PhD, research professor of pediatrics at the Indiana University School of Medicine, Indianapolis, and clinical professor of medicine at the University of Washington, Seattle, noted that the maternal effect with rheumatoid arthritis and celiac disease are understandable given their genetic links (HLA DR4 and HLA DR3, respectively).

However, he added, “ankylosing spondylitis predisposition to T1D is perplexing because HLA B27 is not associated with T1D.” He added that it’s “surprising that HLA DR3 with celiac had so much less effect than DR3 with thyroid. It’s clear we cannot easily explain all of the findings.”

Hagopian also pointed out that it was unclear which maternal effects were conferred by genes rather than a shared body or immune milieu during gestation, and that the lack of adjustment for T1D genes is a “major limitation” not completely overcome by the cousin analysis.

In addition, “it was not corrected for viral exposures, primarily during pregnancy. Viral infections might have been shared by all family members, including during the pregnancy period. And viral diseases vary by HLA type, so that might also be co-analyzed.”

Added Hagopian, who was a co-author of the international consensus for early T1D population screening, “the clinical implications are that parental autoimmune diseases might trigger a greater attention to screening those offspring for T1D autoantibodies. But given the practical difficulty of getting a family history of anything, it may not be worthwhile to screen offspring more based on specific autoimmune diseases. Thyroid is easier than the others to get in the family history, so that might be a practical entree into screening.”

Indeed, Mo said, “overall, we view the study as providing evidence that familial susceptibility is relevant to understanding the intergenerational pattern of type 1 diabetes risk, while highlighting the need for further research before specific screening recommendations can be made.”

The study was supported by grants from the Swedish Heart and Lung Foundation and the Swedish Research Council for Health, Working Life and Welfare. Zhang and Mo reported no further disclosures. Hagopian had no disclosures.

Miriam E. Tucker is a freelance journalist based in the Washington, DC, area. She is a regular contributor to Medscape, with other work appearing in the Washington Post, NPR’s Shots blog, and diaTribe. She is on X @MiriamETucker and BlueSky @miriametucker.bsky.social.