A global view of hypertensive disorders and diabetes mellitus during pregnancy

In the paper

“In the Generation R study142,143 (a large population-based California cohort of singleton births)144, Black women had an increased risk of HDP compared with white women.”

What the sources say

• ?Not checked — no full text of the sourcecites [142] Silva, L. M. et al. Low socioeconomic status is a risk factor for preeclampsia: the Generation R Study. J. Hypertens. 26, 1200–1208 (2008). source
• Disputed

  The Introduction (p. 2) says this analysis was restricted to an ethnically homogeneous population, and Study population (p. 3) specifies that only women of Dutch ethnicity were selected. The paper therefore does not report the Black-versus-white risk comparison attributed to it; it examines educational level and gestational hypertension among Dutch women. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  cites [143] Silva, L. et al. Maternal educational level and risk of gestational hypertension: the Generation R Study. J. Hum. Hypertens. 22, 483–492 (2008). sourceExperimental — accuracy not yet measured
• Partly supported

  The Participants section (p. 3) identifies this as a California cohort, not the Generation R study. The Discussion (p. 9) reports increased preeclampsia risk among Black women compared with White women, but does not establish the claim for hypertensive disorders of pregnancy as a whole. (LLM, conf=0.88)

  cites [144] Ross, K. M. et al. Socioeconomic status, preeclampsia risk and gestational length in black and white women. J. Racial Ethn. Health Disparities 6, 1182–1191 (2019). sourceExperimental — accuracy not yet measured

In the paper

“The application of these broad definitions of pre-eclampsia means patients once diagnosed with gestational hypertension or chronic hypertension were recategorized as pre-eclampsia or chronic hypertension with superimposed pre-eclampsia, respectively17–21.”

What the sources say

• ?Not checked — no full text of the sourcecites [17] Bouter, A. R. & Duvekot, J. J. Evaluation of the clinical impact of the revised ISSHP and ACOG definitions on preeclampsia. Pregnancy Hypertens. 19, 206–211 (2020). source
• ?Not checked — no full text of the sourcecites [18] Khan, N. et al. Impact of new definitions of pre-eclampsia on incidence and performance of first-trimester screening. Ultrasound Obstet. Gynecol. 55, 50–57 (2020). source
• Supported

  The Results (page not supplied) report that women previously classified with gestational hypertension and women with chronic hypertension were diagnosed with pre-eclampsia under the revised ACOG 2013 or ISSHP 2014 criteria. Pre-eclampsia diagnosed in women with chronic hypertension supports the claim’s description of superimposed pre-eclampsia; the finding applies to some women in each group, not all. (LLM, conf=0.92)

  cites [19] Kallela, J. et al. The diagnosis of pre-eclampsia using two revised classifications in the Finnish Pre-eclampsia Consortium (FINNPEC) cohort. BMC Pregnancy Childbirth 16, 221–221 (2016). source
• ?Not checked — no full text of the sourcecites [20] Reddy, M. et al. The impact of the definition of preeclampsia on disease diagnosis and outcomes: a retrospective cohort study. Am. J. Obstet. Gynecol. 224, e211–e217 (2021). source
• ?Not checked — no full text of the sourcecites [21] Saleh, L., Danser, J. A. H., Van Den Meiracker, A. H. & Visser, W. The prevalence of hypertensive disorders according to the old and new criteria of ISSHP and ACOG: risk factors, prediction of preeclampsia. Pregnancy Hypertens. 6, 229 (2016). source

In the paper

“Individuals with HDP or impaired glucose metabolism during pregnancy experience greater maternal mortality and morbidity rates than people with uncomplicated pregnancies.”

What the sources say

• ?Not checked — no full text of the sourcecites [2] Steegers, E. A., von Dadelszen, P., Duvekot, J. J. & Pijnenborg, R. Pre-eclampsia. Lancet 376, 631–644 (2010). source
• Partly supported

  The Results (p. 5) identify hypertensive disorders as a cause of maternal death, and the discussion (p. 10) describes diabetes as a potential indirect contributor to maternal morbidity and mortality. The paper does not establish higher morbidity and mortality rates for either group compared with uncomplicated pregnancies, and its discussion of diabetes does not specifically address impaired glucose metabolism arising during pregnancy. (LLM, conf=0.86)

  cites [3] Say, L. et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob. Health 2, e323–e333 (2014). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [4] Duley, L. The global impact of pre-eclampsia and eclampsia. Semin. Perinatol. 33, 130–137 (2009). source

In the paper

“Notably, the burden of premature deaths from complications of CMDs in pregnancy and associated cardiovascular disease (CVD) later in life falls disproportionately upon LMICs.”

What the sources say

• Partly supported

  The Discussion (Main findings; page unavailable) describes declining cardiovascular burden in high-income countries and greater scope for effective interventions in low-income and middle-income countries. The Results (Global trends; page unavailable) also identify maternal disorders as a leading cause of DALYs among young females. Neither passage establishes that premature deaths from cardiometabolic complications of pregnancy, or associated cardiovascular disease later in life, fall disproportionately on those countries. (LLM, conf=0.78)

  cites [47] Vos, T. et al. Global burden of 369 diseases and injuries in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet 396, 1204–1222 (2020). sourceExperimental — accuracy not yet measured

In the paper

“However, both diseases show an unevenly distributed disease burden for regions with a low income or middle income, or low-income and middle-income countries (LMICs), or regions with lower sociodemographic and human development indexes.”

• Also stated in: § HDP · boosted

  “Countries with lower SDI and HDI generally had a greater disease burden of HDP than those with higher SDI and HDI, demonstrated by a higher prevalence, DALYs and death attributable to HDP (Figs. 2–4).”

What the sources say

• ?Could not verify

  Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.

  cites [47] Vos, T. et al. Global burden of 369 diseases and injuries in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet 396, 1204–1222 (2020). sourceExperimental — accuracy not yet measured

In the paper

“HDP and GDM share many common risk factors and similarities in their pathophysiology, including oxidative stress, inflammation and vascular endothelial dysfunction1”

What the sources say

• Partly supported

  The Introduction states that gestational diabetes and preeclampsia share risk factors and involve oxidative stress, pro-inflammatory factors, and vascular endothelial dysfunction. Preeclampsia is a hypertensive disorder of pregnancy, but the paper’s statement is specific to preeclampsia; it does not establish the same similarities for hypertensive disorders of pregnancy as a whole. (LLM, conf=0.86)

  cites [1] Yang, Y. & Wu, N. Gestational diabetes mellitus and preeclampsia: correlation and influencing factors. Front. Cardiovasc. Med. 9, 831297 (2022). sourceExperimental — accuracy not yet measured

In the paper

“The prevalence of GDM has increased dramatically over the past two decades by more than 30% in numerous countries5–7.”

What the sources say

• ?Not checked — no full text of the sourcecites [5] Ferrara, A. Increasing prevalence of gestational diabetes mellitus: a public health perspective. Diabetes Care 30, S141–S146 (2007). source
• Partly supported

  The Results report a 45% increase in age- and ethnicity-adjusted GDM incidence in New South Wales from 1995 to 2005. The Conclusions also cite U.S. studies reporting increases of up to 68% over a similar period. These passages support an increase exceeding 30%, but cover roughly 11 years and do not establish that it occurred over two decades in numerous countries. (LLM, conf=0.88)

  cites [6] Anna, V., van der Ploeg, H. P., Cheung, N. W., Huxley, R. R. & Bauman, A. E. Sociodemographic correlates of the increasing trend in prevalence of gestational diabetes mellitus in a large population of women between 1995 and 2005. Diabetes Care 31, 2288–2293 (2008). sourceExperimental — accuracy not yet measured
• Supported

  The Introduction states that GDM prevalence increased by more than 30% within one or two decades in a number of countries, including developing countries. This supports the citing sentence’s magnitude, timeframe, and geographic scope. (LLM, conf=0.94)

  cites [7] Zhu, Y. & Zhang, C. Prevalence of gestational diabetes and risk of progression to type 2 diabetes: a global perspective. Curr. Diab. Rep. 16, 7 (2016). source

In the paper

“Several socioenvironmental factors, including poverty, air pollution, educational and sociocultural barriers, and limitations in health-care access and infrastructure12, are responsible for such inequities in disease burden.”

What the sources say

• Partly supported

  The Introduction (page unavailable) links the disproportionate burden of premature deaths in LMICs to disadvantages faced by rural women, including poverty, educational and sociocultural barriers, and limited health-care access and infrastructure. The cited paper does not identify air pollution as a contributor, so it does not support the full list of factors in the claim. (LLM, conf=0.88)

  cites [12] Nagraj, S. et al. Cardiometabolic risk factors in pregnancy and implications for long-term health: identifying the research priorities for low-resource settings. Front. Cardiovasc. Med. 7, 40 (2020). sourceExperimental — accuracy not yet measured

In the paper

“In addition to many common clinical, demographic and behavioural risk factors, the development and clinical consequences of maternal CMDs are substantially influenced by the social determinants of health, such as systemic marginalization.”

• Also stated in: § Race, ethnicity, socioeconomic and environmental factors · plain

  “The stress of systemic racial disparities, such as poverty, living in racially segregated neighbourhoods, a lack of access to health-care services and experience of discrimination, can all negatively affect the health of women of certain ethnic groups, such as non-Hispanic Black women147.”

What the sources say

• Partly supported

  The Discussion (page not provided) says socioeconomic disparities may partly account for differences in cardiovascular risk and adverse pregnancy outcomes, and that systemic racism may contribute to disparities in preeclampsia. The paper did not examine systemic racism directly, so it does not establish a substantial influence on the development and clinical consequences of maternal cardiometabolic disorders generally. (LLM, conf=0.84)

  cites [147] Boakye, E. et al. Nativity-related disparities in preeclampsia and cardiovascular disease risk among a racially diverse cohort of US women. JAMA Netw. Open 4, e2139564 (2021). sourceExperimental — accuracy not yet measured

In the paper

“Therefore, a majority of health authorities, such as the WHO and the American Diabetes Association, have come to support the broad criteria, such as the criteria of the International Association of the Diabetes and Pregnancy Study Groups (IADPSG)26,39.”

What the sources say

• ?Not checked — no full text of the sourcecites [26] Mayo, K., Melamed, N., Vandenberghe, H. & Berger, H. The impact of adoption of the International Association of Diabetes in Pregnancy Study Group criteria or the screening and diagnosis of gestational diabetes. Am. J. Obstet. Gynecol. 212, e221–e229 (2015). source
• Partly supported

  The Background (page unavailable) explicitly says the WHO endorses the IADPSG criteria, and the Discussion says those criteria are widely used. But the paper does not say that a majority of health authorities endorse them or establish that the American Diabetes Association does; the Discussion notes continuing disagreement over diagnostic criteria. (LLM, conf=0.88)

  cites [39] Behboudi-Gandevani, S., Amiri, M., Bidhendi Yarandi, R. & Ramezani Tehrani, F. The impact of diagnostic criteria for gestational diabetes on its prevalence: a systematic review and meta-analysis. Diabetol. Metab. Syndr. 11, 11 (2019). sourceExperimental — accuracy not yet measured

In the paper

“Adopting broad definitions of GDM might result in a considerable increase in the prevalence and incidence of GDM26,39”

What the sources say

• ?Not checked — no full text of the sourcecites [26] Mayo, K., Melamed, N., Vandenberghe, H. & Berger, H. The impact of adoption of the International Association of Diabetes in Pregnancy Study Group criteria or the screening and diagnosis of gestational diabetes. Am. J. Obstet. Gynecol. 212, e221–e229 (2015). source
• Supported

  The Discussion reports that lower diagnostic glucose thresholds identified significantly more women with GDM and increased measured prevalence. The Conclusion says reducing the diagnostic threshold is associated with a significant increase in GDM incidence. Together, these support the hedged claim about broader definitions. (LLM, conf=0.92)

  cites [39] Behboudi-Gandevani, S., Amiri, M., Bidhendi Yarandi, R. & Ramezani Tehrani, F. The impact of diagnostic criteria for gestational diabetes on its prevalence: a systematic review and meta-analysis. Diabetol. Metab. Syndr. 11, 11 (2019). source

In the paper

“A great disparity exists between HICs and LMICs regarding the disease burden of HDP (Table 1).”

What the sources say

• ?Could not verify

  The Results > Global trends section lists maternal disorders among leading causes of DALYs for young females, but does not compare hypertensive disorders of pregnancy between high-income and low- or middle-income countries. Searches for hypertensive disorders, pre-eclampsia, and maternal burden by income or SDI found no passage in our copy establishing the claimed disparity; page numbers were unavailable. (LLM, conf=0.72)

  cites [47] Vos, T. et al. Global burden of 369 diseases and injuries in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet 396, 1204–1222 (2020). sourceExperimental — accuracy not yet measured

In the paper

“The global prevalence of GDM has also steadily increased in the past four decades.”

What the sources say

• Partly supported

  The Screening and Diagnosis section describes an “increasing prevalence of GDM worldwide.” It does not establish that the increase was steady or that it occurred over the past four decades; the Gestational Diabetes Mellitus section gives a current worldwide range, not a historical trend. No page numbers were provided in our copy. (LLM, conf=0.84)

  cites [50] Alejandro, E. U. et al. Gestational diabetes mellitus: a harbinger of the vicious cycle of diabetes. Int. J. Mol. Sci. 21, 5003 (2020). sourceExperimental — accuracy not yet measured

In the paper

“Countries with lower SDI and HDI generally had a greater disease burden of HDP than those with higher SDI and HDI, demonstrated by a higher prevalence, DALYs and death attributable to HDP (Figs. 2–4).”

What the sources say

• ?Could not verify

  Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.

  cites [47] Vos, T. et al. Global burden of 369 diseases and injuries in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet 396, 1204–1222 (2020). sourceExperimental — accuracy not yet measured

In the paper

“Certain ethnic and racial groups have been widely reported to have a disproportionately increased disease burden of maternal CMDs.”

What the sources say

• ?Not checked — no full text of the sourcecites [112] Caughey, A. B., Stotland, N. E., Washington, A. E. & Escobar, G. J. Maternal ethnicity, paternal ethnicity, and parental ethnic discordance: predictors of preeclampsia. Obstet. Gynecol. 106, 156–161 (2005). source
• ?Not checked — no full text of the sourcecites [113] Rao, A. K., Cheng, Y. W. & Caughey, A. B. Perinatal complications among different Asian-American subgroups. Am. J. Obstet. Gynecol. 194, e39–e41 (2006). source
• ?Not checked — no full text of the sourcecites [114] Johnson, J. D. & Louis, J. M. Does race or ethnicity play a role in the origin, pathophysiology, and outcomes of preeclampsia? An expert review of the literature. Am. J. Obstet. Gynecol. 226, S876–S885 (2022). source
• ?Could not verify

  The Methods (Selection of studies; page unavailable) list the risk factors assessed but do not include race or ethnicity. The copy cites a study on ethnicity and obstetric outcomes in its References, but neither that entry nor the searched Results and Discussion passages establish a disproportionate burden of maternal cardiometabolic disorders across ethnic or racial groups. (LLM, conf=0.72)

  cites [94] Bartsch, E., Medcalf, K. E., Park, A. L. & Ray, J. G. Clinical risk factors for pre-eclampsia determined in early pregnancy: systematic review and meta-analysis of large cohort studies. BMJ 353, i1753 (2016). sourceExperimental — accuracy not yet measured
• Supported

  The Abstract reports racial and ethnic differences in the prevalence of maternal hypertensive disorders, chronic hypertension, and diabetes in the US. The Introduction also describes higher risks of hypertension among Black women and gestational diabetes among Hispanic women than among White women. These passages support the broad claim about disproportionate maternal cardiometabolic disease burden. (LLM, conf=0.92)

  cites [115] Bornstein, E., Eliner, Y., Chervenak, F. A. & Grünebaum, A. Racial disparity in pregnancy risks and complications in the US: temporal changes during 2007–2018. J. Clin. Med. 9, 1414 (2020). source
• ?Not checked — no full text of the sourcecites [116] Anderson, N. H., Sadler, L. C., Stewart, A. W., Fyfe, E. M. & McCowan, L. M. Ethnicity, body mass index and risk of pre-eclampsia in a multiethnic New Zealand population. Aust. N. Z. J. Obstet. Gynaecol. 52, 552–558 (2012). source
• Partly supported

  The Background reports that Australian Indigenous women have a 66% greater risk of pregnancy-induced hypertension than non-Indigenous women, supporting a disparity in one maternal cardiometabolic disorder. It does not establish a disproportionate burden across maternal cardiometabolic disorders more broadly. (LLM, conf=0.83)

  cites [117] Campbell, S. K., Lynch, J., Esterman, A. & McDermott, R. Pre-pregnancy predictors of hypertension in pregnancy among Aboriginal and Torres Strait Islander women in north Queensland, Australia; a prospective cohort study. BMC Public. Health 13, 138 (2013). sourceExperimental — accuracy not yet measured
• Partly supported

  The Results (Risk factors for GDM; page unavailable) report higher gestational diabetes risk by maternal region of birth, used as a proxy for ethnicity. The paper supports a disparity for gestational diabetes, but its findings do not establish a disproportionate burden across maternal cardiometabolic disorders more broadly. (LLM, conf=0.84)

  cites [6] Anna, V., van der Ploeg, H. P., Cheung, N. W., Huxley, R. R. & Bauman, A. E. Sociodemographic correlates of the increasing trend in prevalence of gestational diabetes mellitus in a large population of women between 1995 and 2005. Diabetes Care 31, 2288–2293 (2008). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [120] Berkowitz, G. S., Lapinski, R. H., Wein, R. & Lee, D. Race/ethnicity and other risk factors for gestational diabetes. Am. J. Epidemiol. 135, 965–973 (1992). source
• ?Not checked — no full text of the sourcecites [121] Dornhorst, A. et al. High prevalence of gestational diabetes in women from ethnic minority groups. Diabet. Med. 9, 820–825 (1992). source

In the paper

“Racial and ethnic groups with an increased risk of developing GDM include Indigenous Australian, Pacific Islander, South or East Asian, Middle Eastern, Hispanic and African populations6,120–128.”

What the sources say

• Supported

  The Results (Risk factors for GDM; page not specified) report increased GDM risk for women born in every region studied, including South and East Asia and the Pacific, compared with women born in Australia or New Zealand. The Conclusions (page not specified) also report elevated risk for women from the Middle East and Africa and discuss higher risk among Indigenous Australian, Hispanic, and African women. The study uses region of birth as a proxy for ethnicity. (LLM, conf=0.90)

  cites [6] Anna, V., van der Ploeg, H. P., Cheung, N. W., Huxley, R. R. & Bauman, A. E. Sociodemographic correlates of the increasing trend in prevalence of gestational diabetes mellitus in a large population of women between 1995 and 2005. Diabetes Care 31, 2288–2293 (2008). source
• ?Not checked — no full text of the sourcecites [120] Berkowitz, G. S., Lapinski, R. H., Wein, R. & Lee, D. Race/ethnicity and other risk factors for gestational diabetes. Am. J. Epidemiol. 135, 965–973 (1992). source
• ?Not checked — no full text of the sourcecites [121] Dornhorst, A. et al. High prevalence of gestational diabetes in women from ethnic minority groups. Diabet. Med. 9, 820–825 (1992). source
• Partly supported

  The Results (Table 1; page not supplied) report higher GDM prevalence among Hispanics, Asians and Filipinas than among non-Hispanic white women. They do not establish increased risk for Indigenous Australian, other Pacific Islander or Middle Eastern populations, or distinguish South from East Asian populations. African Americans had the lowest reported prevalence, alongside non-Hispanic white women, rather than an increased prevalence. (LLM, conf=0.89)

  cites [122] Hedderson, M. et al. Racial/ethnic disparities in the prevalence of gestational diabetes mellitus by BMI. Diabetes Care 35, 1492–1498 (2012). sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction reports higher GDM risk among Asian, African American and Hispanic women, and higher GDM incidence among women who migrated from Asian and Middle Eastern countries. It does not establish increased GDM risk for Pacific Islanders or Indigenous Australians; the Discussion mentions indigenous populations in the context of diabetes risk after GDM, without identifying Indigenous Australians specifically. (LLM, conf=0.88)

  cites [123] Girgis, C. M., Gunton, J. E. & Cheung, N. The influence of ethnicity on the development of type 2 diabetes mellitus in women with gestational diabetes: a prospective study and review of the literature. ISRN Endocrinol. 2012, 341638 (2012). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [124] Savitz, D. A., Janevic, T. M., Engel, S. M., Kaufman, J. S. & Herring, A. H. Ethnicity and gestational diabetes in New York City, 1995–2003. BJOG 115, 969–978 (2008). source
• ?Not checked — no full text of the sourcecites [125] Pedula, K. L. et al. Ethnic differences in gestational oral glucose screening in a large US population. Ethn. Dis. 19, 414–419 (2009).
• ?Not checked — no full text of the sourcecites [126] Kragelund Nielsen, K., Andersen, G. S., Damm, P. & Andersen, A. N. Gestational diabetes risk in migrants. A nationwide, register-based study of all births in Denmark 2004 to 2015. J. Clin. Endocrinol. Metab. 105, e692–e703 (2020). source
• ?Not checked — no full text of the sourcecites [127] Wan, C. S. et al. Ethnic differences in prevalence, risk factors, and perinatal outcomes of gestational diabetes mellitus: a comparison between immigrant ethnic Chinese women and Australian-born Caucasian women in Australia. J. Diabetes 11, 809–817 (2019). source
• Partly supported

  The Results and Discussion report higher GDM risk among women born in South, East, Southeast, and West/Central Asia than among women born in Australia or New Zealand. The paper does not establish increased GDM risk for Indigenous Australian, Pacific Islander, Hispanic, or African populations; it mentions some of these groups in other contexts. It uses country of birth as a proxy for ethnicity, so its findings also do not establish risk for every Middle Eastern ethnic group. (LLM, conf=0.87)

  cites [128] McDonald, R., Karahalios, A., Le, T. & Said, J. A retrospective analysis of the relationship between ethnicity, body mass index, and the diagnosis of gestational diabetes in women attending an Australian antenatal clinic. Int. J. Endocrinol. 2015, 297420 (2015). sourceExperimental — accuracy not yet measured

In the paper

“By contrast, physical activity before and during pregnancy was reported to be associated with a decreased risk of GDM80,109–111.”

What the sources say

• Supported

  The Results (section 3.4, Physical Activity; page not provided) report reduced odds of GDM associated with physical activity before pregnancy and during early pregnancy. The claim accurately summarizes those associations. (LLM, conf=0.94)

  cites [80] Mijatovic-Vukas, J. et al. Associations of diet and physical activity with risk for gestational diabetes mellitus: a systematic review and meta-analysis. Nutrients 10, 698 (2018). source
• Supported

  The Conclusions report that greater physical activity before pregnancy or during early pregnancy was significantly associated with lower GDM risk. The citing sentence accurately conveys that association; the source specifies early pregnancy for activity during pregnancy. (LLM, conf=0.92)

  cites [109] Tobias, D. K., Zhang, C., van Dam, R. M., Bowers, K. & Hu, F. B. Physical activity before and during pregnancy and risk of gestational diabetes mellitus: a meta-analysis. Diabetes Care 34, 223–229 (2005). source
• ?Not checked — no full text of the sourcecites [110] Zhang, C., Solomon, C. G., Manson, J. E. & Hu, F. B. A prospective study of pregravid physical activity and sedentary behaviors in relation to the risk for gestational diabetes mellitus. Arch. Intern. Med. 166, 543–548 (2006). source
• Supported

  The Discussion reports that higher leisure-time physical activity both before and during pregnancy was associated with lower relative risk of gestational diabetes mellitus. The paper qualifies this by noting that the association for total physical activity during pregnancy was not statistically significant; the citing sentence makes no claim about a specific activity measure or statistical significance. (LLM, conf=0.93)

  cites [111] Aune, D., Sen, A., Henriksen, T., Saugstad, O. D. & Tonstad, S. Physical activity and the risk of gestational diabetes mellitus: a systematic review and dose-response meta-analysis of epidemiological studies. Eur. J. Epidemiol. 31, 967–997 (2016). source

In the paper

“Higher incidence rates of HDP have also been found in Māori, Indigenous Australian, American Indian and Alaskan Native populations94,115–117”

What the sources say

• ?Could not verify

  The paper’s Discussion (> Strengths and limitations; page not provided) discusses pre-eclampsia rates by country income level, not incidence in the named populations. Searches for Māori, Indigenous Australian, American Indian, and Alaskan Native populations found no passage reporting the claimed higher rates; the References’ mention of ethnicity does not establish them. (LLM, conf=0.76)

  cites [94] Bartsch, E., Medcalf, K. E., Park, A. L. & Ray, J. G. Clinical risk factors for pre-eclampsia determined in early pregnancy: systematic review and meta-analysis of large cohort studies. BMJ 353, i1753 (2016). sourceExperimental — accuracy not yet measured
• ?Could not verify

  The Materials and Methods section (page unavailable) says the study included only non-Hispanic White, non-Hispanic Black, and Hispanic women; other racial and ethnic groups were excluded. The Results report HDP prevalence for those three groups, but our copy does not report higher rates among Māori, Indigenous Australian, American Indian, or Alaskan Native populations (searched those population names and related terms). (LLM, conf=0.78)

  cites [115] Bornstein, E., Eliner, Y., Chervenak, F. A. & Grünebaum, A. Racial disparity in pregnancy risks and complications in the US: temporal changes during 2007–2018. J. Clin. Med. 9, 1414 (2020). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [116] Anderson, N. H., Sadler, L. C., Stewart, A. W., Fyfe, E. M. & McCowan, L. M. Ethnicity, body mass index and risk of pre-eclampsia in a multiethnic New Zealand population. Aust. N. Z. J. Obstet. Gynaecol. 52, 552–558 (2012). source
• Partly supported

  The Background reports that Indigenous Australian women have a 66% greater risk of pregnancy-induced hypertension than non-Indigenous Australian women, and the Discussion describes the studied population as having a high prevalence of hypertensive pregnancy. The paper does not address Māori, American Indian, or Alaskan Native populations, so it supports only the Indigenous Australian part of the sentence. (LLM, conf=0.87)

  cites [117] Campbell, S. K., Lynch, J., Esterman, A. & McDermott, R. Pre-pregnancy predictors of hypertension in pregnancy among Aboriginal and Torres Strait Islander women in north Queensland, Australia; a prospective cohort study. BMC Public. Health 13, 138 (2013). sourceExperimental — accuracy not yet measured

In the paper

“but the evidence of the association between smoking during pregnancy and HDP remains controversial101,102.”

What the sources say

• Partly supported

  The Introduction (page unavailable) says evidence is inconsistent about whether quitting smoking during pregnancy changes the apparent reduction in preeclampsia/eclampsia risk. The Discussion (page unavailable) also describes diverse findings from smoking-biomarker studies. These passages support uncertainty about aspects of the association, but do not establish that evidence for smoking during pregnancy and hypertensive disorders as a whole remains controversial. (LLM, conf=0.82)

  cites [101] Kharkova, O. A., Grjibovski, A. M., Krettek, A., Nieboer, E. & Odland, J. Ø. First-trimester smoking cessation in pregnancy did not increase the risk of preeclampsia/eclampsia: a Murmansk County Birth Registry study. PLoS ONE 12, e0179354 (2017). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [102] Yang, Q. et al. Maternal cigarette smoking and the risk of pregnancy-induced hypertension and eclampsia. Int. J. Epidemiol. 35, 288–293 (2005). source

In the paper

“Some genetic variants have been reported to be associated with HDP in women with GDM1, including the MIR146A rs2910164CC131, HNF1A p.I27LTT132 and ACE I/D polymorphism DD133 genotypes.”

What the sources say

• Supported

  The Mechanism and Predictive Markers section reports that the MIR146A rs2910164 CC, HNF1A p.I27L TT, and ACE I/D DD genotypes were significantly more frequent in women with GDM complicated by preeclampsia. Preeclampsia is a hypertensive disorder of pregnancy, so this supports the cited claim. (LLM, conf=0.94)

  cites [1] Yang, Y. & Wu, N. Gestational diabetes mellitus and preeclampsia: correlation and influencing factors. Front. Cardiovasc. Med. 9, 831297 (2022). source
• ?Not checked — no full text of the sourcecites [131] Abo-Elmatty, D. M. & Mehanna, E. T. MIR146A rs2910164 (G/C) polymorphism is associated with incidence of preeclampsia in gestational diabetes patients. Biochem. Genet. 57, 222–233 (2019). source
• ?Not checked — no full text of the sourcecites [132] Beysel, S. et al. HNF1A gene p.I27L is associated with co-existing preeclampsia in gestational diabetes mellitus. Gynecol. Endocrinol. 36, 530–534 (2020). source

In the paper

“indicated a twofold greater risk of reporting pre-eclampsia symptoms in women living in households using biomass and solid fuels than those living in households using clean fuels168.”

What the sources say

• Supported

  The Results section (Effects of cooking smoke on preeclampsia/eclampsia) reports adjusted odds of reporting symptoms 2.21 times higher among women in households using biomass and solid fuels than among those using cleaner fuels. This supports the citing sentence’s approximate twofold comparison. (LLM, conf=0.94)

  cites [168] Agrawal, S. & Yamamoto, S. Effect of indoor air pollution from biomass and solid fuel combustion on symptoms of preeclampsia/eclampsia in Indian women. Indoor Air 25, 341–352 (2015). source

In the paper

“Several studies have shown relationships between perinatal exposure to particulate matter ≤2.5 µm in size (PM2.5) and placental oxidative stress, DNA damage, inflammation, hypercoagulation and thrombosis161–166”

What the sources say

• Partly supported

  The Results and Discussion (page numbers unavailable) report placental inflammation, increased platelets consistent with hypercoagulability, and placental thrombi after PM2.5 exposure in rats. They do not report placental DNA damage. The Results found no significant difference in placental oxidative-stress markers, and the Discussion says oxidative stress did not appear to play a major role. (LLM, conf=0.90)

  cites [161] Liu, Y., Wang, L., Wang, F. & Li, C. Effect of fine particulate matter (PM2.5) on rat placenta pathology and perinatal outcomes. Med. Sci. Monit. 22, 3274–3280 (2016). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [162] Li, Z. et al. Impact of ambient PM(2.5) on adverse birth outcome and potential molecular mechanism. Ecotoxicol. Environ. Saf. 169, 248–254 (2019). source
• Partly supported

  The Introduction and Discussion (page numbers unavailable) report an association between prenatal PM2.5 exposure and placental 3-NTp, a marker of oxidative stress and inflammation. The Introduction places the reported oxidative DNA damage in cord and maternal blood, not the placenta. Our copy does not establish PM2.5 associations with placental hypercoagulation or thrombosis. (LLM, conf=0.88)

  cites [163] Saenen, N. D. et al. Lower placental leptin promoter methylation in association with fine particulate matter air pollution during pregnancy and placental nitrosative stress at birth in the ENVIRONAGE cohort. Environ. Health Perspect. 125, 262–268 (2017). sourceExperimental — accuracy not yet measured
• Partly supported

  The Results and Discussion report that prenatal PM2.5 exposure was associated with an increased placental Alu mutation rate, supporting the DNA-damage component of the claim. The passages do not establish placental oxidative stress, inflammation, hypercoagulation, or thrombosis; the Discussion’s mention of oxidative DNA damage concerns children in another setting, not the placentas studied here. (LLM, conf=0.87)

  cites [164] Neven, K. Y. et al. Placental promoter methylation of DNA repair genes and prenatal exposure to particulate air pollution: an ENVIRONAGE cohort study. Lancet Planet. Health 2, e174–e183 (2018). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [165] Daniel, S. et al. Risk for preeclampsia following exposure to PM(2.5) during pregnancy. Env. Int. 156, 106636 (2021). source
• ?Not checked — no full text of the sourcecites [166] Yi, L., Wei, C. & Fan, W. Fine particulate matter (PM(2.5)), a risk factor of rat gestational diabetes with altered blood glucose and pancreatic GLUT2 expression. Gynecol. Endocrinol. https://doi.org/10.1080/09513590.2017.1318368 (2017). source

In the paper

“The stress of systemic racial disparities, such as poverty, living in racially segregated neighbourhoods, a lack of access to health-care services and experience of discrimination, can all negatively affect the health of women of certain ethnic groups, such as non-Hispanic Black women147.”

What the sources say

• Supported

  The Discussion states that stress from systemic racism, residential segregation, and discrimination negatively affects non-Hispanic Black women's health. It also links neighborhood poverty to harmful lifelong stress and identifies access to health care as a possible contributor to disparities in cardiovascular risk and pregnancy outcomes. (LLM, conf=0.91)

  cites [147] Boakye, E. et al. Nativity-related disparities in preeclampsia and cardiovascular disease risk among a racially diverse cohort of US women. JAMA Netw. Open 4, e2139564 (2021). source

In the paper

“This risk is especially high for individuals with a high severity or postpartum continuation of glucose intolerance and high BMI199–201.”

What the sources say

• Partly supported

  The Discussion (Principal findings; page unavailable) supports a substantially higher later T2DM risk after GDM. It does not establish that risk is especially high with more severe or persistent postpartum glucose intolerance. The Results (Meta-analysis; page unavailable) found no significant association between mean study BMI and the risk estimate, so the high-BMI qualifier is not supported by this analysis. (LLM, conf=0.86)

  cites [199] Vounzoulaki, E. et al. Progression to type 2 diabetes in women with a known history of gestational diabetes: systematic review and meta-analysis. BMJ 369, m1361 (2020). sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction says poorer glucose tolerance during pregnancy has been suggested to increase later T2DM risk, and the Discussion reports higher progression among women with high BMI at follow-up. The cited passages do not establish that glucose intolerance continuing after delivery is a particular risk factor. (LLM, conf=0.85)

  cites [200] Dennison, R. A. et al. The absolute and relative risk of type 2 diabetes after gestational diabetes: a systematic review and meta-analysis of 129 studies. Diabetes Res. Clin. Pract. 171, 108625 (2021). sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion (page not provided) reports a substantially higher later T2DM risk after GDM and says BMI is associated with the prevalence of GDM and T2DM. It does not establish that risk after GDM is especially high with more severe or persistent postpartum glucose intolerance, or specifically with high BMI; its subgroup findings instead highlight maternal age and family history. (LLM, conf=0.78)

  cites [201] You, H., Hu, J., Liu, Y., Luo, B. & Lei, A. Risk of type 2 diabetes mellitus after gestational diabetes mellitus: a systematic review & meta-analysis. Indian J. Med. Res. 154, 62–77 (2021). sourceExperimental — accuracy not yet measured

In the paper

“Women with a history of HDP are more likely to have recurrent HDP in subsequent pregnancies”

What the sources say

• Supported

  The Results passage (labelled “ACCEPTED MANUSCRIPT”; page unavailable) reports that HDP recurred in 20,545 of 99,415 women with a prior affected pregnancy, a recurrence rate of 20.7%. This supports the claim that women with a history of HDP can experience it again in a subsequent pregnancy. (LLM, conf=0.88)

  cites [175] van Oostwaard, M. F. et al. Recurrence of hypertensive disorders of pregnancy: an individual patient data metaanalysis. Am. J. Obstet. Gynecol. 212, 624.e1–624.e17 (2015). source

In the paper

“GDM had similar effects on the risk of women developing future CVDs189,190 (Supplementary Table 4), independent of obesity and at a fairly young age191–194.”

What the sources say

• ?Not checked — no full text of the sourcecites [189] Li, J. et al. Increased risk of cardiovascular disease in women with prior gestational diabetes: a systematic review and meta-analysis. Diabetes Res. Clin. Pract. 140, 324–338 (2018). source
• Partly supported

  The Results report that women with prior GDM had nearly twice the risk of future cardiovascular events, and the discussion says the increased risk is evident in young women within the first decade after delivery (page numbers unavailable). The Results also report an association after pooling adjusted estimates, but adjustment factors varied across studies; the paper does not establish that the association is independent of obesity specifically. (LLM, conf=0.84)

  cites [190] Kramer, C. K., Campbell, S. & Retnakaran, R. Gestational diabetes and the risk of cardiovascular disease in women: a systematic review and meta-analysis. Diabetologia 62, 905–914 (2019). sourceExperimental — accuracy not yet measured
• Partly supported

  The Results section (page unavailable) reports more self-reported CVD among women with prior GDM and a younger age at CVD diagnosis, but the study was limited to women with a family history of type 2 diabetes. Both groups were obese; the reported CVD analyses did not establish that the association was independent of obesity. The study also measured existing CVD rather than following women for future events. (LLM, conf=0.84)

  cites [191] Carr, D. B. et al. Gestational diabetes mellitus increases the risk of cardiovascular disease in women with a family history of type 2 diabetes. Diabetes Care 29, 2078–2083 (2006). sourceExperimental — accuracy not yet measured
• Partly supported

  The Results report that the cohorts had a mean age of 31 and that GDM was associated with subsequent CVD, supporting the young-age portion of the claim. The Methods describe adjustment for subsequent diabetes, while the discussion says clinical cardiovascular risk-factor information was unavailable. The paper therefore does not establish that the association was independent of obesity. (LLM, conf=0.88)

  cites [192] Shah, B. R., Retnakaran, R. & Booth, G. L. Increased risk of cardiovascular disease in young women following gestational diabetes mellitus. Diabetes Care 31, 1668–1669 (2008). sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion reports an association between GDM history and early subclinical atherosclerosis independent of pre-pregnancy obesity, in women followed to ages 38–50. It does not establish an independent effect on future clinical CVD events: the Discussion reports only 13 such events, one in the GDM group, and the atherosclerosis association was found among women who had not developed diabetes or metabolic syndrome. (LLM, conf=0.88)

  cites [193] Gunderson, E. P. et al. History of gestational diabetes mellitus and future risk of atherosclerosis in mid-life: the Coronary Artery Risk Development in Young Adults study. J. Am. Heart Assoc. 3, e000490 (2014). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [194] Chen, L., Mayo, R., Chatry, A. & Hu, G. Gestational diabetes mellitus: its epidemiology and implication beyond pregnancy. Curr. Epidemiol. Rep. 3, 1–11 (2016). source

In the paper

“However, the evidence is inconsistent203.”

What the sources say

• Partly supported

  The Introduction (page unavailable) says studies identifying which women with GDM are more likely to develop later glucose intolerance have produced inconsistent results. It does not say that evidence is inconsistent specifically for early GDM diagnosis; the Results (page unavailable) report no significant association between gestational age at diagnosis and later diabetes risk in this cohort. (LLM, conf=0.82)

  cites [203] Sivaraman, S. C., Vinnamala, S. & Jenkins, D. Gestational diabetes and future risk of diabetes. J. Clin. Med. Res. 5, 92–96 (2013). sourceExperimental — accuracy not yet measured

In the paper

“and this risk increases with decreasing gestational age at delivery in the index pregnancy175.”

What the sources say

• Supported

  The paper’s results summary (Accepted Manuscript) explicitly states that recurrence increased as gestational age at delivery in the index pregnancy decreased. Its discussion of main findings repeats that the chance of recurrence increases with decreasing gestational age at index delivery. (LLM, conf=0.95)

  cites [175] van Oostwaard, M. F. et al. Recurrence of hypertensive disorders of pregnancy: an individual patient data metaanalysis. Am. J. Obstet. Gynecol. 212, 624.e1–624.e17 (2015). source

In the paper

“Some environmental factors, such as passive smoking156 and exposure to persistent organic pollutants (POP) or endocrine disruptors158,159, might contribute to an increased risk of developing GDM.”

What the sources say

• Supported

  The citation to this paper is attached to passive smoking, not to persistent organic pollutants or endocrine disruptors. The Discussion reports that pregnant women exposed to passive smoking at home or at work were more likely to have GDM than those without GDM. (LLM, conf=0.93)

  cites [156] Carroll, X. et al. Socioeconomic, environmental and lifestyle factors associated with gestational diabetes mellitus: a matched case-control study in Beijing, China. Sci. Rep. 8, 8103 (2018). source
• Supported

  The Conclusion (page not available) says that maternal exposure to the persistent organic pollutant PBDE-153 before conception may increase the odds of gestational diabetes. This supports the hedged POP-exposure claim; the separate passive-smoking citation is not attributed to this paper. (LLM, conf=0.90)

  cites [158] Smarr, M. M. et al. Persistent organic pollutants and pregnancy complications. Sci. Total Environ. 551–552, 285–291 (2016). source
• Supported

  The Introduction (page not provided) describes PFOA as an environmental exposure that may disrupt endocrine signaling. The Results and Conclusion (pages not provided) report an association between higher PFOA concentrations and GDM risk and suggest a possible environmental cause. This supports the hedged claim about pollutant or endocrine-disruptor exposure; passive smoking is attached to a different citation. (LLM, conf=0.90)

  cites [159] Zhang, C. et al. A prospective study of prepregnancy serum concentrations of perfluorochemicals and the risk of gestational diabetes. Fertil. Steril. 103, 184–189 (2015). source

In the paper

“Evidence also supports associations between SDOH and diabetes mellitus-related outcomes148.”

What the sources say

• Supported

  The Discussion states directly that evidence supports associations between several social determinants of health and diabetes-related outcomes. The claim closely paraphrases that conclusion. (LLM, conf=0.95)

  cites [148] Hill-Briggs, F. et al. Social determinants of health and diabetes: a scientific review. Diabetes Care 44, 258–279 (2020). source

In the paper

“HDP is also independently associated with a higher risk of T2DM in the future176.”

What the sources say

• Supported

  The Conclusion (p. 10) states that hypertensive disorders of pregnancy are independently associated with a twofold increased risk of subsequent diabetes. The new findings (p. 2) specify that this is type 2 diabetes and that the association is independent of BMI and gestational diabetes. (LLM, conf=0.95)

  cites [176] Zhao, G., Bhatia, D., Jung, F. & Lipscombe, L. Risk of type 2 diabetes mellitus in women with prior hypertensive disorders of pregnancy: a systematic review and meta-analysis. Diabetologia 64, 491–503 (2021). source

In the paper

“Women with GDM have a much higher risk of developing impaired glucose tolerance and T2DM in later life than women with uncomplicated pregnancies7,195–201”

What the sources say

• Partly supported

  The Introduction and ‘Progression from GDM to T2DM’ results report a substantially higher later risk of T2DM in women with GDM than in non-GDM controls. The passages on impaired glucose tolerance concern diagnostic criteria during pregnancy, not a comparative risk of developing it later in life; that part of the claim is unsupported. Page numbers are not available in our copy. (LLM, conf=0.87)

  cites [7] Zhu, Y. & Zhang, C. Prevalence of gestational diabetes and risk of progression to type 2 diabetes: a global perspective. Curr. Diab. Rep. 16, 7 (2016). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [195] Bellamy, L., Casas, J. P., Hingorani, A. D. & Williams, D. Type 2 diabetes mellitus after gestational diabetes: a systematic review and meta-analysis. Lancet 373, 1773–1779 (2009). source
• Partly supported

  The Introduction reports that women with GDM have at least a seven-fold higher risk of later T2DM than women with normoglycaemic pregnancies. The Discussion mentions impaired glucose tolerance as part of a different outcome, but does not establish the claimed higher risk of later impaired glucose tolerance relative to uncomplicated pregnancies. (LLM, conf=0.88)

  cites [196] Li, Z. et al. Incidence rate of type 2 diabetes mellitus after gestational diabetes mellitus: a systematic review and meta-analysis of 170,139 women. J. Diabetes Res. 2020, 3076463 (2020). sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction says that women with GDM can develop type 2 diabetes later in life, and the Discussion (Strengths and limitations) reports an increased risk of future diabetes in women with gestational hyperglycaemia. The paper does not establish the claimed risk of later impaired glucose tolerance or make the stated comparison with women with uncomplicated pregnancies. (LLM, conf=0.86)

  cites [197] Rayanagoudar, G. et al. Quantification of the type 2 diabetes risk in women with gestational diabetes: a systematic review and meta-analysis of 95,750 women. Diabetologia 59, 1403–1411 (2016). sourceExperimental — accuracy not yet measured
• Supported

  The Summary of Findings (section 4.1) reports that women with GDM had a two-fold higher risk of impaired glucose tolerance and a seven-fold higher risk of T2DM later in life than women with normal glucose tolerance during pregnancy. The Results (section 3.3) also report a significantly elevated postpartum T2DM risk. (LLM, conf=0.94)

  cites [198] Benhalima, K., Lens, K., Bosteels, J. & Chantal, M. The risk for glucose intolerance after gestational diabetes mellitus since the introduction of the IADPSG criteria: a systematic review and meta-analysis. J. Clin. Med. 8, 1431 (2019). sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion’s Principal findings report that women with a history of GDM were almost 10 times more likely to develop T2DM than women with a normoglycaemic pregnancy. The paper does not establish the claimed higher risk of later impaired glucose tolerance: its Methods require T2DM to be reported separately from that outcome. (LLM, conf=0.90)

  cites [199] Vounzoulaki, E. et al. Progression to type 2 diabetes in women with a known history of gestational diabetes: systematic review and meta-analysis. BMJ 369, m1361 (2020). sourceExperimental — accuracy not yet measured
• Partly supported

  The Results (Relative risk of T2DM; page not provided) report that women with GDM were 8.3 times more likely to develop T2DM than women with normoglycaemic pregnancies. The Introduction associates GDM with higher long-term risk of glucose intolerance, but does not establish that the risk of specifically impaired glucose tolerance is much higher than in women with uncomplicated pregnancies. (LLM, conf=0.85)

  cites [200] Dennison, R. A. et al. The absolute and relative risk of type 2 diabetes after gestational diabetes: a systematic review and meta-analysis of 129 studies. Diabetes Res. Clin. Pract. 171, 108625 (2021). sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion (page unavailable) reports that women with a history of GDM have nearly nine times the future risk of T2DM compared with women without GDM. The paper does not report a comparable increased risk of impaired glucose tolerance; its references to glucose tolerance concern GDM definitions or postpartum testing. (LLM, conf=0.88)

  cites [201] You, H., Hu, J., Liu, Y., Luo, B. & Lei, A. Risk of type 2 diabetes mellitus after gestational diabetes mellitus: a systematic review & meta-analysis. Indian J. Med. Res. 154, 62–77 (2021). sourceExperimental — accuracy not yet measured

In the paper

“Furthermore, racial residential segregation was associated with higher odds of HDP in areas with higher neighbourhood poverty rates than in those with lower rates146”

What the sources say

• Supported

  The Discussion states that racial residential segregation was associated with higher odds of hypertensive disorder of pregnancy only in areas with higher neighborhood poverty rates. The Results add that the association reversed direction as neighborhood poverty increased; the study concerned non-Hispanic Black women in Chicago. (LLM, conf=0.95)

  cites [146] Mayne, S. L., Yellayi, D., Pool, L. R., Grobman, W. A. & Kershaw, K. N. Racial residential segregation and hypertensive disorder of pregnancy among women in Chicago: analysis of electronic health record data. Am. J. Hypertens. 31, 1221–1227 (2018). source

In the paper

“T2DM is one of the characteristics of patients who are at high risk of severe COVID-19 or death265–268.”

What the sources say

• Supported

  The Introduction identifies diabetes as a common comorbidity in severe COVID-19 and reports higher odds of in-hospital COVID-19 death for people with type 2 diabetes than for those without diagnosed diabetes. The mortality comparison is reported from a companion study, which supports this broad risk statement. (LLM, conf=0.91)

  cites [265] Holman, N. et al. Risk factors for COVID-19-related mortality in people with type 1 and type 2 diabetes in England: a population-based cohort study. Lancet Diabetes Endocrinol. 8, 823–833 (2020). source
• ?Not checked — no full text of the sourcecites [266] Grasselli, G. et al. Baseline characteristics and outcomes of 1591 patients infected with SARS-CoV-2 admitted to ICUs of the Lombardy region, Italy. JAMA 323, 1574–1581 (2020). source
• ?Could not verify

  The main text reports severe outcomes and identifies obesity, male sex, and certain laboratory findings among patients who received invasive ventilation. Searches for diabetes, type 2 diabetes, and T2DM found no passage in our copy linking T2DM to severe COVID-19 or death. (LLM, conf=0.76)

  cites [267] Goyal, P. et al. Clinical characteristics of Covid-19 in New York city. N. Engl. J. Med. 382, 2372–2374 (2020). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [268] Myers, L. C., Parodi, S. M., Escobar, G. J. & Liu, V. X. Characteristics of hospitalized adults with COVID-19 in an integrated health care system in California. JAMA 323, 2195–2198 (2020). source

In the paper

“An overview of Cochrane reviews also found there is insufficient high-quality evidence about the effects of various interventions in GDM246.”

What the sources say

• Supported

  The Authors’ Conclusions (Implications for practice) state that there is insufficient high-quality evidence about relevant health outcomes for many treatment comparisons in women with GDM and their babies. The claim accurately paraphrases that conclusion without asserting that evidence is insufficient for every intervention. (LLM, conf=0.94)

  cites [246] Martis, R. et al. Treatments for women with gestational diabetes mellitus: an overview of Cochrane systematic reviews. Cochrane Database Syst. Rev. 8, CD012327 (2018). source

In the paper

“Neonates exposed to HDP might have higher blood pressure when entering adolescence than neonates from healthy pregnancies205–208.”

What the sources say

• ?Could not verify

  The References section lists a study of blood pressure in 12-year-old children born after maternal preeclampsia, but gives no findings or comparison with children from healthy pregnancies. The Premature Infant section discusses higher offspring blood pressure after other prenatal exposures, not hypertensive disorders of pregnancy. Our copy therefore does not establish the claimed comparison. (LLM, conf=0.70)

  cites [205] Calkins, K. & Devaskar, S. U. Fetal origins of adult disease. Curr. Probl. Pediatr. Adolesc. Health Care 41, 158–176 (2011). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [206] Vatten, L. J. et al. Intrauterine exposure to preeclampsia and adolescent blood pressure, body size, and age at menarche in female offspring. Obstet. Gynecol. 101, 529–533 (2003). source
• ?Not checked — no full text of the sourcecites [207] Tenhola, S., Rahiala, E., Halonen, P., Vanninen, E. & Voutilainen, R. Maternal preeclampsia predicts elevated blood pressure in 12-year-old children: evaluation by ambulatory blood pressure monitoring. Pediatr. Res. 59, 320–324 (2006). source
• ?Not checked — no full text of the sourcecites [208] Hoodbhoy, Z. et al. The impact of maternal preeclampsia and hyperglycemia on the cardiovascular health of the offspring: a systematic review and meta-analysis. Am. J. Perinatol. https://doi.org/10.1055/s-0041-1728823 (2021). source

In the paper

“This finding suggests that a focus only on community-level intervention without facility enhancement is inadequate to improve maternal and neonatal outcomes259.”

What the sources say

• Supported

  The Discussion concludes that community-level intervention without facility enhancement is unlikely to yield the maternal and perinatal improvements needed. The Results also report no effect of the CLIP intervention on maternal or perinatal outcomes, including neonatal outcomes. (LLM, conf=0.93)

  cites [259] von Dadelszen, P. et al. The Community-Level Interventions for Pre-eclampsia (CLIP) cluster randomised trials in Mozambique, Pakistan, and India: an individual participant-level meta-analysis. Lancet 396, 553–563 (2020). source

In the paper

“Among women who received eight or more CLIP contacts (four in Pakistan), the probability of health system and family cost-effectiveness was ≥80%260.”

What the sources say

• Partly supported

  The Abstract Results report a ≥80% probability of cost-effectiveness for women receiving at least eight CLIP contacts, or four in Pakistan. However, the paper specifies that family costs were included only in Pakistan; the claim omits that qualifier and could imply family cost-effectiveness was assessed in all three countries. (LLM, conf=0.90)

  cites [260] Bone, J. N. et al. Economic and cost-effectiveness analysis of the Community-Level Interventions for Pre-eclampsia (CLIP) trials in India, Pakistan and Mozambique. BMJ Glob. Health 6, e004123 (2021). sourceExperimental — accuracy not yet measured

In the paper

“Given that environmental factors such as indoor air pollution168, passive smoking156, POPs, and endocrine disruptors158,159 might contribute to an increased risk of developing either HDP or GDM in pregnancy”

What the sources say

• Supported

  The citation is attached to indoor air pollution, not to passive smoking, POPs, or endocrine disruptors. The Discussion reports an increased risk of symptoms suggestive of preeclampsia/eclampsia among Indian women using biomass and solid fuel for cooking, supporting the hedged claim about a possible contribution to hypertensive disorders of pregnancy. The study assessed reported symptoms rather than confirmed diagnoses. (LLM, conf=0.87)

  cites [168] Agrawal, S. & Yamamoto, S. Effect of indoor air pollution from biomass and solid fuel combustion on symptoms of preeclampsia/eclampsia in Indian women. Indoor Air 25, 341–352 (2015). source
• Supported

  Citation 156 is attached to passive smoking, not to the other listed exposures. The Discussion reports that passive smoking at home and at work was associated with GDM among pregnant women in Beijing, supporting the hedged claim about increased GDM risk. (LLM, conf=0.93)

  cites [156] Carroll, X. et al. Socioeconomic, environmental and lifestyle factors associated with gestational diabetes mellitus: a matched case-control study in Beijing, China. Sci. Rep. 8, 8103 (2018). source
• Supported

  The Conclusion states that preconception exposure to PBDE-153, a persistent organic pollutant, may increase the odds of gestational diabetes. This supports the claim’s POPs-to-GDM link; the sentence’s other environmental factors are not attributed specifically to this source. (LLM, conf=0.89)

  cites [158] Smarr, M. M. et al. Persistent organic pollutants and pregnancy complications. Sci. Total Environ. 551–552, 285–291 (2016). source
• Supported

  The Introduction (page unavailable) describes PFOA as capable of disrupting endocrine signaling. The Results and Conclusion (pages unavailable) report an association between higher PFOA concentrations and increased GDM risk, while cautioning that the finding needs corroboration. This supports the cited possibility that an environmental endocrine-disrupting chemical might contribute to GDM risk; the paper does not address HDP. (LLM, conf=0.88)

  cites [159] Zhang, C. et al. A prospective study of prepregnancy serum concentrations of perfluorochemicals and the risk of gestational diabetes. Fertil. Steril. 103, 184–189 (2015). source

In the paper

“However, the CLIP study did not generate a statistically significant reduction in all-cause maternal and perinatal mortality or morbidity.”

What the sources say

• Supported

  The Discussion states that the CLIP intervention had no effect on the composite of all-cause maternal and perinatal mortality or morbidity compared with usual care. Table 1 in the Results reports a non-significant difference for that primary composite outcome (adjusted OR 1.17, 95% CI 0.90–1.51; p=0.24). (LLM, conf=0.94)

  cites [259] von Dadelszen, P. et al. The Community-Level Interventions for Pre-eclampsia (CLIP) cluster randomised trials in Mozambique, Pakistan, and India: an individual participant-level meta-analysis. Lancet 396, 553–563 (2020). source

In the paper

“In terms of maternal CMDs, it was found that COVID-19 and pre-eclampsia impact perinatal outcomes (such as preterm birth, severe perinatal morbidity and mortality) in an additive fashion264.”

What the sources say

• Supported

  The Comment’s Principal findings state that COVID-19 during pregnancy and preeclampsia increase risks for preterm birth and severe perinatal morbidity and mortality in an additive fashion. The cited sentence closely paraphrases that finding. (LLM, conf=0.95)

  cites [264] Papageorghiou, A. T. et al. Preeclampsia and COVID-19: results from the INTERCOVID prospective longitudinal study. Am. J. Obstet. Gynecol. 225, 289.e1–289.e17 (2021). source

In the paper

“In another Cochrane review248, the average risk reduction from lifestyle interventions on HDP was 0.70 (95% CI 0.40–1.22; four trials, 2,796 women; I2 = 79%; low-quality evidence).”

What the sources say

• Supported

  The review’s maternal primary outcomes section reports an average risk ratio of 0.70 (95% CI 0.40–1.22) for hypertensive disorders of pregnancy, based on four trials and 2,796 women, with I² = 79% and low-quality evidence. The citing sentence calls this a “risk reduction,” but its figures match the reported risk ratio; the review says there was no clear evidence of a difference between groups. (LLM, conf=0.91)

  cites [248] Brown, J. et al. Lifestyle interventions for the treatment of women with gestational diabetes. Cochrane Database Syst. Rev. 5, CD011970 (2017). source

In the paper

“The offspring of women with HDP are reported to be at a greater risk of developing cognitive and psychiatric disorders, such as autism spectrum disorder (ASD), attention-deficit–hyperactivity disorder (ADHD)217–219 or epilepsy during their later life220.”

What the sources say

• Supported

  The Results and Conclusions report increased pooled odds of ASD and ADHD among offspring exposed to hypertensive disorders of pregnancy. Those outcomes are followed by citations 217–219 in the citing sentence; epilepsy is followed by a separate citation, 220, and is not attributed to this paper. (LLM, conf=0.90)

  cites [217] Maher, G. M. et al. Association of hypertensive disorders of pregnancy with risk of neurodevelopmental disorders in offspring: a systematic review and meta-analysis. JAMA Psychiatry 75, 809–819 (2018). source
• Partly supported

  The Main findings (p. 4) report a 32% higher risk of ASD in offspring exposed to pre-eclampsia. That supports the ASD example, but the paper studies pre-eclampsia specifically, not all hypertensive disorders of pregnancy (HDP), and does not establish the ADHD claim. Epilepsy has a separate citation in the citing sentence. (LLM, conf=0.86)

  cites [218] Dachew, B. A., Mamun, A., Maravilla, J. C. & Alati, R. Pre-eclampsia and the risk of autism-spectrum disorder in offspring: meta-analysis. Br. J. Psychiatry 212, 142–147 (2018). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [219] Nahum Sacks, K. et al. Long-term neuropsychiatric morbidity in children exposed prenatally to preeclampsia. Early Hum. Dev. 130, 96–100 (2019). source
• ?Not checked — no full text of the sourcecites [220] Wu, C. S. et al. Preeclampsia and risk for epilepsy in offspring. Pediatrics 122, 1072–1078 (2008). source

In the paper

“Maternal diabetes mellitus, regardless of the type (that is, pre-existing type 1 diabetes mellitus or T2DM, or GDM), has long-term effects on the risk of diabetes mellitus and obesity in offspring172,210–216.”

What the sources say

• Partly supported

  The Offspring Outcomes summary reports increased adiposity and disorders of glucose metabolism in children of mothers with GDM; Childhood Complications also describes higher obesity rates after exposure to diabetes in pregnancy. The paper notes that long-term studies included mothers with some or all types of diabetes, but it does not establish the claimed risks separately for pre-existing type 1 diabetes, pre-existing type 2 diabetes, and GDM. (LLM, conf=0.82)

  cites [172] Szmuilowicz, E. D., Josefson, J. L. & Metzger, B. E. Gestational diabetes mellitus. Endocrinol. Metab. Clin. North. Am. 48, 479–493 (2019). sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [210] Pettitt, D. J., Baird, H. R., Aleck, K. A., Bennett, P. H. & Knowler, W. C. Excessive obesity in offspring of Pima Indian women with diabetes during pregnancy. N. Engl. J. Med. 308, 242–245 (1983). source
• ?Not checked — no full text of the sourcecites [211] Pettitt, D. J., Nelson, R. G., Saad, M. F., Bennett, P. H. & Knowler, W. C. Diabetes and obesity in the offspring of Pima Indian women with diabetes during pregnancy. Diabetes Care 16, 310–314 (1993). source
• Partly supported

  The Introduction (p. 1) reports higher rates of diabetes or pre-diabetes and obesity-related outcomes in offspring of diabetic pregnancies. But the Discussion (p. 7) cautions that evidence by diabetes type is limited, with insufficient data to analyse pre-existing type 2 diabetes; the Abstract (p. 1) also says the BMI association is no longer apparent after adjustment for maternal pre-pregnancy BMI in the limited studies available. The source therefore does not establish long-term effects regardless of maternal diabetes type. (LLM, conf=0.88)

  cites [212] Philipps, L. H. et al. The diabetic pregnancy and offspring BMI in childhood: a systematic review and meta-analysis. Diabetologia 54, 1957–1966 (2011). sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction and Discussion report an association between maternal diabetes during pregnancy and greater offspring BMI or obesity later in life, and the study measured BMI in sons at age 18. The Discussion says the study could not distinguish gestational diabetes from pre-existing type 1 or type 2 diabetes, so it cannot establish an effect for each type. It also did not assess offspring diabetes risk. (LLM, conf=0.88)

  cites [213] Lawlor, D. A., Lichtenstein, P. & Långström, N. Association of maternal diabetes mellitus in pregnancy with offspring adiposity into early adulthood: sibling study in a prospective cohort of 280,866 men from 248,293 families. Circulation 123, 258–265 (2011). sourceExperimental — accuracy not yet measured
• Partly supported

  The Conclusions report increased overweight and abdominal-obesity risk at age 16 among offspring exposed to both gestational diabetes and maternal prepregnancy overweight. They describe similar long-term effects across diabetes types as a postulate, while saying that evidence comparing types is limited. The paper does not assess offspring diabetes risk, and gestational diabetes alone was not associated with increased overweight risk in offspring of normal-weight mothers. (LLM, conf=0.88)

  cites [214] Pirkola, J. et al. Risks of overweight and abdominal obesity at age 16 years associated with prenatal exposures to maternal prepregnancy overweight and gestational diabetes mellitus. Diabetes Care 33, 1115–1121 (2010). sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion (p. 6) reports an association between gestational diabetes and offspring overweight or obesity at ages 9–11, though the estimates were imprecise and attenuated after adjustment for maternal BMI. It also says existing maternal diabetes—mostly presumed type 1—was not associated with later offspring overweight or obesity in this cohort (pp. 6–7). The study does not establish an effect regardless of diabetes type or measure diabetes risk in the offspring. (LLM, conf=0.90)

  cites [215] Lawlor, D. A. et al. Association of existing diabetes, gestational diabetes and glycosuria in pregnancy with macrosomia and offspring body mass index, waist and fat mass in later childhood: findings from a prospective pregnancy cohort. Diabetologia 53, 89–97 (2010). sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction describes a commonly stated association between maternal diabetes exposure and later offspring overweight or obesity, but the Conclusions say the evidence for gestational diabetes is inconclusive. Section 5 cautions that pre-existing and gestational diabetes cannot be assumed to have the same long-term effects. The review does not establish the claimed increased risk of diabetes in offspring. (LLM, conf=0.88)

  cites [216] Kim, S. Y., England, J. L., Sharma, J. A. & Njoroge, T. Gestational diabetes mellitus and risk of childhood overweight and obesity in offspring: a systematic review. Exp. Diabetes Res. 2011, 541308 (2011). sourceExperimental — accuracy not yet measured

In the paper

“The current COVID-19 pandemic has greatly disrupted health service delivery due to lockdown policies, overwhelmed health-care systems and exhausted health-care providers among other effects, such as exacerbation of poverty.”

What the sources say

• ?Could not verify

  The Future directions section discusses transmission-control measures, including travel screening, and protecting health-care providers. It does not address disruption of health service delivery, lockdown policies, overwhelmed health-care systems, or exhausted providers; searches for those terms and paraphrases found no supporting passage. Page numbers were not available in our copy. (LLM, conf=0.74)

  cites [262] Rothan, H. A. & Byrareddy, S. N. The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak. J. Autoimmun. 109, 102433 (2020). sourceExperimental — accuracy not yet measured

In the paper

“A great disparity exists between HICs and LMICs regarding the disease burden of GDM (Table 2).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [53] International Diabetes Federation. IDF Diabetes Atlas 10th edn (IDF, 2021).

In the paper

“Two important maternal cardiometabolic disorders (CMDs), hypertensive disorders in pregnancy (HDP) (including pre-eclampsia) and gestational diabetes mellitus (GDM), result in a large disease burden for pregnant individuals worldwide.”

• Also stated in: § Introduction · plain

  “these two maternal conditions result in a large disease burden for both pregnant individuals and their offspring.”

In the paper

“This diagnostic shift will influence clinical management (for example, increased hospital admission and induction of labour)17.”

What the sources say

• ?Not checked — no full text of the sourcecites [17] Bouter, A. R. & Duvekot, J. J. Evaluation of the clinical impact of the revised ISSHP and ACOG definitions on preeclampsia. Pregnancy Hypertens. 19, 206–211 (2020). source

In the paper

“and psychological stress in women and their families41.”

What the sources say

• ?Not checked — no full text of the sourcecites [41] Kalra, S., Baruah, M. P., Gupta, Y. & Kalra, B. Gestational diabetes: an onomastic opportunity. Lancet Diabetes Endocrinol. 1, 91 (2013). source

In the paper

“The rapid global increase in GDM occurring within the past few decades has created an emerging epidemic in both HICs and LMICs52.”

What the sources say

• ?Not checked — no full text of the sourcecites [52] Guariguata, L., Linnenkamp, U., Beagley, J., Whiting, D. R. & Cho, N. H. Global estimates of the prevalence of hyperglycaemia in pregnancy. Diabetes Res. Clin. Pract. 103, 176–185 (2014). source

In the paper

“Although the debate is still ongoing on these new classification systems, studies published in 2021 revealed that a broad definition of pre-eclampsia could better identify women and babies at risk of adverse outcomes22,23.”

What the sources say

• ?Not checked — no full text of the sourcecites [22] Lai, J., Syngelaki, A., Nicolaides, K. H., von Dadelszen, P. & Magee, L. A. Impact of new definitions of preeclampsia at term on identification of adverse maternal and perinatal outcomes. Am. J. Obstet. Gynecol. 224, e511–e518 (2021). source
• ?Not checked — no full text of the sourcecites [23] Magee, L. A. et al. The impact of pre-eclampsia definitions on the identification of adverse outcome risk in hypertensive pregnancy – analyses from the CHIPS trial (Control of Hypertension in Pregnancy Study). BJOG 128, 1373–1382 (2021). source

In the paper

“However, given different diagnostic criteria for GDM used by different countries, strict cross-country/region comparisons are difficult to interpret (Fig. 6).”

In the paper

“Smoking has been revealed to be a potential protective factor for HDP100”

What the sources say

• ?Not checked — no full text of the sourcecites [100] Wang, J., Yang, W., Xiao, W. & Cao, S. The association between smoking during pregnancy and hypertensive disorders of pregnancy: a systematic review and meta-analysis. Int. J. Gynaecol. Obstet. 157, 31–41 (2022). source

In the paper

“Researchers have found that individuals of African Caribbean origin have a higher risk of developing HDP than white individuals, even after adjusting for markers of social deprivation129.”

What the sources say

• ?Not checked — no full text of the sourcecites [129] O’Gorman, N. et al. Competing risks model in screening for preeclampsia by maternal factors and biomarkers at 11–13 weeks gestation. Am. J. Obstet. Gynecol. 214, 103.e1–103.e12 (2016). source

In the paper

“Inequities in SDOH notably impact disparities in diabetes mellitus risk, diagnosis and outcomes149,150, and diabetes mellitus during pregnancy is no exception151.”

What the sources say

• ?Not checked — no full text of the sourcecites [149] Haire-Joshu, D. & Hill-Briggs, F. The next generation of diabetes translation: a path to health equity. Annu. Rev. Public Health 40, 391–410 (2019). source
• ?Not checked — no full text of the sourcecites [150] Dixon, B., Peña, M. M. & Taveras, E. M. Lifecourse approach to racial/ethnic disparities in childhood obesity. Adv. Nutr. 3, 73–82 (2012). source
• ?Not checked — no full text of the sourcecites [151] Phonyiam, R. & Berry, D. C. Racial and ethnic disparities in health care and health outcomes for pregnant women with diabetes. Nurs. Women’s Health 25, 437–449 (2021). source

In the paper

“HDP was found to mediate the association between racial residential segregation and low birthweight among Black women in New York City, USA145.”

What the sources say

• ?Not checked — no full text of the sourcecites [145] Grady, S. C. & Ramírez, I. J. Mediating medical risk factors in the residential segregation and low birthweight relationship by race in New York City. Health Place. 14, 661–677 (2008). source

In the paper

“Maternal CMDs, such as HDP and GDM, can lead to various obstetric complications such as preterm birth, placental abruption and postpartum haemorrhage33,171.”

What the sources say

• ?Not checked — no full text of the sourcecites [33] Metzger, B. E. et al. Hyperglycemia and adverse pregnancy outcomes. N. Engl. J. Med. 358, 1991–2002 (2008). source
• ?Not checked — no full text of the sourcecites [171] Wong, T., Ross, G. P., Jalaludin, B. B. & Flack, J. R. The clinical significance of overt diabetes in pregnancy. Diabet. Med. 30, 468–474 (2013). source

In the paper

“A systematic review and meta-analysis included 11 studies and found that PM2.5, nitrogen oxides and SO2 exposure increased the risk of GDM167.”

What the sources say

• ?Not checked — no full text of the sourcecites [167] Hu, C. Y. et al. Human epidemiological evidence about the association between air pollution exposure and gestational diabetes mellitus: systematic review and meta-analysis. Env. Res. 180, 108843 (2020). source

In the paper

“In general, the current evidence is highly heterogeneous.”

In the paper

“The diagnosis of GDM early in pregnancy, such as during the first half of pregnancy, might increase the risk of developing diabetes mellitus later in life202.”

What the sources say

• ?Not checked — no full text of the sourcecites [202] Bartha, J. L., Martinez-del-Fresno, P. & Comino-Delgado, R. Postpartum metabolism and autoantibody markers in women with gestational diabetes mellitus diagnosed in early pregnancy. Am. J. Obstet. Gynecol. 184, 965–970 (2001). source

In the paper

“the impact of environmental chemicals (for example, bisphenol A, phthalates and toxic metals) on the development of GDM is not consistent among studies170.”

What the sources say

• ?Not checked — no full text of the sourcecites [170] Robledo, C. A., Romano, M. E. & Alonso-Magdalena, P. Review of current evidence on the impact of environmental chemicals on gestational diabetes mellitus. Curr. Epidemiol. Rep. 3, 51–62 (2016). source

In the paper

“Importantly, these complications might generate long-term health problems for these mothers and their offspring.”

In the paper

“Although study findings have been inconsistent6,143,153–157, poverty and poor living conditions might be associated with the development of CMDs in pregnancy153.”

What the sources say

• ?Not checked — no full text of the sourcecites [153] Bo, S. et al. Low socioeconomic status as a risk factor for gestational diabetes. Diabetes Metab. 28, 139–140 (2002).

In the paper

“To date, very limited evidence exists regarding effective approaches for preventing the development of maternal CMDs and their negative health outcomes.”

In the paper

“The COVID-19 pandemic might therefore generate large negative impacts on this population.”

In the paper

“Available evidence has indicated, in addition to affecting the long-term health of mothers, that maternal CMDs could exert harmful health burdens on their offspring later in life.”

In the paper

“Women with CMDs, such as HDP and GDM, in pregnancy are at a higher risk of adverse perinatal outcomes than those with uncomplicated pregnancies and require more intensive antenatal care.”

In the paper

“Currently, no clear evidence is available of the effectiveness of lifestyle interventions in preventing the development of HDP.”

In the paper

“Two major maternal CMDs, HDP and GDM, are related to substantial short-term and long-term adverse health outcomes for women and their offspring.”

In the paper

“Of note, the role of confounders, mediators and effect modifiers (for example, gestational age at birth, birthweight and SES) were not explored in many of these studies, making it difficult to interpret the current findings.”