Telomere trajectories from early adolescence to adulthood following early institutionalization: Protective effects of foster care in the Bucharest Early Intervention Project

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Previous studies have shown that telomere shortening differs by sex, with males generally having shorter telomeres and a faster rate of decline.

“previous studies have shown that telomere shortening differs by sex (Drury et al., 2012), with males generally having shorter telomeres and a faster rate of decline.”

• cites Drury et al., 2012 sourceDisputed

  The Results (Modification by gender; page unavailable) explicitly report no significant difference in telomere length between boys and girls, contrary to the claim that males generally had shorter telomeres. The sex-related finding concerns how institutional exposure was associated with later telomere length, not a faster rate of shortening in males; the Discussion says the typical rate of telomere change in children is little known. (LLM, conf=0.86)

  Checked by a reasoning model — may be wrong.

  Experimental — accuracy not yet measured

May combine two claims.

People exposed to early life adversity have a higher risk of developing many age-related illnesses at young ages, which shortens the period of life free from chronic disease.

“Individuals exposed to early life adversity are at increased risk of developing a broad spectrum of age-related illnesses at a young age, resulting in shorter health span, referring to the period of life free from chronic disease (Chandan et al., 2020; Hughes et al., 2017).”

• cites Chandan et al., 2020 sourcePartly supported

  The Methods and Results report higher rates of cardiovascular disease, hypertension and type 2 diabetes after childhood maltreatment; the Results give a mean cohort age of 23 at entry. But the study examines maltreatment rather than early-life adversity generally, measures three cardiometabolic conditions rather than a broad spectrum of age-related illnesses, and does not measure disease-free years or health span. No page numbers are available in our copy. (LLM, conf=0.87)

  Experimental — accuracy not yet measured
• cites Hughes et al., 2017 sourcePartly supported

  The Introduction says people with adverse childhood experiences have more physical and mental health problems as adults and greater premature mortality. The Discussion reports that several noncommunicable diseases were substantially more likely among people with at least four ACEs. The paper does not establish that these illnesses develop at a young age or measure a shortened period of life free from chronic disease. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Older adults with a history of childhood adversity have shorter telomeres, which suggests long-term biological consequences.

“Importantly, shorter telomeres have also been observed in older adults with a history of childhood adversity, suggesting long-term biological consequences (Hanssen et al., 2017).”

• cites Hanssen et al., 2017 sourcePartly supported

  The Discussion and Conclusions report an association between childhood psychosocial stressors and shorter telomeres measured in adulthood, and suggest a long-term impact. But participants’ mean age was 42; the paper does not establish the finding specifically for older adults. The indexed passages provide section labels but no page numbers. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

Aging-related processes can accelerate as early as adolescence, contributing to inflammation, metabolic dysfunction, and elevated psychiatric and cardiometabolic risk.

“Acceleration of aging-related processes can emerge as early as adolescence, driving inflammation, metabolic dysfunction, and increased psychiatric and cardiometabolic risk (Henje Blom et al., 2015; Luo et al., 2020; Rasmussen et al., 2020; Slopen et al., 2013; Tang et al., 2020; Widom et al., 2024).”

• cites Henje Blom et al., 2015 sourcePartly supported

  The Discussion (page unavailable) reports shorter telomeres, a marker of cellular aging, in adolescents with major depressive disorder, supporting the point that an aging-related change can be present in adolescence. The Introduction (page unavailable) links cellular-aging markers with psychiatric illness and increased risk of diabetes and cardiovascular disease. The paper does not establish that accelerated aging drives inflammation, metabolic dysfunction, or those risks; it identifies systemic inflammation as a possible mediator for future study. (LLM, conf=0.87)

  Experimental — accuracy not yet measured
• cites Luo et al., 2020 sourcePartly supported

  The Discussion (page unavailable) reports that childhood abuse was associated with greater risk of overweight or obesity at age 19, supporting an adolescent weight-related risk. The paper does not establish accelerated aging-related processes or show that they drive inflammation, metabolic dysfunction, or psychiatric and cardiometabolic risk; its proposed pathway concerns neurocognitive control and weight gain. (LLM, conf=0.78)

  Experimental — accuracy not yet measured
• cites Rasmussen et al., 2020 sourcePartly supported

  The Conclusions report that inflammation associated with childhood stress exposure is apparent by age 18, and the Introduction links early adversity with later physical and mental health problems. The paper does not establish accelerated aging, metabolic dysfunction, or that these processes drive psychiatric and cardiometabolic risk. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Telomeres shorten with each cell division, so average telomere length declines continuously across life.

“Telomeres, protective caps at the ends of chromosomes, shorten with each cell division, resulting in continual decline in average telomere length (TL) across the lifespan (López-Otín et al., 2013).”

• cites López-Otín et al., 2013 sourcePartly supported

  The Telomere Attrition section says most mammalian somatic cells lack telomerase, leading to progressive, cumulative loss of telomere-protective sequences, and that shortening occurs during normal aging. It does not establish that telomeres shorten with every cell division in all cells or that average telomere length declines continuously across the entire lifespan. (LLM, conf=0.82)

  Experimental — accuracy not yet measured

May combine two claims.

Telomere shortening reflects cumulative stress and is strongly associated with early adversity.

“Telomere shortening, a key marker of cellular aging, reflects cumulative stress and is strongly linked to early adversity.”

• cites Coimbra et al., 2017 sourceNot checked — no full text of the source
• cites Drury et al., 2012 sourcePartly supported

  The Results section reports that more time in institutional care was significantly associated with shorter telomeres in middle childhood, supporting a link to this form of early adversity. But the Discussion says telomere length may be a biomarker of adversity and cautions that shortening may reflect a particular aspect of institutional care rather than cumulative psychosocial exposure. The claim states that telomere shortening reflects cumulative stress more definitively than the paper does; page numbers were not available in our copy. (LLM, conf=0.88)

  Experimental — accuracy not yet measured
• cites Humphreys et al., 2016 sourcePartly supported

  The Introduction links shorter telomere length to stress exposure and early adversity, and the Discussion reports significantly greater telomere shortening across childhood in children with a history of institutional care. The paper treats telomere change as a marker of cellular aging, but it does not establish that shortening reflects cumulative stress generally; that part of the claim is stronger than the evidence presented. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Telomere shortening is a key marker of cellular aging.

May combine two claims.

Childhood adversity may speed cellular aging and increase vulnerability to many illnesses at younger ages.

“This indicates that adversity during childhood may accelerate cellular aging and increase susceptibility to a broad spectrum of illnesses at a younger age (Belsky et al., 2017; Colich et al., 2020; Mian et al., 2022).”

• cites Belsky et al., 2017 sourcePartly supported

  The Results report that participants with more adverse childhood experiences showed faster biological aging in their 20s and 30s. The Discussion links early-life adversity to later-life disease and death, but the study measures multi-organ biological aging, not cellular aging, and does not establish greater susceptibility to a broad spectrum of illnesses at younger ages. The indexed passages provide no page numbers. (LLM, conf=0.86)

  Experimental — accuracy not yet measured
• cites Colich et al., 2020 sourceSupported
• cites Mian et al., 2022 sourcePartly supported

  The Abstract (page not provided) says people exposed to adverse childhood experiences show signs of advanced cellular aging as early as childhood and have increased chronic-disease risk. The Introduction (page not provided) says these experiences predispose people to physical and mental diseases. Neither passage establishes that the illnesses occur at younger ages; the paper describes accelerated aging as a potential pathway to poor health later in life. (LLM, conf=0.83)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

The link between early adversity and shorter telomeres is stronger when exposure is closer in time to telomere measurement.

“with larger effects when exposure is closer to telomere measurement (Hanssen et al., 2017).”

• cites Hanssen et al., 2017 sourcePartly supported

  The Abstract reports a trend toward larger effects when less time separates childhood stressors from telomere measurement. However, the Aims and hypotheses section says the authors could not measure that interval directly and used age at measurement as a proxy; the Results report only a trend toward significance (two-tailed P=0.068). The citing sentence presents the pattern more firmly than the analysis supports. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Jopling et al. (2025) demonstrated a developmental cascade whereby early caregiving disruptions predicted delayed pubertal timing, accelerated pubertal tempo, and greater telomere erosion.

“Jopling et al. (2025), using the same BEIP cohort, demonstrated a developmental cascade whereby early caregiving disruptions predicted delayed pubertal timing, accelerated pubertal tempo, and, in turn, greater telomere erosion.”

• cites Jopling et al., 2025 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing).

Parental responsiveness may have protective benefits on telomere shortening among high-risk children aged 3.9-6.5 years with a history of early life stress.

“parental responsiveness may have protective benefits on telomere shortening among high-risk children (ages between 3.9–6.5y) who have a history of early life stress (Asok et al., 2013)”

• cites Asok et al., 2013 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing).

Higher quality parental care is associated with longer TL in young adults aged 20-29 years.

“higher quality parental care is associated with longer TL in young adults (ages between 20–29y) (Enokido et al., 2014)”

• cites Enokido et al., 2014 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing).

In a more recent study with the cohort, frequent disruptions in caregiving during childhood, often higher among those receiving institutional care, predicted greater telomere attrition, partly through accelerated pubertal development.

“In a more recent study with the cohort, frequent disruptions in caregiving during childhood, often higher among those receiving institutional care, also predicted greater telomere attrition, partly through accelerated pubertal development (Jopling et al., 2025).”

• cites Jopling et al., 2025 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Accelerated telomere shortening is proposed to arise from oxidative stress and chronic inflammation, both of which are strongly involved in cardiometabolic disease.

“In this context, accelerative TL shortening is suggested to be a result from oxidative stress and chronic inflammation, both of which are strongly implicated in the development of cardiometabolic disease (Jiang et al., 2024; Sverdlov et al., 2016).”

• cites Jiang et al., 2024 sourcePartly supported

  The Discussion (page unavailable) links telomere shortening in type 2 diabetes to pathological changes that could contribute to cardiometabolic multimorbidity. It does not propose that oxidative stress or chronic inflammation causes accelerated telomere shortening, or discuss those mechanisms in the cited passage. (LLM, conf=0.82)

  Experimental — accuracy not yet measured
• cites Sverdlov et al., 2016 sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

A prior study on BEIP participants found that those who remained institutionalized showed blunted stress reactivity, while those randomized to foster care showed normalization of HPA responses.

“a prior study on stress response among BEIP participants found that those who remained institutionalized showed patterns of blunted stress reactivity which might lead to heightened risk for multiple physical and mental health problems, whereas those who were randomized into foster care showed normalization of HPA responses (McLaughlin et al., 2015)”

• cites McLaughlin et al., 2015 sourcePartly supported

  The Discussion describes normalization of HPA-axis responses in foster-care children relative to those who remained in institutional care, and the Results report blunted stress responses in the latter group. However, the Results also report that foster-care children still had blunted cortisol reactivity compared with never-institutionalized children; the Discussion says the HPA intervention effect was evident for children placed before 24 months. The claim omits those limits on normalization. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Our results confirm that TL declines with age, supporting its role as a marker of cellular aging.

“In line with prior studies, our results confirm that TL declines with age, supporting its role as a marker of cellular aging (López-Otín et al., 2013).”

• cites López-Otín et al., 2013 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing).

A recent meta-analysis found that early exposure to a dysfunctional family environment is associated with shorter TL.

“a recent meta-analysis on the association between childhood exposure to maltreatment, focusing on family violence, and TL found that early exposure to a dysfunctional family environment is associated with shorter TL (Chen et al., 2022)”

• cites Chen et al., 2022 sourceSupported

May combine two claims.

In an earlier BEIP analysis, sex modified the main effect between institutional care and telomere length: institutional care earlier in life (at baseline) was more strongly linked to shorter telomeres in girls, whereas institutional care later (at 54 months) was more strongly linked to shorter telomeres in boys.

“In an earlier BEIP analysis, sex modified the main effect between institutional care and telomere length; institutional care earlier in life (at baseline) was more strongly linked to shorter telomeres in girls, whereas institutional care later (at 54 months) was more strongly linked to shorter telomeres in boys (Drury et al., 2012).”

• cites Drury et al., 2012 sourceSupported

Classified as probably not a substantial claim.

Treatment group differences in TL observed during adolescence and into young adulthood in this study may reflect novel emerging differences of the buffering effect of early parental care.

“It is notable that the treatment group differences in TL, observed during adolescence and into young adulthood, in this current study may reflect novel emerging differences of the buffering effect of early parental care, as suggested by earlier research in BEIP (Wade et al., 2023).”

• cites Wade et al., 2023 sourceSupported

May combine two claims.

Foster care, compared with institutional care, is associated with better developmental outcomes and improved physical and mental health in children.

“Receiving foster care, compared to institutional care, has been associated with better developmental outcomes and improved physical and mental health in children (Bos et al., 2011; van Ijzendoorn et al., 2020).”

• cites Bos et al., 2011 sourcePartly supported

  The Conclusions and Foster Care Intervention results report better attachment, positive affect, and some mental-health outcomes for young children placed in foster care rather than remaining in institutions. The Study Design says physical growth was assessed, but the passages found do not report improved physical health; the paper also found no difference in externalizing disorders. (LLM, conf=0.87)

  Experimental — accuracy not yet measured
• cites van Ijzendoorn et al., 2020 sourcePartly supported

  The Summary and the comparison with the Bucharest Early Intervention Project report better growth and cognitive outcomes for children placed in foster care rather than continuing institutional care. The paper does not establish improvement across physical and mental health generally: its meta-analytical discussion says recovery in socioemotional problems was largely absent and that too few studies assessed health after deinstitutionalisation. (LLM, conf=0.87)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

In 105 young adults with a history of childhood maltreatment, different levels of parental care correlated with TL, with 'affectionless control' parenting style showing the strongest negative association with adult TL.

“Another study of 105 young adults with a history of childhood maltreatment found a correlation between different levels of parental care and TL, where ‘affectionless control’ parenting style, low care and high overprotection, showed the strongest negative association with adult TL (Pesca et al., 2025).”

• cites Pesca et al., 2025 sourcePartly supported

  The Participants section reports 105 young adults, and the Results and Discussion report an association between parental care and telomere length, with affectionless control most associated with shortening. But the 105 participants were not all described as having childhood maltreatment: the Results compare participants who experienced maltreatment with controls. The claim incorrectly applies that history to the entire sample. (LLM, conf=0.90)

  Experimental — accuracy not yet measured

May combine two claims.

Early neglect can compound normative developmental risks, leading to greater telomere shortening and increased long-term health risks.

“early neglect can compound these effects, leading to even greater telomere shortening and increased long-term health risks (Wade et al., 2020).”

• cites Wade et al., 2020 sourcePartly supported

  The Introduction (page not provided) reports that children exposed to profound psychosocial deprivation showed accelerated telomere shortening compared with never-institutionalized children, beyond the natural shortening it describes. The Discussion (page not provided) links telomere erosion to morbidity and mortality, but treats downstream health effects as plausible and in need of further research; it does not establish that early neglect leads to increased long-term health risks. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

The developmental period of adolescence to young adulthood (ages 12-25) is marked by rapid biological, psychological, and social changes, making young people especially sensitive to environmental influences and stress.

“The developmental period of adolescence to young adulthood (ages 12–25) (Jaworska & MacQueen, 2015) is marked by rapid biological, psychological, and social changes, making young people especially sensitive to environmental influences and stress (e.g., depression, anxiety, loneliness) (Danneel et al., 2019).”

• cites Jaworska & MacQueen, 2015 sourceSupported
• cites Danneel et al., 2019 sourcePartly supported

  The Abstract (page not given) says adolescents are particularly vulnerable to loneliness, social anxiety symptoms, and depressive symptoms, supporting the examples attached to the Danneel et al. citation. It does not say that rapid biological, psychological, and social changes make young people more sensitive to environmental influences or stress. The ages 12–25 are attached to a different citation in the citing sentence. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

May combine two claims.

Telomere trajectories were not significantly associated with the cardiometabolic composite score (β = −0.027, 95% CI [−0.131, 0.077]) or the odds of metabolic syndrome (OR = 1.072, 95% CI [0.606, 1.824]).

“Telomere trajectories were not significantly associated with either our cardiometabolic composite score (β = −0.027, 95% CI [−0.131, 0.077]) or the odds of metabolic syndrome (OR = 1.072, 95% CI [0.606, 1.824]).”

May combine two claims.

In FCG versus CAUG sex-stratified analyses, effect sizes were consistent with the main analysis, but differences between declines in TL for treatment groups were not significant (Males: β = 0.015, 95% CI [−0.004, 0.035]; Females: β = 0.014, 95% CI [−0.006 0.035]).

“Results for males and females in the FCG vs CAUG analyses were consistent in their effect sizes with the main analysis, however the differences between the declines in TL for the treatment groups were not significant, likely a result of smaller sample sizes (Males: β = 0.015, 95% CI [−0.004, 0.035]; Females: β = 0.014, 95% CI [−0.006 0.035]).”

Probably not a substantial claim: may not pass S3 (load-bearing).

The AUC of the covariate-only model was 0.714 and increased to 0.715 with the addition of telomere trajectory.

“The AUC of the covariate-only model was 0.714 and with the addition of telomere trajectory, it increased to 0.715, suggesting that its inclusion marginally improved the predictive accuracy of the model.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

For the EIG versus NIG model, the marginal R2 for fixed effects was 0.096 and the conditional R2 was 0.494.

“The marginal R2 for the fixed effects was 0.096, and the conditional R2 was 0.494.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

For the EIG versus NIG analysis, AIC and R-squared indicated a random slope model was the best fit, and results were consistent with a random intercept model, which BIC indicated was best.

“AIC and R-Squared indicated a random slope model was the best fit for the EIG vs. NIG analysis; results for this analysis were consistent when using a random intercept model, which BIC indicated was the best fit.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Male sex was associated with significantly shorter TL (β = −0.09; 95% CI [−0.179, −0.001]; p=0.047).

“Male sex was associated with significantly shorter TL (β = −0.09; 95% CI [−0.179, −0.001]; p=0.047).”

May combine two claims.

There were no significant differences in within-person variability in TL by institutional status; the ratio comparing NIG versus EIG was 0.866 (95% CI [0.70, 1.072]).

“We also did not observe significant differences in within-person variability in TL by institutional status; the ratio comparing the within-person variability in TL in NIG versus EIG was 0.866 (95% CI [0.70, 1.072]).”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims. The quote only partly states this claim.

For the FCG versus CAUG model, the marginal R2 for fixed effects was 0.097 and the conditional R2 was 0.343.

“The marginal R2 for the fixed effects was 0.097, and the conditional R2 was 0.343.”

Probably not a substantial claim: may not pass S3 (load-bearing).

For the FCG versus CAUG analysis, a random intercept model was the best fit according to both AIC and BIC.

“A random intercept model was the best fit for the FCG vs CAUG analysis according to both AIC and BIC.”

Probably not a substantial claim: may not pass S3 (load-bearing).

The ICC for the EIG versus NIG model was 0.44, indicating that 44% of the variance in TL was attributable to between-subject differences.

“In terms of model fit, the intra-class correlation coefficient (ICC) was 0.44, suggesting that 44% of the variance in the TL was attributable to between-subject differences.”

May combine two claims.

In EIG versus NIG sex-stratified analyses, both institutionalization groups experienced declines in TL, and the interaction between institutionalization status and age was not significant.

“For the EIG vs NIG analyses, we observed that for males and females, both institutionalization groups experienced declines in TL over the study period, and the interaction term between institutionalization status and age was not significant.”

May combine two claims.

Age-related differences in TL between treatment groups were primarily driven by differences at ages 12, 14, and 22, with FCG initially having shorter TL but shortening at a slower rate at ages 14 and 22.

“Age-related differences in TL between treatment groups were primarily driven by differences at ages 12, 14, and 22, with those in the FCG group initially having shorter TL but shortened at a slower rate at ages 14 and 22 (Supplementary Table 4).”

Probably not a substantial claim: may not pass S3 (load-bearing). The quote only partly states this claim.

The ICC for the FCG versus CAUG model was 0.27, indicating that 27% of the variance in TL was attributable to between-subject variability.

“The ICC for this model was 0.27, indicating that 27% of the variance in TL was attributable to between-subject variability.”

May combine two claims.

Increased percentage of time spent in institutional care was linked to stronger age-related telomere declines, but not significantly (β = −0.0002, 95% CI [−0.0005, 0.00001]).

“We observed that increased time (as a percentage) spent in institutional care was linked to stronger age-related telomere declines, although not significantly (β = −0.0002, 95% CI [−0.0005, 0.00001]).”

Probably not a substantial claim: may not pass S3 (load-bearing).

Sex-stratified models did not diverge from the main analysis results.

“In general, we did not observe divergence from the main analysis results in sex-stratified models.”

May combine two claims.

The study did not find evidence that the rate of telomere decline over a 10-year period was associated with or could predict cardiometabolic health in early adulthood.

“We did not find evidence that the rate of telomere decline over a 10-year period was associated with or could predict cardiometabolic health in early adulthood.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Our sex-stratified analysis did not identify significant differences, likely due to limited statistical power.

“However, our sex-stratified analysis did not identify significant differences, likely due to limited statistical power.”

May combine two claims.

BEIP is the only randomized controlled trial of foster care as an alternative to institutional care and has followed participants from infancy into young adulthood.

“The Bucharest Early Intervention Project (BEIP), the only randomized controlled trial (RCT) of foster care as an alternative to institutional care, has followed participants from infancy into young adulthood (Zeanah et al., 2003).”

• cites Zeanah et al., 2003 sourceNot checked — no full text of the source

Classified as probably not a substantial claim. May combine two claims.

Less is known about how the rate of telomere shortening from early adolescence to adulthood differs between foster care and institutional care, or the extent to which telomere shortening across adolescence to young adulthood predicts early markers of physical well-being such as cardiometabolic health.

“However, less is known about how the rate of telomere shortening from early adolescence to adulthood differs between those in foster care and those who remain in institutional care, or the extent to which telomere shortening across adolescence to young adulthood predicts early markers of physical well-being, such as cardiometabolic health.”

May combine two claims.

Placement in high-quality foster care may help preserve TL over time in previously institutionalized children, suggesting a buffering effect against accelerated cellular aging.

“Our findings demonstrate that placement in high-quality foster care may help preserve TL over time in previously institutionalized children, suggesting a buffering effect against accelerated cellular aging.”

Probably not a substantial claim: may not pass S3 (load-bearing).

A plausible mechanism linking childhood maltreatment to telomere shortening includes HPA-axis dysregulation and greater cortisol reactivity.

“A plausible mechanism behind this includes dysregulation of the hypothalamic-pituitary-adrenocortical (HPA)-axis and thereby greater cortisol reactivity after been exposed to childhood maltreatment (Danese & McEwen, 2012; Heim et al., 2000).”

• cites Danese & McEwen, 2012 sourceNot checked — no full text of the source
• cites Heim et al., 2000 sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

Samples that failed to amplify or had unacceptably high CVs on two additional reruns were removed from analysis.

“Samples that failed to amplify or had unacceptably high CVs on two additional reruns were removed from analysis (1.70%).”

Probably not a substantial claim: may not pass S3 (load-bearing).

The cardiometabolic health models adjusted for treatment group, institutionalization status, sex, and ethnicity (Roma or non-Roma).

“These models controlled for treatment group and institutionalization status, sex, and ethnicity (Roma or non-Roma).”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The average intraplate CV was 3.85% and the average interplate CV was 2.12%.

“The average intraplate CV was 3.85% and the average interplate CV for samples was 2.12%.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Acceptable PCR efficiency criteria for telomere and albumin reactions were 90-110%, and values must not vary by more than 10% on the same plate.

“Acceptable PCR efficiency criteria for telomere and albumin reactions were 90–110%, and the values must not vary by more than 10% on the same plate.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

All time points from the same individual were required to pass quality control in the same assay; if one sample failed, all related samples were repeated.

“In addition, all time points from the same individual were required to pass quality control in the same assay; if one sample did not pass, all related samples were repeated.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Samples with unacceptably high coefficients of variation (intraplate CV >10% or interplate CV >5%) were repeated.

“Samples with unacceptably high CVs (intraplate CV > 10% OR interplate CV >5%) were repeated (25.48%).”

Classified as probably not a substantial claim.

All time points from a single individual were run in the same assay to reduce batch or plate effects on telomere length.

“All time points from a single individual were run in the same assay to decrease batch or plate effects.”

Probably not a substantial claim: may not pass S3 (load-bearing).

BEIP participants randomized to foster care have shown catch-up growth resulting in accelerated BMI and waist circumference in young adulthood.

“those randomized into foster care have been characterized by catch-up growth resulting in accelerative body mass index (BMI) and waist circumference in young adulthood (results under review).”

• cites results under reviewNot matched

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

Probably not a substantial claim: may not pass S3 (load-bearing).

Sensitivity analyses using individual linear models and a random slope model with full covariate adjustment produced consistent results for the telomere trajectory construction.

“Results were consistent with the following sensitivity analyses to construct the trajectories: 1) running one linear model for each individual and 2) using a random slope model with full covariate adjustment, while the models at age 22 contained only this adjusted trajectory.”

May combine two claims.

A random selection of samples (n=58; 12.53%) was reassessed to quantify reproducibility of T/S ratio estimates using the intraclass correlation coefficient, yielding ICC = 0.909, indicating excellent reliability.

“A random selection of samples (n=58; 12.53%) was reassessed for the explicit purposes of quantifying the overall reproducibility of T/S ratio estimates using the intraclass correlation coefficient (ICC). The resulting estimate was ICC = 0.909, indicating excellent reliability.”

Probably not a substantial claim: may not pass S3 (load-bearing).

All models adjusted for sex and ethnicity (Roma or non-Roma).

“All models adjusted for sex and ethnicity (Roma or non-Roma).”

May combine two claims.

Potential DNA degradation over time may bias telomere length estimates, and because DNA storage duration was correlated with participant age, the study could not adjust for this factor as a separate covariate.

“Potential DNA degradation over time may bias telomere length estimates, and because DNA storage duration was correlated with participant age in our cohort, we were unable to adjust for this factor as a separate covariate”

May combine two claims.

The reported effect sizes were small in magnitude, and the study cannot rule out that these may represent null associations.

“However, our reported effect sizes were small in magnitude, and we cannot rule out that these may represent null associations.”

May combine two claims.

The sample size is relatively small, which may have reduced statistical power and limited the ability to detect subtle effects of changes in telomere shortening.

“Second, our sample size is relatively small, which may have reduced statistical power and limited the ability to detect subtle effects of changes in telomere shortening.”

Probably not a substantial claim: may not pass S3 (load-bearing).

According to stress sensitization theory, early adversity can leave a lasting biological signature.

“according to the stress sensitization theory, such early adversity can leave a lasting biological signature (Hammen et al., 2000; Post, 1992).”

• cites Hammen et al., 2000 sourceNot checked — no full text of the source
• cites Post, 1992 sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

Potential seasonal effects on telomere length remain unmeasured.

“In addition, potential seasonal effects on telomere length remain unmeasured; this is an important limitation”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Participants had an average of 2.8 TL measurements, and DNA samples meeting quality control standards were not available for all participants at every time point.

“although participants in this study had an average of 2.8 TL measurements, DNA samples meeting quality control standards were not available for all participants at every time point due to variability in sample quality over the course of 20 years and participant involvement throughout the study.”

Classified as probably not a substantial claim. May combine two claims.

This study stands out by its robust RCT design investigating early deprivation and effects of randomization into foster care, over two decades of follow-up, and repeated TL measurements spanning adolescence to adulthood.

“Notwithstanding these limitations, this study stands out by its robust RCT design investigating early deprivation and the effects of randomization into foster care, over two decades of follow-up, and repeated TL measurements spanning the critical developmental period from adolescence to adulthood.”

Probably not a substantial claim: may not pass S3 (load-bearing).

In females, longer telomere length may be explained by sex hormones' effects on telomerase expression, such as an estrogen response element in the telomerase gene regulatory region providing protection against age-related telomere shortening until menopause.

“In females, longer telomere length may be explained by the effects of sex hormones on telomerase expression. For example, the presence of an estrogen response element in the regulatory region of the telomerase gene, which provide females with some protection against age-related telomere shortening until menopause (Chico-Sordo et al., 2021).”

• cites Chico-Sordo et al., 2021 sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

Inclusion of high-quality biological data enabled calculation of a comprehensive metabolic score as a proxy for cardiometabolic health, strengthening reliability of findings.

“Additionally, the inclusion of high-quality biological data enabled us to calculate a comprehensive metabolic score as a proxy for cardiometabolic health, collectively strengthening the reliability of our findings.”