22 research outputs found

    Participant characteristics.

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    <p><sup>a</sup> means and standard deviations are reported.</p><p><sup>b</sup> age at the time of the interview.</p><p>Participant characteristics.</p

    Stress increases the risk of type 2 diabetes onset in women: A 12-year longitudinal study using causal modelling

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    <div><p>Background</p><p>Type 2 diabetes is associated with significant morbidity and mortality. Modifiable risk factors have been found to contribute up to 60% of type 2 diabetes risk. However, type 2 diabetes continues to rise despite implementation of interventions based on traditional risk factors. There is a clear need to identify additional risk factors for chronic disease prevention. The aim of this study was to examine the relationship between perceived stress and type 2 diabetes onset, and partition the estimates into direct and indirect effects.</p><p>Methods and findings</p><p>Women born in 1946–1951 (n = 12,844) completed surveys for the Australian Longitudinal Study on Women’s Health in 1998, 2001, 2004, 2007 and 2010. The total causal effect was estimated using logistic regression and marginal structural modelling. Controlled direct effects were estimated through conditioning in the regression model. A graded association was found between perceived stress and all mediators in the multivariate time lag analyses. A significant association was found between hypertension, as well as physical activity and body mass index, and diabetes, but not smoking or diet quality. Moderate/high stress levels were associated with a 2.3-fold increase in the odds of diabetes three years later, for the total estimated effect. Results were only slightly attenuated when the direct and indirect effects of perceived stress on diabetes were partitioned, with the mediators only explaining 10–20% of the excess variation in diabetes.</p><p>Conclusions</p><p>Perceived stress is a strong risk factor for type 2 diabetes. The majority of the effect estimate of stress on diabetes risk is not mediated by the traditional risk factors of hypertension, physical activity, smoking, diet quality, and body mass index. This gives a new pathway for diabetes prevention trials and clinical practice.</p></div

    Longitudinal associations between the hypothesised mediators and type 2 diabetes, using a time lag approach.

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    <p>Each analysis is adjusted for the potential confounders of SES (measured by educational attainment) and age, as well as secular trends (time by survey). The aim here is to identify the relationship between each mediator and the outcome of type 2 diabetes. The combined effect of all the mediators is modelled in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0172126#pone.0172126.t004" target="_blank">Table 4</a>.</p

    Comparison of sociodemographic characteristics between women with incident type 2 diabetes compared with women without a diagnosis of type 2 diabetes over the observation period.

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    <p>Comparison of sociodemographic characteristics between women with incident type 2 diabetes compared with women without a diagnosis of type 2 diabetes over the observation period.</p

    Longitudinal associations between perceived stress and hypothesised mediators using a time lag approach.

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    <p>Each analysis is adjusted for the potential confounders of SES (measured by educational attainment) and age, as well as secular trends (time by survey).</p

    Total causal effects of perceived stress on type 2 diabetes using a time lag approach (assuming physical activity as a time varying mediator).<sup>a</sup><sup>,</sup><sup>b</sup>

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    <p>Total causal effects of perceived stress on type 2 diabetes using a time lag approach (assuming physical activity as a time varying mediator).<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0172126#t004fn001" target="_blank"><sup>a</sup></a><sup>,</sup><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0172126#t004fn002" target="_blank"><sup>b</sup></a></p

    Simplified Directed Acyclic Graph showing hypothesised causal mechanism between perceived stress and type 2 diabetes taking into account potential confounders and mediators.

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    <p>According to the DAG, perceived stress (measured at Survey 2) may be mediated through physical activity, diet quality (or BMI instead of diet), hypertension and smoking status and confounded by age and socioeconomic status (i.e. highest educational qualification).</p

    <i>Sox10</i> is required by bulb melanocytes postnatally.

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    <p>(A–B) <i>Sox10<sup>fl/fl</sup></i> (<i>fl/fl; +/+</i>) and <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> (<i>fl/fl; Cre/+</i>) pups treated with TAM by IP injection to the lactating mother on P0–3 display variegated hypopigmentation on the belly and back and exhibit a white head spot upon the emergence of the morphogenetic coat (P10 shown here, n>5). (C) Number of PAX3<sup>+</sup> melanocytes per hair bulb in skins harvested from these mice at P10 are significantly decreased in <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> animals compared to similarly-treated <i>Sox10<sup>fl/fl</sup></i> animals (*p = 0.002). (D–E) Adult <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> mice treated with TAM by IP injection on 0–3dpp exhibit white hairs within the plucked region upon hair regrowth that is not visible in similarly treated <i>Sox10<sup>fl/fl</sup></i> mice (brackets indicate plucked region, lower image is a magnification of plucked region). (F) Number of PAX3<sup>+</sup> melanocytes per hair bulb in skins harvested from similarly-treated mice at 7dpp are significantly decreased in <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> animals compared to <i>Sox10<sup>fl/fl</sup></i> animals (*p = 0.001). (G–H) Fluorescent and corresponding brightfield images of hair bulbs from mice described in D–E. Arrows and arrowheads indicate PAX3<sup>+</sup>/SOX10<sup>+</sup> and PAX3<sup>+</sup>/SOX10<sup>−</sup> melanocytes, respectively. (I) Distribution of melanocytes double-labeled for PAX3 and SOX10 within pigmented (gray) and non-pigmented (white) hair bulbs in skins from <i>Sox10<sup>fl/fl</sup></i> (n = 3) and <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> (n = 4) harvested on 7dpp from mice treated with TAM on 0–3dpp (*p<0.006).</p

    LPP melanocytes are reduced in <i>Tg(DctSox10)</i> homozygotes during hair morphogenesis.

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    <p>(A) Brightfield images of hairs in <i>Tg(DctSox10)</i> and <i>+/+</i> littermates at P2. (B) Number of DCT<sup>+</sup> melanocytes within the LPP of hairs at P2 (stage 6 hairs) and P7/8. At both time points, LPP melanocytes per hair are reduced in <i>Tg(DctSox10)/Tg(DctSox10)</i> compared to <i>Tg(DctSox10)/+</i> and <i>+/+</i> mice (*p<0.017). (C, D) Quantitative immunohistochemical analysis of stage 6 hairs from P2 skins for DCT and TRP1, or DCT and KIT. The population of DCT<sup>+</sup>/TRP1<sup>+</sup> cells is significantly reduced in <i>Tg(DctSox10)/Tg(DctSox10)</i> in comparison to <i>Tg(DctSox10)/+</i> and +/+ mice (*p<0.008). <i>Tg(DctSox10)</i> also causes a switch in KIT intensity from KIT<sup>hi</sup> in wild type to KIT<sup>low</sup> in <i>Tg(DctSox10)</i> animals (*KIT<sup>lo</sup> and **KIT<sup>hi</sup> comparisons made between +/+ and <i>Tg(DctSox10)/+</i> or <i>+/+</i> and <i>Tg(DctSox10)/Tg(DctSox10)</i>; p<0.005).</p

    <i>Sox10</i> is required by LPP melanocytes postnatally.

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    <p>(A) Number of KIT<sup>+</sup> LPP melanocytes within hairs from <i>Sox10<sup>fl/fl</sup></i> (<i>fl/fl; +/+</i>) and <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> (<i>fl/fl; Cre/+</i>) mice. P0–3/P10 indicates skins harvested from pups on P10 that were maintained by lactating mothers that were IP injected with TAM on P0–3. 0–3dpp/7dpp indicates skins harvested from adult mice on 7dpp after IP injections of TAM on 0–3dpp. (B) White hairs remain visible in adult <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> mice that were treated with TAM by IP injection on 0–3dpp, allowed for complete hair regeneration, replucked and allowed for a second round of hair regrowth (brackets indicate plucked/replucked region, lower image is a magnification of plucked region; mouse in 2E and 3B are the same, imaged prior to and after replucking). (C) Number of PAX3<sup>+</sup> bulb melanocytes within hairs from <i>Sox10<sup>fl/fl</sup></i> and <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> mice treated as described in B but harvested on 7dpp after replucking (0–3dpp/7dpp repluck). (D) Distribution of melanocytes double-labeled for PAX3 and SOX10 within pigmented (gray) and non-pigmented (white) hair bulbs in skins from <i>Sox10<sup>fl/fl</sup></i> (n = 3) and <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> (n = 3) mice treated as described in B but harvested on 7dpp after replucking (*p<0.002). (E) Persistent hair graying is visible in <i>Sox10<sup>fl/fl</sup>; Tyr::CreERT2</i> mice treated with IP TAM for pulse of five days beginning at five weeks old and imaged at one and two years old.</p
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