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Articles by M. Walker
Total Records ( 4 ) for M. Walker
  D Brent , N Melhem , M. B Donohoe and M. Walker

OBJECTIVE: This study examined effects of bereavement 21 months after a parent’s death, particularly death by suicide. METHOD: The participants were 176 offspring, ages 7–25, of parents who died by suicide, accident, or sudden natural death. They were assessed 9 and 21 months after the death, along with 168 nonbereaved subjects. RESULTS: Major depression and alcohol or substance abuse 21 months after the parent’s death were more common among bereaved youth than among comparison subjects. Offspring with parental suicide or accidental death had higher rates of depression than comparison subjects; those with parental suicide had higher rates of alcohol or substance abuse. Youth with parental suicide had a higher incidence of depression than those bereaved by sudden natural death. Bereavement and a past history of depression increased depression risk in the 9 months following the death, which increased depression risk between 9 and 21 months. Losing a mother, blaming others, low self-esteem, negative coping, and complicated grief were associated with depression in the second year. CONCLUSIONS: Youth who lose a parent, especially through suicide, are vulnerable to depression and alcohol or substance abuse during the second year after the loss. Depression risk in the second year is mediated by the increased incidence of depression within the first 9 months. The most propitious time to prevent or attenuate depressive episodes in bereaved youth may be shortly after the parent’s death. Interventions that target complicated grief and blaming of others may also improve outcomes in symptomatic youth with parental bereavement.

  N. J. Leech , J. O`Sullivan , P. Avery , C. Howey , K. Burling , S. Iyer , L. Pascoe , M. Walker and T. Cheetham
  Aims  Obesity and insulin resistance have been linked to rising incidence and earlier onset of Type 1 diabetes. Inherited differences in insulin action might also influence the evolution of Type 1 diabetes. Our aim was to determine whether parental BMI and insulin resistance influences age of onset of Type 1 diabetes in their offspring.

Methods  BMI standard deviation score and age at diagnosis of Type 1 diabetes was examined in 227 children, and in 206 of these was compared with local matched control subjects. Non-diabetic parents of a subgroup of 80 children with Type 1 diabetes were recruited. Parental BMI was compared with local adult control subjects. The relationship between parental BMI, waist-hip ratio, homeostasis model assessment of insulin resistance (HOMA-IR), leptin and adiponectin levels and age at diagnosis of Type 1 diabetes in offspring was examined.

Results  We found no relationship between age at diagnosis of Type 1 diabetes in children and BMI  standard deviation score (P = 0.5). Children with Type 1 diabetes and their parents were heavier than matched control subjects (mean BMI standard deviation score ± sd in children = 0.66 ± 1.06 vs. 0.32 ± 1.16 in control subjects, P = 0.002; mean parental BMI ± sd 27.7 ± 0.4 vs. 25.5 ± 0.4 kg/m2 in control subjects; P < 0.0001). Maternal HOMA-IR accounted for 20% of variation in age at diagnosis (P < 0.001) with increasing maternal insulin resistance associated with later age at diagnosis of Type 1 diabetes.

Conclusions  Children with Type 1 diabetes and their parents have an increased BMI at diagnosis. Maternal insulin resistance is associated with later onset of Type 1 diabetes in children.

  E. L. Edghill , A. Khamis , M. N. Weedon , M. Walker , G. A. Hitman , M. I. McCarthy , K. R. Owen , S. Ellard , A. T Hattersley and T. M. Frayling
  Aim  Genome-wide association studies have identified > 30 common variants associated with Type 2 diabetes (> 5% minor allele frequency). These variants have small effects on individual risk and do not account for a large proportion of the heritable component of the disease. Monogenic forms of diabetes are caused by mutations that occur in < 1:2000 individuals and follow strict patterns of inheritance. In contrast, the role of low frequency genetic variants (minor allele frequency 0.1-5%) in Type 2 diabetes is not known. The aim of this study was to assess the role of low frequency PDX1 (also called IPF1) variants in Type 2 diabetes.

Methods  We sequenced the coding and flanking intronic regions of PDX1 in 910 patients with Type 2 diabetes and 878 control subjects.

Results  We identified a total of 26 variants that occurred in 5.3% of individuals, 14 of which occurred once. Only D76N occurred in > 1%. We found no difference in carrier frequency between patients (5.7%) and control subjects (5.0%) (P = 0.46). There were also no differences between patients and control subjects when analyses were limited to subsets of variants. The strongest subset were those variants in the DNA binding domain where all five variants identified were only found in patients (P = 0.06).

Conclusion  Approximately 5% of UK individuals carry a PDX1 variant, but there is no evidence that these variants, either individually or cumulatively, predispose to Type 2 diabetes. Further studies will need to consider strategies to assess the role of multiple variants that occur in < 1 in 1000 individuals.

  S. A. Finkelstein , E. Keely , D. S. Feig , X. Tu , A. S. Yasseen III and M. Walker


To explore intention to breastfeed and breastfeeding rates in hospital and on discharge across women with pre-gestational or gestational diabetes mellitus, or no diabetes.


A retrospective cohort analysis was conducted using data from four Ontario hospitals. Women who delivered a viable infant between 1 April 2008 and 31 March 2010 were included in the study. Unadjusted and adjusted odds ratios were calculated for each outcome measure and were used to compare the breastfeeding rates among women with and without diabetes.


After controlling for potential confounders, women with insulin-treated diabetes were less likely to intend to breastfeed, when compared with women without diabetes (adjusted odds ratio 0.49, 95% CI 0.27-0.89). In hospital, women with insulin-treated diabetes were least likely to breastfeed (odds ratio 0.42, 95% CI 0.26-0.67), followed by women with non-insulin-treated diabetes (odds ratio 0.50, 95% CI 0.26-0.96) and women with gestational diabetes (odds ratio 0.77, 95% CI 0.68-0.87) when compared with women without diabetes. On discharge, women with insulin-treated diabetes were least likely to breastfeed (odds ratio 0.38, 95% CI 0.24-0.60), followed by women with gestational diabetes (odds ratio 0.75, 95% CI 0.66-0.85); rates of breastfeeding among women with non-insulin-treated diabetes were comparable on discharge with those of women without diabetes. Women seeking care from an antenatal provider other than a physician were 2-3 times more likely to breastfeed in hospital and on discharge.


Women with insulin-treated diabetes had the poorest outcomes with respect to breastfeeding rates. Gestational and non-insulin-treated diabetes were associated with lower rates of breastfeeding in hospital, while gestational diabetes was additionally associated with lower breastfeeding rates on discharge.

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