Aims/hypothesis Experimental evidence suggests that the healing of diabetic foot ulcers is affected by psychosocial factors such as distress. We examined this proposal in a prospective study, in which we considered the role of psychological distress and coping style in the healing of diabetic foot ulcers over a 24 week period. We also explored the role of salivary cortisol and matrix metalloproteinases (MMPs) as potential mechanisms. Methods For this prospective observational study we recruited 93 (68 men; mean age 60 years) patients with neuropathic or neuroischaemic diabetic foot ulcers from specialist podiatry clinics in secondary care. Clinical and demographic determinants of healing, psychological distress, coping, salivary cortisol and both MMP2 and MMP9 were assessed at baseline. Ulcers were assessed at baseline and at 6, 12 and 24 weeks post-baseline. Diabetologia (2010) 53:1590-1598 DOI 10.1007/s00125-010-1743 However, change in ulcer size over the observation period was associated with depression only (p=0.04, d=0.31). Healed ulcers by 24 weeks were also associated with lower evening cortisol, higher precursor MMP2 and a greater cortisol awakening response. Conclusions/interpretation Confrontation coping and depression predict ulcer healing. Our preliminary enquiry into biological mechanisms suggests that cortisol and precursor MMP2 may underlie these relationships.

Patients' beliefs are important determinants of foot-care practices. They may, therefore, also be influential in determining ulcer outcomes. Interventions aimed at modifying illness beliefs may offer a means for promoting self-care and improving ulcer outcomes.

Patient and practitioner factors may contribute to the effective implementation of clinical guidelines regarding education, partnership building and shared decision-making. These findings are discussed in relation to patient education, partnership building and shared decision-making as recommended in NICE guidelines.

Adverse exposures that influence growth in prenatal and early postnatal periods are considered to influence vulnerability to chronic diseases via their effects on the neuroendocrine system. In humans, the assessment of the underlying mechanisms has been restricted. The present study aimed to investigate the effects of adverse early-life exposures, specifically maternal mood, on hypothlamic-pituitary-adrenal (HPA) axis, sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) responses to an acute physiological stressor. In addition, we conducted a preliminary examination into whether these effects varied by time of exposure and sex. One hundred and thity-nine individuals (mean age 15.12 years) were recruited from the ALSPAC (Avon Longitudinal Study of Parents and Children) birth cohort. Participants underwent the CO(2) stress test and indices of the PNS, SNS and HPA axis were measured. Pre-existing data on demographic and psychosocial factors of the mothers during pregnancy (18 and 32 weeks) and postnatally (8 weeks and 8 months) were extracted, as were participants' clinical and demographic data at birth. Increases in both pre- and postnatal anxiety and depression were associated with greater SNS reactivity to the stressor and slower recovery, as well as blunted HPA axis responses. Programming effects on the SNS appeared to be restricted to male offspring only. No consistent relationships were evident for any of the measures of pre-stress function. We have found preliminary evidence that both pre- and postnatal maternal anxiety and depression have sustained programming effects on the SNS and HPA axis. Effects on the SNS were restricted to male offspring.

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