Making time for food when 'doing time'; how enhanced status prisoners counter the indignity of prison foodways.

In contemporary neo-liberal societies, forms of responsible individualism and approaches to everyday foodways that reify healthy home-cooked food prepared from scratch, eaten together around a table are imbued with high cultural capital. What are the implications of this for criminalised individuals incarcerated in a prison system in England and Wales, that works with extremely low budgets, makes heavy use of pre-packaged convenience food and serves food to prisoners in their cells? Indeed, findings from Her Majesty's Inspectorate for Prison Report on food (2016:13), claims that 'the quantity and quality of the food provided [in prison] is insufficient, and the conditions in which it is served and eaten undermine respect for prisoners' dignity', which they argue has implications in terms of increasing the marginalisation and alienation of the prison population from the 'free community'. In this paper I draw on data from 39 in depth interviews at a resettlement scheme in England, conducted with 18 prisoners released on temporary licence from the resettlement wing of a closed and segregated Category C male prison. The enhanced status of prisoners and the benefits of being on the resettlement wing affords opportunities in relation to everyday foodways not available to regular prisoners. Their narrative accounts of prison foodways exemplify some of the HMIP findings and demonstrate how an enhanced prisoner status can counter notions of food as threat and poison, through systems of bartering, solidarity and recompense.

Glucocorticoid antagonist RU38486 fails to block acid-induced muscle wasting in vivo or in vitro.

BACKGROUND: Increased protein degradation during metabolic acidosis contributes to muscle wasting in uraemia. Adrenalectomy experiments in severely acidotic rats (arterial pH approximately 7.15) have shown that this is prevented in the absence of glucocorticoid. It should therefore be possible to block such muscle wasting with glucocorticoid receptor antagonist 11beta-(4-dimethylaminophenyl)-17beta-hydroxy,-17a-(prop-1-ynyl)-estra-4,9-dien-3-one (RU38486). METHODS: The effect of oral RU38486 (50 mg/kg body weight/day) was studied in vivo by administration to rats receiving dietary HCl supplements which yielded moderate acidosis (plasma HCO(3)(-) 19.7 +/- 1.2 mmol/l), comparable with that observed in uraemia. The effect of the glucocorticoid dexamethasone (DEX) (up to 500 nmol/l) and RU38486 (up to 5 micro mol/l) was also studied in vitro in acidified cultures of L6-G8C5 rat skeletal muscle cells. RESULTS: In vivo 15 days of moderate acidosis slowed weight gain and induced muscle wasting (6% weight loss in gastrocnemius with a commensurate decline in muscle protein) but, at this level of acidosis, muscle protein degradation showed no detectable increase. Wasting was not inhibited by RU38486 in spite of blockade of 80% of the glucocorticoid receptors in gastrocnemius. Unexpectedly, weight gain was significantly slower in acidotic rats receiving RU38486 than in acidotic rats receiving vehicle. In vitro acid spontaneously stimulated protein degradation, but even under strongly acidic conditions (pH 7.1) this was only weakly and transiently stimulated by 5 nmol/l DEX and transiently blunted by 5 micro mol/l RU38486. In contrast, as little as 1 nmol/l insulin-like growth factor I (IGF-I) almost abolished the effect of acid and this was partly restored by 5 nmol/l DEX. CONCLUSIONS: IGF-I is a potent determinant of acid-induced protein degradation in vitro and is antagonized by glucocorticoid. If glucocorticoid acts in this indirect way in vivo this may explain why, in moderate metabolic acidosis with intact adrenal glands, the action of RU38486 via glucocorticoid is too weak to be of therapeutic value.