PubMed · 9353494
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M Peel. 1997-10-04. Hunger strikes.. https://doi.org/10.1136/bmj.315.7112.829
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Ernest H. Starling FRS (1866-1927) is remembered as a great physiologist; nevertheless a paper of his that is of substantial historical interest has dropped out of sight. It is a quantitative analysis of the effects of the Allied food blockade during World War I on the energy available to the German population and of the failure by the German government to distribute the available energy fairly. He shows that by 1919 a substantial proportion of the urban Germans were starving. His data are summarized in this article. Starling concluded that empty stomachs were a major reason for the German capitulation. His analysis grew out of his work as the second chairman of the Food [War] Committee of The Royal Society and as one of the two British members of the International Scientific Food Commission, pioneering bodies in using science to help to set public policy.
Patients at a New York City municipal hospital were surveyed in 1985 and 1989 to ascertain the extent of hunger and its possible correlates. Twenty-two percent (22%) of the 382 subjects in 1985 and 23% of the 332 subjects in 1989 experienced hunger. Hunger was related significantly to homelessness, social isolation and the physical inability to buy and/or prepare food. Between 1985 and 1989, there was a large increase in the use of institutional resources for food; a decline in reliance on Food Stamps; and an increase in household density. Inpatients were found to be poorer than outpatients, and to rely more heavily upon soup kitchens. Practice, policy and research implications are noted.
The increased serum reverse T3 and decreased T3 during caloric deprivation and non-thyroidal illness is caused by decreased T3 production (with intact degradation) and reversed T3 degradation (with intact production) respectively. These changes can ensue from two mechanisms i.e. decreased 5'D of T4 and of reverse T3 (possibly caused by a decrease in naturally occurring reducing agents) or by decreased transport of T4 and reverse T3 into the liver (possibly caused by decreased ATP concentrations in the liver). The effects of the low T3 syndrome at the tissue level are in many instances comparable to those seen in hypothyroidism. The effects lead to conservation of energy and decrease of protein breakdown. These effects are considered to constitute a beneficial adaptative mechanism in situations in which the organism is endangered. There is no evidence that treatment of patients with the low T3 syndrome with thyroid hormones is of any benefit. Knowledge at the present moment suggests that administration of thyroid hormones during caloric deprivation or non-thyroidal illness should be avoided.