653
pared with bipolar postmenopausal women. Premenopausal bipolar women had a higher peak G.H. than did unipolar premenopausal women but the difference was not significant. The apparent discrepancy between our findings and those of Gold et al. might be due to the fact that they studied bipolar premenopausal females and bipolar males only, while we investigated both premenopausal (N=3) and postmenopausal bipolar women (N=15). G.H. response in the unipolar group is not significantly influenced by the menopausal status. Furthermore, confirm Gold’s observation of a greater prolactin suppression after levodopa in the bipolar patients. In fact, the opposite seems to be true. There is a paradoxical rise in prolactin secretion 30-90 min after levodopa administration followed by a subsequent suppression in the bipolar patients. This peak is not present in the unipolar group. This paradoxical response to levodopa is more apparent in bipolar premenopausal women than in bipolar postmenopausal patients. Baseline prolactin levels were not significantly different in bipolar and unipolar patients. Our results on G.H. response in affective illness accord with the work of Sachar et awl. who found a reduction in G.H. response to levodopa in postmenopausal women, an observation consistent with the fact that G.H. stimutauon is related to circulating aestrogens.4 Bipolar and unipolar premenopausal women cannot be differentiated on the basis of their G.H. response to levodopa, although there is a trend toward a bigger G.H. response and less prolactin suppression in the bipolar group. The results on prolactin response to levodopa in affective illness are conflicting and more difficult to interpret. On our data, the influence of stress-related factors and oestrogen levels on prolactin response to levodopa cannot be excluded. In future studies in affective illness larger and more clinically homogeneous samples of patients must be investigated and the importance of the menopause in neuroendocrine and neurotransmitter research must be allowed for. we were
unable
J. MENDLEWICZ P. LINKOWSKI H. BRAUMAN
CLINICAL SIGN OF UNILATERAL PNEUMOTHORAX
SIR,-Commonly described signs of thorax include diminution of breath
hyperresonance
on
unilateral pneumo-
sounds, diminution of
percussion,
diminished vocal
resonance, tracheal displacement, or apex-beat displacement. The coin test is of little value in tension pneumothorax.5 A
time with clicking sound may occasionally be heard in heart beat, a sign first described by Hamman.b
the
1 would like to describe an additional neglected sign which I have found useful in the diagnosis of a unilateral pneumothorax. The patient with a suspected pneumothorax is sat upright and a stethoscope is applied in the midline at the upper end of the sternum. Percussion at the midpoint of each clavicle in turn with equal impact will then cause the auscultator to hear an obvious relative hyperresonance over the side of the pneumothorax. Also, the pitch and timbre of the sounds produced is very asymmetrical. A useful adjunct to this technique is to reduce progressively the impact of percussion at the midpoint of one clavicle until virtually no sound is audible. Similar percussion of the other clavicle then causes an easily audible sound if there is an underlying pneumothorax. It is important to sit the patient upright to assist the rise of intrapleural air to the lung apex of the affected side. Some sound heard via the stethoscope will have been transmitted by the bony structures, but this component will be symmetrical and any discrepancy Sachar, D. J., and others, ibid. 1975, 32, 502. Merimee, T. J., Fineberg, S. E. J. clin Endocr. Metab. 1965, 25, 1470. 5 Crofton, J., Douglas, A. Respiratory Diseases. Oxford, 1975. 6 Hamman, L. Ann. intern. Med. 1939, 13, 923. Lawson, J. D. New Engl. J Med. 1961, 264, 88. 3 4
7
metrical scratching of the chest wall results in tatory findings at the midline. Royal Northern London N1
unequal
auscul-
Hospital,
PHILIP D. WELSBY
to
Department of Clinical Biochemistry, Institute of Psychiatry, Brugmann University Hospital, 1020 Brussels, Belgium
movement or
be caused by asymmetry of underlying tissue. Use of the stethoscope also eliminates background ward noise which often interferes with the interpretation of unassisted percussion. The demonstration of this sign relies upon the same principle as the "scratch sign" described by Lawson’in which symmust
GENETIC COMPONENT OF OBESITY
SIR,-Boggl has criticis.ed our suggestionz that individuals become obese within a population as a result of metabolic factors which are genetically determined. We would stress that our views do not relate merely to the "hard-core of idiopathic obese". We would not, however, deny that cultural factors are important in determining the prevalence of obesity within a community-the changing incidence of obesity in the U.S.A. over the past 20 years is not likely to be due to a change in the genetic pool of the population. But whether an individual becomes obese as the population’s overall physical activity diminishes is, in our view, determined by metabolic differences between subjects. Garn et al. have reported that environmental factors are important in determining the clustering of obesity within families in the U.S.A., but metabolic efficiency in obese and lean families has not been studied in detail. Certainly stability of genetic pools and the dominance of cultural factors may not be observed in developing countries where genetic patterns and metabolic efficiency are continuing to shift, particularly where the mortality-rate among the under-5s remains as high as 10-50%. The idea of the selective advantage of a high metabolic efficiency is not new, and the concept of the "thrifty genotype" has been used by Neel4 to explain the continuing incidence of diabetes, associated with obesity. It should not be assumed that, although we emphasised the metabolic aspects of obesity, we neglect the problem of appetite control, for clearly obesity can only develop when food is not limiting. Indeed an important consequence of our views is that an obese person in energy balance continues to consume too much for his energy needs even though his intake may be within the "normal range". A reduction in weight reduces his energy requirements so that once slimmed he needs to control his food intake permanently at a level below the average. This low energy requirement may account for the frequent relapse in the treatment of obesity and the tendency to regain the lost weight-the "set-point" of body-weight merely reflecting the continuing adjustment of weight and energy expenditure until they match the energy ingested. There is also excellent evidence which shows the variable susceptibility to weight gain on increasing food intake,5 and our argument on the defective thermic responses in obese individuals, also noted by Quaade6 and others, led us to favour reduced catecholamine/ free-fatty-acid responsiveness in the characterisation of the obese and pre-obese subjects. This reduced catecholamine "drive" may be evident not only in the reduced thermogenic response to cooling but also in the differences of muscle tone and small physical movements which are not included in the usual definition of physical activity.7 1. 2.
Bogg, R. A. Lancet, 1976, ii, 1205. James, W. P. T., Trayhurn, P. ibid. p. 770. 3. Garn, S. M., Bailey, S. M., Higgins, I. T. T. Am. J. clin.
Nutr.
1976, 29,
1067. 4. 5. 6. 7.
Neel, J. V. Am. J. hum. Genet. 1962, 14, 353. Sims, E. A. H., Danforth, E., Horton, E. S., Bray, G. A., Glennon, J. A., Salans, L. B Rec Progr. Horm. Res. 1973, 29, 457. Quaade, F. in Energy Balance in Man (edited by M. Apfelbaum); p. 135. Paris, 1973. Research on Obesity: a report of the D.H.S.S./M.R.C. group. (compiled by W. P. T. James). H M. Stationery Office, 1976.
pared with bipolar postmenopausal women. Premenopausal bipolar women had a higher peak G.H. than did unipolar premenopausal women but the difference was not significant. The apparent discrepancy between our findings and those of Gold et al. might be due to the fact that they studied bipolar premenopausal females and bipolar males only, while we investigated both premenopausal (N=3) and postmenopausal bipolar women (N=15). G.H. response in the unipolar group is not significantly influenced by the menopausal status. Furthermore, confirm Gold’s observation of a greater prolactin suppression after levodopa in the bipolar patients. In fact, the opposite seems to be true. There is a paradoxical rise in prolactin secretion 30-90 min after levodopa administration followed by a subsequent suppression in the bipolar patients. This peak is not present in the unipolar group. This paradoxical response to levodopa is more apparent in bipolar premenopausal women than in bipolar postmenopausal patients. Baseline prolactin levels were not significantly different in bipolar and unipolar patients. Our results on G.H. response in affective illness accord with the work of Sachar et awl. who found a reduction in G.H. response to levodopa in postmenopausal women, an observation consistent with the fact that G.H. stimutauon is related to circulating aestrogens.4 Bipolar and unipolar premenopausal women cannot be differentiated on the basis of their G.H. response to levodopa, although there is a trend toward a bigger G.H. response and less prolactin suppression in the bipolar group. The results on prolactin response to levodopa in affective illness are conflicting and more difficult to interpret. On our data, the influence of stress-related factors and oestrogen levels on prolactin response to levodopa cannot be excluded. In future studies in affective illness larger and more clinically homogeneous samples of patients must be investigated and the importance of the menopause in neuroendocrine and neurotransmitter research must be allowed for. we were
unable
J. MENDLEWICZ P. LINKOWSKI H. BRAUMAN
CLINICAL SIGN OF UNILATERAL PNEUMOTHORAX
SIR,-Commonly described signs of thorax include diminution of breath
hyperresonance
on
unilateral pneumo-
sounds, diminution of
percussion,
diminished vocal
resonance, tracheal displacement, or apex-beat displacement. The coin test is of little value in tension pneumothorax.5 A
time with clicking sound may occasionally be heard in heart beat, a sign first described by Hamman.b
the
1 would like to describe an additional neglected sign which I have found useful in the diagnosis of a unilateral pneumothorax. The patient with a suspected pneumothorax is sat upright and a stethoscope is applied in the midline at the upper end of the sternum. Percussion at the midpoint of each clavicle in turn with equal impact will then cause the auscultator to hear an obvious relative hyperresonance over the side of the pneumothorax. Also, the pitch and timbre of the sounds produced is very asymmetrical. A useful adjunct to this technique is to reduce progressively the impact of percussion at the midpoint of one clavicle until virtually no sound is audible. Similar percussion of the other clavicle then causes an easily audible sound if there is an underlying pneumothorax. It is important to sit the patient upright to assist the rise of intrapleural air to the lung apex of the affected side. Some sound heard via the stethoscope will have been transmitted by the bony structures, but this component will be symmetrical and any discrepancy Sachar, D. J., and others, ibid. 1975, 32, 502. Merimee, T. J., Fineberg, S. E. J. clin Endocr. Metab. 1965, 25, 1470. 5 Crofton, J., Douglas, A. Respiratory Diseases. Oxford, 1975. 6 Hamman, L. Ann. intern. Med. 1939, 13, 923. Lawson, J. D. New Engl. J Med. 1961, 264, 88. 3 4
7
metrical scratching of the chest wall results in tatory findings at the midline. Royal Northern London N1
unequal
auscul-
Hospital,
PHILIP D. WELSBY
to
Department of Clinical Biochemistry, Institute of Psychiatry, Brugmann University Hospital, 1020 Brussels, Belgium
movement or
be caused by asymmetry of underlying tissue. Use of the stethoscope also eliminates background ward noise which often interferes with the interpretation of unassisted percussion. The demonstration of this sign relies upon the same principle as the "scratch sign" described by Lawson’in which symmust
GENETIC COMPONENT OF OBESITY
SIR,-Boggl has criticis.ed our suggestionz that individuals become obese within a population as a result of metabolic factors which are genetically determined. We would stress that our views do not relate merely to the "hard-core of idiopathic obese". We would not, however, deny that cultural factors are important in determining the prevalence of obesity within a community-the changing incidence of obesity in the U.S.A. over the past 20 years is not likely to be due to a change in the genetic pool of the population. But whether an individual becomes obese as the population’s overall physical activity diminishes is, in our view, determined by metabolic differences between subjects. Garn et al. have reported that environmental factors are important in determining the clustering of obesity within families in the U.S.A., but metabolic efficiency in obese and lean families has not been studied in detail. Certainly stability of genetic pools and the dominance of cultural factors may not be observed in developing countries where genetic patterns and metabolic efficiency are continuing to shift, particularly where the mortality-rate among the under-5s remains as high as 10-50%. The idea of the selective advantage of a high metabolic efficiency is not new, and the concept of the "thrifty genotype" has been used by Neel4 to explain the continuing incidence of diabetes, associated with obesity. It should not be assumed that, although we emphasised the metabolic aspects of obesity, we neglect the problem of appetite control, for clearly obesity can only develop when food is not limiting. Indeed an important consequence of our views is that an obese person in energy balance continues to consume too much for his energy needs even though his intake may be within the "normal range". A reduction in weight reduces his energy requirements so that once slimmed he needs to control his food intake permanently at a level below the average. This low energy requirement may account for the frequent relapse in the treatment of obesity and the tendency to regain the lost weight-the "set-point" of body-weight merely reflecting the continuing adjustment of weight and energy expenditure until they match the energy ingested. There is also excellent evidence which shows the variable susceptibility to weight gain on increasing food intake,5 and our argument on the defective thermic responses in obese individuals, also noted by Quaade6 and others, led us to favour reduced catecholamine/ free-fatty-acid responsiveness in the characterisation of the obese and pre-obese subjects. This reduced catecholamine "drive" may be evident not only in the reduced thermogenic response to cooling but also in the differences of muscle tone and small physical movements which are not included in the usual definition of physical activity.7 1. 2.
Bogg, R. A. Lancet, 1976, ii, 1205. James, W. P. T., Trayhurn, P. ibid. p. 770. 3. Garn, S. M., Bailey, S. M., Higgins, I. T. T. Am. J. clin.
Nutr.
1976, 29,
1067. 4. 5. 6. 7.
Neel, J. V. Am. J. hum. Genet. 1962, 14, 353. Sims, E. A. H., Danforth, E., Horton, E. S., Bray, G. A., Glennon, J. A., Salans, L. B Rec Progr. Horm. Res. 1973, 29, 457. Quaade, F. in Energy Balance in Man (edited by M. Apfelbaum); p. 135. Paris, 1973. Research on Obesity: a report of the D.H.S.S./M.R.C. group. (compiled by W. P. T. James). H M. Stationery Office, 1976.
