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The Siege of Leningrad
- Michael D. Croft (5 January 2004)
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starvation and cvs diseases.
- manan vasenwala (7 January 2004)
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Surviving Leningrad siege starvation
- Par Sparen, Denny Vagero, Dmitri B. Shestov, Rosaria Galanti (15 January 2004)
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No evidence for starvation as the reason for cardiovascular disease in Leningrad survivors
- Christopher Bell (19 January 2004)
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Starvation and stress during the Leningrad siege
- Pär Sparén, Denny Vågerö, Dmitri B. Shestov, Maria Rosaria Galanti (2 February 2004)
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Could a predisposition to development of hypertension confer relative survival advantage during prolonged starvation?
- David Carr (3 February 2004)
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A possible role for post-siege eating behaviour
- Emanuele Cereda, Ettore Corradi, Maria Gabriella Gentile (18 March 2005)
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Michael D. Croft, Salaried GP Gateways Surgery, Shenley, Herts WD7 9LP
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Sir Many thanks for publishing this fascinating study. I am, however, concerned that one crucial confounding factor seems to have been overlooked, and might call into question the conclusions that could be drawn from it. The study has retrospectively analysed outcomes, in terms of cardiovascular mortality, in siege survivors and has selected, as controls, those men of similar age who did not experience the siege. The data indicates that seige survivors have a higher CVS risk. The conclusion is drawn that the process of starvation has adversely affected the physiology of those men who experienced food shortage at a critical stage of their development as juveniles. This conclusion could be drawn if the mortality of the starvation process itself could be shown to have been applicable to all physiological types equally. One might argue that mortality occurring as a result of enemy action (trauma from gunshot wound, or bomb/shell blast) might apply equally to all the men, but one is on much thinner ice if the cause of death is starvation. We know that people with greater fat reserves will outlive people with less in periods of famine, and that ability to withstand protracted famine is very likely related to an efficient metabolism which is substantially genetically inherited. It is quite probable, therefore, that this cohort of siege survivors owes its survival to the possibility that its members, if not overweight themselves at the start of the siege, nevertheless might have been the children of overweight parents. These parents, with better fat reserves themselves, would have been in a better position to survive the siege than their thinner peers, and hence in a better position to ensure the survival of their children. This would have been true whether or not these children had inherited their parents' metabolic type, but especially true if they had. The bread ration for a family would have been distributed in the household as the parents saw fit, and it is not unreasonable to assume that parents with greater fat reserves in the winter of 1941/2 would have been able to hand over a greater proportion of the bread ration to their children. This might suggest that siege survivors in Leningrad represent a selected survival group with the metabolic characteristic of obesity, favourable in a time of famine. It would therefore be hugely surprising if this group, when followed up into old age, did not demonstrate the increased risk of CVS disease that we all know they should have. The siege quite probably selected them, but there is insufficient evidence here to suggest that it affected them in the way that the authors claim it might have done. Michael Croft Competing interests: None declared |
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manan vasenwala, consultant-cardiologist k.k.heart center.aligarh-202002
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it is well know that the human body is programmed to store food during periods of plenty, and expend the stored food in time of scarcity.the mechanisms for storage during plenty are more vigorous. thus in periods of plenty, these same mechanisms are working overtime to store fat resulting in obesity. this genetic mechanisms evolved over millions of years. thus if food is available in plenty obesity will result which is there for all to see. so it appears to be a loose-loose situation. during famine, the factors producing hypertension and cardiac disorders are working overtime and they produce their result in terms of increased morbidity and mortality. when food is made available to them the person refeeds and becomes obese, faces htn, diabetes and ihd and a host of others. in the indian scenario, there has an increase by 300% prevalence of diabetes and ischaemic heart disease. one disturbibg fact that myocardial infacrtion occures at least a decade before their counterparts in europe and west. studies in uk have borne out these facts including severity of diabetes and ihd.till now, speculations have been rife regarding the promoting factors for the upsurge in diabetes and ihd. theories abound including faulty contaminated veg diet,consumption of "gutka", smoking and pan chewing,and genetic predisposition.one must now seriously consider starvation. in india 25% of the population using indian standards are below poverty line. if usa and western data are extrapolated to the indian scene, than 75% of the population are below poverty line.in the last decade the poor have become poorer and many starvation deaths have been reported, but probably for political reasons this is only tip of the iceberg. to some up, i think the increase in prevalence of diabetes and ischaemic heart disease occur in two populations: the starving and the now obese! Competing interests: None declared |
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Par Sparen, senior researcher Dept. of Medical Epidemiology and Biostatistics, Karolinska Institute, SE-171 77 Stockholm, Sweden, Denny Vagero, Dmitri B. Shestov, Rosaria Galanti
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Sir, Michael Croft makes the interesting point that children of fat parents would have had a better chance of surviving the siege of Leningrad. He suggests that if the parents themselves were obese they would be more likely to survive the siege and protect their children; in addition their children would tend to be fatter and therefore also, more likely to survive. He suggests that this could explain our findings of an increased risk of CVS for those exposed to the siege. We have no way of establishing whether the parents of survivors, or the survivors themselves where fatter or thinner than non-survivors (or their parents) when the siege started in 1941. Neither do we know whether obesity did in fact promote survival chances. It might not have. One of the authors of our paper, Professor Shestov, was himself in the siege and recollects a common impression that fat persons were in fact among the first to die. Leyton, who observed Russian prisoners of war in Germany, suggested that fat men lost weight at a faster rate than slim men (Leyton 1946). We do know, however, that the siege survivors were not fatter than other war survivors when both groups were examined in 1975-77. Table 1, in the long (electronic) version of our paper, shows this by comparison of their mean values for BMI. For skinfold thickness measured at the arm there was a non-significant tendency for siege-exposed to be somewhat fatter. However, adjustment for these characteristics did not reduce estimates of starvation effects. Therefore, Croft´s hypothesis (even if it was to be true) seems unlikely to explain our results. Equally important, it would be unable to account for the interaction with age. Interference with puberty for both fat and slim children seems indeed likely to have resulted from protracted starvation. Manan Vasenwala suggests that starvation in India may be one of the determinants of Indian high levels of IHD, hypetension and diabetes. We are aware of some work already going on in this field and it certainly looks like a hypothesis that should be explored further. Denny Vågerö, Dmitri Shestov, Rosaria Galanti, Pär Sparén Reference: Leyton G B. Effect of slow starvation. Lancet 1946; 248:ii:73-79 Competing interests: None declared |
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Christopher Bell, Professor of Physiology Trinity College Dublin, Dublin 2
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Sir I have read Sparén et al's analysis of mortality statistics for survivors of the Leningrad seige repeatedly, with the hope of becoming convinced by their argument. However, I have to conclude that they present any substantive evidence that the increased incidence of cardiovascular disease is due to starvation and that, even if such a relationship does exist, the assumptions made in their study would minimise any chance of its being revealed. Firstly, while the authors are correct that the seige lasted from September 1941 to January 1944, they seriously misrepresent the situation by implying that there was a consistent famine over this period. Pavlov's detailed account emphasises that food stocks did not run seriously low until November 1941 and that deliveries from the East had led to a marked improvement in supply by the end of January 1942. Thus there was only a 3 month window during which calorific and nutritional intakes were likely to be substantially below those in many other parts of Russia. Allocation of subjects to particular age brackets based on the total 2 year seige period is therefore meaningless. Second, the thesis that starvation at puberty might be a particularly potent risk factor for cardiovascular morbidity is based on comparison of data for ages 9-15 with those aged 8 years or younger, and 16-26 years. The authors chose 9 as the beginning of puberty because of evidence for changes in fat metabolism at this age. However, in 1941 Russia at least most pubertal events would have not been likely before age 12. More importantly, from this age Leningrad boys were classed as adult dependents rather than children and their rations were cut by 20%. Therefore, if any link between parapubertal starvation and later life outcome were to be properly investigated, those aged 12-15 over the winter of 1941-2 would be the key group. Combining the 9-11 year olds merely confuses the issue. Third, despite throw-away allusions in the Abstract and the Conclusions that stress might have contributed to cardiovascular changes, this is effectively dismissed, since the authors state repeatedly that their analysis indicates an effect of starvation. Leaving aside the question of the extent to which sustained malnutrition in Leningrad differed from that elsewhere in Russia, long term stress is well established as leading to long term elevation of sympathetic tone, cortisol secretion and blood pressure and there can be no question that two years under seige bombardment constitutes a stressful environment. In addition, Pavlov mentions that once they reached the age of 12, boys were recruited into the squads responsible for defence duties such as bomb disposal. It is difficult not to conclude that the effects of stress alone are an adequate explanation for elevated cardiovascular morbidity in later life. Pavlov DV (1965) Leningrad 1941: the Blockade, University of Chicago Press. Competing interests: None declared |
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Pär Sparén, Senior Researcher Dept. of Medical Epidemiology and Biostatistics, Karolinska Institute, SE-171 77 Stockholm, Sweden, Denny Vågerö, Dmitri B. Shestov, Maria Rosaria Galanti
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Sir, Christopher Bell suggests that the stress of war, especially prolonged bombardment, is sufficient explanation for hypertension and elevated circulatory mortality 30-60 years later, thus rejecting any nutritional link. The siege certainly constituted a considerable stressor; most exposures seen as stressful today are benign in comparison. Food shortage, starvation and threat of starvation may have been as important stressors as were the bomb blasts; most deaths were indeed due to starvation [1]. The endocrine profile of severe starvation in several aspects mimics that of reaction to stress. In the condensed presentation in the BMJ we said that “starvation is entangled with the trauma of the siege”. This trauma obviously has long term psychological effects, and it would not be surprising if they were linked to long term physiological changes. Thus, Bell´s question about the importance of stress is relevant. Boys, aged 9-15 in January 1942 (Bell has misunderstood our definition of age groups, perhaps due to a typo in the first paragraph), were especially prone to the effects of the siege. Sub-dividing this group into 9-11 and 12-15 showed that both groups had an elevated risk of hypertension in adult age, but for those aged 12-15 in Jan 1942 this was more pronounced, in our view reinforcing one of our main hypotheses. Both groups had elevated cardiovascular mortality during follow-up, with almost identical risk estimates. Whatever the biological pathway(s), the fact remains that the effect on cardio-vascular mortality of exposure to siege strongly interacted with (peri-pubertal) age and was partly (but not only) mediated by hypertension. We have been unable to find any precise data on nutrional intake during the spring of 1942, but clearly total caloric intake was still extremely low and lacking in nutrients, even after January 24th, when bread rations went up to 250 g for both children and dependents and after February 11th when they rose again [1]. We doubt very much the suggestion by Bell, that the difference between Leningrad siege starvation and other war time starvation in Russia was small, except for a “three months window”. Nutritional intake in the spring of 1942 was certainly lower than the “slow starvation” rations reported by Leyton [2] for Russian prisoners of war in Germany (1600 cal/day). Keys [3] concluded in 1950: “many factors were involved in the epidemic of hypertension in Leningrad, but the outstanding peculiarity of the period was severe semi-starvation for 6 months, followed by refeeding with the necessity for hard work at all times.” Quite clearly this hypertension epidemic was particularly pronounced among peri-adolescent boys; we suggest that this was so because caloric restriction or deficiency of certain nutrients around puberty [4] may be more likely to interfere with blood pressure regulation than caloric restriction at other ages. Elevated blood pressure was still visible when subjects were examined 1975-77. Surely it is not “redundant” to suggest that the starvation episod also played a role in their elevated circulatory disease mortality in the following decades. Denny Vågerö, Dimitri Shestov, Rosaria Galanti, Pär Sparén References 1. Pavlov D V. Leningrad 1941. The Blockade, p125 and p149. Chicago and London: Univ of Chicago Press, 1965 2. Leyton G B. Effect of slow starvation. Lancet 1946; 248:ii:73-79 3. Keys A, Brozek J, Henschel A, Mickelsen O, Taylor H L. The biology of human starvation. Volume 1, p 621. Minneapolis: Univ of Minnesota Press, 1950 4. Falkner B, Sherif K, Michel S, Kushner H. Dietary nutrients and blood pressure in urban minority adolescents at risk for hypertension. Arch Pediatr Adolesc Med. 2000 Sep; 154(9): 918-22. Competing interests: None declared |
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David Carr, Consultant physician University Hospital of North Tees, TS19 8PE
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Sir, Have the authors of this important study on long-term mortality after severe starvation during the siege of Leningrad considered the possibility of differential survival during such terrible privation as an alternative explanation for the finding of hypertension later among the survivors? For example, could a predisposition (genetic or otherwise) to develop hypertension in middle age be linked in some subtle way with a relative survival advantage during prolonged starvation during adolescence or young adult life? Some 22% of the entire Leningrad population died in the siege. If (to take the extreme case) all those who died would have been destined to remain normotensive had they not starved, then the prevalence of hypertension later on in the survivors of the siege would be increased by a factor of 100/(100-22) = 1.28. It would be necessary to know the rates of survival during the siege for the particular age-cohorts studied in order to examine whether this hypothesis could contribute to explaining the observations described. It would be of interest to know whether the authors have been able to do this analysis. Competing interests: None declared |
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Emanuele Cereda, Clinical Nutritionist Center for Eating Disorders - Niguarda Cà Granda Hospital - Milan, Ettore Corradi, Maria Gabriella Gentile
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In their study of long term mortality in Leningrad siege Sparén et al. hypothesised that starvation and the accompanying chronic stress might have adversely affected survivors' cardiovascular (CV) outcome. Adjustments for occupation, marital status, education, smoking and alcohol consumption apparently had no impact on risk evaluation, in spite of being strongly correlated with mortality. Although lifestyle and socioeconomic circumstances, when considered as possible confounding factors, aim to represent indirectly also the dietetic habit of the population studied, we suggest that starvation, as an experience per-se, might have influenced the future eating behaviour of the survivors, particularly around the age of puberty. After drastic food shortages refeeding opportunities might have supported the development of a relative hyperphagic habit. Moreover nothing is known about the quality of food. General improvement of socio-economic conditions is usually accompanied by an increase in total food availability and consumption of certain food categories (meats, animal-origin and processed foods) to the detriment of others (fruits, vegetables and low-fat diary products). It has been recognised that an unhealthy eating pattern and multiple dietary factors all participate to both an atherogenic lipid profile and raised blood pressure.(2) If, on the one hand, cholesterol concentrations seem to mediate the siege effect on mortality to a lesser extent than blood pressure, 40-50% of patients with coronary artery disease presented normal or mildly increased cholesterol levels.(3) Even so, better genetic resources seem to have been taken into account among possible biases.(1) These considerations look correct above all when considering the age range of the population enrolled (43-49 years) and the one among which CV mortality was detected particularly pronounced (55-65 years). Furthermore, nothing is known about the level of physical activity apart from occupational class status. In this sense we believe that both a dietetic investigation and a physical fitness level evaluation at the time of recruitment, as long as during the follow-up window, would have been of possible interest. Unfortunately at the time of the study (1975-77) most of the notions about the role of diet and lifestyle on main contributors to CVD risk were almost unknown. References: 1. Sparen P, Vagero D, Shestov DB, Plavinskaja S, Parfenova N, Hoptiar V, Paturot D, Galanti MR. Long term mortality after severe starvation during the siege of Leningrad: prospective cohort study. BMJ. 2004; 328(7430):11 2. Krauss RM, Eckel RH, Howard B, Appel LJ, Daniels SR, Deckelbaum RJ, Erdman JW Jr, Kris-Etherton P, Goldberg IJ, Kotchen TA, Lichtenstein AH, Mitch WE, Mullis R, Robinson K, Wylie-Rosett J, St Jeor S, Suttie J, Tribble DL, Bazzarre TL. AHA Dietary Guidelines: revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation. 2000; 102(18):2284-99. 3. de Ferranti S, Rifai N. C-reactive protein and cardiovascular disease: a review of risk prediction and interventions. Clin Chim Acta. 2002; 317(1-2):1-1 Competing interests: None declared |
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