Author
František Bláha, MD, PhD, b. 1896, survivor of Dachau (No. 22526), where he was subject to criminal human experimentation. Forced to work as a prisoner pathologist in the Nazi research laboratory in the camp, he participated in the resistance movement by documenting the criminal medical practices of the Nazi staff.
From the Editors
Prof. Dr František Bláha,1 M.D., the author of this article, was born on 9 June 1896 in Písek, in the South Bohemian region of the Czech territories. Before the Second World War he was a ward physician at Jihlavahospital. At the beginning of 1939, he was arrested and sentenced to death by a court in Breslau, and in 1940 a Leipzig court confirmed the sentence. However, the Nazi German courts did not decide to carry out the verdict, and in early 1941 sent him to Dachau concentration camp as a Rückkehr nicht erwünscht prisoner (i.e. designated as “not wanted to return”), registered as No. 22526 and straightaway sent to the penal commando. Next, he was a human guinea pig used by the Nazi German physicians in the camp for their medical experiments and infected twice with typhus and typhoid. By some miracle, he survived, whereupon he was sent to work as a pathologist in the experimental research laboratory. As a “not wanted to return” prisoner, he was not expected to get the chance to divulge the atrocities he had witnessed. Later he wrote,
We set up an illicit committee made up of German, Austrian, Yugoslav, Russian, French, Polish, and Dutch prisoner-doctors and university professors who worked with us on post-mortems, and over the months and years gradually built up a collection of records. We never expected that any of us would ever be able to draw any scientific conclusions from this work because we could not expect to survive. All we hoped to do was to save these materials — copies of post-mortem reports, lists of the substances used, results and photographs — as documentary evidence for posterity, hiding it all away and using our illicit organisation to smuggle it out of the camp and deposit it in external commandos working in the countryside, so that one day after the war was over it could serve as a historical record.
On 30 April 1945, when the Nazi Germans failed to carry out Himmler’s order and close down the camp, the prisoners chose me as their representative and I handed over all of our materials to the American investigating committee. I supplemented them with numerous oral observations in my statements during the inquiry preceding the 1945 trial of the staff of Dachau before the International Tribunal at Nuremberg, during the German Doctors’ trial in 1946—1947, and the proceedings against the I.G. Farbenindustrie company. The last time I heard of our materials was in 1947, when they were in the hands of Dr Alexander of Chicago,2 who was serving as an expert witness for the American military court at Nuremberg. He put a lot of this material into his publications. Since then, despite many efforts, we have never managed to learn what happened to those materials.
On his return from the concentration camp, Professor Bláha was made chief physician of the central social insurance company in Prague, and in 1948 he was appointed head of the Prague hospitals. In 1945—1955 he served as a deputy to the Parliament of Czechoslovakia and chairman of Department of Health and Social Welfare. In 1952 he was appointed to a professorship at Charles University, Prague, and dean of its newly created Faculty of Hygiene. Currently,3 he is head of the Faculty’s Institute of Social Hygiene.
Professor Bláha wrote this article for Arkhiv Patologii, a journal published in Moscow. In its evaluation, we should not forget that it was written by someone who was not a scientist conducting research in a university laboratory but a prisoner with a death sentence hanging over him in a Nazi German concentration camp. The article has a double value: for the historian it is a testimonial documenting the barbarity of Nazism; for the medical practitioner it is a contribution to the theory on the pathogenesis of atherosclerosis and how to prevent this disease.
This report has yet another special message for those who were persecuted by the Nazi German regime, and for their organisations and legal successors. It presents a large body of evidence to show that imprisonment in a concentration camp gave rise to or aggravated atherosclerosis, which may therefore be regarded as a classic example of “a disease conditioned by confinement in a concentration camp,” even if none of its clinical symptoms were confirmed either for the period when the patient was kept in the camp or following is liberation.
Professor Bláha’s article
I was a prisoner of Dachau concentration camp doing the hardest work involving corpses, and subsequently conducted post-mortems, so I had the opportunity to autopsy all the victims of the Nazi German medical research station. In Dachau there were many of these victims already at the beginning of the war, and their numbers were rising all the time. Until 1942, I was carrying out post- mortems only on the victims of the Nazi German experiments. Later we were ordered to conduct post-mortems on all the prisoners who died in the prisoners’ hospital in the camp. From 1943 on, we autopsied the corpses of all who died in the camp, especially of those who died of infectious diseases.
Occasionally, it was impossible to autopsy every single body because sometimes there were deliveries of as many as two to three hundred bodies of those who had died due to repressive measures or in an epidemic. Whenever this happened, we autopsied only a few of the bodies for the purposes of control. Until 1942, the average number of post-mortems done was 10 a day; in 1942—1943 it was up to 20 a day; and from 1944 it was 35 or more per day. That is how we managed to collect data on, and draw up fairly accurate records of about 10 thousand autopsies. Until 1944, only male prisoners were held in Dachau, and there were only rare instances of female bodies sent in for a post-mortem; these were women who had been sentenced to death and executed. It was not until 1945 that occasionally women arrived in transports for Dachau, so our post-mortem records were almost exclusively for male corpses.
The ancillary staff working in the prisoners’ hospital and mortuary were prisoner-doctors and university professors of diverse nationalities. They assembled illicitly in the early morning in the post-mortem room and discussed the results they had obtained. That was also where a couple of university professors worked as assistants. There were many professors from various medical faculties in Germany, as well as many scientists collaborating with them who were interested in the work of the Nazi German research department and the results it obtained, so they were also interested in our work. Thanks to that, in the final years, 1944—1945, we were able to acquire equipment and funds for histological and bacteriological work, as well as for biopsies. As a result, we could make macro- and microscopic specimens and demonstrate them to one another as well as to visitors from Germany. Previously, materials of this kind, especially from the experimental research department, had been dispatched by road to Munich, where the specimens were preserved and sent to various institutes during demonstrations.
The effects of starvation were a common pathological feature observed in all the corpses. In 1940—1945 we had the chance to carry out clinical examinations and post-mortems on tens of thousands of prisoners suffering from “hunger disease.” We conducted clinical observations on about 25% of the prisoners because the rest had to continue working until they died. We carried out post-mortems on all of those who died, and in 90% of the cases observed complications with characteristic, chronic or recent processes. Moreover, 50% of the prisoners had acute infectious conditions or complications following an epidemic disease they had contracted. The disease which occurred most often was typhus, with over 30 thousand cases among prisoners; we also observed cases of dysentery, typhoid, sepsis, and malaria. The last two conditions occurred in victims of the experimental research department.
From the very outset, we had to assume that there was no such thing as a pure form of “hunger disease.” Hence, there was no such thing as “pure” hypoproteinaemia for hunger disease, as observed in the Minnesota Starvation Experiment of 1951,4 which was carried out in conditions which could be described as in vitro, on volunteers who were students and had the best possible laboratory conditions apart from being kept hungry. In practice, conditions as good as these are never encountered in real situations of hunger disease. Concentration camp prisoners were at the mercy of the effects of various severe neuropsychic traumatic experiences, bad hygienic and weather conditions, and hard labour. So we have to consider the fact that in hunger disease there are other unfavourable factors at play apart from disorders of the metabolism.
From the objective point of view, what we observed in cases of hunger disease was a weight loss at a rate ranging from sudden to slow, down to as much as one-third of the subject’s original weight, or even less (of course, this amount of weight loss could be observed only if there was no oedema). The caloric value of the food rations provided in the camp amounted to 1,000 to 600 calories per day and was falling as the war dragged on to a close, and it comprised approximately 30 g of protein from vegetable foods, 5 g of fats, 200 g of carbohydrates, 10 mg of calcium, 800 mg of phosphorus, and 5 mg of iron. The content of vitamin A was about 140 international units; vitamin B amounted to 250 mg, and vitamin C to 50 mg.
There was certainly no direct correlation between the degree of malnutrition and the size of prisoners’ oedemas or how exhausted and debilitated they were. Usually general or local oedemas developed in prisoners whose weight loss was sudden or considerable. We observed these symptoms especially in individuals who were suddenly transferred to the camp from relatively good living conditions. Those who experienced a gradual shortfall in the food they received were better able to adapt and ended up with a “dry” condition of undernourishment (no oedemas).
One of the symptoms of the disease was a patent fall in brain activity. Our observations showed that both the macro- and microscopic decline in brain and nerve cells proceeded at a much slower rate than the diminishment of other organs. The organ which was particularly vulnerable to damage was the myocardium. The effects we observed were bradycardia, arrhythmia, a tendency to develop haemorrhages, initially on a microscopic scale but later growing into haemorrhagic diathesis with extensive bleeding in all the body’s organs and cavities, and eventually to infarction and /or thrombosis. Also, we observed a gradually progressing achylia or inability to digest food due to the degeneration of the gastric, intestinal and pancreas mucosa. Yet the organ with the most dramatic functional failure was the liver, which stopped converting phytoprotein into albumin. There was a negative nitrogen balance. Disturbances appeared in all the endocrine functions. The thyroid shrank; we observed the flattening of the epithelium, a colloid resistant to pigmentation, and high cholesterol levels. Clinically, this condition led to cases of myxoedema typical for the concentration camp. Curiously, on returning home and adjusting their metabolism, a large number of these patients developed a severe, toxic form of hyperthyroidism. We also observed testicular degeneration in 70% of the patients we examined. Their 17–ketosteroid level dropped to the minimum value, and the condition was very resistant to treatment, even after patients had returned home, although there was a gradual improvement. Nearly all the women held in the camp experienced disorders and dysfunction of the female reproductive organs, such as vulvovaginitis and menstrual disorders.
We observed departures from the norm in the morphology of the adrenal cortex. We had patients with a flat blood sugar curve following a dose of glucose. Some prisoners had a darker skin pigmentation, indicating impaired enzyme activity. There were cases of inhibited activity of the pituitary gland, manifested first in the anterior lobe and disrupting hormone secretion. Usually, there was no impairment to the posterior. No changes were observed in the pineal gland. Calcium levels were low. But we also observed symptoms of the opposite conditions: catabolic changes affecting the skeleton, manifested in the form of osteomalacia and osteoporosis, in which calcium from the bones tended to be deposited chiefly in the pericardium and blood vessels, or excreted in the patient’s stool. We observed many cases of bone atrophy attended by hyperactivity of the osteoclasts and extremely low levels of cholesterol.
Patients’ blood counts gave values typical of anaemia, with haemoglobin levels of 75–70% or even less, but with only a slight fall in blood serum protein. It was a hypo- or hyperchromic, macrocytic type of anaemia with macrocytosis. We tended to observe low reticulocyte counts, leucopenia attended by a relative extent of lymphocytosis and a high red cell sedimentation rate. Total blood counts were well below 5 g/dL, and readings for blood plasma albumin were up to 3% attended by general hydraemia (with solid parts accounting for only 15%). The first fall we observed at the beginning of malnutrition was in prisoners’ level of globulin, while their albumin level was still normal. This was followed by rate of fall in albumin level so rapid that it made for a relatively rising globulin content. According to Gsell, what occurred was a fall in γ-globulin, and a rise in α- and β-globulin, which would have made it a hypoalbuminaemia syndrome, although a rise in water and salt content was a contributing factor.
The first subjective symptoms of hunger disease to occur were associated with the nervous system: paraesthesia (“pins and needles”) in the limbs, followed by a general decline in mobility. With the passage of time, the work of all the organs in the body slumped to the vita minima level. A team of researchers from Leningrad have reported that during the blockade of the city all of the characteristic features marking out an individual were diminished and blurred [due to starvation]; while Polish researchers observed a similar phenomenon in the Warsaw Ghetto5 as what we witnessed in the concentration camp. Even people who were quite young became completely indifferent to the outrages going on around them and didn’t care what would happen to them. They could drop off and fall asleep in any place they happened to be and, as sometimes happens with the elderly, passed from life into death so gradually that it was hard to say when exactly they died. The Muselmänner6 in the concentration camps may serve as a typical example of the condition. An embodiment of the final stage in a wide spectrum of vegetative disorders and decline in physical and mental activity, Muselmänner were literally just like a bag of bones, skeletons encased in a dry, grey skin with the last vestiges of muscles attached to it, slowly slithering along from place to place and tripping over anything that happened to stand in their way. For them, the cause of death was inevitably either hepatic or hypoglycemic encephalopathy, if cardiovascular collapse following even a minor strain or injury did not kill them earlier, which is what usually happened.
Just like other doctors in the camp, in thousands of the post-mortems I conducted I observed very serious changes in the liver, which could shrink down to one-fifth of its initial weight due to a very low level of glycogen (unless stasis had occurred due to complications from infections). Under the microscope we observed extensive fatty streaks with intracellular hydrops. In many cases clinical tests confirmed acute liver depletion proceeding at a dramatically fast rate with all the usual clinical and anatomical pathological symptoms and soon terminating with hepatic encephalopathy.
What we observed in the lungs, apart from specific changes, were numerous oedemas extending over a range of sizes and indicative of pulmonary apoplexy or malacia. This condition often led to erroneous diagnoses of pleural cavities or distensions being made from the clinical observations. The hearts we saw during autopsies of the bodies of prisoners who had been undernourished had clearly shrunk and atrophied. Just like the other organs, the hearts had lost much of their muscle tissue and were no longer able to sustain physical strain. For the overwhelming majority of prisoners, this condition was associated with a considerable fall in blood pressure, particularly diastolic pressure. The cardiac muscle had degenerated and developed cardiomyopathy (“brown atrophy”). Hearts which were small in size were more susceptible to these changes than ones which were large (of the cor bovinum type).
In the overwhelming majority of the post-mortems I did, I observed macroscopic and histological evidence confirming atherosclerosis, which occurred even in very young individuals. Our observations concurred with the reports made by a team of Belgian doctors (Lanny, Halshoffer, Uehlinger and Mollison7), as well the Warsaw Ghetto physicians (Fliederbaum and Stein8). We found that even the bodies of individuals in the 17–30 age group had extensive atherosclerosis with distinct lipid infiltration on the inner wall of the large vessels and oedema on the outer wall and the connective tissue under it.
The blood pressure of all of these individuals had been clearly on the low side (no more than 100 mm Hg for their systolic pressure), and hence they suffered from a distinct bradycardia, with a rate of 40 –50 or even fewer heart beats per minute. They also had a low body temperature, of 35 degrees Celsius or less. At first we thought that the atherosclerotic changes we observed, particularly in the aorta, coronary and cerebral vessels, were the after–effects of infectious diseases such as syphilis or malaria, but when we started to conduct post–mortems during large–scale epidemics of typhus, typhoid, and dysentery, we found we had been wrong about this. There was no difference in the incidence of atherosclerosis between persons who had contracted those diseases and those who had never suffered from them. Most of the victims who died during the epidemics came to the camp straight from communities with a low level of immunity, contracted an infectious disease soon after arriving and died within a short time. The atherosclerotic changes observed in their bodies after death were found to be far less conspicuous than the respective changes in the bodies of prisoners who had been held in a concentration camp for years and were much more resilient to infection. On the grounds of all these observations, we discovered that atherosclerosis along with all of its clinical and anatomical pathological properties was directly correlated with long-term confinement in a concentration camp and occurred more often in association with dry rather than oedematous types of hunger disease.
As I have already said, our post-mortem observations were done almost exclusively on the bodies of persons who for years, right up to their death, never had a gram of animal fat in their diet. The food rations in a concentration camp did not contain animal protein, only vegetable protein, and were made up almost entirely of carbohydrates (but of course with no sugar as such), with a more or less sufficient amount of vitamin C. In the last years of their confinement, prisoners held in German concentration camps (except for those who were working in key production plants for the German war industry) were kept on a diet consisting almost entirely of mangelwurzel (fodder beet). Only rarely did they get a portion of carrot, always in a soup, with a small piece of brown bread. For years on end they never got the chance to have even a drop of alcohol or smoke a cigarette (except for the very few “bigwigs” in the camp, who enjoyed certain privileges). On the other hand, ordinary prisoners were always on the move out in the open air because they had to do heavy labour.
When we autopsied the bodies of persons whose body weight had been half of its original weight for several years before they died, we found they had an advanced stage of atherosclerosis, with plaque developing on the inner wall as well as in the form of aortic calcification. We observed the most conspicuous changes on the endocardium, heart valves, coronary vessels, and on the entire aorta right down to the point where the abdominal aorta bifurcates, and sometimes even down to the pelvic arteries. Cases of cerebral atherosclerosis, especially in the mesencephalon and in the arteries of the brainstem, were just as common, even in young individuals. The fact that we encountered atherosclerotic changes in the kidneys only very rarely was a very interesting phenomenon. In general, instances of kidney diseases were rare, even though there were plenty of reasons for them to occur in a concentration camp. Atheromatous changes in the valves of the heart and endocardium took various forms, for instance papillary concretions in the shape of bundles, or less frequently of flat concretions. The older or more recent plaques on them were so firmly attached that often they would form polypous growths, narrowing the vascular lumen. In other cases, the valves were shortened and damaged by the development of fibrous growths penetrating into the adjoining endocardium. This happened especially in the mitral valve and the valves on the aorta, and less frequently in the pulmonary valve. Sometimes we came across cases of the entire valve breaking off and leaving only shreds.
We also observed other advanced stages of atherosclerosis in the cardiac vessels. If the endocardium was atrophic, we would notice them during a post-mortem as soon as we opened up the chest cavity. In such cases, there would be new and old plaques, or soft or fibrous ischaemic lesions on the brittle branching vessels on the inner and outer wall. Very often we saw haemorrhagic infarcts of various sizes in the myocardium, especially if attended by an infection.
The greatest changes were usually encountered in the aorta, not only in the arch but also in the ascending and descending part. We often saw calcified plaques with necrotic changes below even in the arteries around the clavicle, abdomen and in the lower extremities. Sometimes calcified concretions blocked off the entire lumen in the aorta or other organs. There were blood clots settled firmly on the calcified areas and obstructing the lumen. The pressure of these clots produced ulcers which went down into all the layers of the vascular walls and even into the surrounding tissue.
In the histological specimens, we observed fibrosis in the surrounding tissue and collagen fibres saturated with effusions seen under the microscope or with the naked eye. Overall, the post-mortems showed a general expansion of fibrous tissue in all of the organs. There were cases of pachypleuritis (inflammation of the pleura), pericarditis (inflammation of the pericardium), perisplenitis (inflammation of the tissues surrounding the spleen), perihepatitis (inflammation of the peritoneal capsule of theliver) and perinephritis (inflammation of the tissue surrounding a kidney). Coupled with the specific fibrotic and cirrhotic changes frequently observed in the lungs, these conditions faced us with tremendous problems during post-mortems.
Adhesions and agglutinations of this type which developed in areas with pathological changes or where necrosis or ulceration had set in prevented profuse haemorrhage, which would have quickly led to death. Nonetheless, often we observed haemorrhages into the pericardium, pleural cavity, or peritoneum. Haemorrhages of this type into the cavities and tissues tended to occur with infectious diseases, especially typhus and typhoid, but contributory causes certainly included atherosclerosis, and perhaps nutritional dystrophy as well. Our histopathological tests showed only relatively minor symptoms of inflammation of the inner and outer coat of an artery or the surrounding tissues, or other inflammatory reactions in the blood vessels.
We saw that any injuries sustained in the camp could give rise to a weak inflammatory reaction. This was the general rule both for ulcerations as well as for purulent conditions, post-operative wounds, and other diseases. This was due to the anergy which occurs in the pathological processes which attend serious nutritional deficiency. Our histological tests on the cerebral vessels yielded similar results. Under the microscope or with the naked eye, we could observe numerous haemorrhages or foci of atrophy and malacia developing around stiff, atheromatous arteries containing thrombi. In these cases, we noted glial cell expansion in the surrounding tissues.
Remarkably, none of these persons had ever complained of ailments characteristic of atherosclerosis, which is practically incredible for concentration camp inmates kept in such dire conditions and suffering from such bad disorders. They were up and about and regularly went out to work with practically no rest at all; yet they never complained of dizziness and often had to contend with vastly challenging situations calling for a lot of physical stamina and especially mental and psychological endurance as they were forced to watch torture and executions, experience endless air raids, not knowing at all what the future would bring for them. These were all conditions which could have been a threat even to a perfectly fit person. As I have said, the usual cause of sudden death was not atherosclerosis as such, but the acute infections or infectious diseases which individuals with atherosclerosis are likely to contract. The same happened to those who sustained relatively minor injuries or were victims of violence but showed no outward signs of the condition.
A point of special interest is the question of the provenance of the large quantity of cholesterol which accumulated on the walls of prisoners’ arteries. It may help to explain why the fatty infiltration of the liver we regularly observed was larger than what may be encountered even in patients with a considerable degree of fatty degeneration. We were autopsying the bodies of persons who had been extremely exhausted and emaciated down to a weight of 30 kg. Evidence that these fat resources could have come from other parts of the body was provided by the presence of extensive areas of calcification in the pericardium, around the spleen, liver, or kidneys; moreover, we came across bodies with an armoured heart. The condition reached the point when so much calcium was removed from the long bones that they could easily be cut with a knife or a pair of scissors.
There was definitely a hormonal factor at play in this, but the work of the cerebral cortex most certainly made an even greater contribution. Neither hypertonia nor ailments associated with high blood pressure were observed in the concentration camp, not even in elderly prisoners despite the severe physical and psychic injuries they experienced all the time. Likewise, we never saw any cases of diabetes, bronchial asthma, hyperthyroidism, or other disorders commonplace among patients living in an environment of freedom, but declining and vanishing in concentration camp inmates soon after their confinement. There is a large body of data to show that instances of these diseases re-emerged when survivors returned home, occurred more often than before and developed rapidly in normal conditions, especially whenever they coincided with new situations of stress.
The entire syndrome as observed in the concentration camp may be explained by the atherosclerotic changes I have described occurring in the cerebral arteries, even though in other respects it could be regarded as the outcome of malnutrition leading to the degeneration and atrophy of the neural cells. However, these processes were manifested in the nervous system at a far slower rate than in other organs, as confirmed both by the macroscopic and histological tests as well as by the observation of prisoners’ weight.
Our observations do not concur with reports from certain POW camps or situations such as the siege of Leningrad. Of course, the hunger experienced there was different in many respects. It was gradual and ensued as and when people’s domestic food supplies and the public resources ran out and also as more and more of the inhabitants of Leningrad joined in the fighting and resistance. I regard this last aspect the most important point psychologically. In contrast to that situation, a concentration camp inmate started a new, unspeakably horrific life in terrible hunger as soon as he arrived in the camp, was assigned to a particular barrack, and had his camp number tattooed on his body and all his hair shaved off. Many of those who were obese on arrival lost weight at a rate of 15 to 20 kg a month. Some inmates had been in a concentration camp for 10 or 12 years. There was a linear correlation between the degree to which an inmate’s atherosclerosis had advanced and the time he had spent in the camp. Moreover, as I have already said, psychological factors and even minor brain injuries played an important part.
There was a fundamental difference between taking part in armed combat to defend one’s country, or at least assisting those who were fighting, and life in a concentration camp. Whereas combatants still retained their freedom and could exercise their free will to a certain extent, concentration camp inmates were as good as condemned to death right from the start of their confinement. For example, only 20 thousand survived Dachau, the camp in which we were prisoners and which held 260 thousand inmates in the last six years of its operations (1940–1945). It was the same in other camps. We could observe these differences in ourselves and compared our experiences on the front line during the First World War with what we went through in the concentration camp during the Second World War.
In my opinion, on the basis of the facts I have described it would be a sweeping oversimplification to reduce the issues relating to the pathogenesis and prevention of atherosclerosis to the treatment of obesity and keeping patients’ intake of cholesterol–producing foods under control—in other words, to consider the prevention of atherosclerosis as a question chiefly, or even solely of the right diet. The patient’s condition should first be examined taking all the pathogenic, clinical, and anatomical factors into consideration, and only then use the results of the examination as the basis for a comprehensive preventive and therapeutic procedure. This applies especially to all the internal factors coming from the patient himself, including the psychological ones, because they play a very substantial part in the emergence and development of atherosclerosis.
***
Translated from original article: Bláha, František, “W spramie patogenezy miażdżycy tętnic (na podstawie własnych obserwacji w obozie koncentracyjnym Dachau).” Przegląd Lekarski – Oświęcim, 1964.
Notes
- The spelling of Prof. Bláha’s surname has been corrected throughout this article. The Czech diacritic is missing in the Polish text and the surname is spelled “Blaha.”a
- Probably Prof. Bláha means Leopold “Leo” Alexander (b. 11 October 1905 in Vienna, d. 20 July 1985 in Weston, Massachusetts), an American psychiatrist of Austrian-Jewish origin.b
- The Polish article was published In 1964.a
- In fact, the Minnesota Starvation Experiment was conducted over a 12-month period from November 1944 to December 1945, and a 2-volume report on its results was published in 1950.
“The Minnesota Starvation Experiment, also known as the Minnesota Semi-Starvation Experiment, the Minnesota Starvation-Recovery Experiment and the Starvation Study, was a clinical study performed at the University of Minnesota between November 19, 1944 and December 20, 1945. The investigation was designed to determine the physiological and psychological effects of severe and prolonged dietary restriction and the effectiveness of dietary rehabilitation strategies.
The purpose of the study was twofold: first, to produce a definitive treatise on the subject of human starvation based on a laboratory simulation of severe famine and, second, to use the scientific results produced to guide the Allied relief assistance to famine victims in Europe and Asia at the end of World War II.
The study was developed in coordination with the Civilian Public Service (CPS, 1941–1947) of conscientious objectors and the Selective Service System and used 36 white men selected from a pool of over 200 CPS volunteers.
The study was divided into three phases: A twelve-week baseline control phase; a 24-week starvation phase, causing each participant to lose an average of 25% of his pre-starvation body weight; and 2 recovery phases, in which various rehabilitative diets were tried. The first rehabilitative stage was restricted by eating 2,000-3,000 calories a day. The second rehab phase was unrestricted letting the subjects eat as much food as they would like.
Preliminary pamphlets containing key results from the Minnesota Starvation Experiment. In 1950, Ancel Keys and colleagues published the results in a two-volume, 1,385 page text entitled The Biology of Human Starvation (University of Minnesota Press).” See https://en.wikipedia.org/wiki/Minnesota_Starvation_Experimentb - See note 8 below.a
- The Muselmann condition, a term applied to denote the extreme stage of starvation disease, when all the victim’s defence mechanisms degenerated into a state of atrophy, his sense of hunger and pain disappeared, and his body teetered on the edge between life and death.a
- I have not been able to identify the first three persons. Dr Patrick Loudon Mollison, the last-mentioned, was a captain who served in the Royal Army Medical Corps of the British Army and a member of the Royal Colleges of Physicians. In 1946 he published an article entitled “Observations on cases of starvation at Belsen” in the January 5 issue of The British Medical Journal.b
- Dr Julian Fliederbaum (1898–1943) was a physician in the Warsaw Ghetto and the leader of the team of medical scientists conducting observations on hunger disease in the ghetto. He specialized in biochemical research and wrote a report on the symptoms of hunger disease. In 1943 he and his family committed suicide in the ghetto.
Dr Józef Stein (1904–1943) was an anatomic pathologist and chief physician of Czyste Jewish hospital in Warsaw. He conducted autopsies on persons who died of starvation in the ghetto and wrote the chapter on the anatomic pathology of hunger disease in the report on starvation compiled by the doctors in the ghetto and published after the war as Choroba głodowa: badania kliniczne nad głodem wykonane w getcie warszawskim z roku 1942, ed. Emil Apfelbaum, Warszawa: American Joint Distribution. The English version, Hunger Disease: Studies by the Jewish Physicians in the Warsaw Ghetto, was published in 1979 by Myron Winick of Columbia University. Committee, 1946.b
a—notes by Teresa Bałuk-Ulewiczowa, Head Translator for the Medical Review Auschwitz project; b—notes by Maria Ciesielska, Expert Consultant for the Medical Review Auschwitz project.
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