Hunger disease in Auschwitz

How to cite: Kowalczykowa, J. Hunger disease in Auschwitz. Chłopicki, W., trans. Medical Review – Auschwitz. August 20, 2019. Originally published as “Choroba głodowa w obozie koncentracyjnym w Oświęcimiu.” Przegląd Lekarski – Oświęcim. 1961: 58–60.


Janina Kowalczykowa, MD, PhD, 1907–1970, anatomical pathologist, lectured on medicine in the Polish secret higher education system during the Second World War; held the Chair of Anatomical Pathology at the Kraków Medical Academy.

One of the most notorious experiments perpetrated on Auschwitz prisoners was the hunger disease induced in them by the insufficient quality and quantity of their food.

The basic food for women prisoners in the Birkenau camp was a slice of bread with a scoop of jam or a tiny speck of margarine, or rarely a slice of sausage or salted curd cheese issued in the evening, and unsweetened black coffee, or more usually “leaf” tea, in the morning, of course with no bread. At midday prisoners got a bowl of soup cooked from the Avo food extract.1 In an experiment with rats fed a diet modelled on concentration camp food, the animals developed a typical hunger disease syndrome within three months, even if the quantity of food was unrestricted.

In camp conditions the situation was of course worsened by quantitative restrictions as well as by the fact that camp big shots pilfered ordinary prisoners’ rations.

As a result of malnourishment, Auschwitz prisoners suffered from caloric deficit, particularly of animal protein and fat, along with combined vitamin deficiencies.

In the first weeks of Auschwitz hunger disease, an initial period was observed which could be called the compensation period. The body maintained its (glucose) energy needs from its own tissue reserves. Having exhausted their short-term glycogen reserves, patients metabolised the underlying fat tissue layer, and finally their muscle proteins and the tissues of their internal organs. In outcome their body was emaciated to a considerable extent, accompanied by muscle and organ tissue shrinkage. Their weight served as evidence of the extent of the emaciation: according to the data provided by the Commission for the Investigation of German Crimes2 the weight of woman prisoner no A 27859, who was 155 cm tall, was 23 kg, while woman prisoner no 44884, 160 cm tall, weighed 25 kg. Due to the extensive muscle atrophy, patients literally looked like a bag of bones. Sometimes their emaciation was masked to a large extent by hunger swellings. Slowly the hunger disease developed into its full form, which is sometimes referred to as dystrophia alimentaris (alimentary dystrophy).

The changes within the digestive track led to disruptions in digestion and diarrhoea, which prevented the absorption of even the low-quality food and aggravated malnourishment. This trapped prisoners in a vicious circle, worsening their chances of making full use of the available food.

The detailed assessment of individual aspects of hunger disease was not always easy. I was able to understand some specific changes that I had observed during my stay in the camp only after I was released and read the appropriate medical literature. In experiments on animals, specific food ingredients are withdrawn, and then the assessment of the symptoms is easier. But in this horrific mass experiment on humans a number of disease-generating factors overlapped, distorting the clinical picture. Moreover, hunger disease did not always take the same course with everyone and depended on the specific set of circumstances. It was frequently accompanied by complications such as typhus, purulent infections, or injury.

Nonetheless, the typical syndrome displayed some very characteristic changes, which I will try to discuss. These included emaciation, as discussed above, camp diarrhoea, soft tissue swelling, other skin changes and distortions in the nervous system.

Camp diarrhoea, the notorious Durchfall, was a common pathological change experienced by almost every prisoner. The early diarrhoea which occurred in the majority of prisoners was largely fermentative or infectious and passed relatively quickly. Durchfall, diarrhoea proper, developed in starved and severely ill prisoners, and usually resulted in death. The infectious nature of this diarrhoea cannot be excluded in all the cases with complete certainty, but since it usually did not recede in response to antibacterial medications, but only when food intake improved, it can be regarded as resulting from malnourishment. A radical change of diet, particularly when a prisoner received a parcel from home, could lead to a dramatic deterioration in the prisoner’s health; I observed this phenomenon on a number of occasions. The simplest explanation for the pathogenesis of camp diarrhoea is that it was due to a shortage of wholesome nutrients, particularly proteins and thiamine, as may be concluded by observing analogous processes in animals. Initially, the mucous membranes swell up, causing further deterioration of the digestion process. In the course of the disease, the faeces, which are initially foamy and greenish, turn foul-smelling, and later watery and mixed with blood, with subsequent excretion becoming very frequent and sometimes involuntary. The mucous membrane, which is initially only swollen, undergoes scabbing and then ulceration, leading to a condition very similar to shigellosis.

The swelling on the lower limbs, which sometimes ascended to the trunk, did not affect all prisoners. There were two forms of hunger disease: one with swelling (oedema), and the “dry” form with no swelling, and I can find no explanation—either on the basis of personal experience or of the professional literature—when and why a particular form occurred. The swollen form is generally associated with hypoproteinemia, primarily due to inadequate protein intake. According to Leyton, hypoproteinemic swelling recedes after protein has been administered intravenously. The Russian women in Birkenau who liked to exchange curd cheese or a  piece of sausage for a bowl of soup, which was larger in volume, developed swelling much more frequently than other inmates. In contrast, prisoners with the dry form of nutritional attrition must certainly have suffered from hypoproteinemia but, in spite of that, experienced no swellings, for which I cannot find a convincing explanation on the basis of my observations. The intensifying of swellings on the lower limbs should be treated as the aggregation of the osmotic and hydrostatic factors in hypoproteinemia. An increase in the permeability of the vascular walls could have had some significance, too.

It is not quite clear in terms of pathogenesis what caused the emergence of large sub-epidermal blisters filled with serous fluid. Blisters also appeared on the limbs and specifically on the shins, elbows and shoulders. It cannot be ruled out that the cause of the sub-epidermal blisters was similar to that of the skin swellings. They occurred in highly emaciated patients with sub-epidermal atrophy; perhaps this atrophy could explain the tendency for the serum to penetrate the sub-epidermis and form blisters. We did not observe a considerable amount of local inflammation when the blisters were torn off by the rough surfaces of the blankets or straw mattresses, and the prisoner’s body failed to react. For cases of hypoproteinemia, in which the first stage is hypoalbuminemia followed by hypoglobulinemia, the body’s ability to develop antibodies dropped considerably whenever an infection occurred, and hence many infections, particularly purulent infections, were anergic.

Other changes observed in the skin layers were erythematous, which sometimes became more acute in the spring months. These conditions tended to be pellagroid and were associated with niacin deficiency.

The incidence of hair greying on a mass scale in young inmates should be associated with food shortage, most probably with a shortfall in pantothenic acid. There are obvious analogies with experiments conducted on dogs and rats, which turn grey when starved, but recover their black fur when their proper diet is resumed. Nicholls described similar observations in starved children, who later recovered their original hair colour.

What I saw less of personally was the occurrence of a brownish skin colour reminiscent of Addison’s disease, while occasionally I observed atrophic changes in the epidermis, particularly on the corners of the mouth, with secondary losses due to the generation of scabs which resembled angulus infectiosus (inflammation of the lips) but had a different pathogenesis (cheilosis, dry scaling and fissuring of the lips).

Furthermore, there was a series of other interesting details which could be identified in the clinical picture of hunger disease. For instance, one of the striking features observable in older female prisoners was their dull, muffled, hoarse voice. This change could perhaps also be attributed to a shortage of vitamin A combined with damage to the stratified squamous epithelium.

On the other hand, it would be harder to account for the amenorrhoea commonly observed in prisoners solely by malnourishment; mental processes, mainly the permanent sense of horror and simply fear, were of immense importance in this respect. Amenorrhoea also occurred in women who were better fed but lived in concentration camp or prison conditions.

What was particularly characteristic were the symptoms of nervous system disorders, both mental and neurological. As weight loss progressed, prisoners’ psychological changes increased too: their despondence and apathy as well as their drowsiness intensified. All their reactions slowed down, and sick prisoners followed orders much more sluggishly. Their slow response to orders often evoked attacks of rage on the part of the guards, who considered the prisoners’ behaviour a show of passive resistance. Sick prisoners grew weaker and weaker, their faces turned mask-like, and they preferred to squat instead of sitting up. Such inmates were generally referred to Muselmänner. Always cold and with their blanket wrapped over their body, they were a characteristic sight.

There was another reason for squatting. Some patients suffered from pain in the lower limbs. Page described this as the painful-feet syndrome. The surface of the feet was sore, so when walking, patients tended to support their weight on the outside edges of their feet, which made them waddle. The condition was reported to intensify at night and when the weather changed. What with the considerable weakness in their lower limbs, patients felt better when they squatted. They could also experience spastic conditions in their muscles, sensory disorders, and changes in reflexes. All these changes can be explained by the demyelination of the nervous fibres and partial axonal damage, which is associated with deficiency of group B vitamins,3 especially thiamine.

The women of Birkenau were very clearly affected with sensory disorders. Starved, weakened with illnesses, permanently cold, whenever they were indoors they flocked to the stove, which was more of a brick chimney shaft running horizontally along the barrack. Sick prisoners would often sit on the chimney shaft, as on a bench. Consequently they developed severe burns, even 3rd degree burns, on their buttocks and the back of their thighs. Yet sometimes they did not even feel they had been burnt. The fact that tissue burns occurred much more easily in people whose capillaries had been damaged was another aspect of this matter.

I saw a case of a severely malnourished patient whose feet had been gnawed by rats during the night, leaving only the bare tendons on the surface of her feet—and still she did not react. After her wounds were dressed she lived for another two days. Mitchell and Black have also observed sensory disorders; Lewis and Musselmann observed that changes in the central nervous system receded after nicotinic acid was administered, while changes in the peripheral nerves receded after the administration of thiamine. There were changes affecting the auditory nerves too, and this is why patients’ hearing was muffled; they complained of persistent humming or ringing in their ears.

One could also enumerate many other symptoms in the multifaceted hunger disease complex, and try to explain their pathogenesis. This cannot be done in a short overview, and it was not my aim. My intention was to recall the horrific experiment of hunger disease artificially evoked in Auschwitz prisoners.

Translated from original article: Kowalczykowa, J., “Choroba głodowa w obozie koncentracyjnym w Oświęcimiu.” Przegląd Lekarski – Oświęcim, 1961


  1. An extract made of weeds or fishmeal.
  2. Główna Komisja Badania Zbrodni Niemieckich w Polsce, the central Polish authority for the investigation of German war crimes, set up in 1945.
  3. I.e. beriberi.


1. Lewis, C. F., and Musselmann, ?. ?. Observations on pellagra in American prisoners of war in the Philippines. The Journal of Nutrition. 1946; 32(5): 549–558.
2. Leyton, ?. G. Effects of slow starvation. The Lancet. 1946; 2(6412): 73–79.
3. Mitchell J. B., and Black J. A. Malnutrition in released prisoners of war and internees at Singapore. The Lancet. 1946; 2(6433): 855–862.
4. Nicholls, Lucius. Grey hair in ill-nourished children. The Lancet. 1946; 2(6415): 201.
5. Page, J. A. Painful-feet syndrome among prisoners-of-war in the Far East. British Medical Journal. 1946; 2: 260–262.

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