Proteothesaurismoses (Stored Protein Diseases)

On health consequences of protein overconsumption

excerpted from the book Eiweißspeicherkrankheiten by Prof. Lothar Wendt, University of Frankfurt, Germany, web published and edited for enhanced readability by © Healing Cancer Naturally (incl. appended glossary)

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Corrections of faulty premises

Before we can embark upon our subject of "STORED PROTEIN DISEASES", we have to correct three erroneous premises upheld by the presently valid doctrine of nutrition:

First error: fig. 10

It’s almost a dogma of the current nutritional doctrine that the increase of heart attacks (cardiac infarctions) since World War II, as far as nutrition is concerned, has been caused by the increasing fat consumption among the populations of the western industrialized nations. The yearly publications of the Statistisches Bundesamt (Federal Agency of Statistics) Wiesbaden and the Ministry of Nutrition in Western Germany, as well as the WHO publications, confirm however that during the last 30 years only the increase of animal protein consumption shows a correlation to the increase in the number of heart attacks.

Fig. 10 Between 1934 to 1978, heart attacks increased tenfold (even twentyfold between 1946 and 1978). At the same time, fat consumption remained the same, while potato and cereal consumption even decreased by 45 %. Since potatoes and cereal products constitute the main representatives of both our carbohydrate and vegetable protein consumption, these three nutrients can’t be considered correlatives to the development of the heart attack death graph. During the period of observation, only the consumption of meat increased by 90 percent. Since meat constitutes the main representative of our animal protein consumption, only this nutrient shows a parallel correlation to the development of the heart attack death curve. (Getreide=cereals, Kartoffeln=potatoes, Fleisch=meat, Fette=Fats, Tote=Deaths)

First correction: Fig. 15-18

Not the increase in fat consumption. but the increase in animal protein consumption is the etiological environment factor of alimentary arteriosclerosis.

Second error

According to the current nutritional doctrine, man and other mammalia do not possess a protein store (S. M. Rapoport, 1969). Surplus protein stemming from overfeeding is burned. Regardless in which form the human body takes in calories, the surplus not immediately needed is stored as fat in adipocyts (Errol B. Marliss, 1978). Facts disprove those statements: Fig. 15 shows subcutaneous tissue of a normally nourished man. There are collagen fibres and fat cells.

The subcutaneous tissue of an obese person (Fig. 16) contains almost nothing but fat cells. However in other places of the same fat person’s subcutaneous tissue, we will find nothing but collagen, which is pure protein (Fig. 17).

Fig. 18 on the other hand shows the subcutaneous tissue of a healthy rabbit after an extended period of fasting. Here the fat cells are empty, and the collagen has totally disappeared.

Thus it is proven that overconsumption of calories from mixed food is not only stored as fat but also in the form of protein, and starvation not only consumes fat but also collagen.

Second correction

Man possesses a protein store. The storing molecule for protein is collagen. Subcutaneous tissue is the food store for times of famine, storing all food molecules, in particular one third of the protein content of the body (P. Gedigk et al., 1974), half of the fat content (F. A. Gries et al., 1976), one third of the water content (H. Eppinger, 1949), and probably more than half of the sugar content of the body. Protein is stored in collagen and in the amino group of the mucopolysaccharide, fat is stored in fat cells and water in the vicinity of the mucopolysaccharide. As long as all surplus food is stored in the subcutaneous tissue, overfeeding will lead to obesity but not to illness (Table a). The physiological metabolisation of a hypercaloric meal of mixed food is explained in Table a.

Third error

The predominant opinion of medical sciences is that the same physics - deterministic mechanics - applies to living beings as to inanimate nature. This is an error.

The physics of living beings, of evolution, is the materialistic, deterministic, optimizing teleology: L. Wendt, The physical roots of life (in preparation).

It is a flaw of our physical view of the world that we have not yet succeeded in incorporating the phenomenon of "life" (and of the human being). Therefore, biological science does not possess a scientific foundation as yet. This imperfection is overcome by locating the physical roots of life in our upcoming book.

Fig. 15 Subcutaneous connective tissue of of a normally nourished healthy person. According to A. Maximov, 1927.

Fig. 16 Fat storage in fat cells of subcutaneous connective tissue. According to A. Maximov, 1927.

Fig. 17 Protein storage in the collagen of the subcutaneous connective tissue. According to A. Maximov, 1927.

Fig. 18 Subcutaneous connective tissue in rabbit after long period of starvation. The fat cells are emptied, collagen has disappeared completely. Wide empty spaces appar between the elastic fibres. According to A. Maximov, Handbuch der mikroskopischen Anatomie, 1927.

Table a

The physiological metabolisation of a hypercaloric meal of mixed food takes the following course:

In the bowels, food is digested into a water-soluble pulp of molecules. The diffusion pressure produced pushes these molecules into the blood of intestinal capillaries.

Via the vena portae, they reach the liver.
The liver transforms part of the proteins into urea, which will be excreted into the urine by the kidneys. (This is the specific dynamic effect of proteins.)

The remaining part of the proteins together with the other food molecules flow from the liver into the blood circulation, producing a blood-level elevation of all food molecules.
Hyperaminoacidemia Hyperalbuminemia Hyperglycemia Hyperlipemia Hyperhydremia
Food molecules are transported by the blood circulation

partly to capillaries of interstitial tissues in the large organs, heart, kidney, brain and so on.

partly to capillaries of subcutaneous tissues

food molecules, having arrived in interstitial tissues are metabolised by the organ’s cells for cellular nutrition and cellular function
food molecules, having arrived in subcutaneous tissues, are stored, as there are no cells to be fed

amino acids and protein as collagen

amino acids and glucose as mucopolysaccharides

fat in fat cells
water in the vicinity of the mucopolysaccharide

organ cells excrete metabolic waste matter into tissue fluid.
This is how food is stored in subcutaneous tissues.

Table b

Destorage of subcutaneous tissue during starvation

out of collagen comes  -> protein and amino acids
out of mucopolysaccharide come -> glucose and amino acids

out of fat cells come

-> fatty acids
out of the vicinity of mucopolysaccharides comes -> water

Tissue fluid discharged of food molecules returns via lymphatic capillaries into the blood circulation, getting a new load from the bowels for the next run of the nutrition stream. After 500 runs in about 3 hours the food transportation of the meal is finished.

This process of food metabolisation and storage has lowered the postprandial filtration and diffusion pressures in the blood and tissues to normal, equalizing the pressure differences. The metabolism has again attained its zero state of rest. This metabolisation of a hypercaloric meal is only possible with the cooperation of the subcutaneous tissue store with specific storing molecules for each food molecule. The presently valid doctrine’s assumption that all surplus food is stored as fat is unable to account for the multiplication of all storing molecules in subcutaneous tissues during periods of overfeeding and their gradual fading in periods of starvation.

Table a shows an example of the structure and function of the body’s tissue store for food molecules. In reality, the body has many more storing molecules at its disposal: calcium is stored in the bone, iron in the liver’s Kupffer cells, iodine in the tissue of the thyroid gland, glycogen in liver cells. As long as the next meal is taken only after complete metabolisation of the former meal, metabolical processes will always follow these physiological pathways. The person may grow obese but not ill.

About the urea cycle of liver cells

From the protein contained in a mixed meal, the human body excretes a certain part into the urine in the form of urea.

The liver cells’ urea cycle with a high maximum of urea producing potency is the following.

Table c

Of a hypercaloric protein meal

the normally fed healthy person excretes the surplus nitrogen (N) as urea. The remaining N is built up to human protein. a person who had to endure a long period of protein starvation will excrete no food protein as urea but will build up all food protein to human protein. an overfed person with full protein stores will excrete all food protein as urea.

This phenomenon was more or less known to the founders of the modern nutrition doctrine as early as 100 years ago. They called it "the specific dynamic effect of protein". Many explanations for the phenomenon were given, but not one was satisfactory. In 1972 we were searching for compensating mechanisms enabling the body to defend itself against an overflow of protein in persons indulging in a diet of too much animal protein. Finding and studying this phenomenon, we acknowledged it as an overflow valve for surplus protein.

From our present knowledge we can add:

The etiological hereditary factor in alimentary arteriosclerosis is a weakness of the body’s urea production potency, being smaller than the daily intake of surplus animal protein.

The person with a low maximum of urea production is able to excrete only part of the surplus animal protein food as urea. The unexcreted remainder of the surplus protein goes, together with the other nutrition molecules, into the capillaries of the subcutis and into the interstitial tissues of the organs.

In the subcutis all food molecules are stored physiologically, without negatively impacting the person’s health.

The inflow of superfluous protein molecules into the interstitium, however, can have bad consequences. The organ cells take only as much nourishment as they need, leaving the rest in the interstitial tissue. So with each meal too rich in animal protein, the protein level in the interstitial tissues increases until it oversteps the threshold of storing cells in the tissues which now begin to store the surplus protein molecules.

If no animal protein is consumed in the following days, the needed protein amount is taken from the interstitial tissue store, reducing it in size. If the person, however, persists in overeating protein, the storing of protein in the interstitial tissues will continue. The interstitial tissue thickens and broadens, marking the beginning of the pathological storing of protein and the onset of arteriosclerosis.

About the two kinds of protein stores

The reader is asked to always keep in mind the difference between the two types of stores, the subcutaneous store on the one hand, and the "congestion stores" of blood, blood vessel walls, and interstitial tissues on the other. The subcutaneous store is the physiological store, meant to enable a person to survive a period of starvation. An adequate, even abundant filling of this store is appropriate. The other three stores - we call them "congestion stores" - do not have the same function as the subcutis. On the contrary, under physiological conditions in a healthy person, those stores will never function as stores but merely as a ”soup tureen” in which the food stream flows so that the cells can have their meal; subsequently, the interstitial tissue will be empty again until the next meal, when they refill to serve as a soup tureen for the cells.

Only when more food is flowing into the soup tureen than the cells are able to eat, a rest of the soup will remain in the interstitial tissue. That means congestion in the tissues, and congestion is the adequate impulse for the tissues’ storing cells to store the congested molecules. If that happens after each meal, the interstitial tissue grows thicker and thicker. The doubling of its physiological size in itself has pathological consequences. These consequences are shown in Table d.

The pathogenic storage (Table d)

The Table begins with the thickening of the interstitial tissue which produces a retardation of the tissue stream flowing from the capillary blood through the capillary wall through interstitial tissues to the organ cells in order to feed them. The congestion of the nutritional stream has three consequences, which are explained in the three columns of Table d: the consequences downstream of the hindrance are explained at the first column, interstitially at the second column, and upstream at the third column. Let us begin with the first column, the disturbance downstream of the thickened interstitial tissues.

Table d

Consequences of protein overconsumption

Thickened interstitium Consequences


Column 1


Column 2


Column 3


stagnation rises



hindrance of energy supply (insulin, 02, glucose) for muscular cells.
in capillaries leading to increase in blood levels, to risk factors: amino acids, albumin, glucose, uric acid, cholesterol, fibrinogen, insulin
hindrance of food supply to cells, atrophy and necrosis of cells
Compensation by anaerobic energy metabolism leading to tissue acidosis
hemoconcentration, increase of viscosity, retardation of microcirculation
cells have no sensitive innervation
myalgia (hindrance of removal of metabolical waste products leads to tissue poisoning)
angina pectoris


protein storage of endothelial cells, on basal membranes
death by heart weakness or interstitiogenic cardiac infarction during angina pectoris attack
thickening of basal membranes, reducing permeability
cellular cardiac infarction is painless
microangiopathy, malnutrition of cells


The storage of the congested molecules on the capillary basal membrane continues

amino acids albumin glucose insulin uric acid lipids cholesterol blood proteins growth hormone 02


until the capillary basal membrane store is overfilled.

The overfilled BM can hardly store any more, whereas surplus protein keeps entering the blood due to overeating. This increases the pressure for protein storage in blood again, overstepping at last the threshold of arterial endothelial cells, which now also store congested molecules. That is the beginning of alimentary arteriosclerosis.

Storage on basal membranes eventually leads to BM insufficiency, capillarogenic heart infarction. Storage on intima of arteries: arterial infarction, coronary heart infarction.

Table d, column 1. The congestion in interstitial tissue hinders, downstream, the transportation of food to the muscle cells, leading to cellular atrophy and finally necrosis. As the organ cells have no sensitive innervation, the cellular necrosis would produce no pain. That happening in the heart muscle would be a painless heart attack.

Let us now study the consequences of congestion in the interstitial tissue itself (column 2): In the first column we had examined the consequences of starvation to the cells. The cells, however, not only need food to feed themselves for their wellbeing; each bodily cell has to fulfill a special function for the body. The muscle cells, for instance, have to produce for the body the energy needed for the muscle’s contraction. In order to produce this energy, the cells have to be supplied with glucose, oxygen and insulin (column 2). As the transport through the thickened interstitial tissue is hindered, the muscle cells are lacking the fuel for the production of muscular energy. This leads to a weakness of the heart contraction. The body’s internal control mechanisms compensate for this dangerous situation by activating the anaerobic reserve energy metabolism. This reserve energy metabolism develops contraction energy directly from glucose by breaking it down to lactic acid. Oxygen and insulin are not needed for this type of energy production, however, the energy output of this reserve metabolism is less than the energy output of the glycogen energy metabolism which functions, however, only with a sufficient supply of oxygen and insulin. The other handicap of the reserve metabolism is the fact that its break-down products are acids. Consequently, an acidosis develops in the interstitial tissue.

As glucose breakdown produces less energy output than the splitting of glycogen, glucose energy metabolism is insufficient to keep up the efficiency of the heart action and blood circulation. Therefore, internal control mechanisms have to activate a new energy giving molecule: fat. As 02 is lacking, fat also has to be broken down anaerobically, its split products being acid as well, betaoxybutyric acid, acetic acid and acetone. This increases the energy available for cardiac contraction on the one hand, while increasing tissue acidosis on the other. The thickening of interstitital tissue, however, does not only hinder the transport of molecules from the capillary blood to the cells, but also the backwards transport from the cells to the capillaries, where the waste products and acids of energy metabolism have to flow to be excreted via urine and lungs. Impeded outflow of the waste products created in energy and muscular metabolism produces a congestion edema in the heart muscle’s interstitial tissue which will be rich in acids and split products of muscle metabolism, such as creatinin and uric acid. The walls of the interstitial space are the outside of the capillary walls where the sensitive nerves end as well. So the sensitive nerves are bathed in the acid edema of the tissues. The nerves are irritated by acidity and produce pain in the person. This pain, produced in the skeletal muscles, is myalgia, produced in the heart, the pain of angina pectoris. The progressing stagnation in the interstitial tissue increasingly hinders the transport of food and energy to the muscle cells. The progressing diminution of energy transport makes the heart action continuously weaker, leading to eventual death by blood circulation insufficiency due to untreatable heart weakness. The progressing diminution of nutrition to the cells on the other hand leads to cellular necrosis sooner or later, i.e. cardiac infarction during an angina pectoris attack.

Coming to the third column showing the consequences of congestion in the interstitial tissues, caused by tissue thickening, we see the following: interstitial tissue congestion goes hand in hand with an increased pressure in the tissues, which hinders the food stream flowing from the capillary blood through the capillary wall into the tissues. Consequenly, the congestion spreads upstream into the capillaries. It increases the blood level of all molecules, which have to permeate leads for reaching the interstitium. This blood level elevation caused by congestion is the pathogenesis of risk factors, regarding all food molecules, in particular albumin, amino acids, glucose, fat, cholesterol, insulin etc. This blood level elevation goes together with hemoconcentration, leading to an increase in hematocrit and blood viscosity which again diminishes microcirculation. Increase of blood levels together with retardation of microcirculation means congestion. Congestion, however, is the impulse for the storing cells to store the congested molecules. In blood vessels, the storing cells are the endothelial cells lining the blood vessels inside. Their storing action diminishes the congestion and concentration in the blood, but thickens the capillaries’ basal membranes. Their thickening diminishes the basal membranes’ permeability and hinders, additionally, the nutrition of the cells. Via peptid hormones, the cells inform the regulatory centers of their malnutrition. The centers now give impulses to the stores to the effect that blood levels of all congested molecules are further increased until these elevated blood levels produce diffusion pressures of sufficient force to overcome the thickened basal membranes’ increased resistance, restoring physiological diffusion rates of all molecules and normal cell nutrition.

The compensating blood level elevation of all food molecules is the completion of risk factor developments. So the risk factors of elevated food molecules are produced via two different processes: the first process is a congesting blood level elevation, the second one a compensatory blood level elevation. The storage of food molecules on capillary basal membranes will continue until their storing capacity is exhausted. Now the storing process becomes increasingly slower. However, if the patient’s overintake of protein continues unabated, the protein blood levels rise again, the storing pressure rises as well, until it oversteps the threshold of those endothelial cells which are located on the arteries. Now these also begin to store congested blood molecules. That is the beginning of multifactorial arteriosclerosis.

The pathological storing will now take place in all four of the congestion stores, the arteries, the capillaries, the blood and the interstitial tissues. The place where the storing process occurs the fastest will be the immediate cause of death. So the patient can die of a painless cellular coronary (column 1), or he can die of untreatable heart weakness by blood circulation insufficiency (column 2). On the other hand, if the supply of food to the cell is most impeded, he will die of cellular necrosis, i.e. cardiac infarction (column 2).

If, however, the storage in the blood vessels is happening quicker, either insufficiency of the permeability of the capillary base membrane will lead to a capillarogenic heart attack, or the stenosis of an arteriosclerotic plaque together with an occluding thrombosis will cause death by arteriogenic infarction.

Prophylaxis of hematogenic angiopathies

If man kept his environment clean, most of the presently observed pollutions of his blood (for instance with lead, cadmium, carbon monoxide, nitrosamine and many others) would disappear and with them many of his present angiopathies. More than 50 % of all premature deaths are caused by cardio-vascular diseases (G. Schettler, 1978), only 25% by cancer, and the remaining 25% are deaths from all other diseases combined including traffic accidents. Micro and macro-angiopathies are the last undefeated plague of our times, the most deadly disease of all, double as deadly as cancer, its incidence still growing, cure unknown. Of those premature cardio-vascular deaths, 90 % have their origin in animal protein overconsumption and cigarette smoking. Those patients lose half of their lifespan, dying in their prime of life. They can be cured so that they might live to their physiological life expectation in great age.

Healing therapy

As storage is reversible, storage diseases are curable: no-calorie diet for 4 weeks or animal protein fasting for 1-3 months, encouraged by repeated bloodlettings which work as protein losses, forcing the internal control mechanisms to take protein from the stores: endothelial-perithelial cells break off collagen from intima of arteries and capillary basal membranes, which regain their normal permeability. Under these conditions, elevated risk factors will lower to normal blood levels without further treatment. We have used this therapy for 30 years with great success.

Antigenopathy rather than autoimmune disease

During the last twenty years, immunological research has been performed by chemists in growing numbers. The more this science became a chemical science, the more physicians withdrew from it as it became incomprehensible to them. It is the merit of chemists to have carried immunological chemistry to great success. However, the medical faculty’s retreat from this science was a loss, as unbiological ideas led to faulty conceptions of diseases, for instance with the so-called autoimmune diseases. Faulty diseases led to faulty therapy, for instance the immune suppression in patients whose immune system was already weak in the first place.

In our 1975 book on the subject of "Antigenopathien", we explained that the cause of so-called autoimmune diseases is the antigen of heteroprotein or bacterial or virus antigen. We therefore called those diseases "antigenopathies". They develop because a patient’s weak immune system cannot suppress an antigenemia due to a weakness in antibody production and a weakness of the lysosomal power of protein degradation of capillary endothelial cells. Consequently, the antigenemia attains a high titre. Endothelial cells cannot degrade all antigen. They store the undegraded antigen remainder on the basal membranes and in interstitial tissue. That is the cause of the immunological inflammation of blood vessels and tissues. The cells are degenerated by antigen in many ways: the toxic effect degenerates the protein, deforms the human signal "self". It is the physiological function of the healthy immune system to degrade body tissue which is deformed or destroyed.

The pathogenesis shown in Table d for the course of the alimentary stored protein diseases in cases of protein overconsumption is similarly valid for each other alien protein and for each other antigen which has invaded the blood. The lysosomal degradation power of endothelial cells breaks it down and thereby restores the patient’s health. If, however, the disruptive matter in the blood is excessive, the endothelial cells store the undigested rest on the capillary base membranes and in the interstitial tissues, thus starting the reaction chain depicted in Table d. The interfering matter in the blood in Table d is the euprotein of overconsumption entering our blood in too large a quantity. As it is indifferent to the tissues, it harms the body only by its quantity, thickening BM and interstitial tissues.

The pathogenesis of autoimmune diseases (also known as antigenopathies) is the same as that of arteriosclerosis, except for the difference in the protein stored. In arteriosclerosis the surplus protein of our food is stored in capillaries, arteries, and in interstitial tissues. In autoimmune diseases, it is the antigen of germs and viruses which is stored in those tissues. Both proteins lead to a thickening of blood vessel walls and interstitial tissue. The antigen of germs and viruses, however, in addition to this thickening action also leads to inflammation of the storage tissues.

The blood vessel wall, an instrument of the immune system

The present doctrine of immunity knows only a humoral and a cellular part of the immune system. We found that the blood vessel wall, the endothelial and perithelial cells, the basal membranes and interstitial tissues belong to the immune system as well.

By integrating the immune system into the greater unity of a cleaning system of blood and tissues we restore the unity between immunological and internal diseases. It is thus demonstrated that autoimmune diseases, arteriosclerosis and rheumatism have the same etiology, the same pathogenesis and the same therapy. The common name for all those diseases is "stored protein diseases".


  • adipocyte: a fat cell, a connective tissue cell that has differentiated and become specialized in the synthesis (manufacture) and storage of fat.
  • angiopathy: disease of the blood vessels or lymph ducts
  • antigenopathy: disease triggered by foreign proteins from viruses or bacteria that have entered the blood or tissues.
  • endothelial: relating to the endothelium, the layer of flat cells lining the closed spaces of the body such as the inside of blood vessels, lymphatic vessels, the heart, and body cavities. By contrast, the outside layer of cells that covers all the free, open surfaces of the body including the skin and mucous membranes that communicate with the outside of the body is called the epithelium.
  • hematocrit: the percentage by volume of packed red blood cells in a given sample of blood after centrifugation.
  • hematogenic: pertaining to the formation of blood or blood cells
  • interstitium/interstitial tissue: the matrix or supporting tissue of an organ, as distinguished from its parenchyma or functional element
  • mucopolysaccharide: complex polysaccharides containing an amino group; occur chiefly as components of connective tissue.
  • perithelial: of or relating to the tissue layer around small blood vessels
  • postprandial: following a meal

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