Malabsorption after Small Bowel Resection: Nutrition Therapy

Adaptation of the remaining bowel

The fundamentals of therapy after surgical removal of small bowel segments are the rapid onset of adaptation processes. The processes of adaptation are of considerable importance because the remaining intestine has to take over the tasks of the removed segment as well. During adaptation, the increased use of the remaining intestine leads to proliferation as well as growth of the cells of the small intestinal mucosa. This in turn leads to an increase in the size of the villi as well as the crypts. In addition, enzyme activity in the mucosa of the small intestine is increased. As a result, the absorption capacity in the rest of the intestine improves. However, adaptation of the residual intestine varies from individual to individual and thus continues to determine the extent of malabsorption. Only when maximum adaptation – phase of stabilization – has been achieved can the residual intestine reabsorb essential nutrients and vital substances in sufficient quantities and ensure optimal coverage of nutrient and vital substance requirements. Postoperative adaptation can be divided into three phases

Phase of hypersecretion – immediately after surgical excision, patients experience massive diarrhea lasting approximately 1-4 weeks, accompanied by significant fluid and electrolyte losses. Patients must be fed fluids, nutrients, and vital substances through a venous line (parenterally) during this time and have their serum electrolyte concentrations constantly monitored. If parenteral nutrition is not provided in a timely or adequate manner, energy, nutrient and vital substance deficiencies can develop rapidly
Phase of adaptation – the diarrhea (diarrhea) and thus also the high fluid as well as electrolyte losses decrease slowly. The phase lasts up to a maximum of 12 months. Depending on the extent of adaptation, food can be started in liquid form or via a stomach tube (enteral). Patients with already good adaptation can be fed orally. Establishing nutrition over the intestine is extremely important to prevent atrophy (regression) of the intestine. Oral feeding is the basic requirement for adaptation of the residual bowel.
Phase of stabilization – maximum adaptation is achieved, marked decrease in diarrhea and steatorrhea (fatty stools); stabilization usually occurs 3-12 months after resection, but may take several years; achievement of sole enteral or oral nutrition, although extensive small bowel resections may require lifelong parenteral nutrition in individual cases

As a rule, parenteral nutrition should be supplemented with oral nutrition as soon as possible in the immediate postoperative period. In particular, this must be done to increase the supply of water, vitamins, minerals, as well as trace elements. Oral nutrition is extremely important for stimulating adaptation of the residual bowel. If the adaptation of the residual bowel and thus the oral supply of energy, nutrients and vital elements is sufficient, parenteral nutrition should be progressively reduced. An additional supply of the substrate glutamine can accelerate the adaptation process. Glutamine is essential for the energy metabolism of the small intestinal mucosa and promotes the activity of intestinal cells. The amino acid thus improves the absorption of nutrients and vital substances and contributes to an adequate coverage of requirements.

Importance of growth factors

Parenteral nutrition or nutrition with chemically defined formula diets delays the process of adaptation. For this reason, intact proteins, such as epidermal growth factor, neurotensin, and insulin-like growth factor, and fats of long-chain fatty acids should be administered simultaneously with parenteral or enteral nutrition. These protein and fat molecules are known as growth factors. If patients are fed parenterally without additional administration of growth factors, the epidermal growth factor and transforming growth factor present in the intestine are destroyed by the protein-degrading enzymes of the pancreas present in the intestine. Simultaneous substitution with intact proteins, on the other hand, prevents extensive degradation of the growth molecules. The proteins are able to block the enzymes of the pancreas and thus protect the growth factors from degradation. Additional administration with intact proteins thus increases their number inside the intestine.By stimulating cell growth in the intestinal mucosa, growth factors improve nutrient and vital substance absorption. In return, the growth proteins ensure an increase in mucosal density and a certain growth in length of the residual colon. Finally, growth factors promote adaptation of the remnant colon.

Nutritional recommendations

The therapeutic approach is determined by both the location and extent of the loss of the resorptive surface and the time interval after surgery.

Nutritional medical recommendations above a residual length of the small intestine of 60-80 cm

From a residual length of the small intestine of 60-80 cm, oral nutrition – light whole food – should be started as soon as possible after surgery. The light whole food consists of easily digestible foods with high vital substance and energy content. Such foods, preparation methods and dishes must be avoided that experience has shown to lead more frequently to symptoms of intolerance. In general, spicy fried foods, all dishes prepared with highly heated fats, and foods generally high in fat and sugar should be avoided. The goal is to quickly achieve maximum adaptation of the residual intestine to compensate for the loss of absorptive capacity. As a rule, a complexly composed diet – medium- and long-chain fatty acids, various proteins, such as di- and tripeptides – leads to better adaptation. For this reason, adaptation under oral nutrition is usually completed after a maximum of two years – often after about two to three months. Water-soluble dietary fibers, such as pectins found in fruits, plant gums and mucilages, are essential for restoring intestinal function. Unlike water-insoluble dietary fibers, up to one hundred percent of them are broken down and absorbed by bacteria. Soluble dietary fibers form viscous solutions and have an even higher water-binding capacity than insoluble dietary fibers. By prolonging intestinal transit, reducing stool frequency, increasing water binding and increasing stool weight, soluble dietary fibers counteract diarrhea and thus high fluid and electrolyte losses [6.1]. Fluid intake should occur approximately one hour after the meal, as additional drinking at mealtime accelerates gastric emptying and small bowel passage. It is recommended that water requirements be met via isotonic fluids – electrolyte drinks, such as magnesium– or sodium-rich mineral waters, and carbohydrate-electrolyte mixtures, such as orange or apple juice spritzers. Isotonic drinks have the same concentration of osmotically active particles as those in the blood and are therefore absorbed and reabsorbed at a rapid rate by the rest of the intestine. Because they are enriched with minerals, isotonic liquids make an optimal contribution to meeting nutritional and vital substance requirements. LCT fats If patients suffer from steatorrhea or enteral protein loss syndrome, it is advisable to replace 50-75% of the usual long-chain dietary fats with medium-chain fatty acids – MCT fats1. The importance of MCT fats in the dietary management of steatorrhea and enteral protein loss syndrome

MCTs are cleaved more rapidly in the small intestine than LCT fats under the influence of the pancreatic enzyme lipase2
Due to their better water solubility, the residual intestine can absorb MCT fats more easily
The presence of bile salts is not required for the absorption of MCTs
MCT fats can still be utilized inside the intestine both in the absence and deficiency of lipase and bile salts, respectively – as is the case in short bowel syndrome
The small intestine has a greater absorption capacity for MCT than for LCT.
Binding of MCT fats to the transport lipoproteins chylomicrons is not necessary, because medium-chain fatty acids are transported away via the portal blood and not via the intestinal lymphs
Due to the removal with the portal blood, the lymphatic pressure does not increase during the absorption of MCT and there is less lymph leakage into the intestine, reducing intestinal protein loss – increase in plasma proteins.
In the absorption of long-chain fatty acids, on the other hand, the lymphatic pressure increases and thus the passage of lymph into the intestine – lymphatic congestion leads to a high loss of plasma proteins
MCT are oxidized faster in the tissue than LCT
Medium-chain triglycerides reduce water loss with stool by low stimulation of gallbladder contraction, resulting in low bile salt concentration inside the intestine – reduction of chologenic diarrhea.
MCT fats improve the overall nutritional status
Substitution of MCTs for LCTs subsequently reduces fecal fat excretion – alleviating steathorrhea – and enteral protein loss syndrome.

MCT fatty acids are available in the form of MCT margarine – is not suitable for frying – and MCT cooking oils – can be used as cooking fat. The transition to medium-chain triglycerides should be gradual, otherwise pain in the abdomen, vomiting and headaches may occur – increasing the daily amount of MCT from day to day by about 10 grams until the final daily amount of 100-150 grams is reached. MCT fats are heat labile and should not be heated for too long and never above 70°C. In addition, care should be taken to cover the requirements of fat-soluble vitamins A, D, E and K and essential fatty acids such as omega-3 and omega-6 compounds. When MCTs are administered, fat-soluble vitamins are adequately absorbed.

Nutritional recommendations for massive diarrhea

In short bowel syndrome patients with massive diarrhea and a very high demand for energy, nutrients, and vital substances, replacement with MCT fats does not provide significant benefits. In such cases, the patient should be fed continuously through a nasogastric tube with careful increase in quantity as well as concentration with a formula diet – elemental diet with easily absorbed components. An elemental diet provides the patient with a fully requirement-covering balanced mixture with mono- or low-molecular vital substances, such as amino acids, oligopeptides, mono-, di- and oligosaccharides, triacylglycerides, vitamins, electrolytes as well as trace elements, in ready-to-use liquid or powder form. The composition of the ingredients must be adjusted individually.

Nutritional recommendations from a residual length of the small intestine of 30-50 cm

From a residual length of the small intestine of 30-50 cm, the patient must be fed parenterally in the long term – home parenteral nutrition, since sufficient coverage of the nutrient and vital substance requirements cannot be ensured by oral nutrition.

Nutritional recommendations in resection of the terminal ileum

If the terminal ileum has been resected in patients, vitamin B12 must be administered parenterally. The high losses of fluid, electrolytes, and water-soluble vitamins due to chologenic diarrhea should be compensated by high dietary intake. In addition, the drugs loperamide to inhibit the increased peristalsis in the colon caused by the bile acids and cholestyramine to bind the bile acids in the colon can be used. These drugs relieve chologenic diarrhea and reduce the high water and vital substance losses. Special attention should be paid to low bile acid concentrations in the bile fluid, since fat absorption is significantly impaired by reduced micelle formation. Depending on the extent of steathorrhea, the fat-soluble vitamins A, D, E, and K must be substituted. In addition, the long-chain common fatty acids should be partially replaced with MCT fats to increase fat absorption and improve energy balance. Furthermore, bile acid loss promotes urinary oxalic acid excretion (hyperoxaluria), increasing the risk of kidney stone formation. Patients with a resected ileum should therefore avoid foods containing oxalic acid, such as beet, parsley, rhubarb, spinach, chard, and nuts. Dietary recommendations for intact or resected colon

In cases of short bowel syndrome and simultaneously intact colon, less parenteral energy intake is required under a high-carbohydrate diet. This is due to the ability of the colon to maintain energy balance. With the help of bacteria, it converts carbohydrates not used by the rest of the intestine, as well as dietary fiber, into short-chain fatty acids and reabsorbs them. The short-chain fatty acids can thus be used as energy-providing substrates. Patients can be fed orally if they have a residual length of small intestine of at least 50-70 cm with a preserved and functional colon.If the colon is completely removed, oral feeding is possible exclusively from a residual length of the small intestine of 110-115 cm.

General nutritional recommendations

Overall, patients should maintain a daily energy intake of approximately 2,500 kilocalories. Depending on the location and extent of loss of absorptive surface, it is important to periodically assess patients’ fluid and electrolyte balance–sodium, chlorine, potassium, calcium, magnesium, phosphorus-as well as serum concentrations of vitamins-vitamins A, D, E, K, B9, B12-and trace elements–iron, zinc, selenium. In this way, possible deficiency symptoms can be prevented.

Short bowel syndrome – vital substance deficiency

Vital substance	Deficiency symptoms
Vitamin A	Fatigue, loss of appetite Decreased production of antibodies and weakened immune system. Decreased antioxidant protection Impaired dark adaptation, night blindness Diseases of the respiratory tract, respiratory infections due to changes in the mucous membrane. Disorders of spermatogenesis Anemia (anemia) Increased risk of Tumors of the lung, bladder, prostate, larynx, esophagus, stomach and intestine. Kidney stone formation Drying up to cornification of mucous membranes Attrition of cell and tissue mass of salivary glands and larynx, regression of organs. Dry, brittle nails and hair Dry, rough, itchy skin with rashes Reduced sense of smell, touch, hearing disorders. Deficiency symptoms in children Growth disorders of the long bones Disorders in the formation of dental tissue – dentin disorders. Malformations of the auditory, digestive and genitourinary tracts
Beta-carotene	Decreased antioxidant protection, increased risk for lipid peroxidation as well as oxidative DNA damage. Weakened immune system Increased risk of skin, lung, prostate, cervical, breast, esophageal, stomach, and colon cancers Reduced skin and eye protection
Vitamin D	Loss of minerals from bones – spine, pelvis, extremities – results in Hypocalcemia Decreased bone density Deformities Muscle weakness, especially at the hips and pelvis Increased risk of later osteoporosis Formation of osteomalacia Symptoms of osteomalacia Bone pain – shoulder, spine, pelvis, legs. Spontaneous fractures, often in the pelvic ring. Funnel chest “Map heart shape” of the female pelvis. Loss of hearing, ringing in the ears Disturbed immune system with repeated infections. Increased risk for colon, breast and prostate cancer Deficiency symptoms in children Impairment of the development of bones and teeth. Reduced mineralization of bones with a tendency to spontaneous fractures and bone bending – formation of rickets. Symptoms of rickets Disturbances in the longitudinal growth of bones Deformed skeleton – skull, spine, legs. Atypical heart-shaped pelvis Delayed retention of deciduous teeth, jaw deformity, malocclusion
Vitamin E	Lack of protection against radical attack and lipid peroxidation. Decreases the immune response High susceptibility to infection Disease of muscle cells due to inflammation of muscle tissue – myopathies. Shrinkage as well as weakening of the muscles Disease of the peripheral nervous system, neurological disorders, disorders in neuromuscular information transmission – neuropathies. Reduced number and lifetime of red blood cells. Deficiency symptoms in children Anemia (anemia) Impairment of blood vessels leads to bleeding Disturbances in neuromuscular information transmission. Disease of the retina, visual disturbances – neonatal retinopathy. Chronic lung disease, respiratory distress – bronchopulmonary dysplasia. Cerebral hemorrhage
Vitamin K	Blood coagulation disorders leading to Hemorrhage into tissues and organs Bleeding from body orifices Can cause small amounts of blood in the stool Decreased activity of osteoblasts leads to. Increased urinary calcium excretion. Severe bone deformities
B group vitamins, such as vitamin B1, B2, B3,B5, B6.	Disorders in the central and peripheral nervous system lead to. Nerve disease in the extremities, pain or numbness of the extremities. Muscle pain, wasting or weakness, involuntary muscle twitching Hyperexcitability of the heart muscle, decrease in cardiac output – tachycardia. Memory loss General state of weakness Impaired collagen synthesis resulting in poor wound healing Insomnia, nervous disorders, sensory disturbances. Impaired response of white blood cells to inflammation. Anemia due to decreased production of red blood cells, white blood cells, and platelets Decreased production of antibodies Impairment of cellular and humoral immune defenses. States of confusion, headaches Gastrointestinal disorders, stomach pain, vomiting, nausea. Deficiency symptoms in children Disorders of protein biosynthesis and cell division. Disorders of the central nervous system Disturbance of nervous function and cardiac insufficiency – beriberi Skeletal muscle atrophy Increased risk of cardiac dysfunction and failure
Folic acid	Mucosal changes in the mouth,intestine and urogenital tract lead to Indigestion – diarrhea (diarrhea). Reduced absorption of nutrients and vital substances Weight loss Blood count disorders Anemia (anemia) leads to rapid fatigue, shortness of breath, decreased ability to concentrate, general weakness. Impaired formation of white blood cells leads to the Reduction of the immune response to infections. Decreased antibody formation Risk of bleeding due to decreased production of platelets Elevated homocysteine levels increase the risk for Atherosclerosis (arteriosclerosis, hardening of the arteries). Coronary heart disease (CHD) Neurological and psychiatric disorders,such as. Memory impairment Depression Aggressiveness Irritability Deficiency symptoms in children Disorders in DNA synthesis-restricted replication-and decreased cell proliferation increase the risk for Malformations, developmental disorders Growth retardation Maturation disorders of the central nervous system. Bone marrow alteration Deficiency of white blood cells as well as platelets. Anemia (anemia) Injuries to the mucosa of the small intestine Disorders of protein biosynthesis and cell division
Vitamin B12	Decreased vision and blind spots Functional folic acid deficiency Weakened antioxidant protective system Blood count Anemia (anemia) reduces the ability to concentrate, leads to fatigue, weakness and shortness of breath. Reduction of red blood cells, larger than average and rich in hemoglobin. Impaired growth of white blood cells weakens the immune system Risk of bleeding due to reduced production of platelets. Gastrointestinal tract Tissue atrophy and inflammation of the mucous membranes. Rough, burning tongue Reduced absorption of nutrients and vital substances Loss of appetite, weight loss Neurological disorders Numbness and tingling of extremities, loss of sensation of touch, vibration and pain. Poor coordination of the muscles, muscle atrophy. Unsteady gait Spinal cord damage Psychiatric disorders Memory disorders, confusion, depression Aggressiveness, agitation, psychosis
Vitamin C	Antioxidant deficiency Weakness of blood vessels leads to Abnormal bleeding Mucosal bleeding Hemorrhage into the muscles associated with weakness in heavily used muscles Inflamed as well as bleeding gums (gingivitis). Joint stiffness and pain Poor wound healing Carnitine deficit leads to Symptoms of exhaustion, fatigue, indifference, irritability, depression. Increased need for sleep, decreased performance. Weakness of the immune system with increased risk of infection Decreased oxidation protection increases the risk of heart disease, apoplexy (stroke) Deficiency symptoms in children Weakened immune system Recurrent infections of the respiratory tract, urinary bladder, and the auditory tube, which is connected to the nasopharynx via the tympanic cavity of the middle ear Increased risk of vitamin C deficiency disease- Möller-Barlow disease in infancywith symptoms such as. Large bruises (hematomas). Pathological bone fractures associated with severe pain Wincing after every slightest touch – “jumping jack phenomenon”. Stagnation of growth
Calcium	Demineralization of the skeletal system increases the risk of Decreased bone density Osteoporosis, especially in women with estrogen deficiency. Bone softening as well as bone deformities – osteomalacia. Tendency to stress fractures of the skeletal system. Muscle cramps, tendency to spasm, increased muscle contraction. Cardiac arrhythmias Blood clotting disorders with increased bleeding tendency Increased excitability of the nervous system, depression. Increased risk of Hypertension (high blood pressure) Deficiency symptoms in children Impaired development of bones and teeth Decreased bone density in the newborn. Decreased mineralization of bones with tendency to spontaneous fractures and bone bending – formation of rickets. Symptoms of rickets Disturbances in the longitudinal growth of bones Deformed skeleton – skull, spine, legs. Atypical heart-shaped pelvis Delayed retention of deciduous teeth, jaw deformity, malocclusion of teeth. Additional vitamin D deficiency leads to Hyperparathyroidism – enlarged parathyroid tissue – and increased production of parathyroid hormones – hyperparathyroidism. Hypercalcemic coma
Magnesium	Increased excitability of muscles and nerves leads to Insomnia, difficulty concentrating Muscle and vascular spasms Numbness as well as tingling in the extremities. Heart palpitations and arrhythmias, feeling of anxiety. Increased risk of Decreased immune response Myocardial infarction (heart attack) Acute hearing loss Deficiency symptoms in children Growth retardation Hyperactivity Insomnia, difficulty concentrating Muscle tremors, cramps Heart palpitations and arrhythmias Decreased immune response
Sodium	Fatigability, possible unconsciousness, apathy, confusion, lack of drive, decreased performance – short-term memory. Nausea, vomiting, loss of appetite, lack of thirst. Hypertension (high blood pressure), tendency to collapse, hyperexcitability of the heart muscle, reduction in cardiac output – tachycardia. Muscle cramps Decreased urination
Potassium	Muscle weakness, muscle paralysis Fatigue, apathy Nausea and vomiting, loss of appetite, constipation, decreased intestinal activity until intestinal obstruction. Decreased tendon reflexes Cardiac arrhythmias, cardiac enlargement, tachycardia, dyspnea
Chloride	Acid-base balance disorders Development of metabolic alkalosis Severe vomiting with high salt losses
Phosphorus	Increased mobilization from bone with bone softening as well as bone deformities – osteomalacia. Disturbances in cell formation with impairment of red and white blood cell function. Disorders in the acid-base balance with the formation of metabolic acidosis. Disease of the nerves, which transport information between the central nervous system and the muscles leads to Tingling sensation, pain but also paralysis especially in the arms, hands and legs. Deficiency symptoms in children Increased mobilization from the bones – short stature, formation of rickets. Symptoms of rickets Disturbances in the longitudinal growth of bones Deformed skeleton – skull, spine, legs. Atypical heart-shaped pelvis Delayed retention of deciduous teeth, jaw deformity, malocclusion
Iron	Chronic fatigue syndrome (CFS) Loss of appetite Disorders of thermoregulation High susceptibility to infection of the upper respiratory tract Dry skin with itching Decreased concentration and retentiveness Increased lactic acid formation during physical exertion associated with muscle cramps. Increased absorption of environmental toxins Body temperature regulation may be disturbed Anemia (anemia) Deficiency symptoms in children Disturbance of physical, mental and motor development. Behavioral disorders Lack of concentration, learning disorders Disturbances in the child’s intelligence development Loss of appetite High susceptibility to infection of the upper respiratory tract Body temperature regulation may be disturbed
Zinc	Instead of zinc, the toxic cadmium is integrated into the biological processes,resulting in Inflammatory changes in the mucous membranes of the nose and throat. Cough, headache, fever Vomiting, diarrhea, cramping pain in the abdominal regions. Renal dysfunction and increased protein excretion. Osteoporosis, osteomalacia leads Disturbances in the functioning of the immune system Inhibition of cellular defense leads to increased susceptibility to infection Wound healing disorders and mucosal changes, as zinc is required for connective tissue synthesis Increased keratinization tendency Acne-like symptoms Progressive, circular hair loss Metabolic disorders, such as. Weight loss despite increased food intake Failure of beta cells in the pancreas – high risk of developing adult-onset diabetes (type II diabetes mellitus) Blood clotting disorders, chronic anemia. Reduction of the sense of smell and taste, reduction of vision, night blindness, sensorineural hearing loss. Fatigue, depression, psychosis, schizophrenia, aggressiveness. Male infertility due to hypofunction of the gonads. Deficiency symptoms in children Low zinc concentrations in plasma and white blood cells cause Malformations and deformities especially of the central nervous system. Growth disorders and retardation with delayed sexual development. Skin changes in the extremities – hands, feet, nose, chin and ear – and natural orifices. Wound healing disorders Hair loss Acute and chronic infections Hyperactivity and learning disability
Selenium	Weight loss, intestinal sluggishness, indigestion. Depression, irritability, insomnia. Memory loss, difficulty concentrating, headaches Immunodeficiency Chronic fatigue syndrome (CFS) Thyroid dysfunction due to deficiency of selenium-dependent deiodases. Decreased activity of glutathione peroxidases leads to an increase in peroxides and thus to increased radical formation and increased formation of pro-inflammatory prostaglandins Joint pain due to pro-inflammatory processes. Increased susceptibility of the mitochondria Male infertility Increased risk of Liver damage Muscle pain and stiffness Keshan disease – viral infections, disease of the heart muscle – cardiomyopathy, heart failure, arrhythmia. Kashin-Beck disease – degenerative joint disease with disorders of bone and joint metabolism, which can lead to osteoarthritis and severe joint deformities. Deficiency symptoms in children Immunodeficiency Thyroid dysfunction Increased radical formation Increased susceptibility of the mitochondria Increased susceptibility to infections Increases the need for vitamin E
Copper	Neurological deficits Reduced sperm motility with fertility disorders. Elastin depletion in the vessels, vasoconstriction or occlusion, thrombosis. Anemia (anemia) due to impaired blood formation. Increased susceptibility to infection Increased total cholesterol and LDL cholesterol levels. Glucose intolerance Hair and pigment disorders Osteoporosis due to impaired collagen synthesis Proliferation of smooth muscle cells Weakness, fatigue Copper metabolic disorders Liver damage, hepatitis, cirrhosis – Wilson’s disease. Failure to thrive – Menkes syndrome Skin laxity – Cutis laxa Deficiency symptoms in children Anemia due to impaired hematopoiesis leads to maturation disorders of white blood cells and lack of defense cells in the blood Failure to thrive Skeletal changes with changes in bone age. Increased susceptibility to infections, frequent respiratory infections
Molybdenum	Nausea, severe headache, central visual field defects. Visual disturbances Hyperexcitability of the heart muscle, decrease in cardiac output – tachycardia. Accelerated respiratory rate – tachypnea. Amino acid intolerance with deficient degradation of sulfur-containing amino acids – homocysteine, cysteine, methionine. Kidney stone formation Hair loss
Essential fatty acids- omega-3 and 6 compounds.	Weakened immune system, increased susceptibility to infections. Disturbed heart rhythm Disturbed vision Disturbed wound healing Disturbed blood clotting Hair loss Hypertension (high blood pressure) Hyperlipidemia (lipid metabolism disorder) Kidney damage and blood in the urine Reduced functionality of the red blood cells Skin changes – flaky, cracked, thickened skin. Fertility disorders in women and men Decreased liver function Increased symptoms of arthritis, allergies, atherosclerosis, thrombosis, eczema, premenstrual syndrome – fatigue, poor concentration, marked change in appetite, headache, joint or muscle pain Increased risk of cancer Deficiency symptoms in children Disorders in whole body growth Insufficient development of the brain Reduction in the ability to learn Neurological disorders – poor concentration and performance
High quality protein	Disturbances in digestion and absorption of vital substances and resulting water and electrolyte losses. Muscle atrophy Tendency to accumulate water in the tissues – edema
Amino acids, such as glutamine,leucine, isoleucine, valine, tyrosine,histidine,carnitine	Disturbances in the function of nerves and muscles Decreased performance Limited energy production and resulting fatigue and muscle weakness. Impairment of hemoglobin formation Severe joint pain and stiffness in arthritis patients. High depletion of muscle mass and protein reserves. Insufficient protection against free radicals Weakening of the immune system, since amino acids are the main sources of energy for the immune system Disturbances in the digestive system Fluctuations in blood sugar levels Increased blood lipid and cholesterol levels Cardiac arrhythmias

1 MCT = fats with medium-chain fatty acids; their digestion and absorption is faster and independent of bile acids, so they are preferred in diseases of the pancreas and intestine. 2 LCT = fats with long-chain fatty acids; they are absorbed directly into the body’s own fat depots without much conversion and are released from them only very slowly. They are also known by the term “hidden fats”.