The inadequate nutritional status frequently encountered in Crohn’s patients, which is characterized by underweight, negative nitrogen balance, decreased serum albumin, reduced serum concentration of vital substances (micronutrients), has an extremely negative impact on the patients’ well-being as well as on the course of the disease. In children, malnutrition delays growth in length and puberty [5.1]. Consequently, nutritional therapy or preoperative treatment of Crohn’s disease must consist of a high-energy diet containing sufficient amounts of all important nutrients and vital substances (macro- and micronutrients). The goal of nutritional therapy is to improve the general condition, alleviate symptoms and prevent complications. Treatment is given priority until the relapses of Crohn’s disease – although leaving behind morphological changes in the intestinal mucosa – heal and the inflammatory symptoms subside. In 50-70% of cases, intestinal resection is necessary in the course of the disease because the inflammation of the mucosa does not heal and the intestine shows high-grade changes in the mucosa as well as in the movement pattern. Surgical intervention is also indicated in the development as well as proliferation of carcinomas in the intestine. Nutrition that meets the needs also plays an essential role for the period after surgical interventions, since a poor nutritional status can significantly delay the postoperative course. In order to be protected from pronounced clinical symptoms of deficiency, Crohn’s patients should – depending on their needs – increase their dietary intake of critical vital substances (micronutrients), including fat- and water-soluble vitamins, calcium, magnesium, iron, zinc, selenium, essential fatty acids, proteins and dietary fiber, or be substituted with these. Patients at increased risk of deficiency who have very low serum levels of vitamin B12 and zinc, for example, must be substituted parenterally with these vital substances (micronutrients) [5.1]. In particular, care must be taken to adequately meet the increased requirement for vitamin B12 after resection or loss of function of more than 100 cm of the terminal ileum by parenteral administration. In particular, regular as well as generous intake of vitamins A, E, zinc, and omega-3 fatty acids in Crohn’s patients can reduce the inflammatory process, protect the intestinal wall from ulcers, relieve symptoms, and promote mucosal regeneration.
Dietary recommendations for secondary disaccharidase deficiency
Enteritis regionalis is often associated with secondary lactase deficiency because of the primary inflammatory disease of the small intestine. Depending on the severity of damage to the intestinal villi, many Crohn’s disease patients have decreased lactase activity. In this case, the lactose supplied by milk and dairy products cannot be broken down and consequently not absorbed. In this case, lactose should be largely avoided at the beginning of the dietary treatment of Crohn’s disease in order to avoid typical symptoms of lactose intolerance – flatulence, diarrhea, cramp-like symptoms. Accordingly, low-lactose milk and dairy products must be integrated into the diet to ensure the absorption of the valuable nutrients and vital substances (macro- and micronutrients) contained in milk – including vitamins A, D, E, K, calcium and biologically high-quality protein. As the intestinal villi regenerate during dietary therapy, the activity of the lactase enzyme normalizes and milk and dairy products are again tolerated normally.
Resection or failure of the terminal ileum
Vitamin B12 and bile salts are absorbed exclusively in the lower part of the small intestine – the ileum, or terminal ileum. If the ileum is surgically removed for more than 100 cm or if the intestinal wall is extensively damaged, the intestinal-liver circulation-enterohepatic circulation-which is essential for the regulation of vitamin B12 as well as bile acid circulation, is interrupted
Consequences – resection or failure of the terminal ileum, respectively
As a result of the dysfunction of the enterohapatic circulation, vitamin B12 and bile acids can no longer be reabsorbed by the ileum and thus cannot be absorbed into the bloodstream. Reabsorption of bile acids-again via the liver into the bile, then into the intestine-does not occurAs a result, vitamin B12 absorption is impaired – vitamin B12 deficiency – and unphysiological amounts of bile salts pass into the colon due to the lack of reabsorption. There they increase the contraction waves of the smooth muscles and decrease the reabsorption of water. In this way, bile acids cause chologenic diarrhea with high losses of fluid, electrolytes, and water-soluble vitamins. Bile salts are also excreted in the stool. The liver is unable to compensate for the loss of bile acids by increasing synthesis, resulting in a decrease in bile salt concentration in the bile fluid. As a result of the loss, the primary bile salts are no longer available for micelle formation. The critical micellar concentration leads to decreased utilization of dietary fat and fat-soluble vitamins A, D, E, and K. Since dietary fats cannot be adequately absorbed, the unabsorbed fats as well as fatty lipid products reach deeper parts of the intestine. There, they accelerate the intestinal passage by stimulating peristalsis and finally trigger steatorrhea (chologenic fatty stool) as a result of the increase in fecal fat excretion [5.1]. By also promoting contraction waves in the colon and inhibiting water reabsorption from the intestine, bile salts increase fatty diarrhea. Increased fat loss through the stool also results in increased loss of fat-soluble vitamins A, D, E, and K, as well as essential fatty acids. Depending on the extent of the fat absorption disturbance, a negative energy balance occurs, resulting in weight loss The bile acids produced in the large intestine bind calcium, as a result of which the essential mineral is increasingly excreted together with the bile acids. Calcium deficiencies can rapidly develop as a result. Calcium deficiency is also promoted by the unabsorbed fatty acids, because these combine with calcium to form insoluble calcium soaps and thus inhibit calcium absorption. Furthermore, the loss of bile acid promotes the excretion of oxalic acid in the urine (hyperoxaluria) and thus increases the risk of kidney stone formation. Crohn’s disease patients should therefore avoid foods containing oxalic acid, such as beet, parsley, rhubarb, spinach, chard and nuts. Causes of increased oxalic acid – oxaluria.
- High amounts of glycine enter the colon with bile salts, where it is converted to glyoxalate by bacteria. Glyoxalate is converted to oxalic acid after absorption in the liver.
- High bile salt concentration in the colon increases the permeability of the mucosa to oxalate ions.
- Low bile salt concentration delays the absorption of fatty acids, allowing fatty acids to combine with calcium to form insoluble calcium soaps. Oxalic acid can thus no longer be bound by calcium to calcium oxalate, which means that the free oxalic acid absorbed from food is increasingly absorbed and excreted in the urine[2].
Therapy for hyperoxaluria
A low-fat diet and additional administration of calcium ensures the binding of calcium with oxalic acid and in this way prevents hyperoxaluria and consequent stone formation.
Importance of calcium and vitamin D
Patients with inflammatory bowel disease are often found to have decreased bone density due to steroid therapy Lack of physical activity, inadequate dietary intake of calcium and vitamin D, and the more or less pronounced absorption disorders may also be responsible for low bone density [5.1]. Meeting the increased need for calcium and vitamin D is therefore essential in inflammatory bowel disease. Calcium and vitamin D substitutions promote bone health and prevent deficiencies.
Importance of antioxidants
To fight off bacteria and germs in the area of damaged intestinal mucosa, white blood cells synthesize oxygen free radicals in high amounts. Free radicals multiply in the body in the form of chain reactions, snatching an electron from the attacked molecule and thereby turning it into a free radical itself. The increased formation of radicals – especially in the colonic mucosa – is known as oxidative stress. Oxidative stress is associated with damage to endogenous proteins, enzymes, amino acids, carbohydrates in the cytoplasm as well as cell membranes.In addition, the DNA (genetic material), the cell nucleus and the mitochondria are attacked. Fatty acids are converted into toxic compounds (lipid peroxidation). Impairments of the cell nucleus DNA can lead to gene mutations that impair individual cellular functions. As a result, there is an increased risk that cancer cells – intestinal adenomas or carcinomas – may develop [5.1]. Furthermore, oxidative stress reduces the concentration of antioxidants, which can effectively detoxify free radicals or prevent or inhibit their formation and thus enable the survival of mucosal cells. Without antioxidant protective factors such as vitamins B2, B3, E, D, C, selenium, zinc, manganese and copper, as well as secondary plant compounds – such as carotenoids and polyphenols – harmful oxygen radicals cannot be scavenged. The high level of free oxygen radicals ultimately maintains or promotes the inflammatory reactions of the chronic inflammatory bowel disease. A high dietary intake of antioxidants or substitutions can inhibit the proliferation of harmful radicals in the small and large intestine, reduce its concentration, and decrease the inflammatory reactions of the mucosa[5.1.]
Importance of omega-3 fatty acids and gamma-linolenic acid
In Crohn’s disease, elevated concentrations of the inflammatory mediators leukotriene B4, prostaglandin E2, and thromboxane A2 can be found in the intestinal mucosa and in the irrigation fluid of the rectum[5.1]. In addition, high concentrations of arachidonic acid can be detected in the intestinal mucosa, which promotes the formation of the inflammatory mediators. Evening primrose oil contains abundant gamma-linolenic acid. During drug treatment with evening primrose oil, a high supply of gamma-linolenic acid causes a decrease in the synthesis of the inflammatory mediator prostaglandin E2 and an increased formation of prostaglandins E1. Series 1 prostaglandins in turn inhibit the release of arachidonic acid from cell membranes As a result of the action of the valuable gamma-linolenic acid, the concentrations of inflammatory mediators in the intestinal mucosa decrease, promoting the regeneration of the mucosa. In addition to evening primrose oil, patients are also given fish oil, which is rich in omega-3 fatty acids – especially eicosapentaenoic acid – in the form of gelatin capsules, as a drug therapy. Eicosapentaenoic acid – EPA – has an anti-inflammatory effect in that increased intake leads to increased synthesis of the anti-inflammatory prostaglandin I3 and a significant reduction in the formation of leukotriene B4. Thus, omega-3 fatty acids are of considerable importance for mucosal regeneration of the intestinal wall. In Crohn’s disease, administration of 5 grams of omega-3 fatty acids per day leads to a reduction in the extent as well as the severity of intestinal inflammation and relief of symptoms by influencing inflammatory mediators. In addition, essential fatty acids – omega-3 fatty acids such as alpha-linolenic acid, EPA as well as DHAand omega -6 compounds such as linoleic acid, gamma-linolenic acid and arachidonic acid – are particularly needed to meet the increased caloric requirements of Crohn’s patients. Importance of MCT fats1 in the dietary management of steatorrhea and enteral protein loss syndrome.
- MCTs are cleaved more rapidly in the small intestine than LCT fats2 under the influence of the pancreatic enzyme lipase.
- Due to their better water solubility, the small 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 exploited both in the absence and deficiency of lipase and bile salts inside the intestine, respectively
- 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 removed via portal blood and not via intestinal lymph
- 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.
- During the resorption 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 a low bile salt concentration inside the intestine – reduction of chologenic diarrhea.
- MCT fats improve overall nutritional status
Substitution of MCTs for LCTs subsequently leads to a reduction in fecal fat excretion – alleviation of steatorrhea – and enteral protein loss syndrome. MCT fatty acids are available in the form of MCT margarine – not suitable for frying – and MCT cooking oils – usable 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 meet 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 sufficiently absorbed [5.2]. 1 MCT = fats with medium-chain fatty acids; their digestion and absorption is faster and independent of bile acids, so they are preferred for pancreatic and intestinal disorders. 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 under the term “hidden fats”.
Importance of low-molecular-weight protein
Because of the frequent undersupply of protein-due in part to high intestinal protein loss and hypalbulinemia-Crohn’s disease patients have an increased need for high-quality proteins. In particular, low-molecular-weight protein – high-quality, complete and short-chain protein from milk, soy, potato or egg – should be supplied, since its utilization is almost 100%. This is due to the absorption of this protein, which requires only a greatly reduced effort by the human digestive tract. Even considerably weakened patients can make the effort of protein resorption. Enzymatic degradation of high molecular weight dietary protein produces small amino acid chains (oligopeptides) that are degraded and metabolized almost as rapidly as glucose. In contrast, common long-chain dietary proteins – meat, for example – are only 40-70% broken down and absorbed. In some Crohn’s patients, conventional dietary proteins can trigger allergic reactions and should therefore be reduced in the diet. Crohn’s patients should consume about 100-125 grams of low molecular weight protein per day to increase resistance to disease-causing agents, such as bacteria and germs. The additional intake of the high molecular weight protein in protein deficient people has a positive effect on body weight, total serum protein, serum albumin as well as on the level of gamma globulins. It also supports immune system function, blood circulation, and absorption and utilization of nutrients and vital substances (macro- and micronutrients). Low molecular weight protein provides the amino acid glutamine. This substrate plays an essential role in the energy metabolism of the mucosa of the small intestine, as it is an important source of energy for the intestinal cells. Glutamine counteracts mucosal damage of the intestine and is needed for the healing process of the small and large intestinal wall. Adequate and regular consumption of dietary fiber – protective effects.
- Inhibition of the development of colon tumors – by binding carcinogens as well as by the short-chain fatty acids formed during bacterial degradation – in particular, butyric acid exhibits anticarcinogenic effects. By increasing stool weight, dietary fiber dilutes the concentration of all carcinogens. Since the transit time of stool is shortened by acceleration of intestinal peristalsis in a high-fiber diet, the contact time of carcinogens with the intestinal wall is also reduced. Patients on high-fiber diets show an approximately 40% reduced risk of colorectal cancer, with mortality decreasing as fiber intake increases.
- Cardioprotective effects – dietary fiber grants protection against cardiovascular disease.Just under 30 grams of fiber a day is enough to reduce the risk of heart attack by almost half.
- Lowering LDL cholesterol levels by up to 25%.
- Improvement of carbohydrate tolerance – due to the low glycemic index of fiber-rich foods. Also in diabetics, it comes as a result of high fiber intake to improve carbohydrate tolerance.
- Immunomodulatory properties – especially hemicellulose and pectins. If Crohn’s patients pay attention to a regular fiber intake – about 30 grams a day -, the immune competence can be significantly improved by increasing the non-specific as well as specific defense mechanisms.
- Increased excretion of fat as well as toxic substances with the stool – dietary fiber binds fatty acids and toxic pollutants as well as heavy metals. For example, pectin binds with lead and mercury, increasing the excretion of heavy metals and protecting the body of Crohn’s patients, already weakened by the inflammatory reactions, from oxidative damage
Due to the versatile mechanisms of action of fiber, patients with Crohn’s disease should definitely increase their fiber intake and in parallel ensure adequate fluid intake. Dietary fiber requires fluid to swell. Low fluid intake reduces their swelling capacity, which may cause constipation
Importance of phytochemicals
If Crohn’s patients pay attention to an adequate intake of bioactive substances, such as carotenoids, saponins, polyphenols, and sulfides, the development of colorectal cancer may be inhibited.
- Carotenoids – found, for example, in apricots, broccoli, peas and kale – are able to inhibit the phase 1 enzymes responsible for cancer development.
- Saponins – found primarily in beans, green beans, chickpeas, as well as soybeans – bind primary bile acids, helping to reduce the formation of secondary bile acids. In high concentrations, secondary bile acids can act as tumor promoters. Primary bile acids bound by saponins are increasingly excreted in the stool. The body’s own cholesterol is then used for the new formation of bile acids, which lowers the cholesterol level in the blood. By saponins insolubly bind cholesterol in the intestine, the cholesterol level is also lowered
- Flavonoids belonging to the polyphenols – primarily found in citrus fruits, red grapes, cherries, berries as well as plums – have structural similarities to nucleotides and can therefore mask DNA binding sites for active carcinogens. They also have the ability to prevent the growth of DNA-damaged cells. Furthermore, flavonoids have a positive effect on the vital substance status (micronutrients). They increase the effect of vitamin C and coenzyme Q10 by a factor of ten, have a stabilizing influence on the plasma level of vitamin C and delay the consumption of vitamin E [6.1]. Phenolic acids – especially found in various cabbages, coffee, radishes and whole wheat grains – have a strong antioxidant effect and can therefore inactivate numerous cancer-promoting substances from the environment, such as nitrosamines and mycotoxins.
- Sulfides – abundant in garlic, onions, chives, asparagus and shallots – exhibit similar anti-cancer effects as carotenoids, saponins and polyphenols. They also have an additional immunomodulatory effect, activating natural killer cells as well as cell-killing T lymphocytes to halt carcinogenesis [6.1].
In addition, phytochemicals possess a protective effect against esophageal, gastric, liver, lung, bladder, breast, cervical, prostate, as well as skin cancers. In addition to anticarcinogenic effects, carotenoids, saponins, polyphenols and sulfides also exhibit antioxidant, antimicrobial, antiviral, cholesterol-lowering and anti-inflammatory effects [6.1]. Polyphenols – flavonoids and phenolic acids – are particularly useful in preventing heart attacks.
Importance of growth factors
Growth factors – grow factors – are fat or protein molecules that exhibit protective effects on the intestinal mucosa. Among the most important growth factors are epidermal growth factor, neurotensin, and insulin-like-growth factorThese are able to stimulate the formation and growth of new cells in the mucosa of the small and large intestine, which significantly improves the absorption of nutrients and vital substances (macro- and micronutrients) in Crohn’s patients [5.1]. In addition, as a result of cell proliferation, the barrier function of the intestinal mucosa, which is often reduced in Crohn’s disease patients, can be optimized, so that the uptake of bacteria, germs and endotoxins and the transfer of antigens from the intestines into the lymph and portal blood are largely prevented [5.1]. Crohn’s patients should consequently be fed with additional administrations of growth factors to improve nutritional and general status by increasing nutrient and vital substance absorption (macronutrients and micronutrients), maintaining the mucosal barrier of the intestine, and reducing inflammatory symptoms of the intestinal wall [5.1].
Nutritional therapy during symptom-free or symptom-poor periods-maintenance of remission
If no particular complications are present, a light whole food diet is used to maintain the symptom-free or symptom-poor period, respectively [5.1]. This involves avoiding those foods-mostly dairy, wheat products, and citrus fruits-preparation methods and foods that experience has shown to trigger the typical symptoms. Food sensitivities can aggravate chronic intestinal inflammation. In general, food intolerances are more common in patients with inflammatory bowel disease than in healthy individuals. According to clinical studies, long symptom-free intervals and low relapse rates occurred after elimination of such foods that aggravate the symptoms of Crohn’s disease. In particular, wheat products, milk and dairy products, citrus fruits, yeast, corn, bananas, tomatoes, wine, and eggs were eliminated, as these foods most frequently trigger symptoms [5.1]. Crohn’s disease patients should consume plenty of high-fiber foods, such as whole grain products, rice, wheat bran, oat bran, fruits, vegetables, as well as legumes, in the long term. High fiber consumption ensures a high supply of short-chain fatty acids in the colon. By promoting the metabolic activity and growth rate of the intestinal flora, acetate, propionate and butyrate can optimize the mucosal barrier of the intestine, which is often lowered in Crohn’s patients. Short-chain, low-molecular-weight fatty acids are thus able to reduce the severity of chronic intestinal inflammation and the number as well as the severity of relapses. Most importantly, n-butyrate, as an essential energy-providing substrate of the colonic mucosa, has a positive effect on the disease course of Crohn’s disease. Water-soluble dietary fibers, such as pectins and plant gums found in fruits, are essential for restoring intestinal function. They form viscous solutions and have an even higher water-binding capacity compared to insoluble fiber. By prolonging small intestinal transit, reducing stool frequency, increasing water retention, and increasing stool weight, soluble fiber counteracts diarrhea and consequently high fluid as well as electrolyte losses. It is recommended to avoid refined carbohydrates to a large extent. They promote bacterial overgrowth, aggravate damage to the mucosa of the small and large intestine, and exacerbate absorption disorders as well as vital substance deficiencies (micronutrients). Ultimately, a high-fiber, sugar-free diet can positively influence disease progression. In addition, the rate of required surgical interventions is significantly reduced [5.1].
Nutritional Therapy
Nutrition therapy in acute relapse, general malnutrition or specific substrate deficiencies, and after extensive bowel resection.
Artificial enteral nutrition
If Crohn’s patients suffer from stenosis-related passage obstructions, affected individuals should be careful to eat a diet that is broken down, easily absorbed, and thus low in fiber. In an acute episode of Crohn’s disease with severe nutrient and vital substance utilization disorders (macronutrients and micronutrients) or in cases of general malnutrition or specific substrate deficiencies, it is advisable to provide patients with artificial enteral nutrition in the form of a chemically defined formula diet to preserve intestinal function. Artificial enteral nutrition is also appropriate in cases of intestinal fistulas or after extensive bowel resection.A poorly soluble diet during an acute episode, on the other hand, further irritates the inflammatory intestinal mucosa, increasing the severity of the episode and prolonging its duration. Formula diets – elemental or peptide diets – are administered in ready-to-use liquid or powder form – in some cases via a nasogastric tube. They consist of a fully balanced mixture of mono- or low-molecular nutrients and vital substances (macro- and micronutrients) that can be absorbed without enzymatic cleavage, such as amino acids, oligopeptides, mono-, di- and oligosaccharides, triacylglycerides, vitamins, electrolytes and trace elements. The composition of the ingredients must be individually adjusted. In contrast to nutrient-defined diets – with 20 to 35% fat -, chemically defined formula diets contain only a maximum of 1.5% of energy as fat. Thus, the growth of fungal microorganisms, such as mycoplasmas and mycobacteria, is inhibited inside the intestine. A high fat content, on the other hand, promotes their growth as well as the formation of antigens that can damage the intestinal mucosa both morphologically and functionally A high fat diet, especially high in linoleic acid, increases the conversion to arachidonic acid. Arachidonic acid belongs to the omega-6 compounds and in high concentration inside the intestine promotes the occurrence of lipid peroxidations as well as the formation of inflammatory mediators – especially leukotriene B4. Accordingly, chemically defined formula diets have a positive effect on the intestinal mucosa. They reduce the permeability of the intestinal mucosa as well as the excretion of white blood cells with the stool. In addition, they improve the nutritional status, as they sufficiently cover the increased calorie and vital substance requirements (micronutrients) of the patients. In 50-90%, a temporary decrease in the symptoms of the disease – remission – can be achieved through exclusive nutrition with an elemental diet. However, since the relapse rate is very high at about 50%, surgical intervention to restore bowel function should be sought. In this case, artificial enteral nutrition before surgery improves the general condition in malnourished patients and reduces the rate of postoperative complications. Meeting energy, nutrient, and vital substance (macro- and micronutrient) requirements is of considerable importance, especially in children with Crohn’s disease. Artificial enteral nutrition is well suited for the treatment of short stature. Enteral nutrition is preferable to parenteral nutrition because of its low monitoring requirements, lower complication rate, and lower cost. Parenteral nutrition also carries an increased risk of central venous catheter infections, with bacteria entering the patient’s bloodstream through the catheter (catheter sepsis). In addition, occlusion of the subclavian vein by a blood clot may occur as a result of parenteral nutrition
Total parenteral nutrition-oral nutritional abstinence
If enteral nutrition is not possible, if the course of the disease is exceedingly severe, or if the patient’s general and nutritional status is very poor, the patient must be fed via venous access (parenteral). In about 60% of cases, a temporary reduction in the symptoms of the disease (remission) can be achieved in this way. However, about 40% of patients in remission with total parenteral nutrition relapse within one year. Total parenteral nutrition improves the general condition of malnourished Crohn’s patients. This fact is especially essential for patients who are about to undergo surgery. In addition, parenteral nutrition reduces the rate of complications that can occur during surgery. If chronic oozing bleeding occurs inside the intestine in Crohn’s disease as a result of gastrointestinal symptoms, such as the formation of ulcers, stenoses, granulomas, strictures, fissures or abscesses, the severe or prolonged bleeding leads to high iron losses. Iron should therefore be supplied orally. The trace element is essential for oxygen transport in the human organism [6.2]. If steatorrhea exists in extensive Crohn’s disease, a decrease in fatty diarrhea can be achieved by a low-fat, high-protein diet. When the steatorrhea is relieved, the losses of fat-soluble vitamins decrease and the symptoms triggered by the fatty diarrhea recede [5.1].If patients with steatorrhea do not want to give up dietary fat, medium-chain fatty acids – MCT fats – should be used instead of long-chain triglycerides. Artificial enteral and total parenteral nutrition, respectively – inhibitory effects on chronic inflammation.
- Improvement of nutritional status with a positive effect on the course of the disease.
- Quantitative and qualitative changes in the intestinal flora
- Reduction of the load of the intestine with antigens, such as bacteria, germs as well as endotoxins.
- Normalization of the impaired barrier function of the intestinal mucosa by reducing the permeability of the intestinal mucosa.
- Positive effects of “immobilization” of the intestine
Side effects of medication
In addition to malabsorption, medications commonly used in Crohn’s disease treatment to reduce inflammation or heal inflammatory bowel wall changes can also promote the development of nutrient and vital substance (macro- and micronutrient) deficiencies.
- Synthetically produced steroids-corticosteroids, such as fludrocortisone, prednisone, prednisolone, and methylprednisolone-impede the absorption of calcium, phosphorus, and zinc; increase renal excretion of vitamin C, B6, potassium, sodium, calcium, magnesium, and phosphorus; and increase the need for vitamin D, E, and folic acid [6.6]. Since corticosteroids as immunosuppressants have an inhibitory effect on the immune system, long-term use significantly impairs the immune system – increased susceptibility to infections. In addition, there may be an increase in blood pressure, water retention, muscle wasting, an increased tendency to bruising, acne and mood swings
- The substance sulfasalazine or salazosulfapyridine – is administered for months and years in both Crohn’s disease and ulcerative colitis. Salazosulfapyridine inhibits vitamin B9 absorption in particular, and thus may contribute to the development of folic acid deficiency
- Salicylates, such as mesalazine, decrease serum levels of folic acid as well as iron. Furthermore, salicylates decrease the absorption of vitamin C and impede its uptake into leukocytes (white blood cells). Consequently, the vitamin C level in plasma as well as in platelets (blood platelets) is lowered and the renal excretion of vitamin C increased
- Methotrexate is one of the immunosuppressive agents. In addition to blocking the absorption of folic acid, it also blocks the absorption of vitamin B12 and increases zinc requirements
- Colestyramine binds bile acid and is used to treat diarrhea. This drug contributes to deficiencies of all vital nutrients (micronutrients) by interfering with the absorption of vitamins A, beta-carotene, D, E, K, B9, and iron. Colestyramine also inhibits intestinal absorption of thyroid hormones
Crohn’s disease – vital substance deficiency (micronutrients)
| Vital substance (macro- and micronutrients) | Deficiency symptoms |
| Vitamin A |
Increased risk of
Deficiency symptoms in children
|
| Beta-carotene |
|
| Vitamin D | Loss of minerals from bones– spine, pelvis, extremities- leading to.
Symptoms of osteomalacia
Deficiency symptoms in children
Symptoms of rickets
|
| Vitamin E |
Deficiency symptoms in children
|
| Vitamin K | Blood coagulation disorders leading to
Decreased activity of osteoblasts leads to.
|
| B group vitamins, such as vitamin B1, B2, B3, B5, B6. | Disorders in the central and peripheral nervous systems lead to
Deficiency symptoms in children
|
| Folic acid | Mucosal changes in the mouth, intestines, and urogenital tract lead to
Blood count disorders
Impaired formation of leukocytes (white blood cells) leads to.
Elevated homocysteine levels increase the risk of
Neurological and psychiatric disorders, such as.
Deficiency symptoms in children Disorders in DNA synthesis-restricted replication-and decreased cell proliferation increase the risk for
|
| Vitamin B12 |
Blood count
Gastrointestinal tract
Neurological disorders
Psychiatric disorders
|
| Vitamin C |
Weakness of blood vessels leads to
Carnitine deficit leads to
Deficiency symptoms in children
Increased risk of vitamin C deficiency disease- Möller-Barlow disease in infancy with symptoms such as.
|
| Calcium | Demineralization of the skeletal system increases the risk of
Increased risk of
Deficiency symptoms in children
Symptoms of rickets
Additional vitamin D deficiency leads to
|
| Magnesium | Increased excitability of muscles and nerves leads to
Increased risk of
Deficiency symptoms in children
|
| Sodium |
|
| Potassium |
|
| Chloride |
|
| Phosphorus |
Disease of the nerves, which transport information between the central nervous system and the muscles leads to
Deficiency symptoms in children
Symptoms of rickets
|
| Iron |
Deficiency symptoms in children
|
| Zinc | Instead of zinc, the toxic cadmium is integrated into the biological processes, resulting in
leads.
Metabolic disorders, such as.
Deficiency symptoms in children Low zinc concentrations in plasma and white blood cells cause
|
| Selenium |
Increased risk of
Deficiency symptoms in children
|
| Copper |
Copper metabolic disorders
Deficiency symptoms in children
|
| Manganese | More than 60 enzymes – including decarboxylases, aminopeptidases, hydrolases and kinases – are activated by manganese or contain the trace element as a component. Manganese deficiency results in decreased activity of the enzymes, leading to
can lead to. |
| Molybdenum |
|
| Essential fatty acids- omega-3 and 6 compounds. |
Deficiency symptoms in children
|
| High quality protein |
|
| Amino acids, such as glutamine,leucine, isoleucine, valine, tyrosine,histidine,carnitine |
|
| Secondary plant compounds, such as carotenoids, saponins, sulfides, polyphenols. |
Insufficient protection against
Free radicals lead to
Increased risk of
|
| Dietary fiber | Increased risk of
|
