How interested are you in taking your life and health to the next level? If you're really interested, we suggest you take a complex carbohydrate tolerance test.
Carbohydrates in the diet
The problem is that all organisms are individual and tolerate the same foods in completely different ways. For some, it is absolutely normal to drink milk every morning, accompanied by a large sandwich with butter and cheese. And for some, such a breakfast will provide terrible bloating and uncomfortable flatulence throughout the day.
You've probably heard a lot about lactose and gluten intolerance.
There is also intolerance to complex carbohydrates. Why does this happen?
The fact is that some people have a deficiency of one or more essential enzymes in the intestines. It is their absence that prevents complex carbohydrates from being absorbed normally. Fats and carbohydrates in the diet require special enzymes for complete absorption.
The consequences for the body from such a deficiency are not catastrophic. However, if you regularly consume foods that are not digested normally, your life will be very uncomfortable. The main side effects will be bloating, abdominal pain and strong gas, which can cause colic.
You can determine if you have complex carbohydrate intolerance with this small list of simple questions:
Are you overweight?
Do you often feel tired, especially after eating a meal rich in carbohydrates?
Do you lead a sedentary lifestyle?
Do you feel like you can't control your appetite?
Do you often crave sweet or starchy foods like bread, pasta, potatoes, or legumes?
Do you feel dizzy when you're hungry?
Is your blood sugar higher than normal?
Do you suffer from anxiety, depression, skin problems? Do you have hormonal problems or sleep disorders?
If you answered “yes” to one or more questions, try eliminating all grains, legumes, starchy vegetables (carrots, corn, potatoes) and fruits from your diet.
After two weeks, answer questions number 2, 5, 6 and 8 again. If you see a significant change, most likely you have an intolerance to complex carbohydrates.
If you find out that you have this intolerance, it's not a problem at all! A healthy low-carb diet can help normalize blood pressure and also significantly reduce sugar cravings. The feeling of constant hunger will go away, and your skin and digestion will noticeably improve. HOW EXACTLY SHOULD YOU CHANGE YOUR DIET?
Get rid of sugar and refined carbohydrates. Add more greens and cruciferous vegetables to your diet.
Try to either minimize or completely eliminate starchy vegetables, as well as grains and legumes from your diet. You can only have two or three servings of these foods per week. Stop being afraid of fats. Feel free to add avocado and olive oil to your salads. Limit dairy products, because they are very high in carbohydrates. Protein and carbohydrates in food can play a major role in your daily well-being.
Eat only unsweetened or frozen fruits: fresh berries, citrus fruits, green apples. If possible, you should give up alcohol. In case of a holiday, give preference to dry wine and under no circumstances beer or cocktails.
Complex carbohydrate intolerance is an unpleasant thing, but there is nothing really scary about it. Try to follow these simple rules and replace the foods on the list with lower-carbohydrate options.
Remember that it’s not just carbohydrate intolerance that can cause gas! You can find out more about the causes of flatulence on our website.
Carbohydrate intolerance (carbohydrate intolerance) is the inability to digest certain carbohydrates due to a lack of one or more intestinal enzymes. Symptoms of carbohydrate intolerance include diarrhea, bloating and flatulence. Diagnosis is based on clinical signs and an H2 breath test. Treatment for carbohydrate intolerance involves eliminating disaccharides from food.
ICD-10 code
E73 Lactose intolerance
What causes carbohydrate intolerance?
Enzyme deficiency can be congenital, acquired (primary) or secondary. Congenital deficiency is rare.
Acquired lactase deficiency (primary adult hypolactasia) is the most common form of carbohydrate intolerance. High lactase levels are observed in newborns due to the need to digest milk; In most ethnic groups (80% blacks and Hispanics, almost 100% Asians), lactase levels decrease after breastfeeding, preventing older children and adults from digesting significant amounts of lactose. At the same time, 80-85% of northwestern Europeans have good lactase production throughout their lives, which allows them to digest milk and dairy products. It remains unclear why more than 75% of the world's population is deficient in this enzyme.
Secondary lactase deficiency is associated with conditions that damage the lining of the small intestine (eg, celiac disease, tropical sprue, acute intestinal infections). In infants, temporary secondary disaccharidase deficiency may complicate intestinal infections or abdominal surgery. Recovery from the disease state is accompanied by an increase in enzyme activity.
What happens when you have carbohydrate intolerance?
Disaccharides are normally broken down into monosaccharides from disaccharides [eg, lactase, maltase, isomaltase, sucrase (invertase)], located on the brush border of small intestinal enterocytes. Undigested disaccharides cause an increase in osmotic pressure, which draws water and electrolytes into the intestinal lumen, causing watery diarrhea. Bacterial fermentation of carbohydrates in the colon causes gas formation (hydrogen, carbon dioxide and methane), leading to severe bloating, flatulence and abdominal pain.
Symptoms of carbohydrate intolerance
Symptoms of carbohydrate intolerance are similar for all disaccharidase deficiency conditions. A child with lactose intolerance develops diarrhea after drinking large amounts of milk and may not gain weight. Adults may experience watery diarrhea, bloating, excessive gas, nausea, rumbling in the stomach, and intestinal cramps after taking lactose. Patients notice this early enough and avoid consuming dairy products. Symptoms of carbohydrate intolerance usually appear after eating the equivalent of 8-12 ounces of milk. Diarrhea can be quite severe, causing other nutrients to be eliminated before they are absorbed. Symptoms may be similar to irritable bowel syndrome, requiring differential diagnosis.
Diagnosis of carbohydrate intolerance
Lactose intolerance is usually diagnosed by a thorough history, supported by dietary history. Patients usually have a history of intolerance to milk and dairy products. The diagnosis can be assumed if the stool in the form of chronic or intermittent diarrhea is acidic (pH
In an H2 breath test, the patient takes 50 g of lactose orally and H2, which is formed during the metabolism of undigested lactose under the influence of microflora, is measured by the device when breathing 2, 3 and 4 hours after eating. In patients with significant manifestations of the disease, the increase in H2 reaches more than 20 mmol above the basic value. The sensitivity and specificity of the study is more than 95%.
(Lactose intolerance; lactase deficiency; disaccharidase deficiency; glucose-galactose malabsorption; alactasia)
Carbohydrate intolerance- diarrhea and flatulence associated with impaired digestion of carbohydrates due to a lack of one or more intestinal enzymes.
Pathophysiology
Disaccharides are normally broken down into monosaccharides by lactase, maltase, isomaltase or sucrase (invertase) in the small intestine. Lactase breaks down lactose into glucose and galactose. Unsplit disaccharides remain in the intestinal lumen and osmotically retain fluid, promoting diarrhea. Fermentation of sugar by bacteria in the colon leads to the appearance of large amounts of gas and acidification of the stool. Since enzymes are located in the brush border of mucosal cells, secondary deficiency occurs in diseases accompanied by morphological changes in the jejunal mucosa (for example, celiac disease, tropical sprue, acute intestinal infections, toxic effects of neomycin). In infants, temporary secondary disaccharidase deficiency may be a complication of intestinal infection or abdominal surgery.
Monosaccharides glucose and galactose are absorbed by active transport in the small intestine (fructose is absorbed passively). In glucose-galactose malabsorption, this transport system is defective, and most sugars cause characteristic symptoms.
Prevalence
Lactase deficiency occurs normally in approximately 75% of adults in all ethnic groups except those originating from northwestern Europe, where the prevalence of the condition is less than 20%. Most people of color in North America gradually develop lactase intolerance between 10 and 20 years of age; However, the statistics here are unreliable. This condition is detected in 90% of natives of eastern countries, 75% of American blacks and Indians; it is also very common among the inhabitants of the Mediterranean.
Glucose-galactose intolerance is an extremely rare congenital disorder, as is the deficiency of other intestinal mucosal enzymes (eg, sucrase, isomaltase).
Ed. N. Alipov
"Carbohydrate intolerance" - article from the section
T.E. Borovik, E.A. Roslavtseva, G.V. Yatsyk, V.A. Skvortsova, N.N. Semyonova,
State Institution Scientific Center for Children's Health of the Russian Academy of Medical Sciences
CARBOHYDRATE INTOLERANCE
Disturbances in the hydrolysis and absorption of carbohydrates are manifested by similar symptoms - the so-called fermentative, acidic or osmotic diarrhea, which is explained by the same development mechanisms.
In the absence or insufficient activity of an enzyme involved in the hydrolysis of a particular carbohydrate, disaccharides and/or monosaccharides that are not absorbed and remain in the intestinal lumen, having high osmotic activity, promote the release of water and electrolytes into the intestinal lumen (osmotic diarrhea), stimulate motility upper gastrointestinal tract. As a result, excess carbohydrates enter the colon. In the colon, they are actively fermented by intestinal microflora with the formation of organic acids, hydrogen gas, methane, carbon dioxide and water, which causes flatulence, colic, increased peristalsis and accelerates the passage of chyme through the intestine. The child has frequent (8–10 times a day or more) liquid, foamy stools with a sour odor, leaving a large watery spot on the diaper. In this case, the pH of the intestinal contents changes to the acidic side (pH less than 5.5). In children of the first year of life, carbohydrates are found in the feces - more than 0.25 g%. In some cases, dehydration may develop; rarely, severe malnutrition may develop.
Lactase deficiency (LD)– the most common form of disaccharidase deficiency, which develops as a result of a decrease or complete absence of the enzyme lactase-phlorizin hydrolase in the enterocytes of the mucous membrane of the small intestine. This enzyme is one of the most vulnerable enzymes of the small intestine. It is superficially located, and its concentration is significantly lower than that of other parietal digestive enzymes. Lactase activity in premature infants (from the 28th to the 34th week of gestation) is only 30% of its level in full-term infants. Maximum enzyme activity is achieved by 2–4 months of a child’s life.
The severity of clinical symptoms in LN is determined by the total degree of reduction in enzyme activity, the amount of lactose ingested with food, the nature of the intestinal microflora, as well as individual pain sensitivity to intestinal distension by gases.
Distinguish primary LN associated with congenital enzyme deficiency, and secondary LN, which develops as a result of damage to the enterocyte during infectious, inflammatory, autoimmune diseases of the intestine, as well as lactose intolerance in short bowel syndrome.
Most often, pediatricians encounter hypolactasia in children in the first months of life. Clinical symptoms (flatulence, colic, diarrhea) usually appear in a child at 3–6 weeks of life, which is apparently associated with an increase in the volume of milk or formula. In the anamnesis of such children, as a rule, there are indications of a complicated course of pregnancy and childbirth (hypoxia), and close relatives often show symptoms of adult-type LI. In infants with signs of hypoxic damage to the central nervous system, the so-called “constipated” form of lactase deficiency is sometimes observed, which is characterized by the absence of independent stool in the presence of liquid stool and the other symptoms listed above. Typically, the symptoms in most children stop by 5–6 months (by the time complementary foods are introduced) and are not observed in the future, so this type of lactose intolerance is difficult to classify as primary.
Diet therapy
The approach to treatment should be differentiated depending on the nature of feeding (natural or artificial), the degree of enzymatic deficiency (alactasia, hypolactasia), and the genesis of enzymopathy (Table 1).
Table 1
Scheme for correcting lactase deficiency in children of the first year of life
| With natural feeding | With artificial feeding |
|
Partial or complete replacement of infant formula with low-lactose or lactose-free formula, depending on lactose tolerance and the nature of concomitant pathology |
At primary alactasia of newborns(extremely rare) the child is immediately and completely transferred to feeding with lactose-free formula.
At hypolactasia if the child is on natural feeding, a decrease in the amount of human milk is undesirable. The best option is to use lactase preparations. Lactase Baby (700 units) is prescribed 1 capsule per feeding. A dose of the enzyme preparation is mixed with 20–30 ml (1/3 of the feeding volume) of expressed milk and the baby is given this mixture before breastfeeding. The effectiveness of the drugs increases if expressed milk with lactase is left to ferment for 15 minutes, as well as when the entire volume of milk is treated with lactase. It is possible to use the drug Lactase (3450 units), starting with 1/4 capsule per feeding.
If the use of the enzyme is ineffective (which is usually observed with a pronounced decrease in lactase activity), they resort to reducing the lactose load by replacing 1/3 to 2/3 of the volume of each feeding with lactose-free milk formula, after which the child is supplemented with human milk (Table 2). The lactose-free mixture is introduced into the diet gradually, at each feeding, bringing it to the required amount over 3–5 days, as judged by a decrease in flatulence, restoration of normal stool consistency and stool frequency, a decrease in the excretion of carbohydrates in feces, and an increase in fecal pH. As a rule, the volume of lactose-free product is 30–60 ml for each feeding.
table 2
Chemical composition and energy value of low-lactose and lactose-free milk formulas (in 100 ml of finished mixture)
| Blend name | Chemical composition, g | Energy value, kcal |
|||
| Squirrels | Fats | Carbohydrates | |||
| Total | lactose | ||||
|
Lactose-free mixtures |
|||||
| Babushkino Lukoshko (lactose-free mixture; Russia) |
1,69 | 3,38 | 7,56 | 0 | 67,37 |
| NAN*, ** Lactose-free (Switzerland) |
1,4 | 3,3 | 7,8 | 0 | 67 |
| Nutrilak Lactose-free (Russia) | 1,4 | 3,45 | 7,4 | 0 | 66 |
| Nutrilak Lactose Free Plus* (Russia) |
1,6 | 3,5 | 7,3 | 0 | 66,3 |
| Enfamil Lactofri (USA) | 1,42 | 3,7 | 7,2 | < 0,1 | 68 |
|
Low lactose mixtures |
|||||
| Nutrilak Low-lactose (Russia) | 1,6 | 3,5 | 7,3 | 0,9 | 66,3 |
| Nutrilon Low Lactose (Holland) |
1,4 | 3,6 | 7,1 | 1,33 | 66 |
| Humana LP (Germany) | 1,8 | 2,0 | 9,2 | 1,1 | 62 |
| Humana LP+SCT (Germany) | 1,9 | 2,0 | 8,9 | 0,5 | 61 |
Introduced:
* nucleotides;
** arachidonic and docosohexaenoic acids.
In case of hypolactasia, if the child is bottle-fed, a low-lactose mixture should be selected with the amount of lactose that the patient will tolerate, without allowing the appearance of clinical symptoms and increased excretion of carbohydrates in feces. Low-lactose formula is introduced into each feeding, gradually replacing infant formula with it. Small amounts of lactose entering the colon are a natural prebiotic necessary for the proper formation of microflora. Lactose is also the only source of galactose, which is formed when it is broken down. Galactose is used for the synthesis of galactolipids, including cerebrosides, which are necessary for the formation of the central nervous system and myelination of nerve fibers, as well as for the synthesis of mucopolysaccharides (hyaluronic acid), which are part of the vitreous body and synovial fluid. Complementary feeding dishes for children of the first year of life with LI are prepared not with milk, but with the low- or lactose-free formula that the child receives. From 4–4.5 months of age, industrially produced fruit purees or baked apples are prescribed. It is advisable to prescribe porridge (rice, corn, buckwheat) or pureed vegetables with coarse vegetable fiber (cauliflower, zucchini, pumpkin, carrots) with the addition of vegetable oil as the first main complementary foods (from 5 months). After 2 weeks, meat puree is introduced. Fruit juices (diluted 1:1 with water) are introduced into the diet of such children later, usually after 6 months. In children of the second half of life, it is possible to use dairy products where the lactose content is insignificant: cottage cheese washed from whey, butter, hard cheese.
At primary (constitutional) lactase deficiency low lactose The diet is prescribed for life.
At secondary hypolactasia symptoms of lactase deficiency are transient. Therefore, upon achieving remission of the underlying disease after 1–3 months, the diet should be gradually expanded by introducing lactose-containing milk formulas, under the control of clinical symptoms (diarrhea, flatulence) and excretion of carbohydrates in feces.
Congenital sucrase-isomaltase deficiency– a relatively rare disease among Europeans, inherited in an autosomal recessive manner. Enzyme deficiency is not a life-threatening condition. It appears for the first time when sucrose is introduced into the child’s diet (fruit juices, purees, sweetened water or tea), less often starch and dextrins (porridge, mashed potatoes) in the form of severe “carbohydrate” diarrhea with crises of dehydration. With age, children often acquire the ability to tolerate increasing volumes of dextrins, starch and sucrose without increasing enzyme activity, which is associated with an increase in the absorption surface of the mucous membrane. Often, patients develop an aversion to sweet dishes, fruits, and starchy foods, that is, self-regulation of sucrose intake into the child’s body occurs.
Any damage to the intestinal epithelium can lead to secondary sucrase-isomaltase deficiency (infectious enteritis, giardiasis, celiac disease, radiation enteritis), but the activity of the enzyme does not drop to the extremely low level that occurs with primary deficiency.
Diet therapy
The basis of dietary therapy is the elimination of sucrose and, sometimes, reducing the amount of starch and dextrins in the diet. With primary (congenital) sucrase-isomaltase deficiency, children usually tolerate lactose well. Therefore, when choosing a formula for such a child, it is preferable to maintain breastfeeding for as long as possible, and in its absence, it is necessary to prescribe an infant formula with a lactose carbohydrate component. With secondary (post-infectious) sucrase-isomaltase deficiency, lactase deficiency occurs and combined disaccharidase deficiency is formed.
Children with sucrase-isomaltase deficiency cannot tolerate fruits, berries, vegetables, juices high in sucrose (peaches, apricots, tangerines, oranges, melon, onions, beets, carrots), as well as foods rich in starch (porridge, potatoes, bread , jelly). It is recommended to start introducing complementary foods with pureed vegetables that contain practically no sucrose and starch (Table 3). You can sweeten food with glucose or fructose. In the second year of life, it is usually possible to expand the diet by introducing a small amount of starch-containing foods (vegetables, cereals, potatoes).
Table 3
Vegetables and fruits containing minimal amounts of sucrose and starch
At secondary sucrose intolerance The duration of its exclusion depends on the severity of the underlying disease and the success of treatment. It is recommended to compensate for the carbohydrate deficiency by parenteral and/or enteral administration of glucose solutions. The period of elimination of sucrose, unlike lactose, is shorter and can be limited to 10–15 days.
Starch intolerance may occur in premature infants and children in the first six months of life, in whom the activity of pancreatic amylase is physiologically reduced, as well as in exocrine pancreatic insufficiency, therefore they are not indicated for the administration of mixtures containing starch as part of the carbohydrate component.
With congenital (primary) malabsorption of glucose-galactose, there is a defect in the transport systems of the brush border of enterocytes, while the activity of disaccharidases and carbohydrate hydrolysis are not impaired. This rare pathology is inherited in an autosomal recessive manner; manifests itself as profuse diarrhea and dehydration after the first feeding of the newborn. Replacing milk with lactose-free and dairy-free formulas has no effect. The only monosaccharide that can be absorbed in the small intestine is fructose. The remedy of choice is to transfer the child to total parenteral nutrition. Against the background of parenteral nutrition, feeding begins with a dosed administration of a 2.5% fructose solution, the concentration of which is increased to 7–8% in the absence of diarrhea. Next, a source of protein (protein preparation or meat puree), fat (vegetable oil or fat emulsion, starting with 1-2 drops) is introduced. In the future, the diet is expanded by pureeing fructose-containing vegetables. The prognosis of the disease with total glucose-galactose malabsorption is very serious. Surviving children with a partial defect in the glucose-galactose transport system suffer from chronic diarrhea and are delayed in physical development.
Acquired intolerance to monosaccharides manifests itself as severe chronic diarrhea with delayed physical development. It can accompany the course of severe intestinal infections in children in the first months of life with an unfavorable premorbid background, and occur as a result of atrophy of the villi of the intestinal mucosa in celiac disease, intolerance to cow's milk proteins, and protein-calorie deficiency. The child's diarrhea improves when he fasts and returns with increased oral feeding. Characteristic features are low pH and high concentrations of glucose and galactose in the stool. Therapy with lactose-free and dairy-free formulas is ineffective.
Acquired intolerance to monosaccharides is a transient condition, but it is total in nature: glucose, galactose, fructose are not absorbed, and the hydrolysis of di- and polysaccharides is also impaired. Oral rehydration with standard solutions is ineffective due to the glucose they contain. The patient's condition requires transfer to total parenteral nutrition. Oral administration of glucose is started carefully, with a 2.5% solution against the background of a stable condition and absence of diarrhea, with a gradual increase in the concentration of the solution. When the 5% glucose formula is well tolerated, parenteral nutrition can be discontinued. The introduction of higher concentrations of glucose and starch can again provoke diarrhea, which requires repeated unloading. When good tolerance of glucose, dextrins, and starch is achieved, sucrose solutions are gradually introduced, starting with a 3–5% concentration, fruit puree, juices diluted with water 1:1; and no earlier than 1–2 months later, you can try to introduce infant formula with a moderately reduced lactose concentration.
CELIAC DISEASE (GLUTEN ENTEROPATHY)
This autoimmune disease is characterized by damage to the mucous membrane of the small intestine - T-cell-mediated atrophic enteropathy in genetically predisposed individuals under the influence of proteins (prolamins) in the grain of certain cereals: wheat gliadin, rye secalin, barley hordenin, oat avenin. In the medical literature, cereal proteins that are toxic to patients with celiac disease are usually combined with the term “gluten.” Celiac disease is characterized by persistent, lifelong intolerance to gluten.
Symptoms of typical celiac disease develop in children, as a rule, 4–8 weeks after the introduction of gluten-containing complementary foods (semolina, wheat, oatmeal, cookies, crackers, dryers, vermicelli) into the diet, usually between the ages of 6–8 months and 1. 5–2 years, but they can first appear at any age.
Diet therapy
The only method of treating the disease and preventing complications in celiac disease is a strict and lifelong gluten-free diet. All products and dishes containing wheat, rye, barley and oats are excluded from the diet, as well as industrial products that contain gluten-containing components in the form of additives - thickeners, forming agents, stabilizers (Table 4). Rice, buckwheat, corn, and millet are considered non-toxic cereals for celiac disease. The issue of the safety of oats for young children is debated and needs further study. Flour and starches made from potatoes, tapioca, cassava, sweet potatoes, beans, peas, soybeans, and various nuts are safe.
Table 4
Gluten-containing foods and dishes excluded from children's diets with celiac disease
| Products | Wheat | Rye | Barley | Oats |
| Cereals, porridge | Semolina, wheat, Artek, Poltavskaya, 4 grains, 7 grains, spelt | Nordic porridge with rye flakes | Barley, pearl barley, barley | Oatmeal, Hercules, Sports, oatmeal |
| Flour and bran | Wheat flour and bran | Rye flour and bran | Oat flour | |
| Baby formula | Malyutka plus 2 with oatmeal | |||
| Baby cereals | Based on wheat, semolina and flakes, mixed grain porridge, 7 grains | 7 grains, mixed grain porridge | Gerber barley porridge, Beech Nut barley 7 grains, porridge from mixed cereals |
All ready-made porridges with oatmeal and cereals, multigrain and oat wellings, 7 grains, mixed grain porridges |
| Children's canned food | Canned baby food with meat, fish, vegetables, fruits, yogurt, cream, etc. with the addition of wheat flour, semolina, pasta (see composition on the package) | Children's canned meat, vegetables, fish, fruit with oatmeal (see composition on the package) | ||
| Bread and bakery products, confectionery | Bread, crackers, crackers, cookies, bagels, bagels, straws, crispbreads, baked goods | Rye bread, flatbreads, crackers |
Barley flatbreads ready-made breakfasts with barley molasses | Bread, Hercules |
| Pasta | Pasta, vermicelli, horns, spaghetti, noodles, curly products |
The composition of the diet of a patient with celiac disease depends on the age, severity of the condition and period of the disease and is based on general principles: the carbohydrate component is made up of tolerated cereals, potatoes, legumes, vegetables, fruits and berries; protein and fat - due to meat, eggs, fish, dairy products, vegetable and butter.
For acute period of celiac disease in early childhood, severe dyspeptic disorders and nutritional disorders are characteristic, up to dystrophy and the development of secondary transient food intolerance. Most often this is lactase deficiency, which requires the exclusion of lactose-containing dairy products in almost all patients in the acute period of the disease. 2/3 of young children have intolerance to cow's milk proteins, which requires temporary elimination of all dairy products from the diet. Sensitization to other food proteins is often observed - rice, bananas, chicken egg whites, etc. The missing amount of protein in such patients is compensated with the help of meat-based products - canned children's meat of domestic and foreign production, as well as mixtures based on soy protein isolate.
In children with severe dystrophy and a high degree of polyvalent sensitization, specialized mixtures based on highly hydrolyzed protein can serve as an important source of protein, but their use is limited due to the specific organoleptic properties of these products (children with decreased appetite often refuse them).
In case of severe malnutrition, factors such as severe anorexia and reduced tolerance to food loads must be taken into account, so children are prescribed a diet containing no more than 3–4 g of protein and 120–130 kcal per 1 kg of actual body weight.
The first signs of treatment effectiveness during the period of manifestation of celiac disease are improvement in emotional tone, appetite and the beginning of weight gain, which should be expected after 1–2 weeks of treatment. Unstable stools and abdominal enlargement can persist for quite a long time.
During the period of clinical and morphological remission, the diet is gradually expanded to include foods previously eliminated due to transient intolerance. Dairy products are introduced, starting with low-lactose ones: cheese, butter, cottage cheese washed from whey, low-lactose milk mixtures. Gradually (taking into account tolerance) fermented milk products (kefir, yogurt) are prescribed, and then (after a year) porridge with diluted milk and whole milk. Also carefully, under the control of individual tolerance, other previously excluded products, except those containing gluten, are introduced.
Tatyana Eduardovna Borovik, Head of the Department of Nutrition of Healthy and Sick Children, State Scientific Center for Children of the Russian Academy of Medical Sciences, Professor, Dr. med. sciences
Elena Aleksandrovna Roslavtseva, senior researcher at the State Research Center for Children's Education of the Russian Academy of Medical Sciences, Ph.D. honey. sciences
Galina Viktorovna Yatsyk, Chief Researcher, State Research Center for Children's Health, Russian Academy of Medical Sciences, Professor, Dr. med. sciences
Vera Alekseevna Skvortsova, leading researcher at the State Research Center for Children's Health of the Russian Academy of Medical Sciences, Dr. med. sciences
Natalia Nikolaevna Semyonova, doctor, State Institution Scientific Center for Diagnostics of the Russian Academy of Medical Sciences, Ph.D. honey. sciences
Undigested carbohydrates filling our intestines give rise to signs of food intolerances. Most often we do not tolerate disaccharides, which include:
Lactose is milk sugar separated by the enzyme lactase;
Sucrose – beet and cane sugar broken down by sucrase;
Maltose, broken down by maltase.
To understand what disaccharide intolerance is, you need to become familiar with the digestive process. At the first stage, complex carbohydrates found in porridge, pasta or bread are broken down by the enzyme alpha-amylase, produced by the salivary glands. Consequently, the remaining enzymes - lactase, sucrase and maltase - disassemble disaccharides into monosaccharides. Lactase breaks down lactose, sucrase breaks down sucrose, and maltase breaks down maltose. These enzymes are located in the rim of the intestinal villi cells. It’s worth stopping here and paying attention to the structure of the intestinal villi.
Figure 8. Section of the intestinal villi
Monosaccharides - glucose and fructose - enter the blood. Glucose is necessary for the proper functioning of the human body, since it forms the basis for many significant changes that occur in it.
If the process of metabolism and absorption of disaccharides is disrupted, sugar particles accumulated mainly in the colon are partially eliminated during bowel movements and partially remain in the intestine. This leads to an increase in osmotic pressure and fermentation carried out by bacteria. Fermentation creates excessive amounts of short-chain organic acids, which irritate the intestinal mucosa and cause intestinal motility, resulting in severe diarrhea. This fermentation causes stool to have a sour, vinegary odor. Accumulating gases lead to bloating, abdominal pain, and fecal incontinence during bowel movements. A large amount of gases accelerates intestinal peristalsis, which causes an increase in the frequency of bowel movements - from several times to ten. In infancy, this can lead to dehydration and impaired nutrient absorption. Signs of disaccharide intolerance most often subside with age. In older children and adults, flatulence, abdominal pain, the symptom of “fluid transfusion” in the intestines, and fecal incontinence are more common.
Figure 9. Cross-section of complex carbohydrates
There are several methods for diagnosing disaccharide intolerances:
Stool examination(pH level, presence of sugar and organic acids are examined).
It is done immediately after obtaining a fresh stool sample to avoid fermentation by bacteria. The test is based on identifying the presence of residual substances in the stool. These include undigested sugars (such as lactose, glucose, galactose, fructose, pentose). Due to the lack of enzymes and under the influence of bacteria, they undergo fermentation in the colon. As a result, short-chain organic acids are created and stool acidification occurs. Its pH then becomes< 5,5 (правильный уровень pH – 7,0–7,5). Другие исследования проводятся на пробе стула с суточного сбора.
Test for lactose and fructose intolerance.
The patient is given a lactose solution at the rate of 2 grams/kg body weight (no more than 50 grams). Therefore, after two hours (at 30-minute intervals), the blood glucose concentration is examined. The correct increase in blood glucose levels should be in accordance with the level before the solution is administered by 20 mg%. The examination is done on an empty stomach (you cannot eat 12 hours before the examination).
Hydrogen breath test.
It is done using a device similar to a breathalyzer. The air is exhaled through the tube and the result is read. Therefore, you need to prepare a solution with lactose and give it to the patient to drink. Two hours after the solution is administered, the concentration of hydrogen particles in the exhaled air is measured. Hydrogen concentration > 20 ppm (particles) indicates reduced lactase activity in the mucous membrane of the digestive tract.
Lactic acid bacteria replace unprocessed lactose with hydrogen, which enters the bloodstream through the intestinal mucosa, and therefore into the lungs. If the difference between the first reading recorded and the maximum value measured after taking the lactose solution is 20 ppm, this means that the body is not processing lactose. The study also pays attention to the symptoms that the patient experiences, such as flatulence, a symptom of “fluid transfusion” in the intestines. Unfortunately, this test may not be entirely reliable, for example in the case where the disturbed bacterial flora itself produces hydrogen.
Genetic testing for lactose intolerance– the presence of the LCT gene, as well as fructose intolerance – the absence of the ALDOB gene.
A positive LCT result together with signs of lactose intolerance indicate that the patient does not produce the enzyme lactase, which is responsible for breaking it down from dairy products. It appears that a positive result for the presence of the ALDOB gene together with symptoms of fructose intolerance indicate a lack of tolerance to fructose, such as vegetables. Genetic tests are done from saliva or blood. They are expensive, but the safest for the patient and less painful.
In the office, I diagnose food intolerances based on genetic testing and symptom analysis. I ask each patient to fill out a symptom diary. The point of the diary is to monitor your body and record comments in a specially prepared form.
Added below instructions on how to keep a symptom diary:
We fill out a diary daily, recording the exact date.
We write down all the foods we eat during the day. I suggest adding more intolerable foods to the menu. We can test them for one week and record symptoms with an assessment of increased sensations. For example, if we are testing for lactose intolerance, we drink more sweet milk than usual and eat more dairy products. There is no need to create such a provocation in case of an immediate reaction to the food taken, as this can lead to anaphylactic shock. The symptom diary should cover those foods that cause delayed reactions, that is, reactions that occur 72 hours after exposure to the allergen.
The intensity of each symptom is rated in points on a scale from 1 to 10, with 10 being the most intense symptoms. We mark points by writing them next to the attribute being assessed.
Therefore, it is necessary to exclude the tested product from the diet and monitor the change in the intensity of sensations. We do the test at least six weeks later. I recommend that patients extend the testing time to three months.
(See: “Diary of Intolerance Symptoms” at the end of the book: Tables I–IV.)
The above method of keeping a symptom diary applies to all intolerances described in this guide. The developed diaries differ in the description of symptoms depending on what intolerance they relate to. After all, with lactose and fructose intolerance, different symptoms appear than with histamine or gluten intolerance.
