In which part of the stomach is castle factor produced? Antibodies to intrinsic Castle factor, IgG. Castle factor, what do you eat it with?

Vitamin B12

Vitamins B 12 call the group cobalt-containing biologically active substances, called cobalamins, related to the so-called., ancient natural biocatalysts. These include cyanocobalamin itself, hydroxycobalamin and twocoenzymeforms of vitamin B12: methylcobalamin And adenosylcobalamin . In a narrower sense vitamin B12 called cyanocobalamin, without losing sight of the fact that it is not synonymous with B12, and several other compounds also have B12 vitamin activity. Cyanocobalamin is just one of them. Therefore, cyanocobalamin is always vitamin B12, but vitamin B12 is not always cyanocobalamin.

B12 is a complex of several substances that have similar biological effect. The main one among them is cyanocobalamin - solid dark red crystals. This color is due to the content of a cobalt atom in each large cyanocobalamin molecule. It is this atom that creates all the uniqueness of vitamin B12. No other vitamin in living nature contains metal atoms. Moreover, only in the molecule of this vitamin there is a special chemical bond between cobalt and carbon atoms that is not found anywhere else in living nature. The cyanocobalamin molecule is the largest and bulkiest among the molecules of all vitamins. Each molecule of vitamin B12 has a region in which different atoms can be located. Depending on the type of these atoms, they are distinguished different types vitamin B12 - cyanocobalamin, already known to us, as well as hydroxycobalamin, methylcobalamin and adenosinecobalamin. In the future, we will call all of them by the collective names “vitamin B12”.

True Vitamin B12 (Cobalamin)

A striking feature of the metabolism of classical propionic acid bacteria is a high level of formation of corrinoids, compounds of the vitamin B12 group (the structure of corrin is shown below on the left - is the parent structure of corrinoids and a number of coenzymes.)

Corrinoids are a group of methylated and reduced tetrapyrrole compounds containing a cobalt atom in the center of the corrin ring, which forms a unique covalent bond with the β-ligand carbon, essential for chemical and biochemical reactions(see picture of the spatial structure of adenosylcobalamin, a coenzyme of vitamin B12).

In nature, all corrinoids are synthesized only by prokaryotic microorganisms - representatives of both phylogenetic domains (empires): Bacteria And Archaea. Consequently, all organisms that require corrinoids, including humans, depend on the microorganisms that synthesize them. The entire group of corrinoid compounds is often referred to as “vitamin B12.” However, there is the concept of “true vitamin B12”, which refers to cobalamin.

The latter is characterized by the presence of a “lower” α-ligand of the cobalt atom with a nucleotide, the specific base of which is 5,6-dimethylbenzimidazole (5,6-DMB). It is this corrinoid (cobalamin) that functions in the human body in two coenzyme forms (as adenosyl- or methylcobalamin, β-ligands), which determines medical aspect studying the biochemistry of cobalamin. Cyanocobalamin, containing a CN group as the “top” β-ligand of the cobalt atom, is a commercial form of vitamin B12. Classic PCBs synthesize true vitamin B12 (cobalamin) in large quantities (500-1500 mcg/g).

There are only two enzymes in the human body with coenzymes B12:

Methylmalonyl-CoA mutase, an enzyme that uses as a cofactor adenosylcobalamin, catalyzes the rearrangement of atoms in the carbon skeleton. As a result of the reaction, succinyl-CoA is obtained from L-methylmalonyl-CoA. This reaction is an important link in the chain of reactions of catabolism of proteins and fats.
5-Methyltetrahydrofolate homocysteine methyltransferase, an enzyme from the groupmethyltransferases, using as a cofactor methylcobalamin, catalyzes the conversion of the amino acid homocysteine to the amino acid methionine.

Chemical formula cyanocobalamin: C 63 H 88 Co N 14 O 14 P

HISTORY OF THE DISCOVERY OF VITAMIN B12

Vitamin B12(cyanocobalamin) is one of the more controversial members of the B-complex vitamin family. Although the full chemical structure of vitamin B12 was revealed only in the 1960s, research involving this vitamin has already been recognized with two Nobel Prizes.

As you know, vitamin B12 deficiency leads to the development of pernicious anemia, which in the mid-19th century sounded like a death sentence and could not be treated. Methods to get rid of this disease were discovered by chance during an experiment on dogs. American doctor George Whipple provoked the development pernicious anemia(malignant anemia) in experimental animals, causing bleeding, and then fed to dogs a variety of products in order to identify which foods speed up recovery. During an experiment, the scientist discovered that eating liver in large quantities quickly cured a disease caused by blood loss. Based on these data, George Whipple suggested that daily dosing of this product leads to the elimination of pernicious anemia.

Further clinical studies conducted by doctors William Parry Murphy and George Richards Minot were aimed at isolating the “curing” substance from the liver. During tests, pathophysiologists revealed that completely different liver substances are capable of treating anemia in dogs and people. As a result, Murphy and Minot opened specific factor, found in liver juice. This was the first impetus for the study of the “fatal” disease.

Over the next 2 years, patients with anemia were supposed to drink juice daily and eat liver “flesh” in large quantities (up to 3 kg). However, long-term consumption of raw liver disgusted patients and the search for an alternative medicine became urgent. In 1928, for the first time, chemist Edwin Cohn developed a liver extract that was 100 times more concentrated than animal by-product. The resulting extract became the first active agent in the fight against a merciless disease.

In 1934, “for their discoveries concerning the use of the liver in the treatment of pernicious anemia,” three American doctors, William Parry Murphy, George Maikot, and George Whipple, received the Nobel Prize. This event ultimately led to the birth of soluble vitamin B12. 14 years later, in 1948, Lester Smith (England), as well as Edward Rickes and Karl Folkers (USA), were the first to obtain pure cyanocobalamin in crystalline form. However, it took several more years to determine its structure using X-ray diffraction analysis, which turned out to be extremely complex.In the late 1950s, scientists also developed a method for obtaining large quantities of the vitamin from bacterial cultures. Thanks to this, the fatal disease of that time, called “pernicious anemia,” became treatable. In 1955, the English chemist and biochemist Dorothy Mary Crowfoot Hodgkin determined the spatial configuration, the chemical structure of the molecule, for which she was awarded the Nobel Prize in 1964.

SYNTHESIS OF VITAMIN B12

Vitamin B12 is unusual regarding its origin. Almost all vitamins can be extracted from a variety of plants or specific animals, but no single plant or animal is capable of producing vitamin B12. The exclusive source of this vitamin, according to modern data, are tiny microorganisms: bacteria, yeast, mold and algae... However, despite the fact that only a few microorganisms produce B12, the vitamin itself is required by the entire microbial community due to its unique properties. For more information about this, see the article: .

Propionic acid bacteria synthesize large number , which regulates basic metabolic processes in the body, contributes to increased immune status body, improve overall well-being by activating protein, carbohydrate and fat metabolism, increase resistance to infectious diseases, improves blood quality, participates in the synthesis of various amino acids and nucleic acids. However, the synthesis of vitamin B12 by the human intestinal flora is insignificant. With a lack of vitamin B12, gastrointestinal diseases, dysbacteriosis, and anemia occur. Therefore, probiotic products containing propionic acid bacteria- producers of vitamin B12.

NOTE: It should be especially noted that the content vitamin B12 in products , fermented by the developed starter cultures of propionic acid bacteria is thousands (!) times higher than its amount in products made from traditional starter cultures containing similar cultures, but with the addition of lactic acid bacteria.Among modern methods enrichment fermented milk products vitamins, it is precisely this microbial supersynthesis of vitamin B12 that is most justified, since recent studies by doctors and microbiologists have confirmed that the most effective use of vitamins is in a coenzyme (associated with microbial cell protein), easily digestible form. It should be noted that vitamin B12 is localized inside PCB cells, for which it is endometabolite. Into space gastrointestinal tract the vitamin is supplied only as a result of autolysis of PCB cells. This process is quite pronounced, because (about 30%) dies in the aggressive environment of the gastrointestinal tract (B12 is absorbed mainly in the ileum). This ensures the supply of the human body extra vitamin B12. In this regard, fermented PCB products are of particular importance, where it is possible to increase the accumulation of microbial biomass and, accordingly, the amount of absorbable vitamin B12.

About fermentation, see here: Features of fermentation

About synthesis, see here:

See also:

CASTLE FACTORS

Like most vitamins, B12 can exist in various forms and take different names. The names for vitamin B12 contain the word form "cobalt" because cobalt is the mineral found at the center of the vitamin: cobrinamide, cobinamide, cobamide, cobalamin, hydroxcobalamin, methylcobalamide, aquacobalamin, nitrocobalamin, and cyanocobalamin.

Castle factors and vitamin B12

Vitamin B12 is unusual in that it depends on a second substance called intrinsic factor, which allows the vitamin to pass from the gastrointestinal tract to the rest of the body. Without intrinsic factor, which is a unique protein(more precisely, a compound consisting of a protein part and mucoids- secretion secreted by cells of the gastric mucosa)produced in the stomach, vitamin B12 cannot access the parts of the body where it is needed.

Castle factors (Note: Named after the American physiologist and hematologist W.B. Castle)- these are substances necessary to maintain normal hematopoiesis. Vitamin B12 is one of Castle's external factors. Interior Castle's factor binds vitamin B12 and promotes its adsorption intestinal wall(suction epithelial cells ileum). Secretion of intrinsic factor Castle may be reduced (or even stopped completely) if the gastrointestinal tract is damaged (for example, with inflammatory process, with atrophic gastritis , cancer), when part of the stomach or small intestine is removed, etc. Its release increases under the influence of insulin and decreases under the influence of alcohol. If the release of intrinsic factor is impaired, the binding and absorption of vitamin B12 is impaired, which leads to the development of B12-deficient megaloblastic, or pernicious, anemia.

Functions of vitamin B12

Vitamin B12 is involved in translation folic acid into the active form, in the synthesis of methionine, coenzyme A, antioxidant glutathione, succinic acid, myelin. It controls DNA synthesis (therefore, cell division), maturation of red blood cells, increases the level of T-suppressors, which helps limit autoimmune processes. For information on the functions of vitamin B12, see also here at the link arrow

Perhaps the most well-known function of B12 is its role in the development of red blood cells.As noted above, vitamin B12 is one of Castle’s external factors, which are responsible in the body for maintaining normal hematopoiesis. When red blood cells mature, they require information contained in DNA molecules (DNA or deoxyribose nucleic acids, the substance in the nucleus of our cells that contains genetic information). Without vitamin B12, DNA synthesis fails and the information needed to make red blood cells cannot be obtained. Cells become poorly sized and begin to function ineffectively, a condition called pernicious anemia(or "pernicious anemia"). Most often, pernicious anemia is not caused by a lack of B12, but by a decrease in its absorption due to the lack of intrinsic factor.

Vitamin B12 and the nervous system

The second major task of vitamin B12 is its participation in the development of nerve fibers. Vitamin B12 is involved in the construction of protein and fat structures of the protective myelin layer. The myelin sheath, which covers neurons, forms less successfully with vitamin B12 deficiency. Although the vitamin plays an indirect role in this process, vitamin B12 supplementation has been shown to be effective in relieving pain and other symptoms of nervous system disorders.

One of the main tasks of vitamin B12 is to participate in the production of methionine, an amino acid that affects mental activity and the formation of a person’s emotional background. Vitamin B12, folic acid and methionine (as well as vitamin C) form a kind of working group, which specializes mainly in the functioning of the brain and the entire nervous system. These substances are involved in the production of so-called monoamines - stimulants of the nervous system, which determine the state of our psyche.

Also, vitamin B12 and folic acid promote the production of choline (vitamin B4), which significantly affects mental activity and psyche. In the process of metabolism from it to the so-called. Cholinergic fibers produce the neurotransmitter acetylcholine, a substance that transmits nerve impulses. When a person needs to concentrate, the accumulated choline is converted into acetylcholine, which activates the brain.

A lack of choline threatens a real breakdown of the psyche. With choline deficiency, cholesterol is oxidized, combines with protein waste and clogs the “passages” in cell membranes, so they cannot enter the cell necessary substances. The brain tries to transmit signals, but the passage channels become blocked, and the person loses the ability to think clearly and “falls into depression.” At the same time, sleep is disturbed, and brain cells and nerve endings begin to quickly die: the more cholesterol accumulates in the blood, the faster this process occurs. Since a lack of choline causes entire colonies of cholinergic neurons to die, eventually there is a danger of incurable Alzheimer's disease, which is accompanied by absolute loss of memory and personality disintegration. Modern neurophysiologists are of the opinion that a significant proportion of people over 40 years of age Western countries I have already come close to this disease.

See also: Vitamin B12 in the treatment of diseases of the nervous system

Vitamin B12and musculoskeletal system

At the very lately Evidence has been obtained that vitamin B12 is also of great importance for bone formation. Bone growth can only occur when there is an adequate supply of vitamin B12 in osteoblasts (the cells that make bones). This is especially important for children during the period of active growth, as well as for women in menopause who experience hormonally caused bone loss - osteoporosis.

Vitamin B12 affects muscle growth because it is involved in the processes of protein metabolism and amino acid synthesis. It activates energy exchange in the body. It is also important that it supports the vital activity of nerve cells spinal cord, through which centralized control of the muscles of the body occurs.

Vitamin B12 and metabolism

Vitamin B12 is required to circulate proteins throughout the body that are essential for cell growth and repair. Many of the key components of protein, called amino acids, become unusable in the absence of B12. Vitamin B12 influences the movement of carbohydrates and fats in the body.

In combination with folic acid(vitamin B9) and pyridoxine (vitamin B6), vitamin B12 normalizes the metabolism of methionine and choline, thereby beneficial effect on the liver, preventing its fatty degeneration. This is due to the fact that choline and the essential amino acid methionine are very strong lipotropic substances. Lipotropic substances are very important factors that contribute to the normalization of lipid and cholesterol metabolism in the body, stimulating the mobilization of fat from the liver and its oxidation, which leads to a decrease in the severity of fatty infiltration of the liver.

Also, according to the latest data, vitamin B12 deficiency leads to a lack of carnitine, the so-called quasi-vitamin (vitamin B or B11) - a substance that is a cofactor metabolic processes, ensuring the maintenance of CoA activity. Carnitine promotes penetration through mitochondrial membranes and the breakdown of long-chain fatty acids (palmitic, etc.) from formation of acetyl-CoA, mobilizes fat from fat depots. In other words, carnitine is involved in the transport of fat molecules from the blood to mitochondria - the “energy stations” of cells, where fat is oxidized and provides energy to the entire body. Without carnitine, the content of breakdown products in the blood increases, since fat remains unprocessed. Also, this substance has a neurotrophic effect, inhibits apoptosis (the process of programmed cell death), limits the affected area and restores the structure nerve tissue, normalizes protein and fat metabolism, incl. increased basal metabolism in thyrotoxicosis, restores the alkaline reserve of the blood, promotes economical consumption of glycogen and increases its reserves in the liver and muscles.

Daily intake of vitamin B12.

Physiological requirements for vitamin B12 according toMethodological recommendations MP 2.3.1.2432-08about norms physiological needs in energy and nutrients For various groups population of the Russian Federation:

Upper permissible level not installed.
Physiological requirement for adults - 3 mcg/day

Water-soluble vitamin B12 is non-toxic. Vitamin B12 injections are also found to be safe.Since the vitamin is non-toxic, it is widely used in higher doses for many types of incurable diseases. chronic illnesses, like arthritis and psoriasis. It is also used as a remedy to relieve fatigue, ailments and pain.Upper limit of B12 absorption V normal conditions on average is 1.5 mcg when taken with food up to 50 mcg of the vitamin.When vitamin B12 is taken above its binding capacity, the excess is excreted in urine (and feces). Note ed.: in some pathologies, vitamin B12 supplied with food may not be absorbed at all and may be completely excreted from the body - the causes of B12 deficiency will be discussed separately.

	Age	Daily requirement for vitamin B12, (mcg)
Infants	0 - 3 months
	4 - 6 months
	7 - 12 months
Children from 1 year to 11 years	1 — 3
	3 — 7
	7 — 11
Men (boys, young men)	11 — 14
	14 — 18
	> 18
Women (girls, girls)	11 — 14
	14 — 18
	> 18
	Pregnant and nursing

Vitamin B12 deficiency

The rate at which B12 levels change depends on how much B12 comes from the diet, how much is excreted, and how much is absorbed. In children early age B12 deficiency can appear much more quickly. In the elderly, due to a decrease in the acidity of gastric juice and a decrease in the function of parietal (parietal) cells, there is a high risk of developing B12 deficiency. However, up to 100% of B12 taken from food can be excreted in the feces.

Symptoms potentially associated with vitamin B12 deficiency: dandruff, decreased blood clotting, numbness in the legs, decreased reflexes, red tongue, difficulty swallowing, tongue ulcers, fatigue, tingling in the legs, disorder menstrual cycle.

The signs of vitamin B12 deficiency vary widely. Its insufficient amount manifests itself as a complex syndrome that includes physical, neurological and mental disorders. Physical disorders manifest themselves as weakness, fatigue, memory impairment, headaches, tachycardia, pallor skin, dizziness, dandruff, decreased blood clotting, numbness in the legs, decreased reflexes, red tongue, difficulty swallowing, tongue ulcers, fatigue, tingling in the legs, menstrual irregularities. They also include digestive problems: lack of sense of taste, loss of appetite and eventually weight loss. Neurological disorders often appear first. These include:

paresthesia of fingers;
constant weakness;
sensitivity disorders;
muscle weakness and decreased muscle tone;
atrophy optic nerve(weakened vision, which can result in blindness);
pyramidal syndrome.

Mental disorders include cognitive impairment, dementia, behavioral disturbances, apathy, irritability, confusion, or depression. Vitamin B12 deficiency is detected more often in people susceptible to depression than in “normal” (i.e., not prone to depression).Although B12 deficiency is not the only cause of the symptoms listed, B12 deficiency should be considered as a possible underlying factor whenever any of the symptoms mentioned are present.

CAUSES OF VITAMIN B12 DEFICIENCY

See also: Causes of vitamin B12 deficiency in humans (Stroinski, 1987)

Cause of vitamin deficiency B12 in 50-70% of patients (more often in young and middle-aged people, somewhat more often in women) there is insufficient secretion of the gastric mucosa of intrinsic factor Castle (IFC), caused by the formation of antibodies to the parietal cells of the stomach that produce IFC, or to the binding site of IFC with vitamin B12. In approximately 20% of cases, there is a hereditary history of VPA deficiency. In these cases, the consequence of vitamin B12 deficiency is the development of so-called pernicious anemia. In addition, vitamin B12 deficiency can be caused by a stomach tumor, gastrectomy, malabsorption syndrome, helminthiasis and dysbacteriosis, and an unbalanced diet. Other causes include hereditary diseases characterized by a defect in the production of proteins that bind to vitamin B12 or a defect in the formation of active forms vitamin; metabolic disorders and/or increased need for vitamins (thyrotoxicosis, pregnancy, malignant neoplasms), and also long-term use H2 receptor blockers and inhibitors proton pump. It should be noted that the reserve of vitamin B12 in the body, even with limited supply, is enough for 3-4 years.

Stomach problems. As already indicated (see above), disturbances in the functioning of the stomach can contribute to a lack of vitamin B12. This can happen for two reasons:

Firstly, stomach diseases can cause disruption of the functioning of stomach cells. Cells may stop producing a substance needed to absorb B12 called intrinsic factor. Without intrinsic factor, vitamin B12 cannot be absorbed from the gastrointestinal tract into the body's cells.

Secondly, insufficient secretion of gastric juice. Lack of stomach acid (a condition called hypochlorhydria) reduces the absorption of vitamin B12 because most B12 in foods is attached to food proteins, and stomach acids are needed to separate B12 from these proteins.

Thirdly, excess syndrome bacterial growth in the small intestine ( SIBO), which is caused by a decrease in the secretion of hydrochloric acid in the stomach and impaired motility of the small intestine. During the development of SIBO, various anaerobic and facultative gram-negative aerobes competitively utilize dietary cobalamin. Intrinsic factor inhibits the utilization of cobalamin by gram-negative aerobic flora, but is not able to counteract the gram-negative anaerobic flora that absorb this vitamin.

Intestinal dysbiosis. On the exceptional importance of intestinal microflora in the regulation metabolic processes in the body today is known to everyone. As practice shows, the main cause of B12 deficiency is not the lack of a balanced diet, but a violation of the absorption processes of micronutrients in the small intestine, which are regulated by the host’s own gastrointestinal microflora. Therefore, intestinal dysbiosis is also one of the main causes of B12 deficiency. The causes of microflora imbalance are different (usually secondary), ranging from the diseases described above, to such as: the consequences of intestinal infections, bad habits, other diseases, incl. stress, antibiotic therapy, etc. It is known that in addition to pathogenic bacteria, causing diseases, there are bacteria that use cobalamin for their own purposes, thereby interfering with its absorption by the human body. Based on the above, it would be reasonable to assume that modern conditions probiotic therapy, incl. using propionic acid bacteria - B12 producers, is effective tool in the prevention of hypovitaminosis B12.

Vegetarianism. The ability of a strict vegetarian diet to supply sufficient amounts of vitamin B12 remains controversial, despite growing evidence supporting vegetarianism and its nutritional adequacy.

Firstly, most animals, including humans, are able to accumulate and store vitamin B12.The main place accumulation of vitamin B12 The human body contains the liver, which contains up to several milligrams of this vitamin. It enters the liver with animal foods, in particular meat products, or synthesized intestinal microflora, provided that cobalt (Co) is supplied with food. The daily requirement for cyanocobalamin for an adult (from 14 years of age) is approximately 0.003 mg.

Secondly, the unreliability of the plant as a source of vitamin B12. Since no plant contains B12, the amount of vitamin B12 in plant foods depends on microorganisms (bacteria, yeast, mold and fungi) that produce the vitamin. Fermented bean products (tofu, tempeh, miso, tamari, shoyu) may contain significant amounts of vitamin B12 or none at all, depending on the bacteria, molds, fungi and fungi used to produce them. The B12 content of algae also varies depending on the distribution of microorganisms in the surrounding marine environment. Depending on the environment in which they are grown, brewer's and nutritional yeast can be important sources of vitamin B12 in strict vegetarian diet. Therefore today in plant-based diet It is recommended to consume fortified (fermented with B12 producers) foods. See below for fermentation.

What medications affect vitamin B12?

The category of drugs that can reduce the supply of vitamin B12 to the body includes: antibiotics (kanamycin, neomycin), anticancer drugs (methotrexate), anticonvulsants(phenytoin, primidone), anti-gout drugs (colchicine), antihypertensive drugs(methyldopa), drugs for the treatment of Parkinson's disease (levodopa), antipsychotics (aminazine), anti-tuberculosis drugs (isoniazid), cholesterol-lowering drugs (clofibrate), potassium chloride, sugar-reducing agent.

Smoking and vitamin B12

We will not discuss the relationship between smoking and B12 deficiency here, but will merely comment on one study that some readers have suggested that long-term use of large amounts of B12 may increase the risk oncological diseases. We simply have to make a clarification, since such speculation is presented as evidence, however, of who knows what. This is the study we are talking about: Theodore M. Brasky,et. al. Long-Term, Supplemental, One-Carbon Metabolism-Related Vitamin B Use in Relation to Lung Cancer Risk in the Vitamins and Lifestyle (VITAL) Cohort. Journal of Clinical Oncology, 2017. In this work, it was suggested that in men, long-term consumption of large quantities of vitamins B6 and B12 may increase the risk of developing lung cancer (for women, this conclusion was not confirmed in this statistical study).

However, it is worth describing in detail the conditions of the study: men who took part in the statistical (!) study daily (!)within (!) 10 yearsconsumed high doses vitamin preparations, were aged from 50 to (!) 76 years and had a long (!) smoking history, which in itself raises many questions regarding the level of reliability of the conclusions drawn about the cause-and-effect relationship of the increased risk of lung cancer. The author of the work, Theodore M. Braschi, put an end to the results obtained. He noted that he plans to hold a second more ambitious study to confirm the results of the first. That is why it is simply unacceptable to present these statistical conclusions as proof of anything. In conclusion, we note that the task itself daily multi-year absorption high doses vitamin B12 is not placed at all, because without scientific interest, no one needs it and when used food products(even fermented PCB) or microbiological dietary supplements (not injections or special vitamin preparations) penetration of excess B12 into organs and tissues physically impossible. Moreover, vitamin B12 is non-toxic andsurplusare excreted from the body(cm. ).

Sources of vitamin B12

So what do we have? Humans and animals usually provide themselves with vitamin B12 as a result of the consumption of food of animal origin and its production by microflora digestive tract(cm.: Vitamin B12). However, given that the synthesis of vitamin B12 by intestinal flora is insignificant, the vitamin must enter the body from the outside.

Since vitamin B12 cannot be produced by plants, its content depends on their association with microorganisms (for example, bacteria in the soil). Because of their ability to store vitamin B12, animals contain more of the vitamin than plants.

Therefore, are excellent sources of vitamin B12 limited to animal foods? No. And here, unfortunately, it is not always possible to get a sufficient amount of vitamin B12. This is primarily due to the quality of the products and their industrial processing. If we talk about reliable food sources B12, then today these are the productsfermented by microorganisms that produce cobalamin (B12).The developed technologies now make it possible to obtain B12-containing products from almost any type of food raw material, both plant and animal origin. In this case, propionic acid bacteria are used as powerful B12 producers.

External factor

Castle's extrinsic factor is vitamin B12 (cobalamin, or cyanocobalamin), which is found in raw meat, raw liver, yeast, fish, eggs, and milk.

Internal factor

Castle's internal factor (gastromucoprotein) is a complex compound consisting of peptides that are cleaved from pepsinogen when it is converted into pepsin, and mucoids, a secretion secreted by the cells of the gastric mucosa (mucocytes). The mucoid part of the complex protects it from hydrolysis by digestive enzymes and utilization by intestinal bacteria; the protein part determines its physiological activity. The main role of Castle's intrinsic factor is the formation of a labile complex with vitamin B12, which is absorbed by the epithelial cells of the ileum. Absorption is enhanced in the presence of calcium ions, bicarbonates and pancreatic enzymes. In blood plasma, vitamin B12 binds to plasma proteins, forming a protein-B12-vitamin complex, which is deposited in the liver. It enhances the hematopoietic function of the bone marrow, as well as the functions of nervous tissue and glands. -kish. tract.

Violations

The secretion of intrinsic factor Castle may decrease or completely stop when the gastrointestinal tract is damaged. -kish. tract (for example, during an inflammatory process, cancer), when part of the stomach or small intestine is removed, etc. In these cases, the binding and absorption of vitamin B12 is impaired, which leads to the development of B12-deficient megaloblastic, or pernicious, anemia.

Possible causes of Castle intrinsic factor deficiency:

A congenital genetic defect, when for some reason this substance is not produced enough or is completely absent
Diseases of the stomach in which the work of parietal cells is blocked or their number is sharply reduced (chronic gastritis with atrophy of the mucous membrane or stomach cancer)
Surgical removal of the stomach for various reasons
Often additional pathology from the outside endocrine system, autoimmune diseases are complicated by B12 deficiency anemia

Sometimes enough of it is produced, but the disease still develops. Why could this be?

Castle has an internal factor, but he has nothing to connect with - a strict vegetarian simply deprives himself of vitamin B12 completely
The work of the cells of the small intestine, which is responsible for the absorption of the resulting complex, is disrupted
Complete dysfunction of intestinal absorption, congenital or acquired. This leads to multiple diverticula of the small intestine, some (diphyllobothriasis)
Condition after intestinal resection

Vitamin B12 and Castle factor deficiency clinic

The most well-known form of the disease associated with a deficiency of these factors is pernicious (megaloblastic) anemia. In addition to the expected pallor, brittleness of hair and nails, jaundice is associated with increased destruction of red blood cells. The tongue becomes very characteristic and remarkable - completely smooth due to atrophy of the papillae, shiny and bright - varnished. Often quite painful and unpleasant ulcers appear on it - aphthae. Appetite decreases significantly, aversion to meat appears. The liver and spleen may enlarge, and the activity of the heart may be impaired. Of course, in addition to all this, a person feels weakness, loss of strength, and dizziness and darkening of the eyes are often noted.

From the nervous system The signs are even sadder, and everything begins very innocently, and does not make either the patient or his family wary. Initially, weakness appears in the legs, periodically there is a feeling of pins and needles, and reflexes decrease, which are usually determined at an appointment by neurologists. Over time, muscle weakness increases, the functioning of the pelvic organs is disrupted (the activity of the sphincters of the bladder and rectum, impotence develops in men). In some cases, they may appear mental disorders, from neurosis to severe psychosis with hallucinations, progressive decline in intelligence.

Diagnosis and treatment

For correct diagnosis In addition to the usual peripheral blood test, it is advisable to do a sternum puncture to check the cells bone marrow. In addition, you should definitely consult a hematologist. For the safety of the patient and to make the doctor more informative, it is recommended that a complete examination and initiation of treatment be carried out in a hospital.

Once the diagnosis and its possible cause become clear, therapy begins. The main drug for this pathology is vitamin B12 intramuscularly. The dose depends on the severity and severity of symptoms, the degree of deficiency of this important factor. Initially, injections are prescribed daily, then every other day, gradually switching to maintenance administration of the drug once a week.

Naturally, if it is possible to eliminate the internal deficiency of the vitamin in the blood, for example, by diversifying the menu and switching to less strict vegetarianism, removing helminths, this must be done.

Useful video on the topic - “Vitamin B12 - what you eat it with”

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Clinical picture of stomach inflammation and how to cure...

Castle's internal factor

Castle's internal factor– a protein that is produced in the gastric mucosa that binds, transports and ensures the absorption of vitamin B12. Antibodies to intrinsic Castle factor are complexes that reduce the amount of this glycoprotein. A blood test to determine the content of antibodies of this type is used in gastroenterology, neurology, and hematology. Prescribed in combination with clinical analysis blood test for vitamin B12 and antibodies to myelin basic protein. The results are used for early diagnosis hypoacid gastritis, pernicious anemia, demyelinating diseases of the nervous system, as well as autoimmune pathologies. Blood is taken for testing from a vein. Methods used to detect antibodies enzyme immunoassay. Normally the result is negative. The study is carried out within 11 working days.

Antibodies to intrinsic Castle factor are specific immunoglobulins that interact with intrinsic Castle factor, disrupting its binding to vitamin B12 and absorption by the small intestinal mucosa. Intrinsic Castle factor is classified as a glycoprotein in its chemical structure. It is produced in the cells of the gastric mucosa and enters the small intestine. The main function of this protein is to ensure the absorption of vitamin B12. The internal factor is able to bind, transport and stimulate the absorption of cobalamin even with changes in the aggressiveness of gastric juice, increased exposure to pepsin and perchloric acid, so gastritis does not affect the functions of the glycoprotein.

In clinical and laboratory practice, antibodies to intrinsic Castle factor are considered as a highly specific marker of B12-deficiency anemia. There are two types of these immunoglobulins. Blocking antibodies prevent cobalamin from binding to intrinsic factor. They are more active with increased alkalinity of the internal environment of the stomach. The other type is binding antibodies. They disrupt the attachment of internal factor with vitamin B12 to the receptors of the intestinal mucosa, that is, they interfere with absorption. The result of the action of both types of antibodies is a deficiency of vitamin B12 in the body.

When testing blood for antibodies to intrinsic Castle factor, the total amount of antibodies of two types is revealed, since their separation is not of particular clinical significance. To perform the analysis, blood is taken from a vein. The presence and concentration of antibodies are determined by the enzyme immunoassay method. The main areas of application of the assay are hematology and gastroenterology, and it is used as an auxiliary test in neurology and rheumatology.

Indications

A test for antibodies to intrinsic factor in the blood is indicated for patients with vitamin B12 deficiency and pernicious anemia. Both conditions are accompanied by a decrease in body weight, increasing weakness, disorders of the peripheral nervous system (a frequent manifestation is a change in sensitivity), and inflammation of the tongue. Pernicious or B-12 deficiency anemia most often develops after 40 years. Its combination with autoimmune diseases affecting the endocrine glands is typical. Therefore, as part of a comprehensive diagnosis, an analysis for antibodies to internal factor is prescribed for autoimmune thyroiditis, insulin-dependent diabetes mellitus, Addison's disease, as well as for autoimmune pathologies not related to endocrinopathies.

A test for antibodies to intrinsic Castle factor in the blood is used to early detection autoimmune gastritis (type A) and its differentiation from other diseases. The pathology is practically asymptomatic and rarely becomes the reason for seeking treatment. medical care. Often, autoimmune gastritis is discovered several years after its onset, when, due to a lack of vitamin B12, the production of red blood cells is disrupted and macrocytic anemia develops.

The basis for studying antibodies to the internal factor may be symptoms of anemia, as well as changes in a general clinical blood test - an increase in the size of red blood cells, an increase in erythrocyte hemoglobin, a decrease in the level of reticulocytes, the development of thrombocytopenia, leukopenia. Pernicious anemia with a long course leads to irreversible changes in nervous system, therefore, the study of antibodies to the internal factor may be indicated for polyneuritis, ataxia, and demyelinating pathologies.

The advantage of testing for antibodies to intrinsic Castle factor is its high specificity for vitamin B12 deficiency and pernicious anemia. A limitation of the study is that these antibodies are produced in only 60% of patients with autoimmune gastritis. That's why this test It is recommended to combine it with a blood test for ARVC.

Preparation for analysis and collection of material

The level of antibodies to intrinsic Castle factor is determined in venous blood. The collection procedure is carried out in morning time, before meals. Preparation includes giving up alcohol, limiting physical and psycho-emotional stress during the previous 24 hours, and quitting smoking 30 minutes in advance. Blood is taken from the cubital vein using a puncture, stored and transported in sealed tubes. Before the test, the tubes are placed in a centrifuge unit, and then clotting factors are removed from the plasma.

Antibodies to intrinsic Castle factor are determined in venous blood serum by enzyme immunoassay. The procedure consists of two stages. At the first stage, antigens specific to intrinsic factor antibodies are introduced into the serum. At the second stage, the resulting complexes are colored during an enzymatic reaction. Based on the change in the density of the mixture, the concentration of the antibodies under study is calculated. Preparation of results takes 7-11 days.

Normal values

Normally, the result of a blood test for antibodies to intrinsic Castle factor is negative. Reference values range from 0 to 6 rel. units/ml Physiological factors do not affect the results of the study. It is also worth remembering that the absence of antibodies to the internal factor does not exclude the presence of diseases; the final indicators in any case require interpretation by a specialist.

Level change

The main reasons for increased levels of antibodies to intrinsic factor in the blood are vitamin B12 deficiency and pernicious anemia. If this result is combined with low blood test results for vitamin B12 and characteristic changes V general analysis blood, then the diagnosis of B12-deficiency anemia is confirmed. In addition, the cause of an increase in the level of antibodies to the internal Castle factor in the blood can be atrophic gastritis, autoimmune and neurological diseases.

The reason for the decrease in the level of antibodies to the intrinsic factor in the blood during repeated studies is considered to be a positive response to therapy. Low performance at initial examination are the norm, however negative result does not exclude the diagnosis of pernicious anemia.

Treatment of abnormalities

A blood test for antibodies to intrinsic Castle factor is a highly specific test for diagnosing B12 deficiency and pernicious anemia. In combination with an analysis for ARGC, it is used to identify autoimmune gastritis. The interpretation of the results and the prescription of treatment is carried out by the attending physician - hematologist, gastroenterologist, neurologist, rheumatologist.

Castle factors, named after the American physiologist and hematologist W.B. Castle, are substances that collectively stimulate hematopoiesis.

External factor

This is vitamin B12, which is found in raw meat, raw liver, yeast, fish, eggs, milk.

Internal factor

Castle's intrinsic factor is a complex compound consisting of peptides that are cleaved from pepsinogen when it is converted into pepsin, and mucoids, a secretion secreted by the cells of the gastric mucosa. The mucoid part of the complex protects it from hydrolysis by digestive enzymes and utilization by intestinal bacteria; the protein part determines its physiological activity. The main role of intrinsic factor Castle is to form a labile complex with vitamin B12, which is absorbed by the epithelial cells of the ileum. Absorption is enhanced in the presence of calcium ions, bicarbonates and pancreatic enzymes. In blood plasma, vitamin B12 binds to plasma proteins, forming a protein-B12-vitamin complex, which is deposited in the liver. It enhances the hematopoietic function of the bone marrow, as well as the functions of the nervous tissue and gastrointestinal tract.