Yoga with edema
1. Anatomy, physiology and hormones of the thyroid gland.
1.1. Anatomy of the thyroid gland.
The thyroid gland consists of two parts,connected by isthmus. The lobes are located at the sides, anteriorly and downward from the epiglottis, and the isthmus is anterior and lower than the cricoid cartilage. Sometimes there is also an additional - a pyramidal - a share that extends from the isthmus upward, in the form of a finger, but it can only be palpated when the gland is enlarged.
The weight of the gland is 10 to 30 g. The length of each lobe is 2.5 to 4 cm, width 1.5-2 cm, thickness 1-1.5 cm. Behind the thyroid gland are trachea and esophagus.
The gland is supplied with blood from the upper and lower thyroid arteries. It has both sympathetic innervation (from the cervical ganglia) and parasympathetic (branches of the vagus nerve).
1.2. Physiology and hormones of the thyroid gland.
The thyroid gland consists of follicles. The cavity of the follicle is filled with a colloid and is surrounded by a layer of cubic epithelial cells. With hyperfunction of the gland, they acquire a cylindrical shape, with hypofunction become flat. Numerous microvilli move away from the cells into the lumen of the follicle.
In thyroid cells a protein is synthesizedThyroglobulin, which enters the lumen of the follicle. In each molecule of thyroglobulin, the iodine content is 0.1-1%. Thyroglobulin is involved in the synthesis of thyroid hormones.
Synthesis of thyroid hormones is carried out byiodination of the amino acid tyrosine. As a result of this process, mono- and diiodotyrosines are formed, which, in pairs, form triiodothyronine (T3) and tetraiodothyronine, or thyroxine (T4), respectively. After that, T3 and T4 enter the bloodstream, and along it - into the peripheral tissues.
Thyroid hormones after secretion into the bloodstreamare bound by transport proteins. In this case, only 0.04% of the total T4 remains in the free state. Total T3 and T4 include both free hormones and protein-bound proteins, but the level of protein-related hormones is affected by a variety of physiological and pathological conditions, so the functional activity of the thyroid gland can be judged by the level of free T3 and T4. Among the factors that increase the total T3 and T4 are hyperestrogenic (in pregnancy or estrogen treatment), acute infectious hepatitis, hypothyroidism. Among the reducing factors - androgens, glucocorticoids, poor nutrition, nephrotic syndrome, hyperthyroidism, severe somatic diseases.
In the tissues, a single molecule is cleavediodine from T4 and its transformation into T3. T3 is 3-4 times more active than T4 and is considered as a true hormone, and T4 is a prohormone. In the thyroid gland, only 20% of T3 is formed, and the remaining 80% is formed in peripheral tissues. This process is activated in hypothyroidism, so the normal level of T3 is observed in the blood with reduced T4.
1.3 Regulation of thyroid function.
Regulation of the thyroid glandis carried out on the principle of negative feedback. The thyroid-stimulating hormone (TTG) of the pituitary gland stimulates the gland, and the excess of thyroxine, turning into triiodothyronine, inhibits the synthesis and secretion of TSH.
TSH is under the control of thyrotropin-releasing hormone (TRH), which is synthesized in the hypothalamus.
TTG stimulates all the functions of the thyroid gland, from the transfer of inorganic iodine to the gland before T3 and T4 enter the bloodstream.
In turn, T3 inhibits the secretion of TSH and TGH (see Fig.)
There is also a mechanism of autoregulationactivity of the thyroid gland, depending on the availability of inorganic iodine: in the absence of iodine, iron can support the function by increasing the intake of iodine and increasing the proportion of T3, and in excess, on the contrary, the intake of iodine into the gland and the binding of TSH is reduced.
1.3.3. Regulation by the autonomic nervous system.
The thyroid gland has many endingssympathetic nervous system, located not only around the vessels, but also in the glandular tissue itself. Thus, catecholamines of the SNS influence the thyroid gland both through the blood stream and directly acting on the thyrocytes.
Stimulation by the SNA enhances digestionthyroglobulin thyrocytes, iodine uptake and the synthesis of thyroid hormones. It is believed that the SNS is one of the most important body systems that regulate the level of thyroid hormones in the blood serum and the level of their activity.
The fibers of the parasympathetic nervous system alsofit to follicles and vessels of the thyroid gland. The influence of parasympathetic stimulation is opposite to that of the SNS and leads to a decrease in the secretion of thyroid hormones.
1.4. Physiological effects of thyroid hormones.
Thyroid hormones are necessary for normalgrowth and development of the fetus, including the brain. They have a significant impact on the activity of the central nervous system, cardiovascular and respiratory systems, GAD, endocrine system and skeletal muscles.
Most of the effects of thyroid hormonesis due to two fundamental mechanisms. The first is the action of T3 on the mitochondria. Under the influence of T3, mitochondria increase in size, their activity, cellular respiration, oxygen consumption and ATP formation increase. Thus, thyroid hormones provide all organs and tissues with energy.
The second mechanism is to act oncatecholamines. Thyroid hormones increase the activity of catecholamines by increasing the number of their receptors. Thyroid hormones increase the amount of β-adrenergic receptors in the myocardium, skeletal muscles, adipose tissue, and lymphocytes.
Thyroid hormone action on the heartis to increase oxygen consumption, increase contractile activity of the myocardium, increase the frequency of heart rate and the rate of impulses in the conductive system of the myocardium.
Action on the GI tract is to increase the intestinal motility.
The action on the respiratory system is in maintaining the normal function of the respiratory center, maintaining the balance of oxygen and carbon dioxide in the blood.
Thyroid hormones act on the bone, increasingbone resorption and, to a lesser extent, bone formation. Hyperthyroidism even in young people with prolonged course can contribute to the development of osteoporosis.
On the muscle tissue, thyroid hormones act by increasing the synthesis of structural proteins.
Hypothyroidism - polyethological syndrome,the clinical manifestations of which are a decrease in the function of the thyroid gland, a decrease in the synthesis of thyroxin and its insufficient effect on tissues and organs.
There are primary, central and peripheral hypothyroidism.
Primary hypothyroidism is a consequence of the pathology of the thyroid gland and the inadequacy of its function.
Central hypothyroidism is a consequence of hypofunction of hypophysis (hypopituitarism) or hypothalamus, a lack of synthesis of TSH, a decrease in thyroid stimulation of thyroid gland and a lack of synthesis in it of T3 and T4.
Peripheral hypothyroidism is most often caused by the resistance of target tissues to T4 and T3, caused by genetic defects of T4 and T3 receptors.
The spread of the disease is 0.5-1%,among newborns - 0.025%, and among people older than 65 years - 2-4%. Prevalence among women is about 2%, among men - 0.1%. In the vast majority of cases (more than 95%) hypothyroidism is primary. Secondary (central) hypothyroidism occurs in approximately 1% of cases of hypothyroidism in adults.
Most often, primary hypothyroidism is the outcomeautoimmune thyroiditis, less often - the result of treatment of thyrotoxicosis syndrome, although a spontaneous outcome of diffuse toxic goiter in hypothyroidism is also possible. Allocate congenital and acquired forms of hypothyroidism. The most frequent cases of hypothyroidism in newborns are paladium and dysplasia of the thyroid gland.
Central hypothyroidism develops as a result ofdeficiency of TTG or TRH. Central hypothyroidism can be congenital or acquired. The causes of congenital secondary hypothyroidism are: hypoplasia of the pituitary gland; tumors and cysts; defects of biosynthesis and secretion of TSH.
Acquired secondary hypothyroidism developswith microadenomas of the pituitary gland, operations and irradiation of the hypothalamic-pituitary region; ischemic and hemorrhagic necrosis of the pituitary (Syndrome Shien-Simmonds).
Lack of thyroid hormones affects manyfunctions and metabolic processes in the body. Characteristic is a decrease in metabolic processes, a slowing down of oxidation-reduction reactions. A universal sign is mucinous edema (myxedema), most pronounced in connective tissue. Accumulation of products of protein decay, which have increased hydrophilicity, causes the accumulation of extravascular fluid and sodium. Deficiency of thyroid hormones in childhood inhibits physical and mental development, even to cretinism.
Hypothyroidism is characterized by a wide range of disorders. Their presence and severity depends on the severity of the course of the disease.
• Nervous system: memory disorders, drowsiness, inhibition, depression, hearing loss, slowing of tendon reflexes.
• CCC: bradycardia, reduction of cardiac output, weakening of the heart muscle, low amplitude of the teeth and flattening or absence of a T wave on the ECG. Dysfunction of the heart leads to edema.
• Gastrointestinal tract: constipation, achlorhydria, often in combination with autoimmune gastritis.
• Kidneys: decreased water excretion, which may be due to hyponatraemia. Kidney blood flow is reduced.
• Breathing: shortness of breath; ventilatory reactions to hypoxia and hypercapnia weakened. In severe hypothyroidism, due to hypoventilation of the alveoli, severe hypercapnia may occur.
• ODA: arthralgia, muscle spasms, muscle stiffness, pain in the joints and muscles.
• Blood: anemia may occur.
• Skin and hair: the skin is dry, cold, yellowish, flakes off on the elbows, does not gather in the folds. Myxedema (mucous edema). The face is puffy, with coarse features. Body hair is poor, hair loses its shine. Often there is an outflow of the third third of the eyebrows.
• Violation of sexual function in women. Menorrhagia, often against the background of anovulation. Frequently, menstruation is meager or stops due to the weakening of the secretion of gonadotropic hormones. Girls may experience a delay in sexual development.
• Growth and development: in children, stunting is observed. Epiphyseal areas of bone growth remain open. The delay in growth is caused not only by deficiency of T3 and T4, but also by deficiency of STH, as its secretion is regulated by thyroid hormones.
• Metabolism and energy. Usually there is hypothermia. Reduced the disintegration of lipoproteins, which leads to an increase in the level of cholesterol and triglycerides. Usually there is an increase in weight.
• Thyroid. Thyroid enlargement in children. Goiter in adults.
This is the final manifestation of an untreated orimproperly treated hypothyroidism. Clinical picture: hypothermia, bradycardia, arterial hypotension, hypercapnia, mucous edema of the face and extremities, characteristic skin changes, brain hypoxia, symptoms of CNS damage (confusion, inhibition, stupor or coma). Sometimes there is a delay in urine or intestinal obstruction. D. coma may occur with any form of hypothyroidism. Most often it provokes concomitant diseases, in particular infection or stroke. Other provoking factors: tranquilizers, hypothermia, trauma, hemorrhage, myocardial infarction, hypoxia, hypoglycaemia. Almost all patients die without treatment. Intensive therapy (500 μg of levothyroxine IV, for 1 hour) dramatically reduces mortality.
As a rule, to determine the diagnosis, it is sufficient to determine the total T4, free T4 and TSH in the serum.
Increase in TSH level - sensitive markerprimary hypothyroidism, so a change in the level of TSH is considered the best way to identify the disease among the general population. However, in practice, the common T4 and free T4 are more often determined, since these studies are cheaper.
With secondary hypothyroidism, the functionadenohypophysis or hypothalamus, therefore the concentrations of not only T4 but also TSH are reduced. In some cases, the level of TSH is normal, but its hormonal activity is reduced. CT and MRI can detect changes in the pituitary gland (most often a tumor) in patients with secondary hypothyroidism.
In the treatment of primary hypothyroidism the following medicines are used:
• Levothyroxine. This is a synthetic T4. It is used for hormone replacement therapy. Provides a stable level of not only T4, but also T3. About 70% of levothyroxine is absorbed into the gastrointestinal tract. Taking levothyroxine does not lead to a sharp increase in serum T3 concentration, which could be dangerous in elderly patients or persons with concomitant cardiac pathology. Instead, stabilization of the T3 level, continuously generated from the injected T4, is achieved.
• Tyroid. Extract from the thyroid glands of pigs and cattle, standardized for iodine content. The content of T4 / T3 is approximately 4/1. According to physiological activity, the thyroid is 1000 times weaker than levothyroxine.
• Lyotyronine. Synthetic T3. Lyotyronine is usually not used for long-term therapy. Applied for short-term treatment in cases where it is required to quickly cancel treatment for a short time, as well as for diagnostic purposes. In the gastrointestinal tract, about 90% of the lyotyronine is absorbed.
• Combined preparations of thyroid hormones (lyotriks) were created before it became clear that T4 on the periphery was converted to T3. Currently used rarely.
Most often the metabolic status is neededrestore gradually, especially in elderly patients or with heart disease, since a rapid increase in basal metabolism can deplete the reserves of the myocardium and coronary blood flow. Treatment of adult patients usually begin with a daily dose of levothyroxine of 25 μg and increase it by 25-50 μg every 2-3 weeks until normal metabolic status is achieved. The dose required to maintain the latter is usually about 150 μg per day. In this case, the content of T4 in the blood serum is established, as a rule, at a level slightly higher than the upper limit of normal vibrations. Serum T3 concentration is a more reliable indicator of metabolic status in patients receiving levothyroxine than T4 concentration. Due to the long half-life of the hormone, levothyroxine is usually administered once a day. The optimal dose for an individual patient should be based on clinical criteria and on the results of determining serum levels of TSH and T3. Elevated levels of TSH indicate a failure of treatment, and an increase in the level of T3 - on its redundancy.
With neonatal and pediatric hypothyroidism, it is important tothe possibility to perform full replacement therapy more quickly; otherwise, the chances of providing the child with normal mental development and growth are lost. In infants and children, the necessary doses of levothyroxine are disproportionately high in relation to body size. With confidence or strong suspicions for the presence of pituitary or hypothalamic hypothyroidism, thyroid replacement therapy should not be started without prior treatment with hydrocortisone, as strengthening the basal metabolism can cause adrenal cortex insufficiency.
Some patients with hypothyroidism need to be treatedfast. These are patients with myxedema coma, as well as persons who have an urgent surgical operation, since they are very sensitive to narcotic drugs. In such cases, intravenous administration of levothyroxine in combination with hydrocortisone is indicated.
4. Ayurveda and herbal medicine in the treatment of hypothyroidism.
4.1. Ayurvedic view of hypothyroidism.
From the point of view of ayurveda, hypothyroidism is a Kapha disorder. Most of the symptoms of this disease are described as symptoms of increased kapha:
• Increased weight with low appetite. The decay of lipoproteins has been reduced.
• Accumulation of mucus, mucous edema (myxedema).
• Weakening of the basic cellular exchange.
• Accumulation of ama (metabolic products) in tissues.
• Memory impairment, drowsiness, depression.
• Achlorhydria, indigestion, constipation.
• Shortness of breath, shortness of breath.
• Chilliness, insufficient heat production (hypothermia).
• Skin cold, pale, swollen.
Ayurvedic therapy aimed at lowering Kapha, should be stimulating, drying, lightening and purifying.
Diet: food is light and warm, with an emphasis on sharp, bitterand astringent tastes (to stimulate secretion of digestive secretions). Sugar and sweets are excluded, the amount of salt decreases. To improve digestion, hot spices are recommended: cloves, ginger, cinnamon, black pepper. Periodically, you can fast, if the patient is not weakened.
Exercises: intense exercises, inverted poses, bhastrika.
Cleaning practices: dhauti with the use of expectorant herbs (ayr, lobelia, licorice).
Lifestyle: active, a lot of dynamic exercises, especially in the fresh air. Limit the amount of sleep.
4.2. Phytotherapy for hypothyroidism.
In the case of pronounced hypothyroidism without hormonaltherapy can not be avoided. Severe hypothyroidism should be eliminated immediately, which can only be achieved with thyroid hormone preparations. Prolonged disregard for pharmacological substitution therapy will lead to disastrous results.
Phytotherapy is often used as aadditional therapy for hypothyroidism, allowing you to gradually improve your health, stabilize hormones, and gradually reduce or cancel hormone therapy.
• Herbs that help lose weight: coil, barberry, gentian, myrrh, guggul, phytosorbents of beets, apples, oats, chaga.
• Adaptogens: Eleutherococcus spiny, Aralia Manchu, Ginseng, Rhodiola rosea.
• Herbs containing diiodotyrosine: dyk dye, zheruksa medicinal, kelp, sugary, fucus bubble ¹; lichens: Icelandic cetrarium (yagel, Icelandic moss), sparse parmelia, alpine cladonia. Lichens, in addition to a high content of diiodotyrosine, have a pronounced toning and restoring property due to bitterness and carbohydrates in the thallus composition, and also normalize the stool.
• Soft laxatives: triphala, aloe juice, jaoster, nettle nettle, mountainous pochechuyny, linen ordinary. Strong laxatives are not shown.
• Diuretics: plantain, corn stigmas, horsetail field; herbs and preparations that improve kidney function, for example, mummies.
• Herbs that reduce cholesterol and reduceblood viscosity: quince, aralia high, mountain arnica, elm glabel, licorice, medicinal herb, large burdock, raspberry, coltsfoot, sea buckthorn, oats sowing, dandelion, medicinal, etc.
• Herbs that improve hearing: ayr, cyanosis, dandelion, burdock.
• Herbs that improve nasal breathing: sage, chamomile, yarrow, nettle, picher, horsetail.
• Herbs that improve fluidity of the blood: medicinal clover, creeping knotweed, willow goat, raspberry, peony evading.
5. Yoga in the treatment of hypothyroidism.
5.1. General principles of yoga therapy of hypothyroidism.
Yoga is a very effective methodstimulation of the thyroid gland, which is reflected even in classical yogic texts: "Perfection in hatha yoga is achieved when there is leanness of the body, calmness, the manifestation of inner sound, clear eyes, absence of disease, control over bindu, active digestive fire and purification of nadi "(Hatha yoga pradipika, 2.78).
In the practice of yoga in the case of hypothyroidism, it is necessary to set the following tasks:
• Activation of the sympathetic adrenal system to enhance the activity of the gland (see 1.3.3)
• Stimulation of the production of TRH and TTG by the pituitary and hypothalamus.
• Stimulation of blood flow directly in the thyroid gland.
In addition to direct stimulation of the thyroid gland, hatha yoga in the case of hypothyroidism should include the following mechanisms:
• Improve intestinal peristalsis and gastric juice secretion.
• Stimulation of renal blood flow and water excretion
• Improving mental health
• Increased venous return
• Weight normalization, lowering of cholesterol level
• Stimulation of lung function, reduction of hypercapnia
• Stimulation of ovarian activity in women
• Withdrawal of muscle spasms
5.2. Comparative analysis of the approaches of various schools of yoga to the problem of hypothyroidism.
Hypothyroidism is fairly commonproblem. Despite this, analyzing the recommendations of various schools of yoga seems a challenge. Recommendations are often issued blurred and contradictory. For example, Swami Sivananda considers goitre as a problem, without specifying his character, then how the enlargement of the thyroid gland can be caused by different, including opposite, reasons. Dhirendra Brahmachari generally does not practically describe the influence of asanas on the functioning of the thyroid gland, and judging of these effects is due to indirect data, for example: "Sarvangasana ² ... primarily contributes to the reduction of obesity. Fat accumulations on the abdomen disappear, the body becomes beautiful, the eyes are shiny, and the face is calm. "
Most often in connection with the thyroid gland various authors mention the following asanas: sarvangasana, halasana, shirshasana, matsyasan, ustrasana.
Below I will present the recommendations of four teachers of yoga: Swami Sivananda, Swami Satyananda, BKS Iyengar and Dhirendra Brahmachari - in the form of a summary table.
6. An approximate set of recommendations for hypothyroidism.
2. Vamana-dhauti with the use of expectorant herbs (ayr, lobelia, licorice)
2. Agrisara-dhaouti, Nauli-kriya
3. Surya Namaskar
5. Urdhva dhanurasana
7. Paripurna Navasana
12. Nadi Shoddhana
The approximate composition of the herbal collection, which can be used for hypothyroidism:
Cetraria Icelandic (Thallus) 2 parts
Drok dyeing (grass) 1 part
Donnion medicinal (herb) 1 part
Lazadnii vesolistny (flowers) 2 parts
Common herb (herb) 1 part
Horsetail field (grass) 1 part
Reduce the content of fats, sweets and salt. To improve digestion, you can use spices: cloves, black pepper, ginger, cinnamon.
Recommendations on a way of life:
An active lifestyle with lots of exercise, especially in the fresh air.
7. Conclusion. The problem of the scientific approach to yoga.
Despite the urgency of the problem and, apparently, the high efficiency of practicing yoga in hypothyroidism, no full-fledged study of this effect has been conducted so far.
One study of the thyroidhormones in the practice of asan yoga was conducted by E. Krapivina, E. Musienko (Lviv State University named after I. Frank). Unfortunately, this study can not be called complete. It was conducted on a very small sample (10 people). For some unknown reason, the authors left unexplained TSH (which, as mentioned, stimulates the gland and can change significantly in the practice of asanas). Also, they did not conduct any remote analysis of the hormone level, which, decreasing immediately after the practice, for example, sarvangasana (due to the clamping of the thyroid gland in the posture) may subsequently increase due to the influx of blood, as well as the influence of the TTG of the pituitary gland.
Teachers of yoga and ayurveda, as a rule, do notshow extensive knowledge in the field of Western medicine, so their recommendations are often blurred and contradictory. Thus, from Table 5.2 it can be seen that the recommendations for various asanas are most often reduced to general phrases: "asana has a beneficial effect on the thyroid gland," "asana regulates the activity of the gland," etc. At the same time, it remains completely unclear from the description whether this activity intensifies or depresses asana, it is permissible to use it for hypofunction or, conversely, for hyperfunction of the gland.
Thus, the complex presented in Chapter 7exercises can only be recommended, and in no case should replace hormonal therapy. The primary goal is to reduce the attendant symptoms, and also, perhaps, to a gradual decrease in the thyroid hormone dose. Unfortunately, evidence-based therapy based on yoga is a distant future ...
8. List of used literature.
1. Iyengar BKS "Yoga of dipika."
2. Iyengar BKS "Yoga. The path to health. "
3. Alefirov A.N. "Phytotherapy of autoimmune thyroiditis."
4. The benevolent Ya.V. Shlyakhto E.V. Babenko A.Yu. "Endocrinology".
5. Brahmachari D. "Yogasana Vijnana."
6. Krapivina E. Musienko E. "Study of the content of triiodothyronine, thyroxine and thyrotropin in the blood serum when performing asan hatha yoga".
7. Kubarko A.I. (ed.) "Thyroid gland. Fundamental aspects ».
8. Lavin N. (ed.) "Endocrinology".
9. Lad V. Frowley D. "Herbs and spices."
10. Lesiovskaya E.E. Pastushenkov L.V. "Pharmacotherapy with the basics of herbal medicine."
11. Martynov B.V. "Purification by yoga and ayurveda"
12. Satyananda S. "Asana Pranayama Mudra Bandha."
13. Satyananda S. Muktibodhananda S. "Hatha Yoga Pradipika with comments."
14. Sydney G. Ingbar "Diseases of the Thyroid Gland".
15. Frouli D. "Ayurvedic therapy".
¹ In the case where hypothyroidism is the outcome of autoimmune thyroiditis, the last two are not shown because of the high content of iodides.
² Under this name Dhirendra Brahmachari has asana, in other schools known as halasana.
³ The thyroid and parathyroid glands, tonsils, salivary glands and other formations located in this part of the body belong to the sphere of Visma-granthi.