Muscular System Physiology
Deficiencies of zinc and other micronutrients may occur. Bread dough, cake fillings, artificial whipped cream, processed egg whites. This phenomenon is known as temporal summation. One company is planning to market the sweetener under the name Cweet. Skin of some Florida oranges only. Dextrose is an important chemical in every living organism. While those products may not contain added sodium nitrite, they sometimes are made with celery powder or celery juice, which are naturally high in nitrite.
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One of the bones is pulled towards the other bone, which remains stationary. The place on the stationary bone that is connected via tendons to the muscle is called the origin. The place on the moving bone that is connected to the muscle via tendons is called the insertion. The belly of the muscle is the fleshy part of the muscle in between the tendons that does the actual contraction.
Skeletal muscles are named based on many different factors, including their location, origin and insertion, number of origins, shape, size, direction, and function. Skeletal muscles rarely work by themselves to achieve movements in the body.
More often they work in groups to produce precise movements. The muscle that produces any particular movement of the body is known as an agonist or prime mover. The agonist always pairs with an antagonist muscle that produces the opposite effect on the same bones. For example, the biceps brachii muscle flexes the arm at the elbow.
As the antagonist for this motion, the triceps brachii muscle extends the arm at the elbow. When the triceps is extending the arm, the biceps would be considered the antagonist. Synergists are muscles that help to stabilize a movement and reduce extraneous movements.
They are usually found in regions near the agonist and often connect to the same bones. Because skeletal muscles move the insertion closer to the immobile origin, fixator muscles assist in movement by holding the origin stable. If you lift something heavy with your arms, fixators in the trunk region hold your body upright and immobile so that you maintain your balance while lifting.
Skeletal muscle fibers differ dramatically from other tissues of the body due to their highly specialized functions. Many of the organelles that make up muscle fibers are unique to this type of cell. The sarcolemma is the cell membrane of muscle fibers. The sarcolemma acts as a conductor for electrochemical signals that stimulate muscle cells.
Connected to the sarcolemma are transverse tubules T-tubules that help carry these electrochemical signals into the middle of the muscle fiber.
Myofibrils are made up of many proteins fibers arranged into repeating subunits called sarcomeres. The sarcomere is the functional unit of muscle fibers. See Macronutrients for more information about the roles of sugars and proteins.
The main function of the muscular system is movement. Muscles are the only tissue in the body that has the ability to contract and therefore move the other parts of the body. Muscles often contract to hold the body still or in a particular position rather than to cause movement.
Another function related to movement is the movement of substances inside the body. The cardiac and visceral muscles are primarily responsible for transporting substances like blood or food from one part of the body to another. The final function of muscle tissue is the generation of body heat. As a result of the high metabolic rate of contracting muscle, our muscular system produces a great deal of waste heat.
Many small muscle contractions within the body produce our natural body heat. When we exert ourselves more than normal, the extra muscle contractions lead to a rise in body temperature and eventually to sweating. Skeletal muscles work together with bones and joints to form lever systems. The muscle acts as the effort force; the joint acts as the fulcrum; the bone that the muscle moves acts as the lever; and the object being moved acts as the load.
There are three classes of levers, but the vast majority of the levers in the body are third class levers. A third class lever is a system in which the fulcrum is at the end of the lever and the effort is between the fulcrum and the load at the other end of the lever. The third class levers in the body serve to increase the distance moved by the load compared to the distance that the muscle contracts. The tradeoff for this increase in distance is that the force required to move the load must be greater than the mass of the load.
For example, the biceps brachia of the arm pulls on the radius of the forearm, causing flexion at the elbow joint in a third class lever system. A very slight change in the length of the biceps causes a much larger movement of the forearm and hand, but the force applied by the biceps must be higher than the load moved by the muscle. Nerve cells called motor neurons control the skeletal muscles. Each motor neuron controls several muscle cells in a group known as a motor unit.
When a motor neuron receives a signal from the brain, it stimulates all of the muscles cells in its motor unit at the same time. The size of motor units varies throughout the body, depending on the function of a muscle.
This inappropriate strategy diverted attention from the first need, which is adequate food intake by children. There is now much less emphasis on high-protein weaning foods and on nutrition education efforts to ensure greater consumption of meat, fish and eggs, which are economically out of the reach of many families who have children with PEM.
Protein is an essential nutrient, but PEM is more often associated with deficient food intake than with deficient protein intake. In general, when commonly consumed cereal-based diets meet energy needs, they usually also meet protein needs, especially if the diet also provides modest amounts of legumes and vegetables.
Primary attention needs to be given to increasing total food intake and reducing infection. Sensible efforts are needed to protect and promote breastfeeding and sound weaning; to increase the consumption by young children of cereals, legumes and other locally produced weaning foods; to prevent and control infection and parasitic disease; to increase meal frequency for children; and, where appropriate, to encourage higher consumption of oil, fat and other items that reduce bulk and increase the energy density of foods fed to children at risk.
These measures are likely to have more impact if accompanied by growth monitoring, immunization, oral rehydration therapy for diarrhoea, early treatment of common diseases, regular deworming and attention to the underlying causes of PEM such as poverty and inequity. Some of these measures can be implemented as part of primary health care. Nutritional anaemias are extremely prevalent worldwide. Unlike protein-energy malnutrition PEM , vitamin A deficiency and iodine deficiency disorders IDD , these anaemias occur frequently in both developing and industrialized countries.
The most common cause of anaemia is a deficiency of iron, although not necessarily a dietary deficiency of total iron intake. Deficiencies of folates or folic acid , vitamin B 12 and protein may also cause anaemia. Ascorbic acid, vitamin E, copper and pyridoxine are also needed for production of red blood cells erythrocytes. Vitamin A deficiency is also associated with anaemia.
Anaemias can be classified in numerous ways, some based on the cause of the disease and others based on the appearance of the red blood cells. These classifications are fully discussed in medical textbooks. Some anaemias do not have causes related to nutrition but are caused, for example, by congenital abnormalities or inherited characteristics; such anaemias, which include sickle cell disease, aplastic anaemias, thalassaemias and severe haemorrhage, are not covered here.
Based on the characteristics of the blood cells or other features, anaemias may be classified as microcytic having small red blood cells , macrocytic having large red blood cells , haemolytic having many ruptured red blood cells or hypochromic having pale-coloured cells with less haemoglobin. Macrocytic anaemias are often caused by folate or vitamin B 12 deficiencies. In anaemia the blood has less haemoglobin than normal. Haemoglobin is the pigment in red cells that gives blood its red colour.
It is made of protein with iron linked to it. Haemoglobin carries oxygen in the blood to all parts of the body. In anaemia either the amount of haemoglobin in each red cell is low hypochromic anaemia or there is a reduction in the total number of red cells in the body. The life of each red blood cell is about four months, and the red bone marrow is constantly manufacturing new cells for replacement.
This process requires adequate amounts of nutrients, especially iron, other minerals, protein and vitamins, all of which originate in the food consumed. Iron deficiency is the most prevalent important nutritional problem of humans. It threatens over 60 percent of women and children in most non-industrialized countries, and more than half of these have overt anaemia.
In most industrialized countries in North America, Europe and Asia, 12 to 18 percent of women are anaemic. Although deficiency diseases are usually considered mainly as consequences of a lack of the nutrient in the diet, iron deficiency anaemia occurs frequently in people whose diets contain quantities of iron close to the recommended allowances. However, some forms of iron are absorbed better than others; certain items in the diet enhance or detract from iron absorption; and iron can be lost because of many conditions, an important one in many tropical countries being hookworm infection, which is very common.
Nutritional anaemias have until recently been relatively neglected and not infrequently remain undiagnosed. There are many reasons for the lack of attention, but the most important are probably that the symptoms and signs are much less obvious than in severe PEM, IDD or xerophthalmia, and that although anaemias do contribute to mortality rates they do not often do so in a dramatic way, and death is usually ascribed to another more conspicuous cause such as childbirth.
However, research now indicates that iron deficiency has very important implications, including poorer learning ability and behavioural abnormalities in children, lower ability to work hard and poor appetite and growth. To maintain good iron nutritional status each individual needs to have an adequate quantity of iron in the diet.
The iron has to be in a form that permits a sufficient amount of it to be absorbed from the intestines. The absorption of iron may be enhanced or inhibited by other dietary substances. Human beings have the ability both to store and to conserve iron, and it must also be transported properly within the body. The average male adult has 4 to 5 g of iron in his body, most of it in haemoglobin, a little in myoglobin and in enzymes and around 1 g in storage iron, mainly ferritin in the cells, especially in the liver and bone marrow.
Losses of iron from the body must not deplete the supply to less than that needed for manufacture of new red blood cells. To produce new cells the body needs adequate quantities and quality of protein, minerals and vitamins in the diet. Protein is needed both for the framework of the red blood cells and for the manufacture of the haemoglobin to go with it.
Iron is essential for the manufacture of haemoglobin, and if a sufficient amount is not available, the cells produced will be smaller and each cell will contain less haemoglobin than normal. Copper and cobalt are other minerals necessary in small amounts. Folates and vitamin B 12 are also necessary for the normal manufacture of red blood cells. If either is deficient, large abnormal red blood cells without adequate haemoglobin are produced. Ascorbic acid vitamin C also has a role in blood formation.
Providing vitamin A during pregnancy has been shown to improve haemoglobin levels. Of the dietary deficiency causes of nutritional anaemias, iron deficiency is clearly by far the most important. Good dietary sources of iron include foods of animal origin such as liver, red meat and blood products, all containing haem iron, and vegetable sources such as some pulses, dark green leafy vegetables and millet, all containing non-haem iron.
However, the total quantity of iron in the diet is not the only factor that influences the likelihood of developing anaemia. The type of iron in the diet, the individual's requirements for iron, iron losses and other factors often are the determining factors. Iron absorption is influenced by many factors. In general, humans absorb only about 10 percent of the iron in the food they consume. The adult male loses only about 0. On an average monthly basis, the adult pre-menopausal woman loses about twice as much iron as a man.
Similarly, iron is lost during childbirth and lactation. Additional dietary iron is needed by pregnant women and growing children. The availability of iron in foods varies greatly. In general, haem iron from foods of animal origin meat, poultry and fish is well absorbed, but the non-haem iron in vegetable products, including cereals such as wheat, maize and rice, is poorly absorbed. These differences may be modified when a mixture of foods is consumed.
It is well known that phytates and phosphates, which are present in cereal grains, inhibit iron absorption. On the other hand, protein and ascorbic acid vitamin C enhance iron absorption. Recent research has shown that ascorbic acid mixed with table salt and added to cereals increases the absorption of intrinsic iron in the cereals two- to fourfold.
The consumption of vitamin C-rich foods such as fresh fruits and vegetables with a meal may therefore promote iron absorption. Egg yolk impairs the absorption of iron, even though eggs are one of the better sources of dietary iron. Tea consumed with a meal may reduce the iron absorbed from the meal. The normal child at birth has a high haemoglobin level usually at least 18 g per ml , but during the first few weeks many cells are haemolysed.
The iron liberated is not lost but is stored in the body, especially in the liver and spleen. As milk is a poor source of iron, this reserve store is used during the early months of life to help increase the volume of blood, which is necessary as the baby grows. Premature infants have fewer red blood cells at birth than full-term infants, so they are much more prone to anaemia. In addition, iron deficiency in the mother may affect the infant's vital iron store and render the infant more vulnerable to anaemia.
A baby's store of iron plus the small quantity of iron supplied in breastmilk suffice for perhaps six months, but then other iron-containing foods are needed in the diet. Although it is desirable that breastfeeding should continue well beyond six months, it is also necessary that other foods containing iron be introduced into the diet at this time.
Although most solid diets, both for children and adults, provide the recommended allowances for iron, the iron may be poorly absorbed. Many people have increased needs because of blood loss from hookworm or bilharzia infections, menstruation, childbirth or wounds. Women have increased needs during pregnancy, when iron is needed for the foetus, and during lactation, for the iron in breastmilk.
It is stressed that iron from vegetable products, including cereal grains, is less well absorbed than that from most animal products. Anaemia is common in premature infants; in young children over six months of age on a purely milk diet; in persons infected with certain parasites; and in those who get only marginal quantities of iron, mainly from vegetable foods.
It is more common in women, especially pregnant and lactating women, than in men. In most of the world, both North and South, the greatest attention to iron deficiency anaemia is directed at women during pregnancy, when they have increased needs for iron and often become anaemic. Pregnant women form the one group of the healthy population who are advised to take a medicinal dietary supplement, usually iron and folic acid.
Pregnant and lactating women are a group at especially high risk of developing anaemia. It is only in recent years that the prevalence and importance of iron deficiency apart from anaemia has been widely discussed. Clearly, however, if the causes of iron deficiency are not removed, corrected or alleviated then the deficiency will lead to anaemia, and gradually the anaemia will become more serious. Increasing evidence suggests that iron deficiency as manifested by low body iron stores, even in the absence of overt anaemia, is associated with poorer learning and decreased cognitive development.
International agencies now claim that iron deficiency anaemia is the most common nutritional disorder in the world, affecting over 1 million people. In females of child-bearing age in poor countries prevalence rates range from 64 percent in South Asia to 23 percent in South America, with an overall mean of 42 percent Table Prevalence rates are usually considerably higher in pregnant women, with an overall mean of 51 percent.
Thus half the pregnant women in these regions, whose inhabitants represent 75 percent of the world's population, have anaemia. Unlike reported figures for PEM and vitamin A deficiency, which are declining, estimates suggest that anaemia prevalence rates are increasing. In most of the developing regions, and particularly among persons with anaemia or at risk of iron deficiency, much of the iron consumed is non-haem iron from staple foods rice, wheat, maize, root crops or tubers.
In many countries the proportion of dietary iron coming from legumes and vegetables has declined, and rather small quantities of meat, fish and other good sources of haem iron are consumed. In some of the regions with the highest prevalence of anaemia the poor are not improving their dietary intake of iron, and in some areas the per caput supply of dietary iron may even be decreasing year by year.
In many parts of the world where iron deficiency anaemia is prevalent it is due as much to iron losses as to poor iron intakes. Whenever blood is lost from the body, iron is also lost. Thus iron is lost in menstruation and childbirth and also when pathological conditions are present such as bleeding peptic ulcers, wounds and a variety of abnormalities involving blood loss from the intestinal or urinary tract, the skin or various mucous membrane surfaces.
Undoubtedly one of the most prevalent and important causes of blood loss is hookworms, which can be present in very large numbers. The worms suck blood and also damage the intestinal wall, causing blood leakage. Some million people in the world are infested with hookworms. Other intestinal parasites such as Trichuris trichiura may also contribute to anaemia.
Schistosomes or bilharzias, which are of several kinds, also cause blood loss either into the genito-urinary tract in the case of Schistosoma haematobium or into the gut. Malaria, another very important parasitic infection, causes destruction of red blood cells that are parasitized, which can lead to what is termed haemolytic anaemia rather than to iron deficiency anaemia.
In programmes to reduce anaemia actions may be needed to control parasitic infections and to reduce blood loss resulting from disease as well as to improve dietary intakes of iron. Anaemia resulting from folate deficiency is less prevalent than that from iron deficiency or iron loss.
It occurs when folate intakes are low and when red cells are haemolysed or destroyed in conditions like malaria. The anaemia of both folate and vitamin B 12 is macrocytic, with larger than normal red blood cells. Folic acid or folates are present in many foods including foods of animal origin e.
Iiver and fish and of vegetable origin e. Vitamin B 12 is present only in foods of animal origin. In most countries vitamin B 12 deficiency is uncommon. Haemoglobin in the red blood cells is necessary to carry oxygen, and many of the symptoms and signs of anaemia result from the reduced capacity of the blood to transport oxygen. The symptoms and signs are: These symptoms and signs are not confined to iron deficiency anaemia but are similar in most forms of anaemia.
Most occur also in some other illnesses and thus are not specific to anaemia. Because none of the symptoms seem severe, dramatic or life threatening, at least in the early stages of anaemia, the disorder tends to be neglected. An experienced health worker can sometimes make a preliminary diagnosis by examining the tongue, the conjunctiva of the lower eyelid and the nailbed, which may all appear paler than normal in anaemia. The examiner can compare the redness or pinkness below the nail of the patient with the colour beneath his or her own nails.
Enlargement of the heart may result and can be detected in advanced severe anaemia. Oedema usually occurs first in the feet and at the ankles. There may also be an increased pulse rate or tachycardia.
Occasionally the nails become relatively concave rather than convex and become brittle. This condition is termed koilonychia.
Anaemia is also reported to lead both to abnormalities of the mouth such as glossitis and to pica abnormal consumption of earth, clay or other substances. What is surprising is that many persons with very low haemoglobin levels, especially women in developing countries, appear to function normally.
With chronic anaemia they have adapted to low haemoglobin levels. They may indeed do reduced work, have fatigue and walk more slowly, but they still give the appearance of performing their normal duties even though severely anaemic. Severe anaemia can progress to heart failure and death. Anaemia, as well as producing the symptoms and signs discussed above, also leads to a reduced ability to do heavy work for long periods; to slower learning and more difficulty in concentration by children in school or elsewhere; and to poorer psychological development.
A very important aspect of anaemia in women is that it markedly increases the risk of death of the mother during or after childbirth. The woman may bleed severely, and she has low haemoglobin reserves. There is also an increased risk for her infant. The diagnosis of anaemia requires a laboratory test. In this respect it differs from the serious manifestations of PEM, vitamin A deficiency and IDD; kwashiorkor, nutritional marasmus, advanced xerophthalmia, goitre and cretinism can all be diagnosed with some degree of certainty by skilled clinical observation.
Consequently, whereas few district hospitals and practically no health centres have laboratories set up to test, for example, levels of serum vitamin A or urinary iodine, most are able to do haemoglobin or haematocrit determinations. These tests require quite cheap apparatus and can be performed by a trained technician, nurse or other health worker. Determinations of haemoglobin or haematocrit levels are the most widely used in the diagnosis of anaemia.
It is now realized that although these tests provide information on the absence, presence or severity of anaemia, they do not provide information on the iron stores of the individual. In terms of nutritional assessment to guide nutrition planning and interventions, or for research, it may be important to know more about the iron status of an individual than can be gained from haemoglobin and haematocrit determinations.
Many methods are used to measure haemoglobin levels. These range from simple colorimetric tests to more advanced tests which require a proper laboratory. Some new portable colorimeters can be used in the field; they are simple to use and provide reasonably accurate measurements. In the laboratory of even a moderate-sized hospital the so-called cyanmethaemoglobin method is frequently used; it is accurate and can be used to test blood collected by finger prick in the field.
The different methods and their advantages are discussed in various books, of which some are included in the Bibliography. Haematocrit level or packed cell volume PCV , i. Blood also obtained from a finger prick is placed in a capillary tube and centrifuged, usually at 3 rpm. The centrifuge can be electric run if necessary from a vehicle battery or hand operated. A thin blood film examined under the microscope can be used to judge if the red blood cells are smaller microcytic or larger macrocytic than normal normo cytic.
In iron deficiency they are microcytic and in folate or vitamin B 12 deficiency they are macrocytic.
Pale cells are termed hypochromic. Cut-off points taken from the World Health Organization WHO suggestions for the diagnosis of anaemia based on haemoglobin and haematocrit determinations are given in Table Certain other laboratory tests are useful in judging iron nutritional status rather than for diagnosing anaemia or its severity.
In recent years it has been increasingly recognized that iron status is important because mild or moderate iron deficiency, prior to the development of anaemia, may adversely influence human behaviour, psychological development and temperature control. A person whose diet is low in iron or who is losing iron goes through a period when body iron stores which are mainly in the liver are gradually depleted before he or she develops anaemia as judged by low haemoglobin or haematocrit levels see Figure 7.
Anaemia is the end stage after iron stores have been depleted. To monitor iron stores it is useful to determine serum ferritin levels, because they are the first to decline. This is not a simple or cheap test to do, and few small or medium-sized hospitals in developing countries have the ability to do it, but teaching hospitals and nutrition research laboratories sometimes can.
Unfortunately serum ferritin levels are influenced by infections, which are common in developing countries. Other determinations that may be done to evaluate iron status and which are described in textbooks include free erythrocyte protoporphyrin FEP and transferrin saturation TS Figure 7. Suggested criteria for diagnosis of anaemia using haemoglobin Hb and haematocrit PCV determinations. Changes in body iron compartments and laboratory parameters of iron status during development of iron deficiency due to a continuous negative iron balance.
The treatment of anaemia depends on the cause. Iron deficiency anaemia is relatively easy and very cheap to treat. There are many different iron preparations on the market; ferrous sulphate is among the cheapest and most effective. The recommended dose of ferrous sulphate is usually mg providing 60 mg of elemental iron twice daily between meals for adults. Iron tends to make the stools black.
Because side-effects can occur, particularly involving the intestinal tract, sometimes people do not take their iron tablets regularly. Slow-release iron capsules have become available and seem to be associated with fewer side-effects. Most capsules contain ferrous sulphate in small pellets, so the iron is slowly released. Only one capsule or dose needs to be taken each day, but the capsules cost much more than ferrous sulphate tablets.
Therefore it is unlikely that slow-release preparations will replace standard ferrous sulphate tablets for use in clinics in developing countries. New research conducted in China suggests that ferrous sulphate is as effective when given once every week as when given once a day. If further trials confirm this observation, the finding will alter both the treatment of anaemia and the efforts to prevent it using medicinal iron supplements in prenatal clinics.
In Indonesia, where vitamin A deficiency is a problem, it has been shown recently that giving vitamin A as well as iron improves the haemoglobin levels of pregnant women more than iron tablets alone.
In all cases the underlying cause of the anaemia should be sought and treated if possible. Iron dextran is the injectable preparation most commonly used. Intravenous injection is preferable. The standing rule is to give a very small test dose initially and to wait for five minutes for any sign of an anaphylactic reaction.
If there is no reaction, then mg can be given from a syringe over a period of five to ten minutes. These injections may be given at intervals over a few days. Alternatively, a total dose infusion can be provided at one time. This procedure must be employed only by doctors experienced in the technique and in calculating dosage levels. It is common during pregnancy to provide folate as well as iron, or combined with iron, as part of the treatment of or prophylaxis against anaemia.
For prevention, where anaemia is prevalent, doses of mg of iron and 5 mg of folate daily are recommended. For treatment of established anaemia, doses of mg of iron and 10 mg of folate are suggested. Successful treatment usually leads to a response in haemoglobin levels within four weeks. Persons with iron deficiency anaemia on very poor diets should be advised to consume more fresh fruits and vegetables at mealtimes.
These foods contain vitamin C, which enhances the absorption of non-haem iron in cereals, root crops and legumes. They also contain folic acid and an array of other vitamins and minerals.
If it is feasible and in line with the anaemic patient's budget and culinary habits, he or she could also be advised to consume, even in small quantities, more foods rich in haem iron such as meat, especially liver or kidney.
Creating awareness of the nutritional needs of different family members and helping household decision-makers to understand how these needs can best be met from available resources are important steps in preventing iron deficiency. Iodine deficiency is responsible not only for very widespread endemic goitre and cretinism, but also for retarded physical growth and intellectual development and a variety of other conditions.
These conditions together are now termed iodine deficiency disorders IDD. They are particularly important because: In fact, as H. Labouisse wrote in when he was Executive Director of the United Nations Children's Fund UNICEF , "Iodine deficiency is so easy to prevent that it is a crime to let a single child be born mentally handicapped for this reason" quoted in Hetzel, Nonetheless this crime persists.
Endemic goitre and severe cretinism are the exposed part of the IDD iceberg. These are abnormalities that are visible to the populations where they are prevalent, and they can be diagnosed relatively easily by health professionals without the use of laboratory or other tests.
The submerged and larger part of the iceberg includes smaller, less visible enlargements of the thyroid gland and an array of other abnormalities. In many areas of Latin America, Asia and Africa iodine deficiency is a cause of mental retardation and of children's failure to develop psychologically to their full potential.
It is also associated with higher rates of foetus loss including spontaneous abortions and stillbirths , deaf-mutism, certain birth defects and neurological abnormalities. For several decades the main measure used to control IDD has been the iodization of salt, and when properly conducted and monitored it has proved extremely effective in many countries.
It is also relatively cheap. Several international meetings, including the International Conference on Nutrition held in Rome in , called for the virtual elimination of IDD by the year This goal is achievable, provided the effort receives international support and real national commitment in each of the many countries where the disorders remain prevalent.
The most important cause of endemic goitre and cretinism is dietary deficiency of iodine. The amount of iodine present in the soil varies from place to place and this influences the quantity of iodine present in the foods grown in different places and in the water. Iodine is leached out of the soil and flows into streams and rivers which often end in the ocean. Many areas where endemic goitre is or has been highly prevalent are plateau or mountain areas or inland plains far from the sea. A less important cause of IDD is the consumption of certain foods which are said to be goitrogenic or to contain goitrogens.
Goitrogens are "antinutrients" which adversely influence proper absorption and utilization of iodine or exhibit antithyroid activity. Foods from the genus Brassica such as cabbage, kale and rape and mustard seeds contain goitrogens, as do certain root crops such as cassava and turnips.
Unlike goitrogenic vegetables, cassava is a staple food in some areas, and in certain parts of Africa, for example Zaire, cassava consumption has been implicated as an important cause of goitre. Areas of the world where iodine deficiency is prevalent. Any enlargement of the thyroid gland is called a goitre. The thyroid is an endocrine gland centrally situated in the lower front part of the neck.
It consists of two lobes joined by an isthmus. In an adult each lobe of the normal thyroid gland is about the size of a large kidney bean. In areas of the world or communities where only sporadic goitre occurs or where health workers see only an occasional patient with an enlarged thyroid gland, the cause is not likely to be related to the individual's diet. Sporadic goitre may for example be due to a thyroid tumour or thyroid cancer.
However, if goitre is common or endemic in a community or district, then the cause is usually nutritional. Endemic goitre is almost certainly caused by iodine deficiency, and where goitre is endemic other iodine deficiency disorders can also be expected to be prevalent. Where goitre is endemic, often large numbers of people have an enlargement of the thyroid gland, and some have enormous unsightly swellings of the neck. The condition is usually somewhat more prevalent in females, especially at puberty and during pregnancy, than in males.
The enlarged gland may be smooth colloid goitre or lumpy adenomatous or nodular goitre. The iodine content of foods varies widely, but the amount of iodine present in common staple foods such as cereals or root crops depends more on the iodine content of the soil where the crop is grown than on the food itself.
Because the amount of iodine in foods such as rice, maize, wheat or legumes depends on where they are grown, food composition tables cannot provide good figures for their iodine content. Foods from the ocean, including shellfish, fish and plant products such as seaweed, are generally rich in iodine. In many populations, particularly in the industrialized countries of the North and among affluent groups almost everywhere, diets do not depend mainly on locally grown foods.
As a result many of the foods purchased and consumed may contribute substantially to iodine intakes. For example, persons living in the Rocky Mountains of North America, where goitre used to be endemic, now do not rely much on locally produced foods; they may consume bread made from wheat grown in the North American central plains, rice from Thailand, vegetables from Mexico or California, seafood from the Atlantic coast and so on.
Similarly, affluent segments of society in La Paz, Bolivia consume many foods not grown in the altiplano, and these imported foods will have adequate quantities of iodine. In contrast, the poor in the Bolivian highlands eat mainly locally grown foods and do develop goitre. Many countries of Asia, Africa and Latin America have major iodine deficiency problems, although some countries have made great progress in reducing the prevalence of IDD.
China and India, with their vast populations, still have a high prevalence of IDD. In the Americas, endemic goitre has been largely controlled in the United States and Canada, but many Andean countries including Bolivia, Colombia, Ecuador and Peru still have relatively high endemic goitre and cretinism rates.
During a survey conducted by the author in the s in the Ukinga Highlands of Tanzania, 75 percent of the people examined had goitre.
This was the highest prevalence yet reported in Africa. Prevalence rates of over 60 percent have been reported from communities in many African, Asian and Latin American countries. Generally goitre prevalence rates of 5 to But even with rates of 10 to 15 percent the need for action is important. Where prevalence rates are moderate, urgent action is needed.
Where rates are severe, early action is critical see Table Enlargement of the thyroid gland is the most frequently described and most obvious clinical manifestation of iodine deficiency. Where there is a chronic dietary deficiency of iodine the thyroid often begins to enlarge during childhood, and it becomes more markedly enlarged around the time of puberty, particularly in girls. In many areas where goitre is endemic the majority of people have some evidence of thyroid enlargement.
The thyroid gland secretes hormones vital to metabolism and growth. The gland is made mainly of follicles called acini, minute sacs filled with colloid. Each sac manufactures thyroid hormones, stores them and secretes them into the bloodstream as needed. The main thyroid hormone is thyroxine. The amount of thyroxine secreted is controlled by another endocrine gland, the anterior pituitary, and its hormone, called thyroid stimulating hormone TSH or thyrotrophic hormone.
The function of the thyroid gland is somewhat similar to that of the thermostat of the heating system in a house. It controls the rate of metabolism and influences the Basal metabolic rate BMR , to some extent the heart rate and also growth in children. The normal adult thyroid gland contains about 8 mg of iodine. In simple goitres the total iodine content might be only 1 or 2 mg even though the gland is larger than normal.
Thyroxine contains 64 percent iodine. A lack of dietary iodine makes it increasingly difficult for the thyroid to manufacture enough thyroxine. The gland enlarges to try to compensate and make more thyroxine. This enlargement is described by pathologists as a hyperplasia of the gland. It is triggered by increased production of TSH by the pituitary gland.
Microscopic examination of a gland undergoing hyperplasia shows ingrowths or invaginations of the lining epithelium into the normal architecture of the colloid-containing acini. There is an intense multiplication of cells, with an excess of colloid. This compensatory reaction is an attempt to trap more iodine, and it is partly successful.
Many people with colloid goitres show no evidence of poor thyroid function. Investigation of goitre prevalence is one of the most important means of assessing whether there is an IDD problem of public health importance. Examination of well-chosen samples of schoolchildren has often been recommended as the first step; this survey is relatively easy because schoolchildren are collected together in one place and are usually disciplined, so large numbers can be examined over a short time.
To get a full picture of the prevalence in the area, however, it is important at some stage to examine a representative sample of community members of all ages and both sexes. The thyroid gland of each person should be examined both visually and by palpation to judge its size. Visual examination informs the examiner whether a goitre is visible with the head in normal position or with the head tilted back.
Palpation is usually done with the examiner sitting or standing facing the person being examined; the examiner's eyes should be level with the person's neck.
By placing and rolling the thumbs on either side of the trachea below the Adam's apple or voice box, the examiner can feel the gland and judge its size. A normal thyroid gland is considerably smaller than the last joint terminal phalanx of the thumb. In fact a normal thyroid lobe is perhaps one-fifth that size. If each lobe is larger than this joint, then there is a goitre. Palpation from behind is recommended by some because the fingertips are then used to determine gland size, and they are more sensitive than the tips of the thumbs.
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