What Is Nutritional Disease?/ Nutrient deficiencies And Their List And Explanation
Nutritional disease, any of the nutrient-related diseases and conditions that cause illness in humans. They may include deficiencies or excesses in the diet, obesity and eating disorders. And chronic diseases such as cardiovascular disease, hypertension, cancer, and diabetes mellitus.
Nutrition disorders are diseases that occur when a person’s dietary intake does not contain the right amount of nutrients for healthy functioning. Or when a person cannot correctly absorb nutrients from food. Nutrition disorders can be caused by undernutrition, overnutrition, or an incorrect balance of nutrients.
Nutritional diseases include obesity and eating disorders. And chronic diseases such as protein-energy malnutrition (Kwashiorkor and marasmus). Cardiovascular disease, atherosclerosis, hypertension, cancer (colorectal cancer. Prostate cancer, breast cancer), diabetes mellitus, dental caries.
Nutritional deficiency occurs when the body is not getting enough nutrients such as vitamins and minerals. There are a number of conditions that are caused by nutritional deficiency such as anemia. The body requires vitamins to stay healthy and function properly.
What is Nutrition?
Nutrition is the biochemical and physiological process by which an organism uses food to support its life. It includes ingestion, absorption, assimilation, biosynthesis, catabolism, and excretion. The science that studies the physiological process of nutrition is called nutritional science. Nutrition is nourishment or energy that is obtained from food consumed or the process of consuming the proper amount of nourishment and energy. An example of nutrition is the nutrients found in fruits and vegetables. An example of nutrition is eating a healthy diet.
Nutrition is a critical part of health and development. Better nutrition is related to improved infant, child, and maternal health, stronger immune systems, safer pregnancy and childbirth, lower risk of non-communicable diseases (such as diabetes and cardiovascular disease), and longevity. Healthy children learn better. People with adequate nutrition are more productive and can create opportunities to gradually break the cycles of poverty and hunger.
Malnutrition, in every form, presents significant threats to human health. Today the world faces a double burden of malnutrition that includes both undernutrition and overweight. Especially in low- and middle-income countries. WHO is providing scientific advice and decision-making tools. That can help countries take action to address all forms of malnutrition to support health and wellbeing for all, at all ages. This fact file explores the risks posed by all forms of malnutrition, starting from the earliest stages of development. And the responses that the health system can give directly and through its influence on other sectors, particularly the food system.
What is Disease?
A disease is an abnormal condition that negatively affects the structure. Or function of all or part of an organism, and that is not due to any immediate external injury. Diseases are often known to be medical conditions that are associated with specific signs and symptoms. A disease may be caused by external factors such as pathogens or by internal dysfunctions. For example, internal dysfunctions of the immune system can produce a variety of different diseases, including various forms of immunodeficiency, hypersensitivity, allergies, and autoimmune disorders.
In humans, the disease is often used more broadly to refer to any condition that causes pain. Dysfunction, distress, social problems, or death to the person afflicted. Or similar problems for those in contact with the person. In this broader sense. It sometimes includes injuries, disabilities, disorders, syndromes, infections. Isolated symptoms, deviant behaviors, and atypical variations of structure and function. While in other contexts and for other purposes these may be considered distinguishable categories. Diseases can affect people not only physically, but also mentally. As contracting and living with a disease can alter the affected person’s perspective on life.
Death due to disease is called death by natural causes. There are four main types of disease: infectious diseases, deficiency diseases, hereditary diseases, and physiological diseases. Diseases can also be classified in other ways, such as communicable versus non-communicable diseases. The deadliest diseases in humans are coronary artery disease, followed by cerebrovascular disease and lower respiratory infections. In developed countries, the diseases that cause the most sickness overall are neuropsychiatric conditions, such as depression and anxiety.
What Is Nutritional Disease?
nutritional disease, any of the nutrient-related diseases and conditions that cause illness in humans. They may include deficiencies or excesses in the diet, obesity and eating disorders, and chronic diseases such as cardiovascular disease, hypertension, cancer, and diabetes mellitus.
Nutritional diseases also include developmental abnormalities that can be prevented by diet, hereditary metabolic disorders that respond to dietary treatment, the interaction of foods and nutrients with drugs, food allergies and intolerances, and potential hazards in the food supply.
All of these categories are described in this article. For a discussion of essential nutrients, dietary recommendations, and human nutritional needs and concerns throughout the life cycle, see nutrition, human.
Although the so-called diseases of civilization—for example, heart disease, stroke, cancer, and diabetes—will be the focus of this article, the most significant nutrition-related disease is chronic undernutrition, which plagues more than 925 million people worldwide.
Undernutrition is a condition in which there is insufficient food to meet energy needs; its main characteristics include weight loss, failure to thrive, and wasting of body fat and muscle. Low birth weight in infants, inadequate growth and development in children, diminished mental function, and increased susceptibility to disease are among the many consequences of chronic persistent hunger, which affects those living in poverty in both industrialized and developing countries.
The largest number of chronically hungry people live in Asia, but the severity of hunger is greatest in sub-Saharan Africa. At the start of the 21st century, approximately 20,000 people, the majority of them children, died each day from undernutrition and related diseases that could have been prevented. The deaths of many of these children stem from the poor nutritional status of their mothers as well as the lack of opportunity imposed by poverty.
Only a small percentage of hunger deaths
Only a small percentage of hunger deaths are caused by starvation due to catastrophic food shortages. During the 1990s, for example, worldwide famine (epidemic failure of the food supply) more often resulted from complex social and political issues and the ravages of war than from natural disasters such as droughts and floods.
Malnutrition is the impaired function that results from a prolonged deficiency—or excess—of total energy or specific nutrients such as protein, essential fatty acids, vitamins, or minerals. This condition can result from fasting and anorexia nervosa; persistent vomiting (as in bulimia nervosa) or inability to swallow; impaired digestion and intestinal malabsorption; or chronic illnesses that result in loss of appetite (e.g., cancer, AIDS). Malnutrition can also result from limited food availability, unwise food choices, or overzealous use of dietary supplements.
Chronic undernutrition manifests primarily as protein-energy malnutrition (PEM), which is the most common form of malnutrition worldwide. Also known as protein-calorie malnutrition, PEM is a continuum in which people—all too often children—consume too little protein, energy, or both. At one end of the continuum is kwashiorkor, characterized by a severe protein deficiency, and at the other is marasmus, an absolute food deprivation with grossly inadequate amounts of both energy and protein.
An infant with marasmus is extremely underweight and has lost most or all subcutaneous fat. The body has a “skin and bones” appearance, and the child is profoundly weak and highly susceptible to infections. The cause is a diet very low in calories from all sources (including protein). Often from early weaning to a bottled formula prepared with unsafe water and diluted because of poverty.
Poor hygiene and continued depletion lead to a vicious cycle of gastroenteritis. And the deterioration of the lining of the gastrointestinal tract. Which interferes with the absorption of nutrients from the little food available. And further reduces resistance to infection. If untreated, marasmus may result in death due to starvation or heart failure.
Kwashiorkor, a Ghanaian word meaning the disease that the first child gets when the new child comes, is typically seen when a child is weaned from high-protein breast milk onto a carbohydrate food source with insufficient protein. Children with this disease, which is characterized by a swollen belly due to edema (fluid retention), are weak, grow poorly, and are more susceptible to infectious diseases, which may result in fatal diarrhea.
Other symptoms of kwashiorkor include apathy, hair discoloration, and dry, peeling skin with sores that fail to heal. Weight loss may be disguised because of the presence of edema, enlarged fatty liver, and intestinal parasites; moreover, there may be little wasting of muscle and body fat.
Kwashiorkor and marasmus can also occur in hospitalized patients receiving intravenous glucose for an extended time, as when recovering from surgery, or in those with illnesses causing loss of appetite or malabsorption of nutrients. Persons with eating disorders, cancer, AIDS, and other illnesses where appetite fails or absorption of nutrients is hampered may lose muscle and organ tissue as well as fat stores.
Treatment of PEM has three components
Treatment of PEM has three components. (1) Life-threatening conditions—such as fluid and electrolyte imbalances and infections—must be resolved. (2) Nutritional status should be restored as quickly and safely as possible; rapid weight gain can occur in a starving child within one or two weeks. (3) The focus of treatment then shifts to ensuring nutritional rehabilitation for the long term.
The speed and ultimate success of recovery depend upon the severity of malnutrition, the timeliness of treatment, and the adequacy of ongoing support. Particularly during the first year of life, starvation may result in reduced brain growth and intellectual functioning that cannot be fully restored.
Beneath maximum situations, there may be no absolute dietary requirement for carbohydrates—easy sugars, complicated carbohydrates inclusive of starches, and the indigestible plant carbohydrates called dietary fiber. Positive cells, which includes brain cells, require the simple carbohydrate glucose as gas. If dietary carbohydrate is insufficient.
Glucose synthesis relies upon on the breakdown of amino acids derived from frame protein and nutritional protein and the compound glycerol, which is derived from fats. long-term carbohydrate inadequacy results in expanded production of natural compounds known as ketones (a situation known as ketosis), which imparts a specific sweet odour to the breath.
Ketosis and different untoward consequences of a totally-low-carbohydrate food regimen may be prevented by way of the every day consumption of 50 to one hundred grams of carbohydrate; however, obtaining as a minimum half of the daily electricity consumption from carbohydrates is suggested and is regular of human diets, similar to at the least 250 grams of carbohydrate (1,000 energy in a 2,000-calorie diet).
A various eating regimen containing end result, vegetables, legumes, and entire-grain cereals, which might be all plentiful in carbohydrates, also affords an applicable consumption of dietary fiber.
Essential fatty acids
There is also a minimum requirement for fat—not for total fat, but only for the fatty acids linoleic acid (a so-called omega-6 fatty acid) and alpha-linolenic acid (an omega-3 fatty acid). Deficiencies of these two fatty acids have been seen in hospitalized patients fed exclusively with intravenous fluids containing no fat for weeks, patients with medical conditions affecting fat absorption, infants given formulas low in fat, and young children fed nonfat milk or low-fat diets.
Symptoms of deficiency include dry skin, hair loss, and impaired wound healing. Essential fatty acid requirements—a few grams a day—can be met by consuming approximately a tablespoon of polyunsaturated plant oils daily. Fatty fish also provides a rich source of omega-3 fatty acids. Even individuals following a low-fat diet generally consume sufficient fat to meet requirements.
Although deficiency diseases have been described in laboratory animals and humans deprived of single vitamins, in human experience multiple deficiencies are usually present simultaneously.
The eight B-complex vitamins function in coordination in numerous enzyme systems and metabolic pathways; thus, a deficiency of one may affect the functioning of others.
A vitamin is an organic molecule that is an essential micronutrient that an organism needs in small quantities for the proper functioning of its metabolism. Essential nutrients cannot be synthesized in the organism, either at all or not in sufficient quantities, and therefore must be obtained through the diet.
Vitamin can be synthesized by some species but not by others; it is not a vitamin in the first instance but is in the second. The term vitamin does not include the three other groups of essential nutrients: minerals, essential fatty acids, and essential amino acids.
Vitamin A deficiency is the leading cause of preventable blindness in children and is a major problem in the developing world, especially in Africa and Southeast Asia; in the poorest countries, hundreds of thousands of children become blind each year due to a deficiency of the vitamin.
Even a moderate deficiency can impair immune characteristics, thereby decreasing resistance to ailment. night time blindness is an early sign of vitamin A deficiency, followed via odd dryness of the eye and in the end scarring of the cornea, a circumstance referred to as xerophthalmia. different signs and symptoms include dry skin, hardening of epithelial cells some place else within the frame (along with mucous membranes), and impaired increase and development.
In many areas in which nutrition A deficiency is endemic, the incidence is being decreased by using giving children an unmarried huge dose of nutrition A every six months. A genetically modified form of rice containing beta-carotene, a precursor of vitamin A, has the ability to lessen significantly the prevalence of nutrition A deficiency, but the use of this so-known as golden rice is debatable.
Vitamin D (also known as vitamin D hormone) is synthesized in the body in a series of steps, starting in the skin by the action of sunlight’s ultraviolet rays on a precursor compound; thus, without adequate food sources of vitamin D, a deficiency of the vitamin can occur when exposure to sunlight is limited.
Lack of vitamin D in children causes rickets, a disease characterized by inadequate mineralization of bone, growth retardation, and skeletal deformities such as bowed legs. The adult form of rickets, known as osteomalacia, results in weak muscles as well as weak bones. Inadequate vitamin D may also contribute to the thinning of bones seen in osteoporosis.
Individuals with limited sun exposure (including women who completely cover their bodies for religious reasons), elderly or homebound persons, and those with dark skin, particularly those who live in northern latitudes, are at risk of vitamin D deficiency. Vitamin D is found in very few foods naturally; thus fortification of milk and other foods (e.g., margarine, cereals, and bread) with the vitamin has helped protect those populations in which sun exposure is inadequate. Supplemental vitamin D also may help protect against bone fractures in the elderly, who make and activate vitamin D less efficiently even if exposed to sunlight.
Vitamin E deficiency is rare in humans, although it may develop in premature infants and in people with impaired fat absorption or metabolism. In the former, the fragility of red blood cells (hemolysis) is seen; in the latter, where deficiency is more prolonged, neuromuscular dysfunction involving the spinal cord and retina may result in loss of reflexes, impaired balance and coordination, muscle weakness, and visual disturbances.
No specific metabolic function has been established for vitamin E; however, it is an important part of the antioxidant system that inhibits lipid peroxidation—i.e., it protects cells and their membranes against the damaging effects of free radicals (reactive oxygen and nitrogen species) that are produced metabolically or enter the body from the environment.
The requirement for vitamin E is increased with the increasing consumption of polyunsaturated fatty acids. People who smoke or are subjected to air pollution may also need more of the vitamin to protect against oxidative damage to the lungs.
Vitamin K is necessary for the formation of prothrombin and other blood-clotting factors in the liver, and it also plays a role in bone metabolism. A form of the vitamin is produced by bacteria in the colon and can be utilized to some degree.
Vitamin K deficiency causes impaired clotting of the blood and internal bleeding, even without injury. Due to poor transport of vitamin K across the placenta, newborn infants in developed countries are routinely given the vitamin intramuscularly or orally within six hours of birth to protect against a condition known as hemorrhagic disease of the newborn.
Vitamin K deficiency is rare in adults, except in syndromes with poor fat absorption, in liver disease, or during treatment with certain anticoagulant drugs, which interfere with vitamin K metabolism. Bleeding due to vitamin K deficiency may be seen in patients whose gut bacteria have been killed by antibiotics.
Prolonged deficiency of thiamin (vitamin B1) results in beriberi, a disease that has been endemic in populations where white rice has been the staple. Thiamin deficiency is still seen in areas where white rice or flour constitutes the bulk of the diet and thiamin lost in milling is not replaced through enrichment.
Symptoms of the form known as dry beriberi include loss of appetite, confusion and other mental symptoms, muscle weakness, painful calf muscles, poor coordination, tingling, and paralysis. In wet beriberi, there is edema and the possibility of an enlarged heart and heart failure.
Thiamin deficiency can also occur in populations eating large quantities of raw fish harboring intestinal microbes that contain the enzyme thiaminase. In the developed world, thiamin deficiency is linked primarily to chronic alcoholism with poor diet, manifesting as Wernicke-Korsakoff syndrome, a condition with rapid eye movements, loss of muscle coordination, mental confusion, and memory loss.
Riboflavin (vitamin B2) deficiency, known as ariboflavinosis, is unlikely without the simultaneous deficiency of other nutrients. After several months of riboflavin deprivation, symptoms include cracks in the skin at the corners of the mouth, fissures of the lips, and an inflamed, magenta-colored tongue.
Because riboflavin is readily destroyed by ultraviolet light, jaundiced infants who are treated with light therapy are administered the vitamin. Milk, milk products, and cereals, major sources of riboflavin in the diet, are packaged to prevent exposure to light.
Symptoms of pellagra develop about two months after niacin is withdrawn from the diet. Pellagra is characterized by the so-called three Ds—diarrhea, dermatitis, and dementia—and, if it is allowed to progress untreated, death ensues. Pellagra was common in areas of the southern United States in the early 1900s and still occurs in parts of India, China, and Africa, affecting people who subsist primarily on corn.
The niacin in corn and other cereal grains is largely in bound form, unable to be absorbed well. Soaking corn in lime water, as practiced by Native American populations for centuries, frees bound niacin and thus protects against pellagra. In addition, unlike other cereals, corn is low in the amino acid tryptophan, which can be converted in part to niacin. Sufficient high-quality protein (containing tryptophan) in the diet can protect against niacin deficiency even if intake of niacin itself is inadequate.
Vitamin B6 (pyridoxine and related compounds) is essential in protein metabolism, the synthesis of neurotransmitters, and other critical functions in the body. Deficiency symptoms include dermatitis, microcytic hypochromic anemia (small, pale red blood cells), impaired immune function, depression, confusion, and convulsions.
Although full-blown vitamin B6 deficiency is rare, marginal inadequacy is more widespread, especially among the elderly, who may have a reduced ability to absorb the vitamin. People with alcoholism, especially those with liver diseases cirrhosis and hepatitis, are at risk of deficiency. A number of drugs, including the tuberculosis drug isoniazid, interfere with vitamin B6 metabolism.
Vitamin B12 and folic acid (folate) are two B vitamins with many closely related functions, notable participation in DNA synthesis. As a result, people with deficiencies of either vitamin show many of the same symptoms, such as weakness and fatigue due to megaloblastic anemia, a condition in which red blood cells, lacking sufficient DNA for cell division, are large and immature.
Deficiency of folic acid also causes disruption of cell division along the gastrointestinal tract, which results in persistent diarrhea, and impaired synthesis of white blood cells and platelets. Inadequate intake of the vitamin in early pregnancy may cause neural tube defects in the fetus. Thus, women capable of becoming pregnant are advised to take 400 micrograms (μg) of folic acid daily from supplements, fortified foods (such as fortified cereals).
Or both—in addition to consuming foods rich in folic acids such as fresh fruits and vegetables (especially leafy greens) and legumes. The cancer drug methotrexate interferes with folic acid metabolism, causing side effects such as hair loss and diarrhea. Folic acid deficiency may also result from heavy use of alcohol, which interferes with the absorption of the vitamin.
The deficiency of vitamin B12 (cobalamin), like folic acid, results in megaloblastic anemia. Due to interference with normal DNA synthesis. Additionally, vitamin B12 maintains the myelin sheath that protects nerve fibers. Therefore, an untreated deficiency of the vitamin. This can result in nerve degeneration and eventually paralysis. Large amounts of folic acid (over 1,000 μg per day) may conceal. And possibly even exacerbate, an underlying vitamin B12 deficiency.
Symptoms of vitamin B12 deficiency can include weakness, fatigue, pain, shortness of breath. Numbness or tingling sensations, mental changes, and vision problems. Only animal foods are reliable sources of vitamin B12. Vegans, who eat no foods of animal origin. Are at risk of vitamin B12 deficiency and must obtain the vitamin through fortified food or a supplement. For people who regularly eat animal products, deficiency of the vitamin is unlikely, unless there is a defect in absorption.
In order to be absorbed, vitamin B12 must be bound to an intrinsic factor, a substance secreted by the stomach. If an intrinsic factor is absent (due to an autoimmune disorder known as pernicious anemia) or if there is insufficient production of hydrochloric acid by the stomach, absorption of the vitamin will be limited. Pernicious anemia, which occurs most often in the elderly, can be treated by injections of massive oral doses (1,000 μg) of vitamin B12.
Pantothenic acid is so widespread in foods that deficiency is unlikely under normal circumstances. Deficiency has been seen only in individuals fed semisynthetic diets deficient in the vitamin or in subjects given a pantothenic acid antagonist. Symptoms of deficiency include fatigue, irritability, sleep disturbances, abdominal distress, and neurological symptoms such as tingling in the hands.
Deficiency of the vitamin was suspected during World War II when prisoners of war in Asia who exhibited “burning feet” syndrome, characterized by numbness and tingling in the toes and other neurological symptoms, responded only to the administration of pantothenic acid.
Deficiency of biotin is rare, and this may be due in part to the synthesis of the vitamin by bacteria in the colon, although the importance of this source is unclear. Biotin deficiency has been observed in people who regularly eat large quantities of raw egg white, which contains a glycoprotein (avidin) that binds biotin and prevents its absorption.
A rare genetic defect that renders some infants unable to absorb a form of biotin in food can be treated with a supplement of the vitamin. Long-term use of certain anticonvulsant drugs may also impair biotin absorption. Symptoms of deficiency include skin rash, hair loss, and eventually neurological abnormalities.
Vitamin C, also known as ascorbic acid, functions as a water-soluble antioxidant and as a cofactor in various enzyme systems, such as those involved in the synthesis of connective tissue components and neurotransmitters. Symptoms of scurvy, a disease caused by vitamin C deficiency, include pinpointing hemorrhages (petechiae) under the skin, bleeding gums, joint pain, and impaired wound healing.
Although rare in developed countries, scurvy is seen occasionally in people consuming restricted diets, particularly those containing few fruits and vegetables, or in infants fed boiled cow’s milk and no source of vitamin C. Scurvy can be prevented with relatively small quantities of vitamin C (10 milligrams [mg] per day), although recommended intakes, which aim to provide sufficient antioxidant protection, are closer to 100 mg per day.
Disease states, environmental toxins, drugs, and other stresses can increase an individual’s vitamin C needs. Smokers, for example, may require an additional 35 mg of the vitamin daily to maintain vitamin C levels comparable to nonsmokers.
They include calcium, phosphorus, magnesium, sodium, potassium, chloride, and sulfur. You only need small amounts of trace minerals. They include iron, manganese, copper, iodine, zinc, cobalt, fluoride, and selenium. Most people get the number of minerals they need by eating a wide variety of foods.
Iron deficiency is the most common of all nutritional deficiencies, with much of the world’s population being deficient in the mineral to some degree. Young children and premenopausal women are the most vulnerable. The main function of iron is in the formation of hemoglobin, the red pigment of the blood that carries oxygen from the lungs to other tissues.
Since each milliliter of blood contains 0.5 mg of iron (as a component of hemoglobin), bleeding can drain the body’s iron reserves. When iron stores have depleted a condition arises known as microcytic hypochromic anemia, characterized by small red blood cells that contain less hemoglobin than normal. Symptoms of severe iron deficiency anemia include fatigue, weakness, apathy, pale skin, difficulty breathing on exertion, and low resistance to cold temperatures.
During childhood, iron deficiency can affect behavior and learning ability as well as growth and development. Severe anemia increases the risk of pregnancy complications and maternal death. Iron deficiency anemia is most common during late infancy and early childhood when iron stores present from birth are exhausted and milk, which is poor in iron, is a primary food; during the adolescent growth spurt; and in women during the childbearing years, because of blood loss during menstruation and the additional iron needs of pregnancy.
Intestinal blood loss and subsequent iron deficiency anemia in adults may also stem from ulcers, hemorrhoids, tumors, or chronic use of certain drugs such as aspirin. In developing countries, blood loss due to hookworm and other infections, coupled with inadequate dietary iron intake, exacerbate iron deficiency in both children and adults.
Iodine deficiency disorders are the most common cause of preventable brain damage, which affects an estimated 50 million people worldwide. During pregnancy, severe iodine deficiency may impair fetal development, resulting in cretinism (irreversible mental retardation with short stature and developmental abnormalities) as well as in miscarriage and stillbirth.
Other more pervasive consequences of chronic iodine deficiency include lesser cognitive and neuromuscular deficits. The ocean is a dependable source of iodine, but away from coastal areas iodine in food is variable and largely reflects the amount in the soil. In chronic iodine deficiency, the thyroid gland enlarges as it attempts to trap more iodide (the form in which iodine functions in the body) from the blood for the synthesis of thyroid hormones, and it eventually becomes a visible lump at the front of the neck known as a goiter.
Some foods, such as cassava, millet, sweet potato, certain beans, and members of the cabbage family, contain substances known as goitrogens that interfere with thyroid hormone synthesis; these substances, which are destroyed by cooking, can be a significant factor in persons with coexisting iodine deficiency who rely on goitrogenic foods as staples.
Since a strategy of universal iodization of salt was adopted in 1993, there has been remarkable progress in improving iodine status worldwide. Nonetheless, millions of people living in iodine-deficient areas, primarily in Central Africa, Southeast, and Central Asia, and even in central and eastern Europe, remain at risk.
A constituent of numerous enzymes, zinc plays a structural role in proteins and regulates gene expression. Zinc deficiency in humans was first reported in the 1960s in Egypt and Iran, where children and adolescent boys with stunted growth and undeveloped genitalia responded to treatment with zinc. Deficiency of the mineral was attributed to the regional diet, which was low in meat and high in legumes, unleavened bread, and whole-grain foods that contain fiber, phytic acid, and other factors that inhibit zinc absorption.
Also contributing to zinc deficiency was the practice of clay eating. Which interferes with the absorption of zinc, iron, and other minerals. Severe zinc deficiency has also been described in patients fed intravenously. Solutions inadequate in zinc and in the inherited zinc-responsive syndrome known as acrodermatitis enteropathica. Symptoms of zinc deficiency may include skin lesions. Diarrhea, increased susceptibility to infections, night blindness. Reduced taste and smell acuity, poor appetite. Hair loss, slow wound healing, low sperm count, and impotence.
Zinc is highest in protein-rich foods, especially red meat and shellfish, and zinc status may be low in protein-energy malnutrition. Even in developed countries, young children, pregnant women, the elderly, strict vegetarians, people with alcoholism, and those with malabsorption syndromes are vulnerable to zinc deficiency.
Almost all the calcium in the body is in the bones and teeth, the skeleton serving as a reservoir for calcium needed in the blood and elsewhere. During childhood and adolescence, adequate calcium intake is critical for bone growth and calcification.
A low calcium intake during childhood, and especially during the adolescent growth spurt, may predispose one to osteoporosis, a disease characterized by reduced bone mass, later in life. As bones lose density, they become fragile and unable to withstand ordinary strains; the resulting fractures, particularly of the hip, may cause incapacitation and even death. Osteoporosis is particularly common in postmenopausal women in industrial societies.
Not a calcium-deficiency disease per se, osteoporosis is strongly influenced by heredity; the risk of the disease can be lessened by ensuring adequate calcium intake throughout life and engaging in regular weight-bearing exercise. Sufficient calcium intake in the immediate postmenopausal years does appear to slow bone loss, although not to the same extent as do bone-conserving drugs.
Fluoride also contributes to the mineralization of bones and teeth and protects against tooth decay. Epidemiological studies in the United States in the 1930s and 1940s revealed an inverse relationship between the natural fluoride content of waters and the rate of dental caries.
In areas where fluoride levels in the drinking water are low, prescription fluoride supplements are recommended for children older than six months of age; dentists also may apply fluoride rinses or gels periodically to their patients’ teeth. Fluoridated toothpaste is an important source of fluoride for children and also for adults, who continue to benefit from fluoride intake.
Sodium is usually provided in ample amounts by food, even without added table salt (sodium chloride). Furthermore, the body’s sodium-conservation mechanisms are highly developed, and thus sodium deficiency is rare, even for those on low-sodium diets. Sodium depletion may occur during prolonged heavy sweating, vomiting, or diarrhea or in the case of kidney disease.
Symptoms of hyponatremia, or low blood sodium, include muscle cramps, nausea, dizziness, weakness, and eventually shock and coma. After prolonged high-intensity exertion in the heat, sodium balance can be restored by drinking beverages containing sodium and glucose (so-called sports drinks) and by eating salted food. Drinking a liter of water containing two milliliters (one-third teaspoon) of table salt also should suffice.
Chloride is lost from the body under conditions that parallel those of sodium loss. Severe chloride depletion results in a condition known as metabolic alkalosis (excess alkalinity in body fluids).
Potassium is widely distributed in foods and is rarely deficient in the diet. However, some diuretics used in the treatment of hypertension deplete potassium. The mineral is also lost during sustained vomiting or diarrhea or with chronic use of laxatives.
Symptoms of potassium deficiency include weakness, loss of appetite, muscle cramps, and confusion. Severe hypokalemia (low blood potassium) may result in cardiac arrhythmias. Potassium-rich foods, such as bananas or oranges, can help replace losses of the mineral, as can potassium chloride supplements, which should be taken only under medical supervision.
Water deficiency (dehydration)
Water is the largest component of the body, accounting for more than half of body weight. To replace fluid losses, adults generally need to consume 2 to 4 liters of fluid daily in cool climates, depending on the degree of activity, and from 8 to 16 liters a day in very hot climates.
Dehydration may develop if water consumption fails to satisfy thirst; if the thirst mechanism is not functioning properly, as during intense physical exercise; or if there is excessive fluid loss, as with diarrhea or vomiting. By the time thirst is apparent, there is already some degree of dehydration, which is defined as loss of fluid amounting to at least 1 to 2 percent of body weight.
Symptoms can progress quickly if not corrected: dry mouth, sunken eyes, poor skin turgor, cold hands and feet, weak and rapid pulse, rapid and shallow breathing, confusion, exhaustion, and coma. Loss of fluid constituting more than 10 percent of body weight may be fatal.
The elderly (whose thirst sensation may be dulled), people who are ill, and those flying in airplanes are especially vulnerable to dehydration. Infants and children with chronic undernutrition who develop gastroenteritis may become severely dehydrated from diarrhea or vomiting. Treatment is with an intravenous or oral solution of glucose and salts.
The need for each nutrient falls within a safe or desirable range, above which there is a risk of adverse effects. Any nutrient, even water, can be toxic if taken in very large quantities. Overdoses of certain nutrients, such as iron, can cause poisoning (acute toxicity) and even death. For most nutrients, habitual excess intake poses a risk of adverse health effects (chronic toxicity).
Sustained overconsumption of the calorie-yielding nutrients (carbohydrate, fat, and protein) and alcohol increases the risk of obesity and specific chronic diseases (see below), and the use of isolated amino acids can lead to imbalances and toxicities. However, for most individuals, the risk of harm due to excess intake of vitamins or minerals in food is low.
In 1997 the U.S. Institute of Medicine established a reference value called the Tolerable Upper Intake Level (UL) for selected nutrients, which is also being used as a model for other countries. The UL is the highest level of daily nutrient intake likely to pose no risk of adverse health effects for almost all individuals in the general population and is not meant to apply to people under medical supervision. Discussed below as “safe intakes” for adults, most ULs for infants, children, and adolescents are considerably lower.
Because they can be stored in the liver and fatty tissue, fat-soluble vitamins, particularly vitamins A and D, have more potential for toxicity than do water-soluble vitamins, which, with the exception of vitamin B12, are readily excreted in the urine if taken in excess. Nonetheless, water-soluble vitamins can be toxic if taken as supplements or in fortified food.
Symptoms of acute vitamin A poisoning, which usually require a dose of at least 15,000 μg (50,000 IU) in adults, include abdominal pain, nausea, vomiting, headache, dizziness, blurred vision, and lack of muscular coordination. Chronic hypervitaminosis A, usually resulting from a sustained daily intake of 30,000 μg (100,000 IU) for months or years, may result in wide-ranging effects, including loss of bone density and liver damage.
Vitamin A toxicity
Vitamin A toxicity in young infants may be seen in a swelling of the fontanelles (soft spots) due to increased intracranial pressure. Large doses of vitamin A taken by a pregnant woman also can cause developmental abnormalities in a fetus, especially if taken during the first trimester; the precise threshold for causing birth defects is unknown, but less than 3,000 μg (10,000 IU) daily appears to be a safe intake.
Although most vitamins occurring naturally in food do not cause adverse effects, toxic levels of vitamin A may be found in the liver of certain animals. For example, early Arctic explorers are reported to have been poisoned by eating polar bear liver. The beta-carotene intake, from supplements or from carrots or other foods that are high in beta-carotene, may after several weeks impart a yellowish cast to the skin but does not cause the same toxic effects as preformed vitamin A.
High intake of vitamin D
High intake of vitamin D can lead to a variety of debilitating effects, notable calcification of soft tissues, and cardiovascular and renal damage. Although not a concern for most people, young children are especially vulnerable to vitamin D toxicity. Individuals with high intakes of fortified milk or fish or those who take many supplements may exceed the safe intake of 50 μg (2,000 IU) per day.
Because of its function as an antioxidant, supplementation with large doses (several hundred milligrams per day) of vitamin E in hopes of protecting against heart disease and other chronic diseases has become widespread. Such doses—many times the amount normally found in food—appear safe for most people, but their effectiveness in preventing disease or slowing the aging process has not been demonstrated. Daily intakes greater than 1,000 mg are not advised because they may interfere with blood clotting, causing hemorrhagic effects.
Large doses of niacin
Large doses of niacin (nicotinic acid), given for its cholesterol-lowering effect, may produce a reddening of the skin, along with burning, tingling, and itching. Known as a “niacin flush,” this is the first indicator of niacin excess, and this symptom is the basis for the safe daily intake of 35 mg. Liver toxicity and other adverse effects have also been reported with several grams of niacin a day.
Large doses of vitamin B6 have been taken in hopes of treating conditions such as carpal tunnel syndrome and premenstrual syndrome. The most critical adverse effect seen from such supplementation has been a severe sensory neuropathy of the extremities, including the inability to walk. A daily intake of up to 100 mg is considered safe, although only 1 to 2 mg is required for good health.
Use of vitamin C supplements
The use of vitamin C supplements has been widespread since 1970 when chemists. And Nobel laureate Linus Pauling suggested that the vitamin was protective against the common cold. Some studies have found a moderate benefit of vitamin C in reducing the duration. And severity of common-cold episodes, but numerous studies have failed to find a significant effect on incidence.
The most common side effect of high vitamin C intake is diarrhea and other gastrointestinal symptoms, likely due to the unabsorbed vitamin traversing the intestine. The safe intake of 2,000 mg a day is based on the avoidance of these gastrointestinal symptoms. Although other possible adverse effects of high vitamin C intake have been investigated, none has been demonstrated in healthy people.
A desirable dietary intake of minerals generally falls in a fairly narrow range. Because of interactions, a high intake of one mineral may adversely affect the absorption or utilization of another. Excessive intake from food alone is unlikely, but consumption of fortified foods or supplements increases the chance of toxicity. Furthermore, environmental or occupational exposure to potentially toxic levels of minerals presents additional risks for certain populations.
Widespread calcium supplementation, primarily by children who do not drink milk and by women hoping to prevent osteoporosis, has raised concerns about possible adverse consequences of high calcium intake. A major concern has been kidney stones (nephrolithiasis), the majority of which is composed of a calcium oxalate compound.
For years, a low-calcium diet was recommended for people at risk of developing kidney stones, despite disappointing effectiveness and a fair amount of research challenging the approach.
However, a recent study has provided strong evidence that a diet relatively low in sodium and animal protein with normal amounts of calcium (1,200 mg per day) is much more effective in preventing recurrent stone formation than was the traditional low-calcium diet.
In fact, dietary calcium may be protective against kidney stones because it helps bind oxalate in the intestine. Constipation is a common side effect of high calcium intake, but daily consumption of up to 2,500 mg is considered safe for adults and for children at least one-year-old.
The use of magnesium salts in medications, such as antacids and laxatives, may result in diarrhea, nausea, and abdominal cramps. Impaired kidney function renders an individual more susceptible to magnesium toxicity. Excess magnesium intake is unlikely from foods alone.
High-dose iron supplements
High-dose iron supplements, commonly used to treat iron deficiency anemia, may cause constipation and other gastrointestinal effects. A daily iron intake of up to 45 mg presents a low risk of gastrointestinal distress. Acute toxicity and death from ingestion of iron supplements are major poisoning hazards for young children.
In people with the genetic disorder hereditary hemochromatosis, a disease characterized by the overabsorption of iron, or in those who have repeated blood transfusions, iron can build up to dangerous levels, leading to severe organ damage, particularly of the liver and heart.
It is considered prudent for men and postmenopausal women to avoid iron supplements and high iron intakes from fortified foods. Toxicity from dietary iron has been reported in South Africa. And Zimbabwe in people consuming a traditional beer with extremely high iron content.
Excess zinc has been reported to cause gastrointestinal symptoms such as nausea and vomiting. Chronic intake of large amounts of zinc may interfere with the body’s utilization of copper. Impair immune response, and reduce the level of high-density lipoprotein cholesterol.
A safe intake of 40 mg of zinc daily is unlikely to be exceeded by food alone. Although it may be exceeded by zinc lozenges or supplements. Which are widely used despite a lack of data about their safety or efficacy.
Selenium is toxic
Selenium is toxic in large amounts. Selenosis (chronic selenium toxicity) results in symptoms such as gastrointestinal and nervous system disturbances. Brittleness and loss of hair and nails, a garliclike odor to the breath, and skin rash. There also have been reports of acute toxicity and death from ingestion of gram quantities of the mineral.
Excess selenium can be harmful whether ingested as selenomethionine. The main form found in food, or in the inorganic forms usually found in supplements. A daily intake of up to 400 μg from all sources most likely poses no risk of selenium toxicity.
Impaired thyroid gland function, goiter. And other adverse effects may result from high intakes of iodine from food, iodized salt. Or pharmaceutical preparations intended to prevent or treat iodine deficiency or other disorders. Although most people are unlikely to exceed safe levels, individuals with certain conditions. Such as autoimmune thyroid disease, are particularly sensitive to excess iodine intake.
While the teeth
While the teeth are developing and before they erupt, excess fluoride ingestion can cause mottled tooth enamel; however, this is only a cosmetic effect. In adults, excess fluoride intake is associated with effects ranging from increased bone mass. To joint pain and stiffness and, in extreme cases, crippling skeletal fluorosis. Even in communities where water supplies naturally provide fluoride levels several times higher than recommended, skeletal fluorosis is extremely rare.
High intakes of phosphorus (as phosphate) may affect calcium metabolism adversely. And interfere with the absorption of trace elements such as iron, copper, and zinc. However, even with the consumption of phosphate additives. In a variety of foods and in cola beverages, exceeding safe levels is unlikely.
Manganese toxicity, with central nervous system damage and symptoms similar to Parkinson’s disease. Is a well-known occupational hazard of inhaling manganese dust. But again, it is not likely to come from the diet. Similarly, copper toxicity is unlikely to result from excessive dietary intake. Except in individuals with hereditary or acquired disorders of copper metabolism.
The acute effects of a large intake of alcohol are well known. Mental impairment starts when the blood concentration is about 0.05 percent. A concentration of alcohol in the blood of 0.40 percent usually causes unconsciousness, and 0.50 percent can be fatal.
Accidents and violence, which are often alcohol-related, are major causes of death for young persons. Women who drink during pregnancy risk physical and mental damage to their babies (fetal alcohol syndrome). Alcohol also can interact dangerously with a variety of medications, such as tranquilizers, antidepressants, and pain relievers.
Although numerous studies have confirmed that light to moderate drinkers has less heart disease. And tend to live longer than either nondrinkers or heavy drinkers. Increasing chronic alcohol consumption carries with it significant risks as well: liver disease; pancreatitis; suicide; hemorrhagic stroke; mouth, esophageal, liver, and colorectal cancers; and probably breast cancer.
In alcoholics, the nutritional impairment may result from the displacement of nutrient-rich food. As well as from complications of gastrointestinal dysfunction and widespread metabolic alterations. Thiamin deficiency, as seen in the neurological condition known as Wernicke-Korsakoff syndrome. Is a hallmark of alcoholism and requires urgent treatment.
Diet and chronic disease
The relationship between diet and chronic disease is complicated. Not only because many diseases take years to develop but also. Because identifying a specific dietary cause is extremely difficult.
Some prospective epidemiologic studies attempt to overcome this difficulty by following subjects for a number of years. Even then, the sheer complexity of the diet, as well as the multifactorial origins of chronic diseases. Makes it difficult to prove causal links. Furthermore, many substances in food appear to act in a synergistic fashion. In the context of the whole diet rather than as individual agents. And single-agent studies may miss these interactive effects.
The concept of “risk factors”
The concept of “risk factors” has been part of the public vocabulary for several decades. Ever since the landmark Framingham Heart Study, began in 1948. First reported in the early 1960s that cigarette smoking elevated blood cholesterol. And high blood pressure was a predictor of one’s likelihood of dying from heart disease. Other studies confirmed and further elucidated these findings. And an extensive body of research has since shown that particular conditions. Or behaviors are strongly associated with specific diseases.
Not all individuals with a risk factor eventually develop a particular disease; however, the chance of developing the disease is greater when a known. Risk factor is present and increases further when several risk factors are present. Certain risk factors—such as diet, physical activity, and use of tobacco, alcohol. And other drugs—are modifiable, although it is often difficult to effect such change. Even if one is facing possible disability or premature death.
Others, including heredity, age, and sex, are not. Some risk factors are modifiable to varying degrees; these include exposure to sunlight and other forms of radiation. Biological agents and chemical agents may play a role in causing genetic mutations. That have been associated with an increased risk of certain diseases, particularly cancer.
Cardiovascular disease, is a general term that encompasses diseases of the heart and blood vessels. Is the leading cause of death in developed countries. Coronary heart disease (CHD), also known as coronary artery disease. Or ischemic heart disease, is the most common—and the most deadly—form of cardiovascular disease.
CHD occurs when the arteries carrying blood to the heart, and thereby oxygen and nutrients, become narrow and obstructed. This narrowing is usually the result of atherosclerosis. A condition in which fibrous plaques (deposits of lipid and other material). Build up on the inner walls of arteries, making them stiff and less responsive to changes in blood pressure.
If blood flow is interrupted in the coronary arteries surrounding the heart, a myocardial infarction (heart attack) may occur. Restriction of blood flow to the brain due to a blood clot. Or hemorrhage may lead to a cerebrovascular accident or stroke. And narrowing in the abdominal aorta, its major branches. Or arteries of the legs may result in peripheral arterial disease. Most heart attacks and strokes are caused not by total blockage of the arteries. By plaque but by blood clots that form more readily. Where small plaques are already partially blocking the arteries.
Although atherosclerosis typically takes decades to manifest in a heart attack or stroke. The disease may actually begin in childhood. With the appearance of fatty streaks, precursors to plaque. The deposition of plaque is, in essence. An inflammatory response directed at repairing injuries in the arterial wall.
Smoking, hypertension, diabetes and high blood levels of low-density lipoprotein (LDL). Cholesterol are among the many factors associated with vessel injury. Infection by certain bacteria or viruses may also contribute to inflammation and vessel damage. Particularly vulnerable to premature CHD are middle-aged men. Especially those with a family history of the disease. And individuals with hereditary conditions such as familial hypercholesterolemias.
Diet and weight loss
Diet and weight loss are influential in modifying four major risk factors for CHD. High levels of LDL cholesterol, low levels of high-density lipoprotein (HDL). However, the role of diet in influencing the established risk factors. Is not as clear as the role of the risk factors themselves in CHD.
Furthermore, dietary strategies are most useful when combined with other approaches. Such as smoking cessation and regular exercise. Drug therapy may include cholesterol-lowering drugs such as statins. Bile acid sequestrants, and niacin, as well as aspirin. Or anticoagulants to prevent the formation of blood clots and antihypertensive medication to lower blood pressure.
Although endogenous estrogen (that produced by the body). Is thought to confer protection against CHD in premenopausal women. Recent studies call into question the value of hormone therapy in reducing CHD risk. In women who have gone through menopause.
Because lipids such as cholesterol, triglycerides, and phospholipids are nonpolar and insoluble in water. They must be bound to proteins. Forming complex particles called lipoproteins. To be transported in the watery medium of blood. Low-density lipoproteins. Which are the main transporters of cholesterol in the blood. Carry cholesterol from the liver to body cells. Including those in the arteries, where it can contribute to plaque.
Multiple lines of evidence point to high levels of LDL cholesterol as causal in the development of CHD. And LDL is the main blood lipoprotein targeted by intervention efforts. Furthermore, clinical trials have demonstrated that LDL-lowering therapy reduces heart attacks and strokes in people who already have CHD.
High-density lipoproteins, on the other hand, are thought to transport excess cholesterol. To the liver for removal, thereby helping to prevent plaque formation. HDL cholesterol is inversely correlated with CHD risk; therefore intervention efforts aim to increase HDL cholesterol levels.
Another blood lipoprotein form is the very-low-density lipoprotein (VLDL). Is also an independent CHD risk factor, but to a lesser extent than LDL and HDL. As the major carrier of triglyceride (fat) in the blood. VLDL is particularly elevated in people who are overweight and in those with diabetes and metabolic syndrome.
Although LDL cholesterol is popularly referred to as “bad” cholesterol
Although LDL cholesterol is popularly referred to as “bad” cholesterol. And HDL cholesterol is often called “good” cholesterol. It is actually the lipoprotein form—not the cholesterol being carried in the lipoprotein—that is related to CHD risk. Total cholesterol levels are highly correlated with LDL cholesterol levels. Are typically used for initial screening purposes. Although a complete lipoprotein evaluation is more revealing.
A desirable blood lipid profile is a total cholesterol level below 200 milligrams per deciliter (mg/dl). An HDL cholesterol level of at least 40 mg/dl. A fasting triglyceride level of less than 150 mg/dl, and an LDL cholesterol level below 100, 130. Or 160 mg/dl, depending on the degree of heart attack risk.
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