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Measurements of a child’s growth provide the key information for the presence of malnutrition, but weight and height measurements alone can lead to failure to recognize kwashiorkor and an underestimation of the severity of malnutrition in children.
Although protein energy malnutrition is more common in low-income countries, children from higher-income countries are also affected, including children from large urban areas in low socioeconomic neighborhoods. This may also occur in children with chronic diseases, and children who are institutionalized or hospitalized for a different diagnosis. Risk factors include a primary diagnosis of intellectual disability, cystic fibrosis, malignancy, cardiovascular disease, end stage renal disease, oncologic disease, genetic disease, neurological disease, multiple diagnoses, or prolonged hospitalization. In these conditions, the challenging nutritional management may get overlooked and underestimated, resulting in an impairment of the chances for recovery and the worsening of the situation.
PEM is fairly common worldwide in both children and adults and accounts for 6 million deaths annually. In the industrialized world, PEM is predominantly seen in hospitals, is associated with disease, or is often found in the elderly.
Measures have been taken to reduce child malnutrition. Studies for the World Bank found that, from 1970 to 2000, the number of malnourished children decreased by 20 percent in developing countries. Iodine supplement trials in pregnant women have been shown to reduce offspring deaths during infancy and early childhood by 29 percent. However, universal salt iodization has largely replaced this intervention.
The Progresa program in Mexico combined conditional cash transfers with nutritional education and micronutrient-fortified food supplements; this resulted in a 10 percent reduction the prevalence of stunting in children 12–36 months old. Milk fortified with zinc and iron reduced the incidence of diarrhea by 18 percent in a study in India.
A large percentage of children that suffer from PEM also have other co-morbid conditions. The most common co-morbidities are diarrhea (72.2% of a sample of 66 subjects) and malaria (43.3%). However, a variety of other conditions have been observed with PEM, including sepsis, severe anaemia, bronchopneumonia, HIV, tuberculosis, scabies, chronic suppurative otitis media, rickets, and keratomalacia. These co-morbidities tax already malnourished children and may prolong hospital stays initially for PEM and may increase the likelihood of death.
Growth stunting is identified by comparing measurements of children's heights to the World Health Organization 2006 growth reference population: children who fall below the fifth percentile of the reference population in height for age are defined as stunted, regardless of the reason. The lower than fifth percentile corresponds to less than two standard deviations of the WHO Child Growth Standards median.
As an indicator of nutritional status, comparisons of children's measurements with growth reference curves may be used differently for populations of children than for individual children. The fact that an individual child falls below the fifth percentile for height for age on a growth reference curve may reflect normal variation in growth within a population: the individual child may be short simply because both parents carried genes for shortness and not because of inadequate nutrition. However, if substantially more than 5% of an identified child population have height for age that is less than the fifth percentile on the reference curve, then the population is said to have a higher-than-expected prevalence of stunting, and malnutrition is generally the first cause considered.
Three main things are needed to reduce stunting:
- a kind of environment where political commitment can thrive (also called an "enabling environment")
- applying several nutritional modifications or changes in a population on a large scale which have a high benefit and a low cost
- a strong foundation that can drive change (food security, empowerment of women and a supportive health environment through increasing access to safe water and sanitation).
To prevent stunting, it is not just a matter of providing better nutrition but also access to clean water, improved sanitation (hygienic toilets) and hand washing at critical times (summarised as "WASH"). Without provision of toilets, prevention of tropical intestinal diseases, which may affect almost all children in the developing world and lead to stunting will not be possible.
Studies have looked at ranking the underlying determinants in terms of their potency in reducing child stunting and found in the order of potency:
- percent of dietary energy from non-staples (greatest impact)
- access to sanitation and women's education
- access to safe water
- women's empowerment as measured by the female-to-male life expectancy ratio
- per capita dietary energy supply
Three of these determinants should receive attention in particular: access to sanitation, diversity of calorie sources from food supplies, and women's empowerment. A study by the Institute of Development Studies has stressed that: "The first two should be prioritized because they have strong impacts yet are farthest below their desired levels".
The goal of UN agencies, governments and NGO is now to optimise nutrition during the first 1000 days of a child's life, from pregnancy to the child's second birthday, in order to reduce the prevalence of stunting. The first 1000 days in a child's life are a crucial "window of opportunity" because the brain develops rapidly, laying the foundation for future cognitive and social ability. Furthermore, it is also the time when young children are the most at risk of infections that lead to diarrhoea. It is the time when they stop breast feeding (weaning process), begin to crawl, put things in their mouths and become exposed to faecal matter from open defecation and environmental enteropathies.
Vitamin poisoning is the condition of overly high storage levels of vitamins, which can lead to toxic symptoms. The medical names of the different conditions are derived from the vitamin involved: an excess of vitamin A, for example, is called "hypervitaminosis A".
Iron overload disorders are diseases caused by the overaccumulation of iron in the body. Organs commonly affected are the liver, heart and endocrine glands in the mouth.
A positive diagnosis test for thiamine deficiency can be ascertained by measuring the activity of the enzyme transketolase in erythrocytes (Erythrocyte Transketolase Activation Assay). Thiamine, as well as its phosphate derivatives, can also be detected directly in whole blood, tissues, foods, animal feed, and pharmaceutical preparations following the conversion of thiamine to fluorescent thiochrome derivatives (Thiochrome Assay) and separation by high-performance liquid chromatography (HPLC). In recent reports, a number of Capillary Electrophoresis (CE) techniques and in-capillary enzyme reaction methods have emerged as potential alternative techniques for the determination and monitoring of thiamine in samples.
The normal thiamine concentration in EDTA-blood is about 20-100 µg/l.
Obesity is caused by eating too many calories compared to the amount of exercise the individual is performing, causing a distorted energy balance. It can lead to diseases such as cardiovascular disease and diabetes. Obesity is a condition in which the natural energy reserve, stored in the fatty tissue of humans and other mammals, is increased to a point where it is associated with certain health conditions or increased mortality.
The low-cost food that is generally affordable to the poor in affluent nations is low in nutritional value and high in fats, sugars and additives. In rich countries, therefore, obesity is often a sign of poverty and malnutrition while in poorer countries obesity is more associated with wealth and good nutrition. Other non-nutritional causes for obesity included: sleep deprivation, stress, lack of exercise, and heredity.
Acute overeating can also be a symptom of an eating disorder.
Goitrogenic foods can cause goitres by interfering with iodine uptake.
Many people with beriberi can be treated with thiamine alone. Given thiamine intravenously (and later orally), rapid and dramatic recovery can occur within hours. In situations where concentrated thiamine supplements are unavailable, feeding the person with a thiamine-rich diet (e.g. whole grain brown bread) will lead to recovery, though at a much slower rate.
Following thiamine treatment, rapid improvement occurs, in general, within 24 hours. Improvements of peripheral neuropathy may require several months of thiamine treatment.
Obesity increases health risks, including diabetes, cancer, cardiovascular disease, high blood pressure, and non-alcoholic fatty liver disease, to name a few. Reduction of obesity lowers those risks.
A 1-kg loss of body weight has been associated with an approximate 1-mm Hg drop in blood pressure.
In the US, the Dietary Reference Intake for adults is 55 µg/day. In the UK it is 75 µg/day for adult males and 60 µg/day for adult females. 55 µg/day recommendation is based on full expression of plasma glutathione peroxidase. Selenoprotein P is a better indicator of selenium nutritional status, and full expression of it would require more than 66 µg/day.
Social conditions such as poverty, social isolation and inability to get or prepare preferred foods can cause unintentional weight loss, and this may be particularly common in older people. Nutrient intake can also be affected by culture, family and belief systems. Ill-fitting dentures and other dental or oral health problems can also affect adequacy of nutrition.
Loss of hope, status or social contact and spiritual distress can cause depression, which may be associated with reduced nutrition, as can fatigue.
In the United States, the prevalence of obese or overweight adult dogs is 23–53%, of which about 5% are obese; the incidence in adult cats is 55%, of which about 8% are obese.
In Australia, obesity is the most common nutritional disease of pets; the prevalence of obesity in dogs in Australia is approximately 40%.
Overnutrition or hyperalimentation is a form of malnutrition in which the intake of nutrients is oversupplied. The amount of nutrients exceeds the amount required for normal growth, development, and metabolism.
The term can also refer to:
- Obesity, which "usually" occurs by overeating, as well as:
- Oversupplying a "specific" nutrient, such as dietary minerals or vitamin poisoning. This is due to an excessive intake or a nutritional imbalance caused by fad diets.
For mineral excess, see:
- Iron poisoning, and
- Low sodium diet (a response to excess sodium).
Overnutrition may also refers to greater food consumption than appropriate, as well as other feeding procedures such as parenteral nutrition.
Infants and children who have had unpleasant eating experiences (e.g. acid reflux or food intolerance) may be reluctant to eat their meals. Additionally, force feeding an infant or child can discourage proper self-feeding practices and in-turn cause undue stress on both the child and their parents. Psychosocial interventions can be targeted at encouraging the child to feed themselves during meals. Also, making mealtimes a positive, enjoyable experience through the use of positive reinforcement may improve eating habits in children who present with FTT. If behavioural issues persist and are affecting nutritional habits in children with FTT it is recommended that the child see a psychologist.
There is no single, specific test for malabsorption. As for most medical conditions, investigation is guided by symptoms and signs. A range of different conditions can produce malabsorption and it is necessary to look for each of these specifically. Many tests have been advocated, and some, such as tests for pancreatic function are complex, vary between centers and have not been widely adopted. However, better tests have become available with greater ease of use, better sensitivity and specificity for the causative conditions. Tests are also needed to detect the systemic effects of deficiency of the malabsorbed nutrients (such as anaemia with vitamin B12 malabsorption).
FTT may be evaluated through a multifaceted process, beginning with a patient history that notably includes diet history, which is a key element for identifying potential causes of FTT. Next, a complete physical examination may be done, with special attention being paid to identifying possible organic sources of FTT. This could include looking for dysmorphic features, abnormal breathing sounds, and signs of specific vitamin and mineral deficiencies. The physical exam may also reveal signs of possible child neglect or abuse. Based on the information gained from the history and physical examination, a workup can then be conducted, in which possible sources of FTT can be further probed, through blood work, X-rays, or other tests.
Compared to non-obese animals, obese dogs and cats have a higher incidence of osteoarthritis (joint disease) and diabetes mellitus, which also occur earlier in the life of the animal. Obese animals are also at increased risk of complications following anesthesia or surgery.
Obese dogs are more likely to develop urinary incontinence, may have difficulty breathing, and overall have a poorer quality of life compared to non-obese dogs, as well as having a lower life expectancy. Obese cats have an increased risk of diseases affecting the mouth and urinary tract. Obese cats which have difficulty grooming themselves are predisposed to dry, flaky skin and feline acne.
It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also in persons of advanced age (i.e., over 90).
People dependent on food grown from selenium-deficient soil may be at risk for deficiency. Increased risk for developing various diseases has also been noted, even when certain individuals lack optimal amounts of selenium, but not enough to be classified as deficient.
For some time now, it has been reported in medical literature that a pattern of side-effects possibly associated with cholesterol-lowering drugs (e.g., statins) may resemble the pathology of selenium deficiency.
Alcoholic polyneuropathy is very similar to other axonal degenerative polyneuropathies and therefore can be difficult to diagnose. When alcoholics have sensorimotor polyneuropathy as well as a nutritional deficiency, a diagnosis of alcoholic polyneuropathy is often reached.
To confirm the diagnosis, a physician must rule out other causes of similar clinical syndromes. Other neuropathies can be differentiated on the basis of typical clinical or laboratory features. Differential diagnoses to alcoholic polyneuropathy include amyotrophic lateral sclerosis, beriberi, Charcot-Marie-Tooth disease, diabetic lumbosacral plexopathy, Guillain Barre Syndrome, diabetic neuropathy, mononeuritis multiplex and post-polio syndrome.
To clarify the diagnosis, medical workup most commonly involves laboratory tests, though, in some cases, imaging, nerve conduction studies, electromyography, and vibrometer testing may also be used.
A number of tests may be used to rule out other causes of peripheral neuropathy. One of the first presenting symptoms of diabetes mellitus may be peripheral neuropathy, and hemoglobin A1C can be used to estimate average blood glucose levels. Elevated blood creatinine levels may indicate renal insufficiency and may also be a cause of peripheral neuropathy. A heavy metal toxicity screen should also be used to exclude lead toxicity as a cause of neuropathy.
Alcoholism is normally associated with nutritional deficiencies, which may contribute to the development of alcoholic polyneuropathy. Thiamine, vitamin B-12, and folic acid are vitamins that play an essential role in the peripheral and central nervous system and should be among the first analyzed in laboratory tests. It has been difficult to assess thiamine status in individuals due to difficulties in developing a method to directly assay thiamine in the blood and urine. A liver function test may also be ordered, as alcoholic consumption may cause an increase in liver enzyme levels.
The treatment is some form of Vitamin E supplementation.
Aggressive vitamin E replacement therapy has been shown to either prevent, halt or improve visual abnormalities.
Vitamin E deficiency is rare and is almost never caused by a poor diet. Instead, there are three specific situations when a vitamin E deficiency is likely to occur:
- Premature, very low birth weight infants - birth weights less than 1500 grams, or 3.5 pounds. A neonatologist, a pediatrician specializing in the care of newborns, typically evaluates the nutritional needs of premature infants.
- Rare disorders of fat metabolism - There is a rare genetic condition termed isolated vitamin E deficiency or 'ataxia with isolated with vitamin E deficiency', caused by mutations in the gene for the tocopherol transfer protein. These individuals have an extremely poor capacity to absorb vitamin E and develop neurological complications that are reversed by high doses of vitamin E.
- Fat malabsorption - Some dietary fat is needed for the absorption of vitamin E from the gastrointestinal tract. Anyone diagnosed with cystic fibrosis, individuals who have had part or all of their stomach removed or who have had a gastric bypass, and individuals with malabsorptive problems such as Crohn's disease, liver disease or exocrine pancreatic insufficiency may not absorb fat (people who cannot absorb fat often pass greasy stools or have chronic diarrhea and bloating). Abetalipoproteinemia is a rare inherited disorder of fat metabolism that results in poor absorption of dietary fat and vitamin E. The vitamin E deficiency associated with this disease causes problems such as poor transmission of nerve impulses, muscle weakness, and degeneration of the retina that can cause blindness.
Treatment is directed largely towards management of underlying cause:
- Replacement of nutrients, electrolytes and fluid may be necessary. In severe deficiency, hospital admission may be required for nutritional support and detailed advice from dietitians. Use of enteral nutrition by naso-gastric or other feeding tubes may be able to provide sufficient nutritional supplementation. Tube placement may also be done by percutaneous endoscopic gastrostomy, or surgical jejunostomy. In patients whose intestinal absorptive surface is severely limited from disease or surgery, long term total parenteral nutrition may be needed.
- Pancreatic enzymes are supplemented orally in pancreatic insufficiency.
- Dietary modification is important in some conditions:
- Gluten-free diet in coeliac disease.
- Lactose avoidance in lactose intolerance.
- Antibiotic therapy to treat Small Bowel Bacterial overgrowth.
- Cholestyramine or other bile acid sequestrants will help reducing diarrhoea in bile acid malabsorption.
In dairy breeds, the disease may occur in calves between birth and 4 months of age. In rustic breeds or beef cattle, heifers and young steers up to 12 months of age can be affected. In calves, muscles in upper portion of the front legs and the hind legs are degraded, causing the animal to have a stiff gait and it may have difficulty standing. The disease may also present in the form of respiratory distress.