Intellectual Disability

Is the most common developmental disability and is characterized by significantly below average intellectual functioning along with related limitation in two or more of the following area: communication, self-care, functional academics, home-living, self-direction, health and safety, leisure, or work and social skills.1 Principles of nutrition care: Numerous nutritional problems have been identified in the individual with developmental disability, including growth retardation, obesity, failure to thrive, feeding problems, metabolic disorders, medication-nutrient interactions, constipation, and renal problems. Other health problems exist, depending on the disorder. In designing the medical nutrition therapy plan, four areas considered: nutrition assessment (anthropometrics, biochemical, dietary intake, feeding issues such as oral-motor problems, positioning problems and feeding skills) nutritional diagnosis, intervention, and monitoring and evaluation. Nutritional Assessment: Anthropometrics It altered when an individual is unable to stand, suffers from contractions, or has other gross motor problems. Measure body weight may require special equipment such as chair scales. Wheelchair scale is used in some clinics but require that the wheelchair weight be known.

Obtaining height for the non ambulatory individual requires either a recumbent board that can be purchased or constructed. Other measure of height include arm span, knee to ankle height, or sitting height. Biochemical assessment: Use of some medications can lead to low blood levels of folic acid, carnitine, ascorbic acid, calcium, vitamin D, alkaline phosphate, phosphorus, and pyridoxine. Assessment of thyroid status is part of the protocol for children with Down syndrome, and glucose tolerance test is recommended for Prader-Willi syndrome. Feeding Issues: Feeding problems have been defined as the inability or refusal to eat certain foods because of neuromotor dysfunction, obstructive lesions such as strictures, and psychosocial factors. Other causes of feeding problems in this population includes: oral-motor difficulties, positioning problems, conflict in parent-child relation ships, sensory issues, and tactile resistance post intubation. Nutrition diagnosis: problem identification: Once the nutrition assessment has been completed, problems should be identified related to growth, including weight, dietary adequacy or inadequacy; fluid intake; and clinical problems such as constipation, diarrhea, allergies, reactions to medication, and feeding issues. The problems in addressing them should be listed so that priorities can be set. When possible this information is shared with the parent or caregiver and the adult client before the intervention process begins. Intervention:

Before intervention or medical nutrition therapy can begin, consideration must be given to the motivational level of the parent or client, his or her cultural background, and how the therapy can be community based and family centered. This means that consideration must be given to where the client will be served so that it becomes a part of the individualized education plan or the individualized family plan.2 Attention – deficit hyperactivity disorder (ADHD): Is a neurobehavioral problem seen in children with increasing frequency it has been associated with learning disorders, inappropriate degrees of impulsiveness, hyperactivity, and attention deficit. Diagnostic criteria were developed by the American psychiatric association and have designated three types: (1) combined type of hyperactivity and attention deficit; (2) predominately inattentive type; and (3) predominately hyperactive – impulse type. ADHD affects the child at home, and in social situations. Numerous studies have demonstrated that some children are sensitive to dyes. Thus, you might start by eliminating only foods (and vitamins, drugs, and toothpastes) that contain artificial colorings. The Feingold diet, which is based mostly on unconfirmed reports from parents and doctors, eliminates additional additives, as well as “Salicylates containing” foods. That diet eliminates: • Artificial colorings (look for names like Red 40 and Yellow 5 on labels) • Artificial flavorings (including vanillin, used in synthetic vanilla) • Artificial sweeteners (acesulfame-K, aspartame, saccharin, sucralose)3

Down syndrome: Etiology:
• •

Due to older maternal age at onset of pregnancy. Trisomy 21from non-disjunction or translocation.

Clinical findings:

Hypotonia, Hyper flexibility/mobility of the joints , Hip subluxation or dislocation .

• Scoliosis, Foot deformity, Microbrachycephaly. • Short neck, depressed nasal bridge and small nose, upward slanting eyes. • Abnormally shaped ear, Enlarged, protruding tongue, Single simian crease in center of the palm. • Excessive space between large and second toe, Mental retardation, speech and motor delay. • Cardiac anomalies, G1 atresia or stenosis, Hearing loss. • Hypothyroidism, Dental problems. Nutrition Assessment: Anthropometric Measures: Height, weight, head circumference, triceps skin fold, and arm circumference are obtained for the child with DS with the usual measurements. (BMI can be taken but may be higher than normal because of short stature.

Growth measures are an important part of the assessment and ongoing nutrition therapy since these individuals tend to be short, Muscle tone is low, and gross motor ability is often delayed, leading to the possibility of the individual becoming overweight. 2 Dietary Intake: During infancy the food intake of the infant with DS may differ from that of the normal infants. Although human breast milk is recommended, many infants with DS are formula fed .One recent study found that out of 560 children with DS, 57% were formula fed. The main reasons reported by the mothers were infants, illness and admission to the neonatal unit, frustration or depression, perceived milk insufficiency, and difficulty in suckling by the infant. Progression to solid food has been found to be delayed in children with DS, mostly as a result of delays in feeding and motor development. Introduction of solid food may not be offered at 6 months if the infant has poor head control or is not yet sitting. Low tone and sucking problems also delay weaning from the breast or bottle of the cup. IEPs include feeding and feeding progression instruction and practice. An important part of evaluating the dietary intake is determining energy and fluid needs since children with DS have a high prevalence of obesity. Studies have indicated that the resting energy expenditure of the child with DS is lower than for controls without DS and may be as much as 10% lower than the dietary reference intake for energy. For the child over the age of 5, calculation for energy requirements may need to be based on height rather than weight.2 Feeding Skills: Feeding skills are delayed in the infant and child with DS. Some parents have found difficulty in initiating oral motor skills such as

suckling and sucking. The infant with DS often has difficulty in coordinating sucking, swallowing, and breathing, which are the foundations for early feeding. When the infant has congenital heart defect, which occurs in 40% to 60% of the DS infants, sucking is weakened, and fatigue interferes with the feeding process. Gastrointestinal anomalies are found in 8% to12% of infants with DS, and these infants often require nasogastric or gastrostomy feedings. Weaning and self-feeding are usually late when compared to the normal infant and frequently do not emerge until 15 to 18 months of age. The DS infant strives for independence and autonomy about 6 months later than the child without DS. Estimated caloric needs for special conditions Condition Normal child Prader-Willi Kcal/cm 16 maintain growth: 10-11 Slow weight loss: 8.5 Down syndrome Girls: 14.3 Boys: 16.1
Heindicles E: Nutrition and feeding for person with special needs, Interdisciplinary center for Disability, 1992.2

comments for all children & adolescent for all children & adolescent

Reliable for ages 5-11 yr

Prader-willi syndrome (PWS):

It is a genetic condition caused by the absence of chromosomal material from chromosome 15. It characteristics by developmental delays, poor muscle tone, short stature, small hands and feet, incomplete sexual development, and unique facial feature, insatiable appetite leading to obesity, the problem with hypotonia interferes feeding, learning disability, and mental retardation. Metabolic abnormalities: Short stature in PWS is due to growth hormone deficiency. This child has low serum insulin-like growth factor-1 (IGR-1), low IGF binding protein-1, and low insulin compared to normal obese children. Appetite and obesity: Appetite control and obesity are common problems with PWS. After the initial period of failure to thrive, children begin to gain excessively between the age of 1 & 4, and appetite is excessive. The cause of uncontrollable appetite involves the hypothalamus and the oxytocin neurons, which are decreased in PWS brain. They have abnormal body composition, decreased lean body mass, and increased fat even in infancy. Body fat is generally deposited in the thighs, buttocks, and abdominal area. The lower energy expenditure is found in young children, adolescents, and adult with PWS, total energy expenditure may be lowered to 53% of that of normal obese adolescents. The lower the muscle tone contributes greatly to the lack of interest in physical activity.2 Alzheimer’s disease:

Is the most common form of dementia with “patterns and rates of cognitive decline that are far from uniform”. Etiology: Due to: atherosclerosis Genetic factors: three genes have been discovered that cause early-onset, familial AD. Apolipo-protein-E4 (Apo-E4) is a protein located on chromosome19; it binds b-amyloid and is involved in the transport of cholesterol. Damage to key mitochondrial components, impaired insulin signaling, and the factors related to heart disease and stroke. Risk factors: Down syndrome, mother’s age at birth, low level of education, birth order, head injury and old age. Symptom: Poor judgment, restlessness, mood swings, personality changes. With loss of: memory, speech, and intellectual function. Fats Much of the evidence linking AD and diet is either epidemiological or the result of long-term cohort studies. Many of the studies have shown a positive association between saturated fat (SFA) intake and the incidence of dementia, whilst also showing an inverse relationship between its incidence and polyunsaturated fatty acid (PUFA) intake.

One study looking at the total fat intake of eleven countries found a correlation between higher levels of fat consumption and higher levels of AD amongst the over 65. It has also been observed that older Japanese people, known for their high fish consumption, have very low levels of AD and this finding has been supported by cohort studies with other older populations. Similarly, the “Mediterranean diet”, characterized by high intakes of monounsaturated fatty acids, has been linked to low rates of dementia in Italy68, while high intakes of cereals and fish appears to decrease risk in North American and northern European countries. One controlled trial in this field looked at the effect of a mixed PUFA supplement on 100 older adults with AD, over a period of four weeks. Of the 60 that received the supplement, 49 reported improvement in mood, cooperation and short-term memory. Vitamins and Minerals A different field of research examines the association between high vegetable consumption and decreased incidence of AD. For example, one study compared groups of meat eaters and vegetarians, matched for age, sex and residence, finding that the meat- and fish-eaters were more than twice as likely to develop AD as their vegetarian counterparts.

It is unclear whether this outcome was the result of higher fat consumption by the meat eaters or of higher vegetable consumption by the vegetarians. However, the possible protection offered by vegetable consumption has also been explored in studies on antioxidants. One long-term population-based study found that high intakes of vitamins C and E were linked to a lower risk of AD, particularly amongst smokers, and this finding has been replicated in other long-term prospective studies. Methylation & Homocysteine Methylation is the process our brain depends on to create, maintain and repair brain cells and the neurotransmitters that pass between those cells. One amino acid – homocysteine – determines how effectively methylation occurs; that is, how effectively the methyl groups in the brain respond to the myriad demands placed upon them each second. If the level of homocysteine is low, the methyl groups are able to carry out repairs quickly and effectively, keeping our body healthy and balanced. Higher rates of homocysteine indicate that methylation is happening more slowly and ineffectively, leading to declining memory, mood and cognitive function. Poor methylation and high levels of homocysteine are strongly associated with an increased risk of AD. Research in the US measured homocysteine levels in 3,766 males and 4,918 females and concluded that a diet

low in folate, vitamin B12 or vitamin B6 can be a cause for homocysteine build-up. As such, the United States Department for Agriculture (USDA) emphasizes the need for older adults to consume nutrient-dense foods, fiber and water, recommending that they drink at least 8 [250ml] glasses of water a day. The Alzheimer’s Prevention Plan also suggests a diet that improves methylation and reduces homocysteine, avoiding harmful fats, refined carbohydrates; sugar and excesses of caffeine and alcohol are also recommended.3

Phenylketonuria: It is a genetic abnormality due to deficiency of enzyme phenylalanine hydroxylase so increase phenylalanine in blood at newborn screening. Increasing in phenylalanine and abnormal phenylalanine/tyrosine ratio in blood left untreated or inadequate treatment of mental retardation. Clinical finding: • Blood phenylalanine > 6-10 mg/dl. • Blood tyrosine < 3 mg/dl. Medical management: regular monitoring of blood phenylalanine to maintain at 1-6 mg/dl.

Nutritional care: Phenylalanine free formula / medical food. Low phenylalanine foods. Supplement with tyrosine. Education of family and child about formula/medical food preparation. Adequate nutrition intake . Regular monitoring of growth. Education on label reading and food choices. 4

References:
1. American Psychiatric Association. "Mental Retardation."

In Diagnostic and Statistical Manual of Mental Disorders, 4th ed., text revision. Washington, DC: American Psychiatric Press, Inc., 2000. 2. Harriet cloud, MS, RD, FADA, MNT for Developmental Disabilities, Krause’s Food & Nutrition Therapy, 2008. 1170-94.
3.

Dr. Deborah Cornah, the Mental Health Foundation report: Feeding Minds- http://www.sustainweb.org

4.

Cristine M. Trahms, MS, RD, CD, FADA. Beth N. Ogata, MS, RD CD, MNT for Genetic Metabolic Disorders, Krause’s Food & Nutrition Therapy, 2008.1141-65.

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