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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.

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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 problemsin 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:

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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 theclient 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

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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, tricepsskin 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.

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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, anddifficulty 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

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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 Kcal/cm comments

Normal child 16 for all children & adolescent

Prader-Willi maintain growth: 10-11 for all children & adolescent

Slow weight loss: 8.5

Down syndrome Girls: 14.3 Reliable for ages 5-11 yr

Boys: 16.1

Heindicles E: Nutrition and feeding for person with special needs, Interdisciplinary center for Disability,

1992.2

Prader-willi syndrome (PWS):

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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 toobesity, 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:

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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.

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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 decreaserisk 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.

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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 thebrain 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

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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.

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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: AmericanPsychiatric 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 Foundationreport: Feeding Minds- http://www.sustainweb.org

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4. Cristine M. Trahms , MS, RD, C D, FADA. Beth N. Ogata, MS, RD

CD , MNT for Genetic Metabolic Disorders, Krause’s Food &

Nutrition Therapy, 2008.1141-65.

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