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Eating Disorders. In Adolescence Dr. Franco Navazio MCB 135E - Lecture 38. Adolescence. From the Latin Ad Olesco : to grow up Most adolescents have VORACIOUS APPETITE A response to the increased energy requirement generated by the GROWTH SPURT. Body Mass Index.
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Eating Disorders In Adolescence Dr. Franco Navazio MCB 135E - Lecture 38
Adolescence From the Latin Ad Olesco : to grow up Most adolescents have VORACIOUS APPETITE A response to the increased energy requirement generated by the GROWTH SPURT
Body Mass Index • Weight in kg divided by height in m2 • NORMAL BMI : 18 to 24 years of age BMI < 18 : suspect malnutrition BMI 24 to 30 : overweight BMI 30 to 40 : obesity BMI above 40 = morbid obesity
Why do we eat? The hypothalamus is the controller stimulated by: • OREXIGENIC PEPTIDES (appetite inducers) e.g. agouti-protein and neuropeptide Y • ANOREXIGENIC PEPTIDES (appetite suppressants) e.g. melano-cortin which, with effects on specific receptors (MC1R), decreases food intake and increases energy expenditure
Central Controls are Influenced by Circulating HORMONES: • INSULIN: provides signals related to blood glucose levels • LEPTIN: signaling consistency of body fat stores and, in addition • The GUT HORMONES
The GUT HORMONES • GRELIN: secreted by the stomach fundus (when empty) increases appetite and hence food intake • NO: nitric oxide (not a hormone but dilates the empty stomach hence very orexigenic) • CHOLECYSTOKININE and PEPTIDE YY3-36: secreted by endocrine lining cells of the distal gut and colon when food present hence appetite suppressants (anorexigenic) Can these hormones be manipulated therapeutically? Not easily!ANY LOSS OF BODY FAT stimulates a defensive system which acts in order to RESIST THE LOSS OF FAT IN CONCLUSION: the GUT TALKS to the BRAIN
Anorexia Nervosa: A Classic Eating Disorder • A disease of the mid-adolescent period characterized by: • INTENSE FEAR OF GAINING WEIGHT • DENIAL OF THE SERIOUSNESS of the CURRENT LOW WEIGHT • PRESENCE of AMENORRHEA in post-menarchal females for at least 3 consecutive periods periods occurring following estrogen administration DO NOT COUNT
Anorexia Nervosa: Clinical Aspects • WEIGHT: very decreased • FEMALE to MALE ratio = 10 : 1 • MENSTRUATION : absent • BINGE-EATING: 25 to 50% of patients • MORTALITY : 5% per decade
Anorexia Nervosa:Clinical & Laboratory Findings • LANUGO and EDEMA of the skin, bradycardia and hypotension, constipation, normochromic anemia and leukopenia, hyponatremia, hypoglycemia, low hormonal levels (estrogen or testosterone, LSH, FSH) but normal TSH and increased cortisol • SKELETAL CHANGE: OSTEOPENIA
Anorexia Nervosa: Signs of Malnutrition • Easy pinching in the posterior region of the arms, due to to loss of fat • Hollowing temporal muscles • Wasting of the thigh muscles • Easily plucked hairs MEMO: the laboratory signs of malnutrition are HYPOALBUMINEMIA and HYPOPREALBUMINEMIA
Anorexia Nervosa • Definite neuro-psychiatric disorder • More frequently encountered in young post-pubertal females of college age
Bulimia Nervosa • Characterized episodes of binge eating alternating with purging • Female to male ratio 10:1 • Some genetic factors may be involved, but and above all cultural attitudes toward standards of physical attractiveness • 3 modalities are the most frequent: • Self induced vomiting via “fingers” or ipecac • Abuse laxatives (e.g. bisacodyl, cascara or senna) • Misuse diuretics • In addition to diuretics also diet pills (containing ephedrine)
Bulimia Nervosa: Complications • Oral: loss of enamel of the anterior teeth and dental caries • GI tract: frequent vomiting can induce GE-reflux (occasionally tears in the esophagus). The abuse of laxatives can lead to constipation due to damage of the myo-enteric plexus • Abnormalities of the electrolytes: • Metabolic alkalosis due to frequent vomiting • HYPOKALEMIA present in 5% of the patients
Bulimia Nervosa: Treatment • Replenish potassium losses • Eventually I.V. fluids and lytes • Monitor lytes frequently and, of course • Refer for psychiatric or psychologic counseling
The Female Athlete Triad • Dysmenorrhea or amenorrhea • Dietary inadequacy or disordered eating • Osteopenia and eventually osteoporosis
The Female Athlete Triad:The Risk Profile 1) Athletes in the elite and highly competitive levels: e.g. gymnastics, figure skating, ballet dancing, distance running 2) Individual sports more at risk than TEAM SPORTS 3) During adolescence and young adulthood skeletal integrity is at significant risk due to the rapid growth occurring at this time MEMO: Some male sports (such as wrestling) place athletes at risk due to pressure “to make weight.” Some males may become affected also by delayed puberty and anorexia (especially in long distance runners) in parallel to the female triad (but incidence is 9 : 1)
The Female Athlete Triad:Prevention and Treatment • Prevention: Develop educational models and evaluate all women with changes in menstruation and weight • Medical care: Remove athletes at risk from competition and develop guidelines for hormonal-nutritional treatment and bone mass assessment • Education: Facilitate development of educational material and courses
Obesity • In the USA in the year 2000: • 97 million overweight (BMI < 24) • 50 million obese (BMI < 30) • 15 million morbid obese (BMI < 40) • An overall increase of 30% in 7 years and the ever more frequent presence of obesity in children
Types of Obesity The APPLE The PEAR The TRUNCAL The PEAR type much less related to eventual complications
Obesity and Related Morbidities: CAD - DJD - CANCER- GOUT Type 11 DM (66% of diabetics Type II are obese) The deadly triad: diabetes II + obesity + smoking Sleep APNEA - Pulmonary embolism
Obesity Treatments • Caloric restrictions: with necessity to restrict fats to less than 30% of the total caloric intake • Modification of lifestyle and exercise: • A walk of 1 mile (1.5 m) burns 100 Kcal Walk 2 - 3- or even 4 miles, 4 or 5x weekly, and add some resistance exercise 2 or 3 times weekly (all under some supervision). • The dietary variations: The Atkins Diet or the high protein low carbohydrate (only 20 grams of CHO/day)
Comments • Even if the Atkins Diet permits a gradual increase in CHO after the initial weight loss (5g per week after a loss of 10 lbs. or 4.5 kg) still it provokes: • Calciuria • Not indicated in renal or hepatic diseases • Atherogenic (high in saturated fats, trans-fats and cholesterol while in adequate for fruits, vegetables, whole grains • Drug treatments: Redux, Meridia, Leptin, Orlistat, etc., etc. • And finally surgery shunts and/or restrictive today • Even with laparoscopic procedures
Final Comments The recipe for effective weight loss is a combination of: • Motivation • Physical activity • Caloric restriction And all this with a lifelong adherence BUT MEMO: Prevention of weight gain is the first step EVEN IN CHILDREN