Anorexia nervosa (AN)
Persistent restriction of energy intake leading to significantly low body weight.
Intense fear of gaining weight or of becoming fat or persistent behaviour that interferes with weight gain.
Disturbance in the way one’s body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, persistent lack of recognition of the seriousness of the current low body weight.
Bulimia nervosa (BN)
Recurrent episodes of binge eating: eating, in a discrete period, an amount of food that is definitely larger than most people would eat with a sense of lack of control over eating during the episode.
Recurrent inappropriate compensatory behaviour to prevent weight gain (self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or excessive exercise).
Self-evaluation is unduly influenced by body shape and weight.
Binge eating disorder (BED)
Recurrent episodes of binge eating not associated with the recurrent use of inappropriate compensatory behaviours.
Binge Eating Disorder is associated with more subjective distress regarding the eating behaviour
Avoidant/restrictive food intake disorder (ARFID)
Persistent failure to meet appropriate nutritional and/or energy needs associated with:
Significant loss of weight or failure to achieve expected weight gain or faltering growth in children
Significant nutritional deficiency
Dependence on enteral feeding or oral nutritional supplements
Marked interference with psychosocial functioning
Other specified feeding or eating disorder (OSFED)
Atypical Anorexia Nervosa: all criteria are met, except despite significant weight loss
Night Eating Syndrome: Recurrent episodes of night eating (…)
In adolescents strictly selective food intake, recurrent functional gastrointestinal symptoms impairing normal feeding and physical activity measured on estimated caloric intake are very common behaviours. Therefore, they often move in a “grey area” of eating disorders, sometimes presented as healthy habits, more difficult to discover.
From the point of view of the gynaecologists, the identification of an ED is pivotal in clinical situations where the reduced energy availability disrupts hypothalamus-pituitary-ovarian axis function inducing pubertal delay or amenorrhoea. It is important to stress that all eating disorders, especially bingeing, are associated with later overweight and gaining weight could promote the clinical expression of a polycystic ovary syndrome. The emergence of these disorders is mainly the consequence of several promoting factors acting during infancy, pubertal development, and early adolescent years. The knowledge of different pathogenic and risk factors is important to orient the history taking. Various studies have put in evidence the possible genetic transmission of vulnerability to ED, so girls coming from family where restrictive disorders or bingeing or struggling for being overweight are common are at risk for unhealthy relation with feeding. Recent evidences pointed out the possibilities of epigenetic modifications occurring in the intrauterine life or related to adverse events in childhood. Sexual abuse, maltreatments, and neglect are frequent in the history of subjects with emotional feeding and tendency to loss of control [3, 4]. The genetic background and the family climate influence the development of typical personality traits that in subjects with tendency to restrictive eating are shyness, insecurity, cognitive rigidity, perfectionism, and respect for rules. In subjects with tendency to bingeing, depressed mood, low self-esteem, high stress reactivity are described. The comorbidity with anxiety disorders is elevated in all the cases. The increase of steroid hormones in post-pubertal years seems to facilitate the clinical expression of ED, with a critical peak between 13 and 17 years. Social pressure on thinness and fitness play a major role in the spread of attention to body image and caloric control. The current feminine dominant models ever-present in the messages of the mass media and the social networks magnify the difficulties with the changes of body image typical of adolescence.
The hypothalamus-pituitary centres are highly sensitive to energy availability. The evolution in all living beings has selected homeostatic mechanisms to avoid reproduction in circumstances at risk of failure. In humans, several sophisticated feedback mechanisms (Fig. 8.1) link growth, pubertal maturation, and menstrual function to signals coming from fat, GI tract, and stress response activation, in order to consent ovarian activity only when a metabolic equilibrium is present [5–7]. The same mechanisms, with similar thresholds, control the neo-apposition of bone mass and consequently reduce bone turnover. Oestrogen deficiency and hypercortisolism promote bone resorption. Physical hyperactivity, use of SRIs, specific nutritional deficiency, and genetic predisposition are additional pathogenic factors. These adaptive repercussions of energy deficiency are particularly evident in very young girls during puberty or in the first years of gynaecological age [8].
Fig. 8.1
Simplified overview of peripheral signs of energy availability to hypothalamic centres
For the following hormones, a key role in response to food restriction is well documented in human beings:
- 1.
Leptin a protein hormone [9] produced by adipocytes in a pulsatile fashion regulates food intake at hypothalamic level stimulating the production of anorexigenic hormones (NPYY, ARP) and indirectly inhibits the production of GnRH during pubertal maturation (threshold effect) and during the fertile period of life. This hormone displays multiple regulatory functions on ovarian folliculogenesis, bone marrow, bone turnover, and on liver triglycerides metabolism.
- 2.
Ghrelin an orexigenic peptide [10] produced by specific cells in stomach and duodenum increases hunger and stimulates food intake. It acts on neuropeptide NPY and, unlike many other endogenous peptides, is able to cross the blood–brain barrier. Moreover, Ghrelin produced inside the CNS, stimulates growth hormone and is involved in stress reaction; the peptide is also a stimulus on osteoblasts formation.
- 3.
Insulin [11] the protein hormone produced by endocrine pancreas, besides the well-known effects on glucose cell uptake and fat deposition, acts at hypothalamic level as a sign of energy availability and is involved in the gratification related to food experience.
Other gastrointestinal peptides (PP, GLP-1, amylin, PYY), oxytocin, produced by neurohypophysis but not exclusively, endocannabinoids, adiponectin, and various nutrients (glucose, specific amino acids, long chain fatty acids) all interact [12] in the signalling of energy status to CNS. The adaptive response to energy deficiency is mainly based on:
- 1.
The activation of autonomic nervous system, comprehensive of secretion of adrenalin by adrenal medulla, with imbalance of the sympathetic/parasympathetic physiological equilibrium (mainly reduced sympathetic/exaggerated parasympathetic nervous system activity)
- 2.
The increased activity of CRH-ACTH-cortisol axis as a trigger of stress reaction, a modulator of behavioural and metabolic adjustments, an inhibitor of GnRH activity and of bone reabsorption
- 3.
The reduction of peripheral conversion of thyroxine in 3-jodo-thyronin (FT3 the bioactive form) in peripheral tissues
- 4.
The uncoupling at hepatic level between Gh stimulus and IGF-1 production; the reduced IGF-1 concentrations slow down all mitotic processes in the body.
8.2 Diagnostic Work-Up
The assessment of an adolescent with suspected ED should start with a comprehensive history and a complete physical examination.
The history should focus on:
Psychiatric disorders, weight concern, or food habits in the family
Family conflicts or difficulties in recognizing and managing emotions
Growth and nutritional problems in infancy
Previous overweight and recent weight changes
Stress, depression, or bereavement
Perfectionism, obsessive traits
Selective eating
Functional or painful gastrointestinal disorders
Diseases requiring food control (diabetes, coeliac disease…)
Quality and quantity of physical activity
Body reaction to cold (Raynaud phenomenon)
Recent fainting fits
Use of drugs or nutritional supplements
The physical examination can also be perfectly normal if the ED is at its beginning, but it is important to check, just with a handshake, the finger temperature, to consider the dryness of skin appendages, to look at the clothes (if baggy or layered). The signs of autonomic dysregulation are rather precocious: bradycardia, orthostatic hypotension.
The measurement of BMI is the starting point of body evaluation, but even if 18.5 has been proposed as a cut-off for menstrual function, this figure is only approximate. If the history does not give clear evidences, it is useful to propose an evaluation of body composition. A rapid, non-invasive and relatively low-cost method of orientation is the BIA. The technique determines the body tissue electrical impedance, which can be used to calculate an estimate of Total Body Water (TBW) and to derive Fat-Free Mass (FFM) and, by difference with body weight, Body Fat (BF). It must be kept in mind that dehydration is a recognized factor affecting BIA results and that moderate exercise before the measurements lead to an overestimation of fat-free mass and an underestimation of body fat percentage; an extremely reduced BMI is another limit to application of this method. BIA has a good accuracy in the prediction of resting energy expenditure (REE), the esteem of the energy required from the body in 24 h, always reduced as adaptation to negative energy balance, traditionally measured by calorimetry. As additional assessment the BCM, the measure of metabolically active body cells inside FFM, indexed to height, if lower than seven is a clue of catabolic phenomena. BIA (and BCMI) is also very useful for tracking body composition in an individual over a period [13, 14].
The US scan points out the degree of functional regression of internal genitalia. Reduced uterine size and endometrial thickness reveal the hypo-oestrogenization. Ovarian structure is often multifollicular (Fig. 8.2) in response to adaptation to reduced energy availability or during weight recovery. In situations of serious energy deficiency, the ovaries may appear compact; liver steatosis, evident as a diffuse increased echogenicity, is also often present due to the accumulation of triglycerides within hepatocytes. In anorexia nervosa can be useful to control the kidney to exclude a nephropathy linked to hypokalaemia and malnutrition.
Fig. 8.2
Multifollicular ovary (slightly increase volume, multiple follicles of diameter >8 mm, without stroma visualization)
Routine blood tests can be normal if the metabolic situation is not particularly compromised; alterations are present when catabolic processes take place: an increase in albumin with a decrease in globulins, a relative increment in creatinine and liver enzymes, especially SGOT. A reduction in white blood cells and erythrocytes is present when the medulla function is impaired. Total cholesterol can be elevated because of mobilization of fat stores; high ferritin concentrations are a marker of inflammatory status. In special conditions, specific nutritional markers can be tested as retinol binding globulin and transferrin. The monitoring of plasma electrolytes is mandatory in case of suspect of purging behaviours (vomiting or laxative abuse) or during weight rehabilitation, together with amylase dosage. Standard urine analysis can show higher concentrations linked to dysregulation of ADH with altered osmoregulation.
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