Week 4 - Eating Disorders Flashcards
disordered eating occurs in __% of women
80% Low calorie intake Excessive exercise Vegetarianism* Fat restriction Carbohydrate restriction Candida diets, wheat free, dairy free*
Men comprise what percentage of individuals with ED in clinical settings?
5-10%
with significantly more gay and bisexual men suffering from these disorders compared with heterosexual men .
However, there is evidence that more men in the general population have ED and that ED in men are under-diagnosed and under-treated. Men may not seek treatment due to experiencing fewer severe symptoms or because they may not consider themselves at risk for eating disorders (Woodside).
Describe the spectrum of eating disorders
- anorexia nervosa; restrictive; binge-eating, purging
- bulimia nervosa
- binge eating disorder
- eating disorders not otherwise specified; female athlete triad; anything else (e.g. orthorexia)
Diagnostic criteria for anorexia nervosa
Body weight <85% expected weight
Intense fear (pathological) of becoming fat
Inaccurate perception of own body size, weight or shape
Excessive dieting leading to severe weight loss
Criterion removed:
Amenorrhea of at least 3 consecutive mos.
(in girls or women after menarche)
Mortality rates for AN: __% at 10 years; __% at 20 years
Mortality rates: 10% at 10 years; 20% at 20 years
More than __% of patients with AN become chronically ill over 10 years
More than 30% of patients with AN become chronically ill over 10 years
What is the profile of high risk for death that causes AN to have the highest mortality rate of any psychiatric disorder?
Profile of high risk for death:
Chronic illness (> 2yr)
Very low weight (BMI <19) – irrespective of dx.
History of suicidal behaviour or self harm
Presence of affective disorders
Alcohol misuse
History of hospitalization for mental health problems
Daily vomiting; Daily bingeing
Laxative misuse &/or Diuretic misuse
Ipecac use; Stimulant use (cocaine, ephedrine)
14 signs of AN
Emaciation Hyperactivity Bradycardia Tachycardia Hypotension Dry skin Brittle hair Hair loss on scalp "Yellow” skin especially on palms Lanugo - very fine, soft, and usually unpigmented, downy hair as can be found on the body of a fetus or newborn baby; d/t malnutrition Peripheral cyanosis Raynaud’s phenomenon Edema: ankle, periorbital Sialadenosis - Enlargement of the salivary glands, usually the parotids, often seen in conditions such as alcoholism and malnutrition.
16 symptoms of AN
Weight loss Amenorrhea Irritability Sleep disturbances Fatigue Headache Dizziness Food sensitivities/allergies Faintness Constipation Nonfocal abdominal pain or bloating Feeling of “fullness” Polyuria Cold intolerance Leg pains Infertility
Temperament of person with AN
Cautious Inhibited Controlled thinking Restricted Rigid Fearful of intimacy < New experience Extremely persistent Fear Decreased self directedness Perfectionist Anxious (even as child) Struggle with identity Low self esteem Hyperactivity (cycle) (zinc defic, malnutrition)
8 physiological sequelae of AN
Electrolyte imbalance (K+, Cl-, Na+) Cardiac insufficiency Reproductive stunting/imbalance Gastrointestinal dysfunction Osteoporosis Immune stress - infections Organ failure (heart, liver, kidney) Death – due to physiological shut down or suicide
Symptoms of electrolyte imbalance
Weakness Muscle twitches Constipation Hypotension Dizziness Polyuria Depression Polydipsia Fatigue Paraesthesia Leg (muscle) pain
Cardiac complications found in eating disorders
Fatigue bradycardia small HT, EKG changes (AN) Syncope orthostatic/systolic hypotension (AN, BN, EDNOS) Acrocyanosis poor peripheral circulation (AN) Palpitations abnormal EKG (AN, BN, EDNOS) Chest pain mid-systolic click MVP & TVP (AN) Calf pain hypokalemia * (AN, BN)
Dyspnea rapid respiratory rate (AN)
Factors For Increased Cardiac Risk In Person With AN
Severe and/or rapid weight loss Purge frequency Ipecac use Co-morbid physiological disorder Underlying cardiac disease Older age
Red Flags (physical aspect) of AN
Very low weight
High frequency of binge/vomiting
Low vitals – HR & BP
Arrhythmia
Appearance – weak, peripheral edema
Abnormal lab- electrolytes, liver enzymes
Patient complains of chest pain, leg cramps
History – alcohol misuse; self harm/suicide, hospitalization, chronic illness, etc
Effects on Reproductive System in Anorexia Nervosa
Normally, pulsatile GnRH release induces LH-FSH
In AN, LH-FSH pulses diminish with reversion to prepubertal pattern
60% women with oligomenorrhea or amenorrhea seen at infertility clinics have eating disorders
Amenorrhea not likely due to starvation alone
Study: Nutrition (fats) and reproductive hormones:
non-dieters, intense dieters, risk group
–> women who ovulated consumed more energy from fat vs. non-ovulating women
Factors Contributing to the Development of Osteoporosis in Anorexia Nervosa
Estrogen deficiency state –> high turnover bone resorption state –> osteoporosis
Osteoclast-stimulating cytokines:
- IL-1, IL-6, IL-11, TNF
High cortisol implicated also.
Mechanisms of estrogen regulation of bone resorption
- Bone cells contain E receptors
- L-1, IL-6, TNF-α, granulocyte macrophage colony-stimulating factor, macrophage colony-stimulating factor (M-CSF), and prostaglandin-E2 (PGE2). These factors increase bone resorption, mainly by increasing the pool size of pre-OCs in bone marrow (2, 3), and are downregulated by E.
- E upregulates TGF-β, an inhibitor of bone resorption that acts directly on OC to decrease activity and increase apoptosis
Effects of ED on GI system
- gastroparesis
- GERD
- gall stones
- constipation - reflex hypo functioning of colon; cathartic colon syndrome
- abdominal pain
- dysphagia, hoarseness
- stomach rupture via gastric dilation (binges) BN
cathartic colon syndrome
Cathartic colon is the anatomic and physiologic change in the colon that occurs with chronic use of stimulant laxatives (> 3 times per week for at least 1 year). Signs and symptoms of cathartic colon include bloating, a feeling of fullness, abdominal pain, and incomplete fecal evacuation. Radiologic studies show an atonic and redundant colon. Chronic use of stimulant laxatives can lead to serious medical consequences such as fluid and electrolyte imbalance, steatorrhea, protein-losing gastroenteropathy, osteomalacia, and vitamin and mineral deficiencies. When the drug is discontinued, radiographic and functional changes in the colon may only partially return to normal because of drug-induced neuromuscular damage to the colon.
Anthranoid laxatives (aloe, cascara sagrada, and senna) are derived from naturally occurring plants and are considered to be stimulant laxatives. Short-term use of stimulant laxatives is safe, but abuse of these drugs can cause melanosis coli and possibly increases the risk of colonic cancer. Melanosis coli, a benign condition, is characterized by dark pigmentation of the colonic mucosa that usually develops 9 months after initiating the use of these drugs and disappears just as quickly after the drug is discontinued.
Bulimia Nervosa diagnostic criteria
Recurrent binge eating
Recurrent purging, excessive exercise or fasting
Excessive concern about body weight or shape
Absence of anorexia nervosa
Usually normal weight
12 Symptoms Found in Patients with Bulimia Nervosa
Irregular menses Esophageal burning Nonfocal abdominal pain Abdominal bloating Lethargy Fatigue Constipation Diarrhea/Irritable Bowel Syndrome Frequent sore throats Depression Water retention Swollen cheeks
12 Signs of Bulimia Nervosa
Can be seen in AN also if vomiting
Russell’s sign (calluses on the knuckles or back of the hand due to repeated self-induced vomiting over long periods of time) Sialadenosis Perimolysis (Decalcification of the teeth from exposure to gastric acid in people with chronic vomiting) Periodontal disease Gingivitis Dental caries Perioral irritation Mouth ulcers Hematemesis Edema (ankle, periorbital) Periorbital petechiea Arrhythmia Injected sclera (red eye)
Temperament of a person with BN
Distracted easily Aware of others’ opinion of them Impulsive; but can be fearful Chemical dependency High risk behaviours Dependent on praise Give up easily
Relationship of CCK with Bulimia
Studies have shown that CCK is decreased in individuals with BN when compared with healthy controls. Decreased CCK functioning may contribute to impaired satiety and thus binge eating in this patient population. Depending on the macronutrient composition of food choices, CCK release can be differentially influenced. For instance, protein is a potent stimulator of a CCK response. Eating more protein-rich meals increases the release of CCK, increasing satiety and ending a meal.
Knowledge of CCK functioning and the utility of manipulating the macronutrient composition of meals may inform standard behavioral treatment strategies for those who suffer from BN.
6 Physical Sequelae to Bulimia Nervosa
- Electrolyte imbalance
- Cardiac arrest
- Gastric dysfunction
- Endocrine abnormalities – reproductive,
thyroid, adrenal etc - Immune insufficiency
- Blood sugar dysregulation
Binge Eating Disorder description
Distinct group among the obese
Less severely disturbed compared to individuals with BN
Uncontrollable episodes of binge eating without the inappropriate physical compensatory behaviours ie no purging or over exercise
Individuals feel extremely upset after bingeing
Often feel calm when bingeing
Affects 4-5% of all adults in US
Approximately 40% of people who are mildly obese and who try to lose weight
Binges & willpower
“Binges are purposeful acts, not demented journeys. They do not signify a lack of willpower or the inability to care for yourself. On the contrary, a binge can actually be an urgent attempt to care for yourself when you feel uncared for. Bingeing is the only way many of us know how to give to ourselves without holding back.” Geneen Roth
6 comorbidities with bulimia & binge eating disorder
ADHD Bipolar disorder Depression OCD Substance Abuse Personality Disorder
General Temperament of Person with Binge Eating Disorder
Responsible Sensitive Rebellious Perfectionist in work Critical (internally or externally of others) Mixed messages Impatient Assertive – not afraid to voice opinion
Sequelae to Binge Eating Disorder
Diabetes mellitus Hypothyroidism; adrenal exhaustion High blood pressure High cholesterol Gall stones Inflammatory state – arthritis, skin infections (fungal) Metabolic syndrome (HBP, HChol, DM)
Eating Disorders Not Otherwise Specified;
What is the Female Athlete Triad?
Syndrome found in athletic women, consisting of three inter-related components:
4a1. Disordered eating
4a2. Amenorrhea (in women)
4a3. Osteoporosis
Eating Disorders Not Otherwise Specified;
Orthorexia
Excessive focus on righteous eating (ultra puritan, vitamin obsession)
7 Potential Risk Factors for Developing an Eating Disorder
- Perinatal stress and low birth weight
- Genetics
- Temperament – often seen at 18mos
- Early puberty
- Dieting
- Standard North American diet
- Comorbid mental health ailments: Anxiety, OCD, Depression etc
Explain the Correlation of Perinatal Stress and Anorexia Nervosa
Swedish study (Cnattingius, 1999)
All live born girls in Sweden from 1973-1984
Relative to controls – individuals with AN
Were 3x more likely to have been born pre-term
More likely low birth weight and multiple birth; 2x more likely to have experienced birth trauma; more likely to have instrumental delivery
Inner beliefs/perceptions of Anorexia Nervosa
Anorexia nervosa: (gases, muriaticum, oxidatum)
“I need nothing/no one, but I am afraid”
“I don’t deserve to take much”
Inner beliefs/perceptions of Bulimia Nervosa
Bulimia nervosa: (father, carbonicum, snake family)
“I am not worthy of holding/taking this in.”
i.e. struggle with praise, success etc
Inner beliefs/perceptions of Binge Eating
AN + BN?
“I need nothing/no one, but I am afraid”
“I don’t deserve to take much”
“I am not worthy of holding/taking this in.”
i.e. struggle with praise, success etc.
5 possible aetiologies of eating disorders
- Nutritional Deficiencies: Zn, EFA, B12
- Genetics: AN – family hx – 1st degree relatives of indiv with AN have 10x incr.; 12x BN
- Family dynamics:
Boundary violation (emotional & physical)
Family Hx: depression, alcoholism, death
History of sexual, physical or emotional abuse
Expectations - Society and Culture: media, dieting, over exercise
- Self and sensitivity: CNC theory [confirmed negativity condition]
Explain the Confirmed Negativity Condition
Although a person can have C.N.C. without an eating disorder, all eating disorder sufferers must have C.N.C. According to Claude-Pierre, there are many self-negating manifestations of C.N.C. and these can include depression, agoraphobia, panic attacks, obsessive compulsive disorder, or somatic disorders. An eating disorder is one such manifestation, albeit one of greater concern because of high mortality rates associated with eating disorders.
Sufferers of C.N.C. feel a sense of self-loathing and unworthiness. They have a negative “voice” inside their head who’s sole purpose is to destroy them. With a person who has an eating disorder, the “voice” will often concentrate on their main weakness of food. For example, it might say “You’re fat, you don’t deserve to eat”, “You’ll never get better, you’ll only get worse”, or “You deserve to die, therefore you don’t deserve to eat.”
Claude-Pierre describes this constant battle as being like a civil war in the person’s mind. The “voice” or Negative Mind is totally powerful when the eating disorder symptoms are present. However, the “voice” is louder for some than it is for others. For some people, it is loud and constant, whereas for others it may be like a whisper or a number of whispers that are hard to distinguish.
Sufferers of C.N.C. feel guilty about not being perfect, that they are not worthy of anybody’s attention and that they are to blame for things that are clearly beyond their control. Inevitably, this leads to a sense of failure and reinforces the Negative Mind’s opinion that they are useless and unworthy. Many sufferers feel they are so unworthy to the point that they refuse to eat in front of other people for fear of being in the way.
C.N.C. sufferers will often punish themselves for going back on a bargain with their Negative Mind or for things that they perceive as being their fault, even if in reality they are not. Punishments usually take the form of denying themselves pleasure and happiness. Food is the obvious example (after all, we all need food to survive) but the Negative Mind is also often telling the sufferer that they deserve to die.
Punishment may also include self-injury. The sufferer will cut, scratch, pinch, hit, burn or slap themselves in order to repent for “breaking the rules” in some way. Even if the individual is not self-injuring in that regard, it is likely they are using starvation, binging and/or purging as indirect methods of punishment.
What are the 6 general treatment goals for an ED?
Build trust and rapport
Stabilize weight (loss or gain)**
Strengthen coping skills
Empower the individual – connection to self
Assist them to decrease fear of food/living
Develop regular eating patterns
5 requirements of recovery
- Willingness or desire to think differently
- Physical: sleep, diet, exercise, supps etc
- Emotional: support (friends, family)
- Therapy: CBT, Non specific supportive psychotherapy, NLP, Homeopathy etc
- Spiritual: Yoga, meditation, breath work, creativity, art work; nature, etc.
Process of recovery
Mourning, shame and guilt Regaining hope Taking responsibility for the healing process Regaining a purpose in life * Developing choices Helping others Disappearance of symptoms
How to calculate BMI?
weight (kg) / height (m2)
What constitutes a PE for a suspected or known ED?
State of hydration Vitals Weight and height* Teeth and gums CDV (EKG) BP: lying, seated and standing Abdominal Neurologic Gynecologic
Recommended lab tests
CBC* Serum electrolytes* EKG* Serum glucose* Dual energy x-ray absorptometry (DEXA) Liver function* KI function Serum; salivary amylase levels Serum BUN, creatine levels T3, T4 and TSH Urinalysis* Stool (GI bleeding, abdominal, anemia) Serum zinc levels Zinc tally
AN is a symptom or complication of which 4 conditions?
Clinical marker of Beriberi (Thiamine Def)
AN also an early symptom of Pellagra (Niacin B3 deficiency)
AN – complication of Scurvy (Vit C Def)
AN is a symptom of zinc deficiency
Symptoms of zinc deficiency?
Depression Attention difficulties Decreased appetite Meat avoidance* Amenorrhea Inhibition of EFA metabolism Decreased taste & Hypercarotenemia (chrnc) Poor wound healing Poor sleep Decreased melatonin Nausea Bloating/GI discomfort Distorted body image Vulnerability to stress Change in opiate receptors Rough, dry skin
10 supplements/modalities for a nutritional approach to EDs
- zinc - (liquid) 15-60mg daily divided doses
- 5HTP - 50-1200mg/day (Bulimia & BEDs)
- homeopathy - individualize
- St. John’s Wort: 3% hypericin: 300mg tid ; caution w antidepressants (serotonin syndrome)
- GABA - for anxiety
- EFAs - Low levels of EFA’s lead to weight gain
without omega 3 intake during periods of weight loss, patients regain weight more readily because omega 3 deficiency results in poor insulin regulation and slow metabolism
** Long term effect of omega 3 deficiency is sluggish metabolism - Theanine - 200mg 1-2x/d as needed
- rhodiola - 50-500mg/d (high % rosin = use lower dose)
- thiamine (B1) - anorexia is a beriberi symptom
- acupuncture: HT7, PC6, CV16
What is serotonin syndrome
Serotonin syndrome occurs when you take medications that cause high levels of the chemical serotonin to accumulate in your body.
Serotonin syndrome can occur when you increase the dose of such a drug or add a new drug to your regimen. Certain illegal drugs and dietary supplements also are associated with serotonin syndrome.
Serotonin is a chemical your body produces that’s needed for your nerve cells and brain to function. But too much serotonin causes symptoms that can range from mild (shivering and diarrhea) to severe (muscle rigidity, fever and seizures). Severe serotonin syndrome can be fatal if not treated.
Milder forms of serotonin syndrome may go away within a day of stopping the medications that cause symptoms and, sometimes, taking drugs that block serotonin.
Serotonin syndrome is not an idiopathic drug reaction; it is a predictable consequence of excess serotonin on the CNS and/or peripheral nervous system. For this reason, some experts strongly prefer the terms serotonin toxicity or serotonin toxidrome which more accurately reflect that it is a form of poisoning.
No laboratory tests can currently confirm the diagnosis. Hence it is diagnosed based on symptoms, disease course (that is, the progression of the disease) and the exclusion of other possible causes of the presenting symptoms.
Sxs: increased heart rate, shivering, sweating, dilated pupils, myoclonus (intermittent tremor or twitching), as well as overresponsive reflexes
Factors contributing to zinc deficiency
Phytates impair zinc absorption
Easiest sources of zinc are animal products
High number of individuals with AN avoid meat &/or have been vegetarian for years *
Puberty – zinc demands increased (B12, EFAs)
High stress (glucocorticoids)
BCP’s (reduce albumin decr. Zn)
Strenuous physical activity
Poor diet
What is the relationship between zinc deficiency and appetite control?
- Majority of digestive enzymes are Zn-dependent
- Aminopeptidase A is a Zn-dependent enzyme which metabolizes CCK
- CCK secreted in duodenum to decr gastric emptying and enhance satiety
- After a meal, AN patients show peak levels of CCK that is 2x normal levels
- Zinc also controls appetite by stimulating
Norepinephrine, Dopamine, Serotonin, GABA
& Opiate receptors of CNS
Why is zinc awesome for EDs?
- Zinc increases serotonin uptake
- Study of children with ADHD showed improved attention levels with Zn supplementation
- AN patients supplemented with Zn gained more weight that AN patients without Zn supplementation
Dosage & form of zinc for teens/adults?
- elemental zinc
- 30-60mg/d
- max 90mg/d in divided doses
add 1-2mg of copper after approx 2-3 months of higher doses of zinc
