Physiology of Eating - L10&11

1. increase of wanting/eating palatable foods -> increase in insulin resistance, more FFA release and uptake -> more MESENTERIC AT

2. increased fructose consumption -> activation of 11beta-HSD-1 -> stimulates release of more glucocorticoids

3. increased gluconeogenesis, insulin (resistance), LPL (enzyme that directs energy to various tissues)  -> more MESENTERIC AT

1.

a. endocrine changes (increased ghrelin, decreased leptin) -> increased hunger 

b. Hedonic factors -> increased time/opportunity to eat, increased food reward 

2. 

a. decreased thermogenesis

b. increased fatigue

c. decreased physical activity 

-> increased energy intake + decreased energy expenditure 

(+ another factor is gut dysbiosis -> disrupted intestinal barrier + increased LPS translocation)

1. Inhibiting effect on food intake -> major effect is enhancement of CCK satiation by acting in hindbrain

2. estradiol receptors are all over brain -> also in many areas involved in eating regulation/energy homeostasis

3. Estradiol can act in all these areas! (and thus has an effect on food intake)

1. high fluctuations of estrogen/progesterone 

2. depends on individual differences -> genetics, stress, history of mood disorders 

3. women show disturbed eating! -> changes coincide with changes in serotonin activity (depression..)

1. menopause: dramatic drop in estrogen levels + estrogen dominance (over progesterone) 

2. leads to disrupted estrogen-related systems (e.g. thermoregulation, sleep, circadian rhythm etc.)

3. thus MAINLY neurological symptoms -> hot flushes, insommnia, mood changes, depression, eating, impaired cognitive function

4. Estradiol receptors: ESR1, ESR2, GPER 

estrogen & FSH levels decrease, which leads to a decrease in muscle mass & strength, energy expenditure and adipose cell metabolism -> increased body weight

1. factors that trigger the cycles: genetics, stress, poor diet

-> Neuroendocrine effects (HPA-axis, leptin, insulin dysregulation)

-> Gut Microbiota (Dysbiosis)

-> Adipose tissue (increased lipogenesis, pro-inflammatory cytokines) 

2. All of this leads to neuroinflammation (also via IDO, which is a key enzyme involved in the synthesis of monoamines (serotonine, dopamine)

3. Altered brain activity for mood&food 

4. Depression <-> Obesity 

1. simulates biosynthesis of serotonin

2. inhibits serotonin degradation

3. blocks serotonin uptake

4. potentiates serotonin receptor activation 

1. anorexia nervosa

2. bulimia nervosa

3. binge eating disorder

4. orthorexia nervosa 

1. violations lead to self-punishement

2. guilt/self-loathing

3. risk for social isolation

1. no direct causes are known

2. genetics & familial influences

3. obesessive- compulsive personality type (perfectionism, poor coping with stress, rigidity)

4. dysfunction of monoaminergic neurotransmission

5. sociocultural influences equating beauty with an overly thin physique 

6. almost always begins with dieting -> positive feedback -> obtain reward for not eating 

7. some imbalance in the dopaminergic (reward) & serotonic system is involved 

1. depression

2. obsession with food

3. low sociability

4. poor attention & concentration (mainly AN)

5. loss of libido/lack of interest in sex (mainly AN)

1. low leptin (mainly AN)

2. low estrogn, FSH, LH (mainly AN)

3. Amenorrhoea

4. low BMD (mainly AN)

5. impaired gastric system

6. impaired immune system

7. impaired dental status (AN and BN, but more BN) 

Dieting -> increased attention to nutrient caloric content -> increased attention to BW/shape, size -> strict rules (what, when, how much eating) -> exercise -> routine of eating/exercise becomes rigid -> obession with food -> practice deception to hide habits, wear loose clothes -> social avoidance -> psycholocial signs of starvation

Diet -> cravings -> break rule/eat -> guilt -> binge -> guilt/shame -> compensatory behavior (purge/vomit/laxatives) -> guilt/depression -> diet 

1. dont want to be treated

2. nutritional rehabilitation + restoring weight is essential

3. family therapy

4. highly controlled & structural environment 

5. cognitive-behavior therapy most effective 

6. the sooner start, the better, intenste treatment not always better

7. outcome better for adolescents 

1. want to be treated

2. cognitive-behavioral therapy -> short term, focus on restructuring maladaptive thoughts&m behaviors

3. Drug Treatment -> Antidepressants reduce binge/purge behavior, serotonin reuptake inhibitors have the least side effects