12.2 Nutrition, Obesity & Metabolism Syndrome Flashcards
Define obesity
BMI >30 kg/m2
- Class 1 (30-34.9)
- Class 2 (35-39.9)
- Class 3 (>40)
BMI is not accurate tool for identifying obesity-related complications
- ⬆️ BMI = ⬆️ health complications
- Waist-hip/ waist circumference proposed as alternate measure
- At individual level: complications due to excess adiposity, location and distribution of adiposity and also other factors (Environmental; Genetic; Biologic; Socioeconomic)
Potential consequences of stigmatisation of pt with obesity
- ⬆️ risk for depression
- low self-esteem
- poor body image
- ⬆️ risk of eating disorders & binge eating
- exercise avoidance
- further weight gain
- avoidance of medical consultation
- suicide
Pathogenesis of obesity
- Food intake and energy balance
- Family history, lifestyle, psychology
- Microenvironment and gut microbiome
- Genetic factors and causes
- Epigenetic modification
- complex interplay of numerous genetic, metabolic, behavioural and environmental factors
- Appetite regulation
- crosstalk between homeostatic and hedonic eating is influenced by mediators from adipose tissue, the pancreas, gut and other organs.
- Cognitive functions in the prefrontal cortex exert executive control on food choices and the decision to eat.
- interconnectivity of these neural networks drives eating behaviour and has been shown to be altered in obesity.
- Growing consensus that obesity is a disorder of energy homeostasis, rather than only passive accumulation of excess weight
- Upward setting of the defended level of body fat mass – acquired/ inherited
- Two distinct processes:
• Sustained positive energy balance (energy intake>expenditure)
• Resetting of the body weight “set point” - Latter process explains why difficult to lose weight with lifestyle changes
- Ongoing study of the pathogenesis (especially why increased body weight becomes to be “defended”) – inform better treatment, public policy, advocacy and awareness
- Diet influences calorie intake, not conferring changes in energy expenditure or metabolic milieu (“calorie is a calorie”)
What parts of the brain is part of controlling ingestive behaviour and energy balance?
- visual, olfactory & auditory stimuli and cues
- cortico-limbic systems (reward, learning & memory, executive control)
- hypothalamus (master nutrient sensor, incentive motivation)
- hindbrain (oromotor & autonomic controls, sensation)
Endogenous factors that lead to pre-obesity
- genetic predisposing
- epigenetic
- family profile
- physiological (pregnancy)
- endocrine abnormalities
- others
Exogenous factors that leads to pre-obesity
- environment
- occupation
- lifestyle
- energy intake (food & drinks)
- eating behaviour (speed of eating, pleasure while eating)
- inactivity
- smoking cessation
- short sleep duration
- chronic stress
- eating disorders (binge eating, night eating syndrome, bulimia, severe restriction)
- psycho-social factors
- depression, anxiety, psychosis
- drugs
What is the best method for identifying adiposity related complications?
- BMI + Waist circumference
Waist circumference independently associated with ↑CVS risk , but not good predictor of individual visceral adiposity
What is Visceral adipose tissue an increased risk to?
Increase metabolic risk
Risk assessment of obesity
Slide 21
Common endocrine conditions that predisposes to obesity
- androgen deficiency (men) -> hypogonadism
- androgen excess (women) -> irregular menses
- drug-induced endocrine dysfunction -> anti-depress, lithium
- ovarian failure -> menopause
- cushing’s disease / syndrome
- GH deficiency
- hypopituitarism
Disease consequences of obesity due to ⬆️ fat cell size
- diabetes
- NAFLD (non-alcoholic fatty liver disease)
- CVD
- GB disease (guillian-barre)
- cancer
Disease consequences due to ⬆️ fat mass
- stigma
- osteoarthritis
- sleep apnea
Physical health and economic consequences of overweight and obesity
- cancer
- type 2 diabetes
- cardiovascular disease
- hypertension
- stroke
- dyslipidemia
- reproductive disorders
How does obesity (adiposopathy) contribute to type 2 DM?
Sick Fat Disease
->
Immunopathies
+
Endocrinopathies
+
Increased circulating free fatty acids
=
Insulin resistance & beta cell dysfunction
Endocrine changes associated with obesity
Increased
- leptin in plasma
- TSH (upper normal range)
- Insulin
- IGF-I
- Androgens
- Progesterone
- Cytokines (IL-6)
- ACTH/cortisol
- Sympathetic nervous system activity
Decreased
- GH
- Ghrelin
- Adiponectin
