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Lecture 8

PSY333H1 Lecture 8

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University of Toronto St. George
Lisa Lipschitz

PSY333H1F L8 Nov 07, 2013 Brain-Body Relationships: The Role of Obesity HPA (Hypothalamic-pituitary axis) (Deborah Schwartz) Methods of brain-body communication Autonomic Nervous System  CNS communicates w body via PNS  Hypothal secretes CRH  Anterior pituitary releases ACTH   Autonomic NS: Parasympathetic (rested state, slows body Adrenal Cortex releases Cortisol (recs everywhere  strong down) & Sympathetic (non-essential fns on hold; stress effects) response) o Regulates glucose (blood sugar) levels o Quick response o Increases body fat o Unconscious o Helps to defend the body against infection o Direct synapses from brain onto muscles o Helps the body respond to stress Hormone Communication (HPA axis, insulin, cytokines) Insulin  Hormone: a chemical msger produced in 1 part of the body & travels via blood to a target organ or cell o The target organ or cell has recs specific to certain hormones  Slower response o Takes time for hormone to be created, excreted, to travel thru blood o Systemic reaction – any cell in the body can react t Controls blood-glucose levels the hormone as long as it has the receptor for it  Insulin rises after eating  Sympathetic NS stimulates Adrenal Medulla  NE, E  systemic effects on multiple tissues  Beta cells in pancreas release insulin when blood-glucose  Type 2 diabetes levels are high o Hyperinsulinemia (too much blood insulin)  Targets liver & muscles to use glucose  convert into glycogen or use it for energy Blood Brain Barrier  Some hormones have neutral effects in body, strong effects in Cytokines brain  Immune system o So need to separate systemic circulation from body  Heal infections by signaling to other cells in body that circulation  Blood brain barrier infection is occurring o Regulate immunity, inflammation o Recs determine entry  Can have far reaching effects since by blood o Insulin can get in via recs, then can attach to recs on neurons & astrocytes in:   Olfactory bulb How obesity can impact brain health  Cerebral cortex  Hippocampus Insulin resistance in obesity  Hypothal  Amygdala o  Feeding bhvr, Peripheral glucose metabolism, Learning & memory  Chronic peripheral (in the body) hyperinsulinemia  o Decreased #s of insulin recs at BBB o Reduced insulin transport into brain o Reduced cognitive fn’ing Increased Sympathetic NS activity in Obesity  Could be seen as advantage o Burn more calories (since uses more energy)  Elevated BP o BP: resistance of vessels during blood flow o Increased rennin secretion & sodium reabsorption in kidney  increased bp  hypertension, constrict vasculature (also increases bp)  Insulin resistance common in obesity  Normally insulin binds to recs at surface of muscle cell  biochemical pathway  GLUT4 rec to surface  glucose enters cell to be used as energy  Bp in brain needs to be kept constant o Natural fluctuation in bp when we move, neurons very sensitive  Cerebral autoregulation: keeps cerebral blood flow constant at dif bp’s o Regulated by carotid arteries to affect whole brain  Obesity: insulin recs resistant to insulin  cells don’t respond o Body responds by producing more insulin into the blood  2 types of insulin resistance: o Hyperglycemia (excess blood glucose) Maury et al. (2007)  Obesity is often characterized as a state of chronic low-grade inflammation  Normotension: normal BP  Hypertension: chronic high BP  Adipocytes (fat cells) o cerebral autoregulatory curve shifted to right  less o Obese: bigger adipocytes (storing lipids), more adipocytes, staining for macrophages (inflammatory blood in brain reaction)  What adiposities are secreting: o Increasing secretion of pro-inflammatory cytokines o Can cross BBB using:  Rec mediated transport or  Phospholipid byproducts o  Reduce concentration  Like when you’re sick Measuring obesity  Not all obesity is equally dangerous to our health  Body mass index (BMI) = body weight (kg) / height (m ) o Overweight: BMI above 25 o Obese: BMI above 30  Problem: doesn’t take into account muscle mass (heavier than Functional Hyperemia:  coupling of blood flow to energetic needs of brain regions fat), bone density  MRI – measuring blood flow o More active  need more blood  Blood vessels contain smooth muscle cells o Can harden from pounding less elastic  less responsive to changes in blood flow  Vascular Resistance o SMCs surrounding blood vessels can also harden from LDL plaques  Two women w BMI 29 o  can’t fn as well since can get oxygen  Woman on right has lots of muscle mass (good since can take glucose of out body and burn energy)  Miss out on changes in body composition if we just look at Inflammation in Obesity BMI Subcutaneous fat vs. Visceral fat  Fat storage: o Histology stain of adipose cell o 90% storage is lipids Lipolysis  MRI scan of abdomen (belly button at top, spinal cord in middle)  Not all fat is dangerous  Subcutaneous fat: fat we can see, right under the skin  Visceral fat: grows underneath abdominal muscles, around internal organs o Higher lipid weight then other fat so more dangerous o Higher lipolytic rate o Drained by the venous portal system o This person is skinny so there isn’t much  In order for fat cells to enter blood stream, need to break down TGs into components  Lipolysis: hydrolysis of TAGs into glycerol & 3 free fatty acids (FAAs) o TAG  DAG  MAG  components o Hormone sensitive lipase  Hormones can act on this to make it active or inactive  Ex. Epinephrine induces lipolysis  Triglyceride (TAG) = 3 fatty acids + glycerol   So can control how fast our fats are  Fatty acids can differ in # of carbons & saturation broken down & pushed into bloodstream o Monounsaturated: one double bond  Double bonds cause bends o Polyunsaturated: multiple double bonds  Increase dyslipidemia (altered LDL & HDL levels)  Hypertension  Type 2 Diabetes  Lipolytic rate o Stimulated by beta adrenergic recs (1,2,3) Study Schwartz et al., (2013) o Stimulated by glucocorticoids (cortisol) o Inhibition by insulin  Obesity is risk factor for developing dementia  Visceral fat: Increased density of adrenergic recs  Will there be a relationship w cognition o Also increased density of glucocorticoid recs  983 adolescents (age 12-18) o Therefore more metabolically active  From Saguenay Youth Study (SYS) o Decreased sensitivity to insulin  Measure abdominal circumference, scanned everyone w MRI, o Net effect: Increased lipolysis  passes fat thru liver measured whole body fat w electric pulse, cognitive battery test Venous portal system:  Executive fn’ing: 1. Processing Speed: Ruff 2&7 Selective Attention Test, WISC-III Symbol Search & Coding 2. Working Memory: Digit-span, Self-Ordered Pointing 3. Resistance to Interference: Stroop Colour-Word Test 4. Cognitive Flexibility: Semantic & Phonemic Fluency  Control for total body fat o Want to see if specific visceral fat affecting  Females tend to put on more fat subcutaneously  Men tend to take on more fat viscerally  Negative correlation btwn cognitive performance & visceral fat on all tasks of executive fn’ing o Unrelated to totally body fat (contributed positively) Bjorntorp (1990)  Females w low visceral fat – did better than females w more o Didn’t have this difference for males  When fat cells in abdominal cavity break down TGAs  pumped into Liver: 1. Synthesizes TGAs; secrete lipoproteins, dependent on Conclusions:  Visceral fat (-)ly associated w executive fn’ing FFA availability o consistent w past studies showing (-)ve associations o Don’t want to throw level off 2. Synthesis of glucose btwn obesity & executive fns o Stimulation by FFAs o adolescent cardiometabolic health is predictive of adult cardiometabolic health o So affect what goes out of liver 3. Insulin clearance o such visceral fat-cognition relationships could have o Inhibited by FFAs cumulative effects if elevated visceral fat persists across the lifespan, potentially resulting in dementia  Females are more sensitive to the negative impacts of visceral fat on cognition than males  Visceral fat-cognition relationships were independent of total body fat  Total body fat could be protective, when controlled for visceral fat o Elevated subcutaneous fat (when controlled for visceral fat) is associated w lower bp, triglycerides & reduced risk of the metabolic syndrome (Pausova et al., 2012; Porter et al., 2009; Demerath et al., 2008)  Adipocytes might be able to create their own hormones, like cortisol  Stress is related to more visceral fat  Fat releases estrogen-like hormones Schwartz et al., (2013)  Also since visceral fat is more metabolically active, is more sensitive to body processes – so when we lose fat, we’ll specifically lose visceral fat  Hunger on one end, Satiety on the other  When need food for survival reasons – on Hunger end Eating Pathology (prof’s lecture)  When so full you can’t eat another bite – at Satiety end Survival  Whenever you’re sort of hungry, in the middle o So why are we eating if it isn’t for survival purposes,  Carbohydrates: energy, from glucose (quicker than protein or fats) and why do we stop eating if we aren’t completely full?  Meats & Beans: protein, iron, zinc, vitamin B12 o Influences: cognitive reason, emotional reasons, social reasons, cues (sight of food), availability of food  Vegetables & Fruit: vitamins, minerals, natural sugars, fiber, vitamins  Dairy: calcium, vitamin D, protein  Physiological factors vs. other (non biological) influences of eating  Oils/Fats: trans fat & saturated = worst for you, limited the amt of unsaturated  Boundary model takes both into consideration  Satiety & hunger on the opposite ends of the spectrum  Middle range = appetitive control (nature is satisfied)  Survival isn’t always the reason we eat o Often we don’t know why...  In the middle range – psychological factors influence eating (cognitive, envt, etc) Food Guide  Indiv difs in regards to model o Everyone will have dif hunger & satiety levels at the ends of the model Social Influences 1. Social Facilitation 2. Modeling 3. Impression Management 1. Social Facilitation Clendene, Herman, & Polivy, 1994  Movie then dinner  120 female U of T undergraduates o Ate in grps of 4, pairs, or alone (control group) o Ate w strangers or friends o Each had own platter, could share w each other o Given dif bite sizes, snacks o Turkey, ham, provolone cheese, swiss cheese, white bread, rye bread, and mini-oreo cookies  Results: o Subjects in pairs (703kcal) & grps of 4 (721 kcal) consumed more than did control grp (374 kcal)  Almost double  Recommened to mostly have carbs > veggies > meat & dairy > o Subjects in grps of friend consumed more than did fats, oils, sweets subjects in grps of strangers Boundary Model o Pairs took longer to eat than did grps of 4 who took longer than the alone grp  Social facilitation occurs when we’re eating w other ppl  When ppl eat in grps they tend to eat more than they do when alone  Family dinners, out w friends  30-50% more in grps  Theories: o Time-extension hypothesis – spending more time at the meal, spending more time w the food o Special social occasions – making more food since  Just altering the type of meal (big or small) influences how ppl worried about running out  excess food are rated
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