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49 Cards in this Set
- Front
- Back
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Insulin/Diabetes
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The hormone made by the pancreas that allows glucose to enter the cells.
Type 1: Lack of Insulin Type 2: Cell does not hear the Insulin |
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Excess Glucose
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Damage to artery walls which leads to cardiovascular disease, poor circulation, loss of eyesight and risk of infection.
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Glycogen
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The body's storage form of carbohydrates. 1600 calories are stored in muscle and liver. Lasts about 24-36 hours at rest, 2-3 hours during exercise.
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Anaerobic
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"Without Oxygen" - Breakdown from C6 glucose to C3 glucose
-Brain and central nervous system uses glucose for fuel anaerobically -Body needs energy when there is no oxygen. Can be used for short time during exercise. Fat and protein can not be utilized this way. |
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Aerobic
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"With Oxygen" - Breakdown from C3 glucose to C2 glucose
- Muscles and most cells uses glucose for fuel aerobically - This is a one way process |
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End Product of Carbohydrate Energy Metabolism
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Energy (4kcal/g) + CO2 + H2O
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Carbohydrate Excess
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Glucose is broken down to C2 units and converted to and stored as fat
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A carbohydrate deficiency may occur when:
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- During a fast
- low carb diet - Insulin is lacking so that glucose does not get in the cells |
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Function of Fat
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Energy: 9kcal/g
Regulation: Sex hormones and essential fats (prostaglandin) Structure: Insulation and cell membrane structure |
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Triglycerdies
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The chemical form in food fat and body fat. Consists of 3 fatty acids and glycerol (carbon backbone)
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Fatty Acids
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- Two categories (saturated and unsaturated)
- Long chains of carbon that are typically even in number range from 4 to 26 |
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Saturated Fatty Acids
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- Each carbon fully saturated with hydrogen
- Straight and stiff (no C-C double bond) - Solid at room temperature |
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Unsaturated Fatty Acids
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- Each carbon is not fully saturated with hydrogen
- Contains one (mono) or more (poly) C-C double bonds - Liquid at room temperature - Chemically unstable and susceptible to oxidation (rancidity) |
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Essential Fatty Acids
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18:2 linoleic acid - carbon double bond sixth from left (two in total)
ex: corn oil 18:3 linolenic acid - carbon double bond sixth from left (three in total) ex: flaxseed oil Role in health: Maintain cell membrane structure and make prostaglandins which mediate blood clot formation and inflammatory response. |
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Hydrogenation
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- Process of adding hydrogens to double bonds of unsaturated fatty acids which removes bonds and makes it saturated (trans fat)
- Makes it more resistant to oxidation, but loses EFA. - Does not change cholesterol or calorie content. |
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Animal vs Vegetable Fats
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Animal greater in saturated fat, vegetable greater in unsaturated fat (vegetables higher EFA and liquid at room temp)
Exceptions for animal: Fish, Chicken, Egg Exceptions for vegetable: Coconut, Palm Oil |
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Emulsification
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This process allows fat to be accepted by the body. Water and fat don't mix which influences digestion, absorption and transport.
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Fat Digestion
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- Triglycerides mix with substance called bile (made from cholesterol in the liver) to emulsify the fat
- Lipase (secreted in pancreas) chemically digests triglycerides. It breaks off the fatty acids leaving monoglycerides (single fatty acid attached to the glycerol) - Fat droplets form micelles, which is a combination of fatty acids and monoglycerides. They migrate to surface of small intestine and are absorbed. |
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Fat Absorption
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Once micelles are absorbed, the triglycerides reform. A protein coat is put on the outside of the triglyceride so it can be transported. This fat and protein combination is called a chylomicron (a lipoprotein).
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Fat Transport
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- The chylomicron (dietary fat) circulates in the blood, delivering TG to tissues (muscle and adipose). It also travels to the liver where it is repackaged to form a VLDL.
- The VLDL is released and circulates in the blood, delivering TG to tissues (muscle and adipose). Loss of some TG transforms the VLDL into an LDL - The LDL drops off cholesterol at cells and returns to liver - The liver also forms HDL which it releases into the blood. HDL receives cholesterol from LDL and travels back to the liver |
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Fat Energy Metabolism
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Fatty Acids contains potential energy and are broken down into C2 units. The end product is:
Energy (9kcal/g) + CO2 + H2O |
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Olestra
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- Fat Replacement (along with protein, starch, mono and triglyceride fats and water)
- not digestible - made from sugar and fatty acids - reduces absorption of fat soluble minerals - 0 calories |
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Cholesterol Functions
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A fatty, waxy-like substance in the body and is handled like fat
Functions: Precursor to bile, sex hormones, vitamin D and component of cell membrane structure. However, it is not essential. |
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Energy Metabolism (After eating a meal)
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Following a meal, energy nutrients are put away into storage.
Carbohydrate (Glucose) - stored as glycogen in muscle and liver. Excess is converted to fat. Fat (triglyceride) - stored as body fat cells. Protein (Amino Acids) - Used for protein replacement needs. Excess amino acids are stripped of their nitrogen (goes into urine) and carbon skeleton is converted into fat. |
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Energy Metabolism (Several hours after eating)
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Energy nutrients are brought out of storage when you haven't eaten for several hours.
Carbohydrate (Glycogen) - Glycogen is broken down to glucose and moves out into the circulation. Used for brain energy and fuel. Fat (fat stores) - Triglycerides are taken out of storage and broken into C2 units and are then used as energy. Protein - Not touched since you have enough carbohydrate fuel |
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Energy Metabolism (Without food for at least 24 to 36 hours)
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With fasting, glycogen stores in both the liver and muscle have run out
Carbohydrate - stores of glycogen run out Protein (Amino Acid) - Nitrogen is disposed of through urine. Carbon skeletons are converted to C3/C2 units, and the C3 units are glued together to form glucose. It is then sent out into the circulation to fuel the brain and other needy tissues. Fat (fat stores) - used for energy. Ketones form as C2 units because carbohydrates are lacking to turn the cycle efficiently. |
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Coronary Artery Disease:
Risk Factors |
Cigarette smoking
Hypertension Hypercholesterolemia (high LDL; low HDL) Diabetes Heredity Increasing age Obesity (abdominal fat) Male sex Inactivity Dietary factors |
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Optimal cholesterol levels
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Overall: <200mg/dL
LDL: <100mg/dL HDL: >65mg/dL |
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Coronary Artery Disease:
Dietary factors |
Total fat intake: less than 30%
Type of fat: Saturated and trans fat under 10% (raise LDL). Monosaturated 10-20% (lower LDL). Polysaturated fat under 10% (lower LDL, HDL). Cholesterol: <300 mg/day Fiber: >25g/day Soduim: <2400mg/day Limit alcohol intake Achieve healthy weight Exercise |
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Daily Value for Total Fat and Saturated Fat
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Total Fat: 65 grams
Saturated Fat: 20 grams |
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Metabolic Syndrome
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NCEP consider a cluster of certain coronary artery disease risk factors to determine risk for heart disease.
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Obesity
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1. Condition of excess body fat that
2. Results in adverse health effects. 3. Classification: Body weight > 20% above desirable Body fat > 20-25% men > 30% women |
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BMI
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Weight (KG)/Height2 (M)
Normal 18-25 Overweight 25-29 Obese 30+ |
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Lower-Body Obesity
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-Pear shaped
-Excess fat stored in hips and thighs -Common in women -This fat is resistant to weight loss -No significant health risk |
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Upper-Body Obesity
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-Apple shaped
-Excess fat stored in abdomen -Common in men -Greater risk of health problems -Visceral fat is near vital organs |
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Determining Upper-Body Obesity
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Waist-to-hip ratio indicator of abdominal obesity
Men: >.95 Women: >.80 |
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Obesity Health Risks
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1. Cardiovascular disease
2. Hypercholesterolemia 3. Hypertension 4. Diabetes 5. Cancer (certain types) 6. Osteoarthritis 7. Emotional disturbances |
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Lipoprotein Lipase (and influencing factors)
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Enzyme vital to storage of triglycerides in adipose cells.
-LPL activity increases at certain fat depot sites (hips anc thighs) -LPL activity increases during hormone changes (pregnancy) -LPL activity increases during weight loss -LPL activity decreases during exercise |
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Fat Cell Development
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- 3rd trimester of pregnancy
- Adolescent growth spurt 12-14 yrs. - Once a fat cell is made, it does not go away. With weight loss, fat cells shrink but they do not go away. - During critical period can cause increase in cell number and size. During adult years results in increase cell size and sometimes cell number |
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Food Intake Control
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The basics of why we eat. The body is designed to defend against weight loss.
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Food Intake Control
1. Central Nervous System |
-Brain Centers (hypothalamus)
-Brain Chemicals (serotonin) |
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Food Intake Control
2. Peripheral Factors |
-Hormones
-Fat mass and cell size (leptin sginals the brain) -Stomach signals -Exercise (increases) |
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Food Intake Control
3. Conditions/Diseases |
-Pregnancy and breast-feeding
-Obesity -Eating disorders -Cancer -Psychological disturbances |
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Food Intake Control
4. External Factors |
-Time of day
-Temperature (when cold) -Eating cues (buffets) |
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Obesity Causes
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1. Calorie imbalance-kcal in >kcal out i.e. consumption of calories in excess of need, leading to increased fat stores
2. Inactivity- decreased calorie expenditure, lower BMR, positive kcal balance leading to increased fat stores (kcal out < kcal in) 3. Genetic Influence: 40-60% of all obesity is due to genetics, the chance of becoming obese is greater if a parent is obese. 4. Thrifty metabolism: Decreased BMR kcal out < kcal in increased fat stores 5. Set point: the body strives to maintain fat cell size/mass; if fat cell size reduces, mechanisms encourage fat cell “filling” and fat gain 6. Meal pattern- skipping meals may increase fat stores by encouraging greater fat storage 7. Meal composition- high fat diet may increase fat stores since food fat is preferentially stored and it’s easier to consume more calories with high fat foods/diet |
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3 components to successful weight loss
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1. Reduced energy diet (get nutrients, minimize fatigue and hunger, meeting individual tastes)
2. Behavior modification (changing eating behavior, understanding response to environmental cues, cognitive restructuring) 3. Physical activity or exercise (food intake control, weight and fat loss, increased BMR, weight maintenance, improved sense of well-being, disease prevention) |
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Poor Obesity Treatments
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-Very low-calorie diets
-Special formulas or products -Extremes in macro nutrient restrictions -Surgery -Drug therapy |
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Anorexia Nervosa
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Self induced starvation
-Fear of becoming fat -Distorted body image -Body weight 15% below expected -Amenorrhea (loss of regular menstrual cycle) -low calorie intake and therefore, nutrient deficiencies: Protein Calcium Zinc Iron Vitamins |
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Bulimia
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Recurrent episodes of binge eating and purging
-Starts with dieting to loose weight by restricting food intake and types of foods -After a period of restricted eating, they “give in”, and binge eat -This is followed by guilt from loss of control, then purging -Occurs 2 times wk in 3 mths Risks: -Potassium loss -Fat-soluble vitamin loss (use of laxatives) -Teeth erosion due to stomach acid -Heat and organ failure |
