Midterm #2 Flashcards

(207 cards)

1
Q

What determines protein structure?

A

the sequence of amino acids

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2
Q

What determines protein function?

A

Its shape, determined by primary/secondary/etc. structure

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3
Q

What is a protein?

A

one or more polypeptide chains folded into a three dimensional shape

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4
Q

Describe the connection between form and function for collagen/connective tissue proteins.

A

elongated, used to for structural benefits

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5
Q

How can you denature a protein?

A

change in pH, heat, etc.

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6
Q

What is transamination?

A

Can be used in synthesis of nonessential amino acids; transferring an amino group from one AA to another compound to create a new AA

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7
Q

What are essential amino acids?

A

AAs that the body can’t make at all/enough of, so we need to supply in diet

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8
Q

What are the four components of an amino acid?

A

H, amino, carboxyl (acid), R-side chain

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9
Q

What are the building blocks of protein?

A

Amino acids

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10
Q

Why is fever so dangerous?

A

High body temperature shuts down enzyme systems due to protein denaturation effects

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11
Q

What nutrients are in animal protein sources?

A

some B vitamins, and minerals (iron, zinc, calcium); BUT low in fiber and potentially high in fat)

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12
Q

What nutrients are in plant protein sources

A

B vitamins, minerals (iron, zinc, calcium); BUT in less absorbable forms

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13
Q

When protein is absorbed in the small intestine, what gets passed through to the blood?

A

ONLY amino acids, no peptides!

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14
Q

How are proteins related to food allergies?

A

Allergy when we absorb the protein whole instead of broken into amino acids

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15
Q

Describe the relationship between Americans and proteins.

A

Deficiency is rare, and 2/3 of dietary protein comes from animal sources

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16
Q

Describe the relationship between the rest of the world and proteins.

A

Vegans do get enough, and most of the world gets dietary protein from plant sources (grains and vegetables)

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17
Q

Describe the relationship between economic status and protein sources

A

The higher the economic status, the more animal protein you have available to eat

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18
Q

How can you use diet to reduce risk of heart disease?

A

Plant-based diets: phytonutrients

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19
Q

What food increases risk of heart disease?

A

Not saturated fat in general, but from red meats (dairy fat and eggs are okay)

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20
Q

What is the effect of PUFAs on heart disease?

A

Increase lipid oxidation and increase risk

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21
Q

What is the main source of PUFAs?

A

vegetable seed oils and red meats

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22
Q

What are reduced fat foods?

A

when fat is removed, replaced, or is a form that cannot be absorbed

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23
Q

Give some examples of reduced-fat foods

A

Nonfat/skim milk (removed), carb/protein/fat replacements (Olestra = sucrose polyester)

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24
Q

What can you make from the amino acid pool in the body?

A

energy, glucose or FAs, nitrogen-containing compounds, other amino acids

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25
What are the two steps to protein synthesis?
transcription and translation
26
What happens at the end of protein digestion?
Nitrogen made into urea and excreted
27
Is using % dietary lipid for recommendations supported by the research literature?
no
28
What kind of nutrient reduces the risk of heart disease?
phytonutrients: plant based diet
29
What kinds of animal foods are related to heart disease risk?
Red meat; not dairy fat, not eggs
30
What is the main cause of red meat's contribution to heart disease risk?
PUFAs: some vegetable seed oils, but mostly in red meats; increases lipid oxidation
31
What is the effect of reduced fat foods?
Doesn't have same satiety effects of fat; doesn't really show benefits for weight control
32
What are some ways of making reduced fat foods?
Remove, replace, or put in undigestable/unabsorbable fats instead (non-fat and skim milk; replacement with a carb; sucrose polyester Olestra, etc.)
33
What nutrients are supplied by animal and plant protein foods?
Animal (B vitamins and minerals, low fiber), Plant (B vitamins, fiber)
34
What is the relationship between shape and function of protein?
Shape determines function: hemoglobin, connective tissue, etc.
35
How can you denature proteins?
change in pH, heat, agitation, etc.
36
What part/form of protein passes from the intestinal lumen to the blood stream?
Amino acids
37
What is a food allergy?
absorbing the protein whole and causing an immune response
38
What are some protein functions?
enzymes, transport proteins, antibodies, contractile, some hormones, regulating fluid balance and acid-base balanec
39
Name two protein deficiencies
Kwashiorkor and Marasmus
40
What is Kwashiorkor?
protein-only deficiency; have enough energy but no protein, and immune system functions
41
What is marasmus?
Protein and energy deficiency; wasting, like in AIDS and cancer
42
How to make trans FAs?
hydrogenation: add hydrogens to unsat FAs; double bonds become saturated
43
What are the health issues of trans fats?
increase risk of heart disease and cancer
44
Where can you find trans fats?
in foods with long shelf life
45
What are phospholipids?
TGA with phosphate group (2 FAs, one phosphate on the glycerol)
46
What is the function of phospholipids?
emulsifiers (allow suspension of fat in water; forms micelles; detergent) and lipid bilayer
47
What are sterols?
lipid found in plants and animals; doesn't dissolve in water welll; cholesterol
48
What is cholesterol?
sterol found only in animal foods; more than 90% of our cholesterol is in our cell membranes
49
what do we need to emulsify lipids?
bile
50
Where is bile stored?
gallbladder
51
what are lipases?
enzymes that remove FAs from TGs
52
what are two kinds of lipase?
Gastric: in stomach, but minimal digestion of lipids there; Pancreatic: digests TG into monoglyceride and 2 free FAs
53
What are lipoproteins?
proteins that carry water-insoluble lipids (TG, cholesterol), phospholipids;; can also transport fat-soluble nutrients; complex of the lipid and protein
54
What does the protein part of the lipoprotein do?
gives the lipid a charge to allow it to stay in fluid
55
What are four types of lipoproteins?
chylomicrons, VLDL, LDL, HLDL
56
what are chylomicrons?
lipoprotein; transports long chain FAs into lymphatic system; delivers TGs to body's cells (carries diet-derived lipids: TGs, cholesterol, phopshoplipids, etc.; made in intestinal tract)
57
What do chylomicrons carry?
mostly diet-derived lipids; TGs, cholesterol, phospholipids, (mostly TG but can carry cholesterol)
58
What are VLDLs?
produced from the liber; takes extra energy from carbs (glucose) and protein (AAs) and catabolize to 2C acid for FA anabolism; VLDLs carry this fat from liver to body cells
59
What does fasting TGs mean?
what you measure with blood test in fasting state; NOT the chylomicrons
60
What is LPL?
lipoprotein lipase: removes TG from VLDL and creates IDL (intermediate density LP)
61
What are LDLs?
1/3 of IDL have additional TG removed and become LDLs: main carrier of blood cholesterol (if high blood cholesterol, often have high LDL); cells have LDL receptors to bring cholesterol into cell
62
What does it mean to have elevated LDL?
most likely due to genetic effect in LDL receptor; can't get it out of system; receptors mainly on liver; elevated oxidized LDLs increase risk for heart siease
63
what are HDLs?
bring cholesterol back to liber, help decrease LDL oxidation; primarily genetically determined
64
What is the relationship between blood TG and HDL levels?
inverse
65
Can you increase HDLs with exercise?
not really; and can't change more than 10% at all
66
What is the relationship between HDL and heart disease risk?
positive! HDLs are good
67
What is the function of stored lipid?
stored energy as TGs in adipose tissue; insulation; protection/cushioning
68
What is the function of cholesterol?
used to make some hormones (sex hormones, cortisol); Vitamin D; bile; component of cell membranes, only in animal foods!
69
What is the function of PUFAs?
essential; growth, skin integrity, fertility, structure and function of cell membranes; omega-3 and -6
70
What do Omega3/6 FAs do?
make eicosanoids (competition at first enzyme); hormone-like (act where synthesized)
71
What do omega-3 do?
decrease inflammation, clotting, BP
72
What do omega-6 do?
increase inflammation, clotting, BP
73
what are the health benefits of omega3?
we're inefficient at converting 18C to 20C, which we need; therefore we can't get benefit from plant products; have to get from fish: better for heart disease risk than Omega6
74
what happens with an excess of oxidation from too many PUFA?
oxidation of DNA (cancer); LDL (atherosclerosis), and cell membranes
75
Are plant sources good sources of Omega-3/6?
No: they only have the 18C version, which we cannot convert to 20/22C (which we need)
76
What sources of Omega3 and Omeg6 are 20c vs 22c?
EPA (fish oil) and arachidonic (red meat) are 20c /// DHA (fish oil) is 22c
77
How do we get energy from TGs?
Beta-oxidation: breaking up the FAs in groups of 2C (acetyl-CoA)
78
What happens to lipid metabolism during feasting?
excess energy stored in liver as TGs (in adipose cells)
79
Where is excess lipid energy stored, and in what form?
In adipose cells of the liver; as TGs
80
How is excess lipid energy stored in the liver? (process)
LPL breaks fats into TG and stores in adipose tissue
81
What happens to lipid metabolism during fasting?
TGs from adipose tissue are broken down and released for energy bia HSL
82
What is HSL?
hormone sensitive lipase: breaks down TGs from adipose cells for energy during fasting; releases fat into the blood
83
How does insulin affect HSL?
Inverse -- if low insulin (fasting), then HSL ON; if high insulin (feasting) then HSL OFF
84
How do lipids affect health in the US?
Major cause of death: CVD (via excess/improper lipid intake)
85
What is atherosclerosis?
lipids and fibrous materials deposited in artery walls; oxidized LDL taken up by scavenger pathways
86
How do SFAs affect lipids/LPs?
Saturated fats: (ldl) UP, (hdl) UP, (tg) no change
87
How do MFAs affect lipids/LPs?
Monounsaturated fals: (ldl) DOWN, (hdl) UP, (tg) no change (also, no oxidation of LDL)
88
Do MFAs oxidize LDLs?
no
89
How do PFAs affect lipids/LPs?
(ldl) DOWN, (hdl) DOWN, (tg) no change (also oxidation of LDL)
90
Do PFAs oxidize LDLs?
yes
91
How do transFAs affect lipids/LPs?
Worse case scenario: (ldl) UP, (hdl) DOWN, (tg) no change
92
Do any types of FA affect triglycerides in the body?
No, just affect levels of LDL/HDL/oxidation
93
What types of FAs increase/decrease LDL?
Increase: SFA, trans Decrease: MFA, PFA
94
What types of FAs increase/decrease HDL?
Increase: SFA, MFA Decrease: PFA, trans
95
Why are low-fat diets ineffective?
Increase carb intake to compensate, more overall calories
96
What happens for lipids during excessive carb consumption?
No longer stored as glycogen, but rather as fat (glycolysis -- acetyl-CoA -- FA)
97
What LP is for measuring fasting?
VLDL
98
Explain the pathway of excess glucose stored as fat?
Glucose -- glycolysis -- acetyl-CoA -- FAs -- picked up by VLDLs (consequent decrease in LDLs and HDLs)
99
Where does the extra glucose end up as lipid?
in the liver: made into TGs from FAs (increases VLDL, lower LDL)
100
How is total dietary fat related to heart disease?
it's not: it's about saturated red meat fat
101
What is EVOO?
juice of olives
102
What are health benefits of EVOO?
decrease heart disease (BP, blood oxidation, coagulation), decrease BG, improve insulin function; independently increases HDL
103
Does the USA regulate olive oil?
Nope
104
What is nutrition transition?
when a country moves from less nutritive diets to more (plant-based to processed)
105
What are the consequences of nutrition transition?
hydration and kidney function issues (excrete more nitrogen); bone hhealth issues (loss of calcium in urine), kidney stones, increased risk of CVD
106
Why is red meat related to chronic disease?
Grilling makes HCA; EAAs increase insulin in body (disease risk); arachidonic acid PUFA; methionine increases homocysteine; increase in body weight; fewere phytonutrients
107
What is PKU?
Phenylketonuria: inhereted genetic condition; aspartame contains phenylalanine, which cannot be metabolized (because it's in most proteins, must screen during infancy)
108
What is the approximate protein requirement for adults?
0.8 g/kg of body weight
109
When do protein needs increase?
Growth, pregnancy, lactation
110
How to consider protein quality?
Chemical/AA socre, protein digestibility-corrected AA score
111
What is the Chemical/AA score?
Method for assessing protein quality; compare EAA content of protein in a good with reference protein; the lowest AA ratio calculated in chemical score (mg of limiting AA/g test protein) // (mg limits AA/g reference protein)
112
What is protein-digestibility-corrected AA score
another method for assessing protein quality
113
What is protein complementation?
Combining two foods for full necessary protein amount (rice and beans, etc.)
114
What nutrients are at risk with a vegan/vegetarian diet?
protein, B12, Ca, Vit D, Fe, Zn, I, O3FA
115
When did ED get recognizes as problem?
mid-1800s
116
When were ED recognized as mental illness?
1980
117
What are the four main categories of ED?
AN, BN, EDNOS, BED
118
Overall, ED are more prevalent in ...
women than men
119
Prevalence of ED is higher than...
Prevalence of Alzheimer's, Schizophrenia, HIV/AIDS
120
How is disordered eating potentially manifested in males, besides the typical four EDs?
Muscle dysmorphia: cannot be assessed using current tools
121
What are the four diagnostic criteria for AN from DSM IV?
Refusal to maintain 85% body weight; intense fear of weight; disturbance in experience of weight/shape (denial, etc.); amenorrhea in females
122
What are DSM IV's two AN subtypes?
Restricting; Binge-eating/Purging
123
What are the four criteria for BN from DSM IV?
Recurrent binge-eating (at least 2x per week for 3 mo); recurrent inapprorpiate compulsive behavior to prevent weight gain; persistent concern with body weight/shape; not AN
124
What are the DSM IV's two subtypes of BN?
Purging vs Non-purging
125
What is a particular danger of BN, esp. purging?
electrolyte imbalance -- dangerous
126
What are the changes in diagnostic criteria for AN in DSM V?
persistent restriction of energy intake RELATIVE TO age/gender/development/etc; ELIMINATED objective weight criterion, amenorrhea, or "refusal" to eat
127
What are the changes in diagnostic criteria for BN in DSM V?
Change requirements of episode to discrete amount of time eating and sense of lack of control; reduced symptom frequency to once a week
128
What happened to BED from IV to V?
included!
129
What happened to EDNOS from IV to V?
changed into OSFED and UFED (other specific, unspecified)
130
What are some risk factors for EDs?
genetics' social and psychological; gender, ethnicity, athletes, bariatric candidates, adolescents
131
What is ON?
not in DSM; "righteous eating" -- more common in athletes
132
How is the mortality rate for ED?
highest of any mental illness
133
What are complications of AN?
bradycardia, orthostasis, hypothermia, edema, atrophy of breasts and muscles, emaciation, osteopenia, osteoporosis
134
What are complications of BN?
bradycardia, orthostasis, dry skin, parotid gland swellin, Russell's signs, mouth scores and dental erosion, ruptured esophagus, cardiac arrhythmia
135
What are the complications of BED?
weight-related HT; abnormal lipid profile, diabetes/prediabetes; obesity, altered hormone secretion
136
How is multidisciplinary treatment used for ED?
Medical stability, psychotherapy, psychiatry, nutritional
137
What is the typical order of treatments in a multidisciplinary approach to EDs?
Medical, psychotherapeutic, psychiatric, nutritional
138
What are the five levels of care for EDs in order of decreasing severity?
Inpatient hospitalization, residential treatment, day treatment, intensive outpatient, outpatient
139
How long can treatment for severe ED be?
2-7 years or more
140
What are some nutritional management treatment goals for EDs?
Weight restoration, elimination or reduction of symptom use; normalization of eating behavior; improving body image/acceptance; promoting healthy physical activity when appropriate, independent meal planning
141
What is a better way to talk about abnormal eating behavior, besides "triggers" or "addiction?"
Fear foods
142
What is refeeding syndrome?
problem with severe malnourishment; metabolism switches from the catabolic to anabolic state -- start building body back again; leads to severer drops in certain nutrients
143
What is the hallmark of refeeding syndrom?
Hypophosphatemia: rapid reduction of already-low K, Mg, P
144
What are some metabolic changes associated with refeeding syndrome?
Conservation of protein and use of ketone bodies switches to insulin secretion in response to increased blood sugar; depletion of intracellular minerals to maintain serum levels switches to glycogen/fat/protein synthesis (store it all); suppressed insulin and increased glucagon switch to reduction in glucose and thiamine
145
What are the consequences of refeeding syndrome?
cardiac arrhythmias, possible death; heart failure due to electrolyte and fluid shifts that strain the heart
146
How to prevent refeeding syndrome?
Go slow: replenish electrolytes first (establish stable biochemistry); start low and go slow; be careful with carbs
147
What important ED legislation was passed in 2000/2008 nationally?
Parity Act for ED: serious mental illness with medical consequences, mandated coverage (but companies find loopholes)
148
What has a better recovery stats, AN or BN?
BN
149
What affects AN recovery?
young onset of treatment is better, longer duration of follow up is better
150
What affects BN recovery?
Prevention of cross-over to another ED; duration of follow up strongest predictor of recovery (4-9 years)
151
How is weight discrimination related to obesity?
Increased discrimination increases risk of suffering from obesity -- discourages from seeking treatment, reduced social support, disordered eating, chronic stress
152
What are hidden vs visible sources of fat?
Visible - you can see it; Hidden - don't actually know how much is there (like in cupcakes)
153
Why are EAAs a risk factor for CVD?
increase insulin secretion (insulin associated with disease - growth hormone)
154
What causes oxization, the fats or the AAs in red meat?
The AAs!
155
What is portion distortion?
Increase in portion sizes over the past 40 years (62% increase)
156
How is body weight assessed?
BMI: kg/m^2
157
What BMI is considered normal?
=< 25 kg/m^2
158
What are the four energy uses?
BMR, physical activity, TEF, NEAT
159
What is BMR?
basal metabolic rate: anything the body needs to function at minimal energy use; 60-70% of energy needs
160
How can you change your BMR?
fever increases; starvation decreases
161
What is the only energy use that we can control?
Physical activity
162
What is TEF?
Thermic effect of food: diet-induced thermogenesis; if you eat fewer larger meals, not snacks (keep more energy from the snacks, requires more energy relative to food amount of digest larger meals)
163
What is NEAT?
non-exercise activity thermogenesis; overeating and regulating body heat; two groups (if you fidget, will have higher NEAT); cooler environment means need more calories to stay warm
164
How does body energy use/storage affect weight?
If you use it, lose it; if you store it, gain it
165
How is energy stored as fat?
Glucose --> pyruvate --> acetyl CoA --> FAs --> TGAs (measure as VLDL for fasting); AAs -- acetyl-CoA --> FAs -- TGAs
166
What is the hunger obesity paradox?
chances of being overweight are higher if food-insecure (associated with low-income and low-education, minority populations)
167
What might cause the hunger obesity paradox?
May overeat when food is available, may become more efficient at storing fat; erratic eating (grazing), etc.
168
What is passive overconsumption?
overeating and energy-dense foods
169
what is energy density for food?
calories per weight/volume of food
170
What are some higher energy dense foods?
refined grains, products with added sugar/salt/fat; less expensive, worse for you
171
What are some lower energy dense foods?
fruit, vegetables, whole grains; more expensive
172
Why is there such a different in cost for energy density foods?
US gov subsidizes crops used for high energy density foods
173
How can you measure energy expenditure?
direct calorimetry, indirect calorimetry, double-labeled water
174
What is direct calorimetry?
measure heat produced by person
175
What is indirect calorimetry?
gas exchange measurements
176
What is double-labeled water?
drink water that radiated/tagged to figure out energy expenditure
177
Why is excess fat related to disease risk?
Excess fat increases insulin, which is a risk for disease
178
What are five methods for assessing body composition?
BIA, skinfold thickness, underwater weighing, dilution methods, radiologic methods
179
What is BIA?
body impedance analysis: put a current through body, which is different based on fat/muscle/water composition
180
What is skinfold thickness measuring?
Body composition: amount of fat; difficult to do properly
181
What are dilution methods for body composition assessment?
Double-labeled water, drinking a tagged isotope, etc.
182
What is apple vs pear shape?
If fat collects around midsection or hips/thighs (latter is better)
183
What are the two types of fat in body composition?
Visceral (worse bc close to organs) and subcutaneous (not as bad, right underneath skin, can grab it)
184
How is waist circumference related to disease risk?
Smaller waist means less visceral fat, which decreases risk
185
How do we maintain our weight?
SET POINT! we resist weight change
186
How can we change our set point?
Long-term overeating or long-term physical activity
187
What's the difference between hunger and appetite?
Hunger is physiological, appetite is psychological
188
What two hormones help us regulate hunger short-term?
Ghrelin (hunger) and CCK (satiety)
189
What is ghrelin? Where is it produced and used?
Hunger hormone released and produced in stomach; stimulates desire to eat
190
What is CCK? Where is it produced and used?
Cholecystekinen: produced in SI and works at pancreas to send signals of satiety to brain; produced when you eat lipid/protein (not carbs)
191
How we do regulate hunger long-term?
Leptin! (Hormone made in adipose cells)
192
Where is leptin made?
adipose cells
193
How is leptin related to hunger and weight?
When you lose weight, decrease adipose tissue so decrease amount of leptin (decreased satiety, makes you hungrier and gain the weight back); when you gain weight, increase adipose tissue so increase leptin (more satiety, don't continue to gain weight or even lose weight because of decreased hunger)
194
What is MOST LIKELY the cause of incorrect leptin function in obesity?
Receptors are broken -- can't read satiety or hunger signals; it's not just a matter of providing more leptin, because the receptors can't recognize
195
What is thrifty metabolism?
Store energy really well; obesity
196
What is futile cycling/adaptive thermogenesis?
Store energy poorly; a lot of it is lost as heat
197
What is brown adipose tissue? What does it do?
Higher in mitochondria content; produces more heat; we lose it because we most likely "phased out" the need for it by having external temperature regulation; prevalent in babies
198
What is the treatment for obesity?
Classified as a chronic disease and treated as such; behavioral and medical changes (eating habits, bariatric surgery, etc.)
199
What is considered successful weight loss?
If you manage to keep off 50% of the weight at least
200
What are the requirements for treatment for obesity?
Should be overfat (not overweight); have risk factors for chronic diseases (otherwise considered metabolically-healthy obese people); motivation!!! (key component)
201
What is it called when you are overfat but have no risk for other disease?
Metabolically-Healthy Obese People
202
What should be the diet composition for weight management?
Higher in plants and phytonutrients, have to eat less, compliance is key, NOT low carb diets, EVOOOOOOO
203
What are components of a healthy weight loss program?
Control of energy (calories do count), diet composition doesn't really matter much, but compliance is key; not low-fat (else hungry), SLOW weight loss (1-2 lbs/week), have to change behavior, have to increase energy expenditure (to change set point)
204
What are components of a fad diet?
Don't require a change in eating habits, restrict/focus on certain kinds of foods, selling a product, advertised by a celebrity, disregard/criticize science; promise fat/targeted weight loss
205
What are the five steps to weight management through behavior modification?
Identify antecedent, recognize behavior, see consequences, modify behavior, enjoy new consequences
206
What is bariatric surgery?
For BMI over 35 with risk factors; altering the stomach's capacity to reduce energy intake
207
What are the three kinds of bariatric surgery?
Band (constrict stomach to reduce size), Sleeve (remove part of stomach), Bypass (go from stomach egg-size directly to small intestine)