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Nutrition [BIOL0030] > Midterm #2 > Flashcards

Midterm #2 Flashcards

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
Q

What are the two steps to protein synthesis?

A

transcription and translation

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26
Q

What happens at the end of protein digestion?

A

Nitrogen made into urea and excreted

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27
Q

Is using % dietary lipid for recommendations supported by the research literature?

A

no

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28
Q

What kind of nutrient reduces the risk of heart disease?

A

phytonutrients: plant based diet

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29
Q

What kinds of animal foods are related to heart disease risk?

A

Red meat; not dairy fat, not eggs

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30
Q

What is the main cause of red meat’s contribution to heart disease risk?

A

PUFAs: some vegetable seed oils, but mostly in red meats; increases lipid oxidation

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31
Q

What is the effect of reduced fat foods?

A

Doesn’t have same satiety effects of fat; doesn’t really show benefits for weight control

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32
Q

What are some ways of making reduced fat foods?

A

Remove, replace, or put in undigestable/unabsorbable fats instead (non-fat and skim milk; replacement with a carb; sucrose polyester Olestra, etc.)

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33
Q

What nutrients are supplied by animal and plant protein foods?

A

Animal (B vitamins and minerals, low fiber), Plant (B vitamins, fiber)

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34
Q

What is the relationship between shape and function of protein?

A

Shape determines function: hemoglobin, connective tissue, etc.

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35
Q

How can you denature proteins?

A

change in pH, heat, agitation, etc.

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36
Q

What part/form of protein passes from the intestinal lumen to the blood stream?

A

Amino acids

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37
Q

What is a food allergy?

A

absorbing the protein whole and causing an immune response

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38
Q

What are some protein functions?

A

enzymes, transport proteins, antibodies, contractile, some hormones, regulating fluid balance and acid-base balanec

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39
Q

Name two protein deficiencies

A

Kwashiorkor and Marasmus

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40
Q

What is Kwashiorkor?

A

protein-only deficiency; have enough energy but no protein, and immune system functions

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41
Q

What is marasmus?

A

Protein and energy deficiency; wasting, like in AIDS and cancer

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42
Q

How to make trans FAs?

A

hydrogenation: add hydrogens to unsat FAs; double bonds become saturated

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43
Q

What are the health issues of trans fats?

A

increase risk of heart disease and cancer

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44
Q

Where can you find trans fats?

A

in foods with long shelf life

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45
Q

What are phospholipids?

A

TGA with phosphate group (2 FAs, one phosphate on the glycerol)

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46
Q

What is the function of phospholipids?

A

emulsifiers (allow suspension of fat in water; forms micelles; detergent) and lipid bilayer

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47
Q

What are sterols?

A

lipid found in plants and animals; doesn’t dissolve in water welll; cholesterol

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48
Q

What is cholesterol?

A

sterol found only in animal foods; more than 90% of our cholesterol is in our cell membranes

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49
Q

what do we need to emulsify lipids?

A

bile

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50
Q

Where is bile stored?

A

gallbladder

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51
Q

what are lipases?

A

enzymes that remove FAs from TGs

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52
Q

what are two kinds of lipase?

A

Gastric: in stomach, but minimal digestion of lipids there; Pancreatic: digests TG into monoglyceride and 2 free FAs

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53
Q

What are lipoproteins?

A

proteins that carry water-insoluble lipids (TG, cholesterol), phospholipids;; can also transport fat-soluble nutrients; complex of the lipid and protein

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54
Q

What does the protein part of the lipoprotein do?

A

gives the lipid a charge to allow it to stay in fluid

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55
Q

What are four types of lipoproteins?

A

chylomicrons, VLDL, LDL, HLDL

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56
Q

what are chylomicrons?

A

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)

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57
Q

What do chylomicrons carry?

A

mostly diet-derived lipids; TGs, cholesterol, phospholipids, (mostly TG but can carry cholesterol)

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58
Q

What are VLDLs?

A

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

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59
Q

What does fasting TGs mean?

A

what you measure with blood test in fasting state; NOT the chylomicrons

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60
Q

What is LPL?

A

lipoprotein lipase: removes TG from VLDL and creates IDL (intermediate density LP)

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61
Q

What are LDLs?

A

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

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62
Q

What does it mean to have elevated LDL?

A

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

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63
Q

what are HDLs?

A

bring cholesterol back to liber, help decrease LDL oxidation; primarily genetically determined

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64
Q

What is the relationship between blood TG and HDL levels?

A

inverse

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65
Q

Can you increase HDLs with exercise?

A

not really; and can’t change more than 10% at all

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66
Q

What is the relationship between HDL and heart disease risk?

A

positive! HDLs are good

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67
Q

What is the function of stored lipid?

A

stored energy as TGs in adipose tissue; insulation; protection/cushioning

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68
Q

What is the function of cholesterol?

A

used to make some hormones (sex hormones, cortisol); Vitamin D; bile; component of cell membranes, only in animal foods!

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69
Q

What is the function of PUFAs?

A

essential; growth, skin integrity, fertility, structure and function of cell membranes; omega-3 and -6

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70
Q

What do Omega3/6 FAs do?

A

make eicosanoids (competition at first enzyme); hormone-like (act where synthesized)

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71
Q

What do omega-3 do?

A

decrease inflammation, clotting, BP

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72
Q

What do omega-6 do?

A

increase inflammation, clotting, BP

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73
Q

what are the health benefits of omega3?

A

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

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74
Q

what happens with an excess of oxidation from too many PUFA?

A

oxidation of DNA (cancer); LDL (atherosclerosis), and cell membranes

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75
Q

Are plant sources good sources of Omega-3/6?

A

No: they only have the 18C version, which we cannot convert to 20/22C (which we need)

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76
Q

What sources of Omega3 and Omeg6 are 20c vs 22c?

A

EPA (fish oil) and arachidonic (red meat) are 20c /// DHA (fish oil) is 22c

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77
Q

How do we get energy from TGs?

A

Beta-oxidation: breaking up the FAs in groups of 2C (acetyl-CoA)

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78
Q

What happens to lipid metabolism during feasting?

A

excess energy stored in liver as TGs (in adipose cells)

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79
Q

Where is excess lipid energy stored, and in what form?

A

In adipose cells of the liver; as TGs

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80
Q

How is excess lipid energy stored in the liver? (process)

A

LPL breaks fats into TG and stores in adipose tissue

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81
Q

What happens to lipid metabolism during fasting?

A

TGs from adipose tissue are broken down and released for energy bia HSL

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82
Q

What is HSL?

A

hormone sensitive lipase: breaks down TGs from adipose cells for energy during fasting; releases fat into the blood

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83
Q

How does insulin affect HSL?

A

Inverse – if low insulin (fasting), then HSL ON; if high insulin (feasting) then HSL OFF

84
Q

How do lipids affect health in the US?

A

Major cause of death: CVD (via excess/improper lipid intake)

85
Q

What is atherosclerosis?

A

lipids and fibrous materials deposited in artery walls; oxidized LDL taken up by scavenger pathways

86
Q

How do SFAs affect lipids/LPs?

A

Saturated fats: (ldl) UP, (hdl) UP, (tg) no change

87
Q

How do MFAs affect lipids/LPs?

A

Monounsaturated fals: (ldl) DOWN, (hdl) UP, (tg) no change (also, no oxidation of LDL)

88
Q

Do MFAs oxidize LDLs?

A

no

89
Q

How do PFAs affect lipids/LPs?

A

(ldl) DOWN, (hdl) DOWN, (tg) no change (also oxidation of LDL)

90
Q

Do PFAs oxidize LDLs?

A

yes

91
Q

How do transFAs affect lipids/LPs?

A

Worse case scenario: (ldl) UP, (hdl) DOWN, (tg) no change

92
Q

Do any types of FA affect triglycerides in the body?

A

No, just affect levels of LDL/HDL/oxidation

93
Q

What types of FAs increase/decrease LDL?

A

Increase: SFA, trans

Decrease: MFA, PFA

94
Q

What types of FAs increase/decrease HDL?

A

Increase: SFA, MFA

Decrease: PFA, trans

95
Q

Why are low-fat diets ineffective?

A

Increase carb intake to compensate, more overall calories

96
Q

What happens for lipids during excessive carb consumption?

A

No longer stored as glycogen, but rather as fat (glycolysis – acetyl-CoA – FA)

97
Q

What LP is for measuring fasting?

A

VLDL

98
Q

Explain the pathway of excess glucose stored as fat?

A

Glucose – glycolysis – acetyl-CoA – FAs – picked up by VLDLs (consequent decrease in LDLs and HDLs)

99
Q

Where does the extra glucose end up as lipid?

A

in the liver: made into TGs from FAs (increases VLDL, lower LDL)

100
Q

How is total dietary fat related to heart disease?

A

it’s not: it’s about saturated red meat fat

101
Q

What is EVOO?

A

juice of olives

102
Q

What are health benefits of EVOO?

A

decrease heart disease (BP, blood oxidation, coagulation), decrease BG, improve insulin function; independently increases HDL

103
Q

Does the USA regulate olive oil?

A

Nope

104
Q

What is nutrition transition?

A

when a country moves from less nutritive diets to more (plant-based to processed)

105
Q

What are the consequences of nutrition transition?

A

hydration and kidney function issues (excrete more nitrogen); bone hhealth issues (loss of calcium in urine), kidney stones, increased risk of CVD

106
Q

Why is red meat related to chronic disease?

A

Grilling makes HCA; EAAs increase insulin in body (disease risk); arachidonic acid PUFA; methionine increases homocysteine; increase in body weight; fewere phytonutrients

107
Q

What is PKU?

A

Phenylketonuria: inhereted genetic condition; aspartame contains phenylalanine, which cannot be metabolized (because it’s in most proteins, must screen during infancy)

108
Q

What is the approximate protein requirement for adults?

A

0.8 g/kg of body weight

109
Q

When do protein needs increase?

A

Growth, pregnancy, lactation

110
Q

How to consider protein quality?

A

Chemical/AA socre, protein digestibility-corrected AA score

111
Q

What is the Chemical/AA score?

A

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
Q

What is protein-digestibility-corrected AA score

A

another method for assessing protein quality

113
Q

What is protein complementation?

A

Combining two foods for full necessary protein amount (rice and beans, etc.)

114
Q

What nutrients are at risk with a vegan/vegetarian diet?

A

protein, B12, Ca, Vit D, Fe, Zn, I, O3FA

115
Q

When did ED get recognizes as problem?

A

mid-1800s

116
Q

When were ED recognized as mental illness?

A

1980

117
Q

What are the four main categories of ED?

A

AN, BN, EDNOS, BED

118
Q

Overall, ED are more prevalent in …

A

women than men

119
Q

Prevalence of ED is higher than…

A

Prevalence of Alzheimer’s, Schizophrenia, HIV/AIDS

120
Q

How is disordered eating potentially manifested in males, besides the typical four EDs?

A

Muscle dysmorphia: cannot be assessed using current tools

121
Q

What are the four diagnostic criteria for AN from DSM IV?

A

Refusal to maintain 85% body weight; intense fear of weight; disturbance in experience of weight/shape (denial, etc.); amenorrhea in females

122
Q

What are DSM IV’s two AN subtypes?

A

Restricting; Binge-eating/Purging

123
Q

What are the four criteria for BN from DSM IV?

A

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
Q

What are the DSM IV’s two subtypes of BN?

A

Purging vs Non-purging

125
Q

What is a particular danger of BN, esp. purging?

A

electrolyte imbalance – dangerous

126
Q

What are the changes in diagnostic criteria for AN in DSM V?

A

persistent restriction of energy intake RELATIVE TO age/gender/development/etc; ELIMINATED objective weight criterion, amenorrhea, or “refusal” to eat

127
Q

What are the changes in diagnostic criteria for BN in DSM V?

A

Change requirements of episode to discrete amount of time eating and sense of lack of control; reduced symptom frequency to once a week

128
Q

What happened to BED from IV to V?

A

included!

129
Q

What happened to EDNOS from IV to V?

A

changed into OSFED and UFED (other specific, unspecified)

130
Q

What are some risk factors for EDs?

A

genetics’ social and psychological; gender, ethnicity, athletes, bariatric candidates, adolescents

131
Q

What is ON?

A

not in DSM; “righteous eating” – more common in athletes

132
Q

How is the mortality rate for ED?

A

highest of any mental illness

133
Q

What are complications of AN?

A

bradycardia, orthostasis, hypothermia, edema, atrophy of breasts and muscles, emaciation, osteopenia, osteoporosis

134
Q

What are complications of BN?

A

bradycardia, orthostasis, dry skin, parotid gland swellin, Russell’s signs, mouth scores and dental erosion, ruptured esophagus, cardiac arrhythmia

135
Q

What are the complications of BED?

A

weight-related HT; abnormal lipid profile, diabetes/prediabetes; obesity, altered hormone secretion

136
Q

How is multidisciplinary treatment used for ED?

A

Medical stability, psychotherapy, psychiatry, nutritional

137
Q

What is the typical order of treatments in a multidisciplinary approach to EDs?

A

Medical, psychotherapeutic, psychiatric, nutritional

138
Q

What are the five levels of care for EDs in order of decreasing severity?

A

Inpatient hospitalization, residential treatment, day treatment, intensive outpatient, outpatient

139
Q

How long can treatment for severe ED be?

A

2-7 years or more

140
Q

What are some nutritional management treatment goals for EDs?

A

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
Q

What is a better way to talk about abnormal eating behavior, besides “triggers” or “addiction?”

A

Fear foods

142
Q

What is refeeding syndrome?

A

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
Q

What is the hallmark of refeeding syndrom?

A

Hypophosphatemia: rapid reduction of already-low K, Mg, P

144
Q

What are some metabolic changes associated with refeeding syndrome?

A

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
Q

What are the consequences of refeeding syndrome?

A

cardiac arrhythmias, possible death; heart failure due to electrolyte and fluid shifts that strain the heart

146
Q

How to prevent refeeding syndrome?

A

Go slow: replenish electrolytes first (establish stable biochemistry); start low and go slow; be careful with carbs

147
Q

What important ED legislation was passed in 2000/2008 nationally?

A

Parity Act for ED: serious mental illness with medical consequences, mandated coverage (but companies find loopholes)

148
Q

What has a better recovery stats, AN or BN?

A

BN

149
Q

What affects AN recovery?

A

young onset of treatment is better, longer duration of follow up is better

150
Q

What affects BN recovery?

A

Prevention of cross-over to another ED; duration of follow up strongest predictor of recovery (4-9 years)

151
Q

How is weight discrimination related to obesity?

A

Increased discrimination increases risk of suffering from obesity – discourages from seeking treatment, reduced social support, disordered eating, chronic stress

152
Q

What are hidden vs visible sources of fat?

A

Visible - you can see it; Hidden - don’t actually know how much is there (like in cupcakes)

153
Q

Why are EAAs a risk factor for CVD?

A

increase insulin secretion (insulin associated with disease - growth hormone)

154
Q

What causes oxization, the fats or the AAs in red meat?

A

The AAs!

155
Q

What is portion distortion?

A

Increase in portion sizes over the past 40 years (62% increase)

156
Q

How is body weight assessed?

A

BMI: kg/m^2

157
Q

What BMI is considered normal?

A

=< 25 kg/m^2

158
Q

What are the four energy uses?

A

BMR, physical activity, TEF, NEAT

159
Q

What is BMR?

A

basal metabolic rate: anything the body needs to function at minimal energy use; 60-70% of energy needs

160
Q

How can you change your BMR?

A

fever increases; starvation decreases

161
Q

What is the only energy use that we can control?

A

Physical activity

162
Q

What is TEF?

A

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
Q

What is NEAT?

A

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
Q

How does body energy use/storage affect weight?

A

If you use it, lose it; if you store it, gain it

165
Q

How is energy stored as fat?

A

Glucose –> pyruvate –> acetyl CoA –> FAs –> TGAs (measure as VLDL for fasting); AAs – acetyl-CoA –> FAs – TGAs

166
Q

What is the hunger obesity paradox?

A

chances of being overweight are higher if food-insecure (associated with low-income and low-education, minority populations)

167
Q

What might cause the hunger obesity paradox?

A

May overeat when food is available, may become more efficient at storing fat; erratic eating (grazing), etc.

168
Q

What is passive overconsumption?

A

overeating and energy-dense foods

169
Q

what is energy density for food?

A

calories per weight/volume of food

170
Q

What are some higher energy dense foods?

A

refined grains, products with added sugar/salt/fat; less expensive, worse for you

171
Q

What are some lower energy dense foods?

A

fruit, vegetables, whole grains; more expensive

172
Q

Why is there such a different in cost for energy density foods?

A

US gov subsidizes crops used for high energy density foods

173
Q

How can you measure energy expenditure?

A

direct calorimetry, indirect calorimetry, double-labeled water

174
Q

What is direct calorimetry?

A

measure heat produced by person

175
Q

What is indirect calorimetry?

A

gas exchange measurements

176
Q

What is double-labeled water?

A

drink water that radiated/tagged to figure out energy expenditure

177
Q

Why is excess fat related to disease risk?

A

Excess fat increases insulin, which is a risk for disease

178
Q

What are five methods for assessing body composition?

A

BIA, skinfold thickness, underwater weighing, dilution methods, radiologic methods

179
Q

What is BIA?

A

body impedance analysis: put a current through body, which is different based on fat/muscle/water composition

180
Q

What is skinfold thickness measuring?

A

Body composition: amount of fat; difficult to do properly

181
Q

What are dilution methods for body composition assessment?

A

Double-labeled water, drinking a tagged isotope, etc.

182
Q

What is apple vs pear shape?

A

If fat collects around midsection or hips/thighs (latter is better)

183
Q

What are the two types of fat in body composition?

A

Visceral (worse bc close to organs) and subcutaneous (not as bad, right underneath skin, can grab it)

184
Q

How is waist circumference related to disease risk?

A

Smaller waist means less visceral fat, which decreases risk

185
Q

How do we maintain our weight?

A

SET POINT! we resist weight change

186
Q

How can we change our set point?

A

Long-term overeating or long-term physical activity

187
Q

What’s the difference between hunger and appetite?

A

Hunger is physiological, appetite is psychological

188
Q

What two hormones help us regulate hunger short-term?

A

Ghrelin (hunger) and CCK (satiety)

189
Q

What is ghrelin? Where is it produced and used?

A

Hunger hormone released and produced in stomach; stimulates desire to eat

190
Q

What is CCK? Where is it produced and used?

A

Cholecystekinen: produced in SI and works at pancreas to send signals of satiety to brain; produced when you eat lipid/protein (not carbs)

191
Q

How we do regulate hunger long-term?

A

Leptin! (Hormone made in adipose cells)

192
Q

Where is leptin made?

A

adipose cells

193
Q

How is leptin related to hunger and weight?

A

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
Q

What is MOST LIKELY the cause of incorrect leptin function in obesity?

A

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
Q

What is thrifty metabolism?

A

Store energy really well; obesity

196
Q

What is futile cycling/adaptive thermogenesis?

A

Store energy poorly; a lot of it is lost as heat

197
Q

What is brown adipose tissue? What does it do?

A

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
Q

What is the treatment for obesity?

A

Classified as a chronic disease and treated as such; behavioral and medical changes (eating habits, bariatric surgery, etc.)

199
Q

What is considered successful weight loss?

A

If you manage to keep off 50% of the weight at least

200
Q

What are the requirements for treatment for obesity?

A

Should be overfat (not overweight); have risk factors for chronic diseases (otherwise considered metabolically-healthy obese people); motivation!!! (key component)

201
Q

What is it called when you are overfat but have no risk for other disease?

A

Metabolically-Healthy Obese People

202
Q

What should be the diet composition for weight management?

A

Higher in plants and phytonutrients, have to eat less, compliance is key, NOT low carb diets, EVOOOOOOO

203
Q

What are components of a healthy weight loss program?

A

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
Q

What are components of a fad diet?

A

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
Q

What are the five steps to weight management through behavior modification?

A

Identify antecedent, recognize behavior, see consequences, modify behavior, enjoy new consequences

206
Q

What is bariatric surgery?

A

For BMI over 35 with risk factors; altering the stomach’s capacity to reduce energy intake

207
Q

What are the three kinds of bariatric surgery?

A

Band (constrict stomach to reduce size), Sleeve (remove part of stomach), Bypass (go from stomach egg-size directly to small intestine)

Nutrition [BIOL0030] (3 decks)

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