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Human Nutrition > Exam > Flashcards

Exam Flashcards

1
Q

What Factors influence your diet?

A

Food preferences, availability, convenience, cost, culture/ religion, and overall health

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2
Q

Function of Carbohydrates

A

the primary energy source for all cells in the body, the sole source of energy for brain function, includes fibers vitamins, and minerals

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3
Q

Function of Fats

A

Facilitates absorption of fat-sol;uble vitamins, production of hormones

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4
Q

Function of protein

A

building block for all tissues, production of hormones and enzymes

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5
Q

Reasons to change your diet (5)

A

Fat loss, muscle gain, exercise performance, nutrient deficiency, overall health

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6
Q

Ways to expend energy

A

Basal metabolic rate, exercise activity, non-exercise activity, thermic effect of food

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7
Q

Def: Neutral Energy Balance

A

When energy in = energy out

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8
Q

Def: Positive Energy Balance

A

Energy in is greater than energy out (caloric surplus)

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9
Q

Def: Negative Energy balance

A

energy in is less than energy out (caloric deficit)

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10
Q

Ketogenic Diet

A

Mostly fats low carbs

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11
Q

Whole 30

A

Eat vegetables, fruit, nuts, oils, seeds, seafood and meat, dont eat grains, dairy, sugar, legumes and processed food

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12
Q

Intermittent fasting

A

Fast for a certain period of time and then eat for a certain period of time

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13
Q

Macro Tracking

A

Track what you are consuming

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14
Q

How to preserve muscle while losing fat

A

Adequate dietary protein (1.4g/kg), resistance training and appropriate rate of weight loss

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15
Q

How to assess effectiveness of a diet

A

is it practical, flexible, sustainable, working. Need to strategize, implement, evaluate and assess constantly

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16
Q

Factors effecting protein quality

A

Digestibility and amino acid composition

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17
Q

Def: Digestibility

A

The ability to digest and absorb the protein in a given food

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18
Q

Digestibility of Animal Protein

A

90-99%

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19
Q

Digestibility of soy and legume protein

A

less than 90%

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20
Q

digestibility of plant protein

A

70-80%

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21
Q

Def: Complete protein sources

A

Protein sources that contain all essential amino acids

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22
Q

Complete protein sources examples

A

all animal based proteins, quinoa, soy and whey

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23
Q

What does PDCAAS stand for?

A

Protein digestibility-corrected amino acid score

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24
Q

What is PDCAAS?

A

scale of protein quality that goes from 0 to 100

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25
Q

What is the PDCAAS of Dairy, egg whites, beef and chicken

A

100

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26
Q

What is the PDCAAS of soybeans

A

94

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27
Q

What is the PDCAAS of legumes

A

50s and 60s

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28
Q

What is the PDCAAS of gluten (wheat protein)

A

25

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29
Q

Def: Complementary Proteins

A

Combining plant proteins with various essential amino acids to create full amino acid complement

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30
Q

Recommendation of CFG regarding protein

A

Eat plant based proteins more often

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31
Q

Reasons of eating plant based protein

A
  1. plant-based proteins create significantly lower greenhouse gas emissions
  2. low quality can be overcome by consuming complimentary proteins
  3. plant-based diet reduces risk of diabetes and cardiovascular disease
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32
Q

How does a plant-based diet reduce risk of diabetes and cardiovascular disease

A

decreased saturated fat, increased fiber, decreased cholesterol and more conscious abut nutrient consumption due to restricted diet

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33
Q

Def: Vegan

A

No animal productd

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34
Q

Def: Lacto-ovo vegetarian

A

consume eggs and dairy

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35
Q

Def: Pesco vegetarian

A

consume fish, eggs and dairy

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36
Q

Def: Semi-vegetarian

A

consume dairy and eggs and red meat/poultry once a week

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37
Q

Def: Protein-energy undernutrition (PEU)

A

Insufficient intake of protein, energy or both

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38
Q

Impacts of (PEU)

A

Poor growth (height and/or weight) in children, infections from degradation of antibodies

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39
Q

Marasmus

A

prolonged period with out enough protein, occurs in babies less than 2 years, slow onset, skin and bones

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40
Q

Kwashiorkor

A

Sudden change in protein levels, occurs usually around 1 to 3 years, rapid onset (during weening), causes edema (including swollen belly)

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41
Q

How to reverse PEU

A

Rehydration, electrolyte balance, gradually add protein to diet

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42
Q

Infections caused by PEU

A

Dysentery, anemia, heart failure and death

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43
Q

Protein recommendations

A

AMDR 10-35% of total daily energy intake

RDA 0.8g/kg body weight/ day

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44
Q

Def: Nutrigenetics

A

Examines how gens influence the activities of nutrients

nutrient absorption, nutrient use and metabolism, nutrient requirements and food and nutrient tolerances

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45
Q

Def: Nutrigenomics

A

Examines how nutrients influence the activities of genes

gene mutation, gene expression and gene programming

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46
Q

Def: Nutritional Genomics

A

Examines the interactions of genes and nutrients, including both nutrigenetics and nutrigenomics

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47
Q

Single Gene disorders

A

mutations inherited at birth, influences a single gene, damage to the individual exerted early in life

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48
Q

Multigene disorders

A

influence several genes, sensitive to interactions with the environment

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49
Q

Single Nucleotide polymorphisms

A

Change to a single nucleotide in a DNA sequence

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50
Q

Transcription

A

From DNA to RNA

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51
Q

Translation

A

from RNA to polypeptide chain

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52
Q

Gene expression

A

Genes switched on and off through methylation, expressed goes form DNA to mRNA to tRNA to proteins

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53
Q

Pathway of eating impacting gene expression

A
  1. Nutrients or phytochemicals consumed
  2. Directly interact with genetic signals to turn on or off a gene or indirectly interact with genetic signals through substances generated during metabolism
  3. Gene is activated of silenced
  4. Protein synthesis increases or decreases
  5. leads to affect of individuals health such as disease prevention or progression
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54
Q

Anabolic reactions

A

Building reactions, requires energy

ex: glu+glu=gycogen, Glycerol+fatty acid=triglyceride, AA+AA=protein

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55
Q

Catabolic reaction

A

Breaking down, releases energy

ex: glycogen= Glu, trigly=Glycerol+fatty acid, protein=AA

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56
Q

ATP

A

High energy storage compound that captures energy, holds energy through negative charges of phosphates that are vulnerable to hydrolysis, cleaving P groups releases energy

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57
Q

Enzymes

A

almost always required, facilitates reactions, remains unchanged

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58
Q

Coenzymes

A

Complex, organic molecules, not proteins, associated with enzymes, required for enzyme function (E.g. Vitamins)

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59
Q

Pyruvate

A

3-C structure, can be used to make glucose in the liver

60
Q

Acetyl CoA

A

2-C structure, cannot make glucose

61
Q

How does protein enter the metabolism cycle

A

AA can enter as pyruvate, acetyl CoA or into the TCA cycle

62
Q

How does carbohydrates enter the metabolism cycle

A

Glucose to pyruvate (can go back and fourth)

63
Q

How do fats enter the metabolism cycle

A

Glycerol enters as pyruvate and fatty acids enter as acetyl CoA

64
Q

Glycolysis

A

Starts as glucose, Required ATP to start, 6C split into 2 3C, Net ATP production, Hydrogen attaches to coenzyme (NADH) ends in pyruvate

65
Q

Anaerobic pyruvate

A

Converted into lactate when there is not enough oxygen, coenzyme returns H allowing it to grab more, ATP is used in the liver to convert lactate into glucose (shift the burden of energy use to the liver over the muscles)

66
Q

Aerobic pyruvate

A

pyruvate enters the mitochondria, a carbon is removed to convert to acetyl CoA (irreversible) process

67
Q

Acetyl CoA options

A

Can be converted into fat or can make energy though the TCA Cycle

68
Q

Converting Fatty acids to Acetyl CoA

A

oxidize 2 carbons at a time, releases a H in process (more energy), requires oxygen

69
Q

Glucogenic vs ketogenic

A

ketogenic can only be converted into acetyl CoA, gulcogenic can be converted to pyruvate and other glucose precursors

70
Q

Glucogenic entry points

A

As pyruvate or into TCA cycle (need deamination first)

71
Q

Ketogenic entry points

A

Acetyl CoA (need deamination first)

72
Q

TCA cycle

A

acetyl CoA comines with oxaloacetate (from carbs) produces H which attach to coenzymes that are sent to the Electron transport chain

73
Q

Electron Transport Chain

A

accepts electrons form NADH using oxygen to produce ATP and Water, occurs in the inner mitochondrial membrane

74
Q

Alcohol Metabolism

A

Absorbed through the stomach walls and small intestine, liver breaks down alcohol with alcohol dehydrogenase (ADH), produces acetyl CoA and NADH, which is most often converted into fat due to the livers low metabolic needs

75
Q

Macronutrient uses post-prandial

A

carbs - stored, fats - used first, protein -build protein in body

76
Q

Priorities for excess CHO

A
  1. Fill glycogen stores
  2. Used for energy
  3. Converted to fat
77
Q

Priorities for excess Protein

A
  1. Body proteins
  2. Used for energy
  3. Converted to fatty acids
78
Q

Priorities for excess Fat

A
  1. Use for energy

2. Store

79
Q

Post-absorptive (2-3 hours)

A

break down liver and muscle glycogen stores and body fat stores for energy use

80
Q

Beyond Glycogen completion

A

Body protein broken down and converted into glucose to supply, brain, nervous system and red blood cells and protein and fats broken down to provide energy for other cells

81
Q

Prolonged fasting

A

acetyl CoA broken down to make ketone bodies to fuel tissues and brain, energy is conserved by reducing metabolic functions and suppressing appetite, energy used from all sources not just target fat loss

82
Q

Result of changes in energy balance

A

Rapid water changes and gradual fat changes

83
Q

Def: Appetite

A

Psychological and physical cues (see food, know popcorn at movies even though not actually hungry)

84
Q

Def: Hunger

A

Physiological response, hypothalamus, presence or absence of nutrients in blood, can be overridden

85
Q

Def: Satiation

A

Stop eating, feeling of fullness

86
Q

Def: Satiety

A

opposite to hunger, sensing nutrients in blood, do not start eating again, overriding factors include stress, boredom, favorite food, social cues

87
Q

Food Intake cycle

A
  1. Hunger (psychological influences)
  2. Seek food and start meal (sensory influences)
  3. Keep Eating (Cognitive influences)
  4. Satiation - end meal (postingestive influences)
  5. Satiety - several hours later (postabsorpitive influences)
88
Q

Physiological influence of food intake

A 
empty stomach
gastric contractions
absence of nutrients in small intestine
GI hormones
Endorphins are triggered by the smell, sight or taste of foods, enhancing the desire for them
89
Q

Sensory influences of food intake

A 
Thought
sight
smell
sound
taste of food
90
Q

Cognitive influence of food intake

A

Presence of others/ social stimulation
Perception of hunger/awareness of fullness
Favorite foods/ foods with special meanings
Time of Day
Abundance of available food

91
Q

Postingestive influences of food intake

A

food in stomach triggers stretch receptors

nutrients in small intestine elicit hormones (CCK)

92
Q

Postabsorptive influence of food intake

A

nutrients in the blood signal the brain about their availability, use and storage
nutrients dwindle, satiety diminishes
hunger develops

93
Q

Components of energy expenditure

A
  1. Basal metabolism - basal metabolic rate and resting metabolic rate (50-65%)
  2. physical activity (highly variable) (30-50%)
  3. Food consumption - thermic effect of food (10%)
  4. adaptation responses
94
Q

Factors increasing BMR

A

Height, growth, body composition, fever, stress, environmental temperature (increases at both extremes), hormones

95
Q

Factors decreasing BMR

A

age, fasting/starvation, malnutrition, sleep

96
Q

Influences of estimating energy requirements

A

sex, growth, age, physical activity, body composition and size

97
Q

Low-Carbohydrate diet

A

Uses glycogen stores first, then body proteins through gluconeogenesis, ketones found in urine from incomplete breakdown of fat, causes rapid weight loss due to glycogen loss, lean muscle loss, fluid loss and some fat loss

98
Q

Ketogenic diet for athletic performance study

A

3 groups - high CHO, periodized CHO and ketogenic diet (tested over 3 week training camps with 2 workouts a day)
ketogenic diet performed worse, was less efficient, more oxygen required for the same race speed

99
Q

Ketogenic Diet on Bone Health

A

Preliminary research showed reduced markers of bone health after just 3.5 weeks, values did not fully rebound when returned to normal diet

100
Q

Total body mass

A

includes body fat (makes up about 20%), muscle, bones and organs

101
Q

Lean body mass

A

includes muscle, bones and organs

102
Q

lean soft tissue mass

A

includes muscles and organs

103
Q

Total body muscle mass

A

includes muscle

104
Q

Body fat composition distribution

A

ideal amount depends on gender (F25% - 12% essential, M15% - 3% essential)

105
Q

Body fat location distribution

A

Visceral fat - surrounds vital organs causes central obesity

Subcutaneous fat- other regions

106
Q

Waist circumference as an indication of visceral fat

A

women less than 35 in

men less than 40 in

107
Q

Apple shape

A

android obesity, high health risk

108
Q

Pear shape

A

gynoid obesity, less high health risk, may even improve health

109
Q

Methods to assess body fat

A

Waist circumference - common with healthcare practitioners
Skinfolds - at several sites
Bioelectrical impedance - fat provides more resistance to electrical current ( more accurate than above)
Dual energy x-ray absorptiometry (DEXA) - low dose x-ray, gold standard
MRI- also gold standard, used to compare and contrast with DEXA

110
Q

Body Mass Index (BMI)

A

relative weight for height weight in kg /height in m^2

based on population averages, related to disease risk, increased accuracy with waist measurements

111
Q

BMI Classifications

A

Underweight: < 18.5
Healthy Weight: 18.5 to 24.9
Overweight: 25.0 to 29.9
Obese: 30.0+

112
Q

Obesity

A

Excess or abnormal body fat that can impair health

113
Q

Obesity Diagnosis

A

Anthropometric - BMI, waist circumference, boy fat %, body fat location
and
Impact on health - BP, lipids, glucose, physical symptoms, psychopathology, functional limitations/well being

114
Q

Obesity prevalence

A

Obesity prevalence increasing, overweight prevalence remain the same (overweight becoming obese)

115
Q

Health Risks associated with being over wieght

A

CVD, diabetes, cancer, inflammation and metabolic syndrome, increase mortality rate

116
Q

BMI affect on mortality

A

BMI 22.5-24.9 = optimal survival
BMI 30-34.9 = 3 years loss of life
BMI greater than 40 = 10 years loss of life

117
Q

Social and psychological affects of obesity

A

Discrimination and judgment
perceived laziness and lack of self-control
embarrassment, rejection, shame and depression

118
Q

Fit fat paradox

A

Being overweight but fit counteracts increased risks and is healthier than normal weight unfit individuals

119
Q

Health risks associated with underweight

A

fighting against wasting diseases (lack of energy stores)
menstrual irregularities and infertility
osteoporosis and bone fractures
increased risk of mortality

120
Q

Fat Cell development

A

Energy in greater than energy out causes it to be stored as adipose tissues, body fat reflected in number of fat cells - grow must rapidly in first year, obese individuals have more fat cells
increase # of cells then cells increase in size then increase # of cells again
when lose fat # of cells remain

121
Q

Lipoprotein Lipase (LPL)

A

Uptake of triglycerides into tissues, higher in obese people (Predisposed, have more LPLs), active in varying body regions depending on sex, weight loss increases activity

122
Q

Set-point theory

A

Body likes to maintain homeostasis even with weight, adjusts to original weight, increased metabolism during weight gain and reduce metabolism during weight loss

123
Q

genetic causes of overweight and obesity

A

genetics may determine a predisposition to obesity, identical 2 x more likely to be same weight, but genes interact with diet and physical activity

124
Q

ob gene

A

Codes for leptin protein produced in adipose tissue, nicknamed obesity gene, promotes negative energy balance by suppressing appetite and increases energy expenditure, mutations are rare, leptin resistance

125
Q

Adiponectin

A

protein regulation energy homeostasis
Lower concentration in obesity
secreted from adipose tissue
increases insulin sensitivity

126
Q

Ghrelin

A

protein regulation energy homeostasis
Increases in concentration with fasting, decreases after a meal
Secreted form the stomach
Stimulates appetite

127
Q

Leptin

A

Protein regulation energy homeostasis
high concentration in obesity
secreted from adipose tissue
suppresses appetite and increases energy expenditure

128
Q

PYY

A

Protein regulation energy homeostasis
increases in concentration after a meal
Secreted form the CNS and GI tract
suppresses appetite

129
Q

Types of fat

A

white adipose tissue - stores fat for other tissues to use, main type for fat in adults
Brown adipose tissue - releases stored fat as heat, abundant in newborns, lots of mitochondria, activated by uncoupling proteins

130
Q

Environmental causes of overweight and obesity

A

Overeating - abundance of high kcal, inexpensive, tasty and advertised foods
Physical inactivity - sedentary behaviors which require little energy and replace more vigorous activity

131
Q

Obesity treatments

A

WHO recommends 5-10% reduction in body weight as treatment through negative energy balance achieved by exercise training and hypocaloric diet

132
Q

Weight loss strategies

A

small changes, moderate losses (10-20lbs/yr), reasonable goals

133
Q

Physical activity recommendations

A

150 min of moderate to vigorous activity per week

134
Q

Discretionary kcal allowance

A

Window between energy intake required to meet nutritional needs and energy expenditure, increased with exercise

135
Q

Strategies for weight gain

A

energy dense foods, regular meals and snacks, use of nutrient-dense caloric beverages, exercise(ST), if aerobic training HITT, balance is key

136
Q

Relative Energy deficiency in sport

A

Low energy availabilities effect on immunological, menstrual, bone health, endocrine, metabolic, hermatological, growth + development, psychological, cardiovascular and gastrointestinal function

137
Q

Energy availability equation in athletes

A

energy availability =energy intake - exercising energy expenditure, includes energy needed to recover from workouts

138
Q

Early symptoms of RED-S

A

Menstrual disturbances, initial weight loss, decreased mood status, decreased RMR, lower Resting HR, low BP

139
Q

Mid Symptoms of RED-S

A

weight gain+ swelling, stress reactions/fractures, decreased sex hormones and leptin, decreased T3, decreased IGF-1, decreased ferritin, increased cortisol, decreased fasting

140
Q

Long-term symptoms of RED-S

A

Recurrent stress fractures year to year, increased MSK injuries, increase illnesses, impaired performance, gut issues, inability to lose weight

141
Q

Menstrual disorder symptoms

A

lower RMR, lower estradiol, higher cortisol, trend towards lower T3

142
Q

Consequences of RED-S

A

Osteopenia or osteoporosis, low of adaptation to training, inability to lose weight, reduced fertility, thyroid dysfunctions

143
Q

What drives RED-S in athletes

A

body image - societal and sport pressures
drive for thinness - lighter = faster
exercise dependency and eating disorders
making weight
unintentional LEA due to increased training volume
lack of understanding differences in male and female maturation

144
Q

Puberty in male athletes

A

primarily increase in muscle mass and strength
increased testosterone brings about sex differences
greater cardiac blood and lung volumes
increased Hemoglobin

145
Q

Puberty in female athletes

A

primarily increase in adipose tissue

initial dip in performance to adapt to new body

146
Q

How to heal from RED-S

A

fuel around training, no fasted training or diets, CHO are essential, within day energy balance - no 3-4 hours blocks without food, low fiber, strength training, seek professional help early

Human Nutrition (3 decks)

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