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NUTRITION > Exam 2 - Lecs 1-6 > Flashcards

Exam 2 - Lecs 1-6 Flashcards

1
Q

Is protein deficiency common in the US?

A

No, rare

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2
Q

What is most common dietary source of protein in US? How much of dietary protein does it comprise?

A

Animal sources—meat, poultry, seafood, eggs, dairy

>2/3

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3
Q

What is most common dietary source of protein in the world?

A

Plant sources—grains and veggies

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4
Q

What is the correlation btwn economic status and animal foods consumption?

A

W/ increase in economic status → increase in proportion of animal foods consumed

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5
Q

What is avg amount of protein consumed/day in US?

A

90g protein/day

>High burden of disease

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6
Q

What are nutrients supplied by animal protein foods? Drawbacks?

A

> B vitamins, iron, zinc, calcium

>Low in fiber, can be high in fat

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7
Q

What are nutrients supplied by plant protein foods? Drawbacks?

A

> Fiber, phytochemicals, and monounsaturated and polyunsaturated fats.
Less absorbable forms of protein and vitamins

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8
Q

What are amino acids (AAs)?

A

> Building blocks of protein

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9
Q

What are essential AAs?

A

AAs that can’t be synthesized by the human body in sufficient amounts to meet needs
>Need to include in diet

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10
Q

How many AAs in total? How many are essential vs. not?

A

20 AAs total—9 essential, 11 not

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11
Q

What are conditional essential AAs?

A

They need to be obtained via the diet when one is sick or in some conditions

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12
Q

What is unique about the 11 non-essential AAs?

A

We can convert all 11 non-essential AAs into one another

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13
Q

What is a protein?

A

1+ polypeptide chains (many AAs) folded into a 3D shape

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14
Q

What determines a protein’s fxn?

A

Its shape

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15
Q

What is protein denaturation?

A

alteration in protein’s 3D structure

>Normal fxn ceases

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16
Q

What are causes of protein denaturation?

A

> Change in pH (digestion)
Heat (cooking)
Agitation (whipping an egg white)

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17
Q

What is AA structure?

A

Central C bound to H, Amino group (NH2), Acid group (C(O)OH), R Chain (differs by AA)

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18
Q

What are peptide bonds, dipeptide bonds, and polypeptides?

A

> Peptide bonds—chemical bonds that link AA together
Dipeptide bonds—2 AAs
Polypeptides—many AAs

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19
Q

How is protein digested and absorbed?

A

> Mouth—Mechanical breakdown via chewing
Stomach—HCL starts chem digestion
Small intestine
»Active transport into mucosal cell, where dipeptides and tripeptides are broken down into single AAs
AA pass into blood, travel to liver

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20
Q

What causes food allergies?

A

Absorbing a protein whole = allergy

>Most common allergens = milk, eggs, nuts, wheat, soy, fish and shellfish, and peanuts

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21
Q

What is Anaphylaxis?

A

rapid, severe allergic rxn
>Life-threatening
>Epi-pen—epinephrine is used to treat allergic reactions

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22
Q

What is AA Pool?

A

We don’t store AA, but there are AAs floating in our blood from digestion and mscl breakdown (body proteins)

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23
Q

What are AAs used for?

A

> Energy,
Synthesis of glucose or fatty acids,
Synthesis of nonprotein molecules that contain nitrogen (e.g. DNA and RNA)

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24
Q

Protein Synthesis: Transcription and Translation

A

Nucleus (DNA to mRNA) ⇒ cytosol (mRNA to ribosomes) ⇒ ribosomes (tRNA reads code and synthesizes the protein)

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25
Q

What determines proportion of AAs in AA pool?

A

AA composition of the diet

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26
Q

What organ can excess protein consumption damage and why?

A

Kidneys bc we don’t store protein, we excrete it

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27
Q

What are some fxns of protein in the body?

A

> Enzymes → speed up metabolic rxns
Hormones → chemical messengers, E.g. insulin and glucagon
Antibodies → immune system (antigens/foreign bodies)
–
Transport proteins → move substances in and out of cells
Contractile proteins → help mscls move, E.g. Actin and myosin
Regulate fluid and acid-base balance

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28
Q

What is US and global impact of protein deficiency?

A

Not a problem in US but major cause of early mortality globally

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29
Q

What is Protein-Energy Malnutrition (PEM) and 2 types?

A

> Range of protein deficiency conditions

|&raquo_space;Kwashiorkor and Marasmus

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30
Q

What is Kwashiorkor?

A

PURE protein deficiency

>Characterized by swollen belly

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31
Q

What is Marasmus?

A

energy AND protein deficiency
>Depletion of fat stores
>Wasting of mscl

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32
Q

Diets that contain animal protein can result in what?

A

consuming protein in excess of need

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33
Q

What are consequences of excess protein consumption over long periods of time?

A

> Hydration and kidney fxn issues
»From need to excrete excess Nitrogen

> Bone health issues from loss of Ca2+ in urine
»High meat diet → excrete more Ca2+ in urine

> ## Increased body fat (excess protein not stored –> converted to fatty acids –> stored in adipose tissue)Kidney stones
Increased risk of heart disease and cancer (red meat)

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34
Q

Why might red meat be related to an increased risk of chronic diseases?

A

> GRILLING (any high-dry/high-heat cooking) makes heterocyclic amines (HCA), which appear as blackened surfaces
»HCA is carcinogenic, acts like nicotine

> INCREASE IN BODY WEIGHT
»Associated w/ cancer risk, e.g. breast, colon, and prostate cancer

> Decrease in plant products

> Insulin secretion from essential AAs
»High lvls of Insulin can cause cell damage

> Arachidonic acid content (PUFA)

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35
Q

What is the implication of excess Nitrogen in the urine (N out > N in)?

A

Means you’re burning up body tissue (protein is seen as N in urine)

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36
Q

What is the implication of N in > N out?

A

Indicates tissue growth

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37
Q

How much protein do adults require by bodyweight?

A

0.8g/kg bodyweight

>Assumption: not excess body fat

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38
Q

When do we need more protein?

A

during periods of growth, pregnancy, and lactation

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39
Q

Do we need protein supplements?

A

> No – unregulated
Amino acid is brought to mscl right after exercise
»Need INSULIN to get AA into mscl
»Flavored milk is best to have after exercise

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40
Q

What is protein complementation?

A

Putting together foods to get all your amino acids, e.g. rice + beans

> Rice has a lot of Met + Cys but not Lys
Beans have a lot of Lys but not Met + Cys
Combine them and get enough of both

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41
Q

Why are we eating more as a population?

A

Portion Distortion – portions are larger = more cals

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42
Q

How is body weight assessed on popul’n lvl?

A

BMI = Weight in kg/ height in m2

>Tells whether overweight [BMI 25 – 29.9] or obese [BMI 30+]

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43
Q

Issues with BMI measurement?

A

> Does not measure fat

>Not useful for individuals but for popul’n measures

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44
Q

What is energy balance?

A

energy consumed equals energy expenditure

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45
Q

What constitutes an individual’s total energy expenditure?

A

Basal metabolic rate (BMR), physical activity, Thermic effect of food (TEF)

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46
Q

What’s Basal metabolic rate (BMR)?

A

energy you need to run your body, equals 60-75% of energy expenditure
>Varies by size, body composition, age, gender

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47
Q

What are 2 types physical activity?

A

> Daily, e.g. chores, walking, normal activity

>Strucutred, e.g. sports, gym

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48
Q

What’s the Thermic effect of food (TEF), aka diet-induced thermogenesis? What is Non-exercise activity thermogenesis (NEAT)?

A

> Energy used to digest/absorb food → inherent to food size
On avg = 10% of total energy in food, e.g. if you eat 100 cals you use 10 of those cals to digest food
We store more energy from smaller amounts of foods (why snacking causes weight gain)

> NEAT= Overeating and regulating body heat

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49
Q

When are body energy stores used or built?

A

> Weight loss = stores are used

>Weight gain= stores are built

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50
Q

Extra protein is stored as what?

A

FAT!
>Not stored as mscl or AA but as fat!
»»(converted to fatty acids and stored in adipose tissue)

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51
Q

What is the Hunger-Obesity Paradox?

A

Says that your chances of being overweight are higher if you’re

> Food insecure → associated w/ low-inc
Low-income
Low-education
Minority → associated w/ low-edu, low-inc

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52
Q

Define food insecure

A

For at least some part of the month you don’t know if you will have food at next meal
>Most of the time due to financial circumstances

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53
Q

What are reasons for the Hunger-Obesity Paradox?

A

> If you’re food insecure:
»You may overeat when food is available
»You may become more efficient at storing fat (survival)
»Erratic eating – you don’t consistently eat the same # of meals a day

> You’re going through feast and famine all the time
Increase activity of lipoprotein lipase? (theory)

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54
Q

What is passive overconsumption?

A

> When you keep eating a food, unaware you’re doing it
[taste, cost, convenience]

> Energy density—-calories for a weight/volume of food
»Higher energy density = high cals for low weight/volume food, e.g. refined grains (“white” pasta, rice, bread), products w/ added sugar/salt/fat-snack foods, candy
*LOWER COST → US gov’t subsidizes crops used to make high energy density foods

> > > Lower energy density: low cals for a low-weight/volume food, e.g. fruit, veggies, whole grains (have more water/fiber)

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55
Q

What are eating disorders?

A

Diagnostic and Statistical Manual (DSM) IV:
>Anorexia Nervosa (AN)
>Bulimia Nervosa (BN)
>Eating Disorder Not Otherwise Specified (EDNOS)
»>Binge Eating Disorder (BED)

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56
Q

About how many women struggle w/ an eating disorder or disordered eating in the U.S.?

A

1 in 5 women

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57
Q

What is DSM-IV diagnostic criterion for Anorexia Nervosa (AN)?

A

A. Refusal to maintain body weight at or above 85% of expected weight for age + height
B. Intense fear of gaining weight or becoming fat, even though underweight
C. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of seriousness of current low weight
D. (AMENORRHEA) In post postmenarcheal females: amenorrhea - the absence of at least 3 consecutive menstrual cycles

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58
Q

What are the 2 AN subtypes?

A

> Restricting types

>Binge-eating/purging type

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59
Q

Restricting Type

A

(AN subtype)

During current episode of AN, no regular binge eating or purging behavior

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60
Q

Binge-eating/purging type

A

(AN subtype)
During current episode of AN, regular binge eating or purging

> DIFFERENTIATED from bulimia bc of presence of a body weight

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61
Q

What is DSM-V diagnostic criterion for Anorexia Nervosa (AN)?

A

A. Persistent restriction of energy intake relative to reqs leading to a significantly low body weight in context of age, sex, developmental trajectory, and physical health
aa. ELIMINATES specificity of below 85% ideal body weight
B. Intense fear of gaining weight or becoming fat even though underweight
C. Disturbance in the way in which ones body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or the denial of the seriousness of the current low body weight

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62
Q

CHANGES in diagnostic criterion for Anorexia Nervosa (AN) from DSM-IV to DSM-V?

A

ELIMINATES objective weight criterion (specificity of below 85% ideal body weight), amenorrhea, and use of the word “refusal”

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63
Q

What is DSM-IV diagnostic criterion for Bulimia Nervosa (BN)?

A

A. Recurrent binge eating (at least 2x/ wk for 3 mos duration)
»>Usually normal weight bc 50% cals are absorbed when consumed, despite purging
B. Recurrent, inappropriate, compulsive behavior to prevent weight gain (e.g. self-induced vomiting, abuse of laxatives, diuretic or other meds, or excessive exercise)
C. Persistent overconcern w/ body shape and/or weight
D. Absence of Anorexia Nervosa

64
Q

What are the 2 BN subtypes?

A

> Purging type

>Non-purging type

65
Q

Purging type

A

(BN subtype)

self-induced vomiting, laxative abuse, diuretic abuse

66
Q

Non-purging type

A

(BN subtype)

Fasting, over-exercise

67
Q

What is DSM-V diagnostic criterion for BN?

A

A. Recurrent episodes of binge eating characterized by BOTH of the following:
»>Eating in a discrete amount of time (w/i a 2hr period) large amounts of food
»>Sense of lack of control over eating during an episode (i.e. feeling that one cannot stop eating)
B. Recurrent, inappropriate compensatory behavior in order to prevent weight gain (e.g. purging)
C. The binge eating and compensatory behaviors both occur on avg at least 1x/week for 3 mos
D. Self-evaluation is unduly influenced by body shape and weight
E. The disturbance does not occur exclusively during episodes of AN

68
Q

CHANGES in diagnostic criterion for BN from DSM-IV to DSM-V?

A

> ## Reduced frequency of symptom use to 1x/week vs. 2x/wkMy own observation:
In (B), Changes “compulsive behavior” to “compensatory behavior”

69
Q

What is DSM-V diagnostic criterion for Binge-Eating Disorder (BED)?

A

A. Recurrent episodes of binge eating. An episode is characterized by:
»>Eating a larger amount of food than normal during a short period of time (w/i any 2 hr period)
»> Lack of control over eating during binge episode (i.e. feeling that one cannot stop eating)
B. Binge eating episodes are associated w/ 3+ of the following:
»>Eating until feeling uncomfortably full
»>Eating large amounts of food when not physically hungry
»>Eating much more rapidly than normal
»>Eating alone bc you’re embarrassed by how much you’re eating
»>Feeling disgusted, depressed, or guilty after overeating
C. Marked distress regarding binge eating is present
D. Binge eating occurs, on avg, 2x/week for 6 mos
E. The binge is not associate w/ the regular use of inappropriate compensatory behavior and does not occur exclusively during the course of BN or AN

70
Q

What is The Binge Cycle?

A

Binge → feel better → feel bad/guilty → want to feel better → binge again → cycles

71
Q

CHANGES in diagnostic criterion for BED from DSM-IV to DSM-V?

A

BED became its own separate category

72
Q

CHANGES in diagnostic criterion for EDNOS from DSM-IV to DSM-V?

A

> Eliminated as a category
Development of OSFED (other specified feeding and eating disorder)
Development of UFED (unspecified feeding and eating disorder)

73
Q

What is OSFED (other specified feeding and eating disorder)?

A

> Atypical AN (AN features w/o low weight)
BN of low frequency and/or limited duration
BED of low frequency and/or limited duration
Purging disorder
Night eating syndrome

74
Q

What is UFED (unspecified feeding and eating disorder)?

A

Individuals uncategorized as OSFED or w/ insufficient info to make a diagnosis

75
Q

Purging disorder

A

recurrent purging behavior to influence shape or weight w/o prior bingeing

76
Q

Night eating syndrome

A

sleep-wake cycle disturbance, causing very low food intake during the day and very high intake at night
>or waking up in the middle of the night to eat

77
Q

What are some risk factors for EDs?

A

> Genetic: 50-83% of the variance in ED is related to genetics
Social: Societal pressured for thinness
Psychological: anxiety, depression, OCD, trauma
DIETARY RESTRAINT– one of the predisposing factors for EDs
Gender (>prevalence in females)
Low self-esteem
Body dissatisfaction

78
Q

What are high-risk popul’ns for EDs?

A

> Athletes
[Female Athlete Triad]
Bariatric (weight loss surgery) candidates
Adolescents

79
Q

Female Athlete Triad

A

disordered eating, amenorrhea, bone loss

>Drop in estrogen + lack kcals = osteoporosis

80
Q

Orthorexia Nervosa

A

> Fixation on righteous eating
»Rigid rules about food quality and purity
»Food choices often become so restricted in variety and calories that health suffers
A more frequent eating disordered behavior in athletes (28%)

81
Q

Dangers of EDs

A

EDs have highest mortality rate of any mental illness!!!

82
Q

Complications of EDs

A

> AN – bradycardia, orthostasis, hypothermia
BN – bradycardia, orthostatis, dry skin
BED – diabetes/pre-diabetes, obesity, altered hormone secretion

83
Q

What is Hunger-Obesity Paradox? Reasons for it?

A

food insecurity increases risk of obesity

> Overeating when food is available
Ppl may become more efficient at storing fat (survival)!
Erratic eating

84
Q

What helps with weight control?

A

Meal planning

85
Q

What makes us choose food? How does this relate to income?

A

Taste, cost, convenience

>When ppl increase income, they typically don’t change food choices – only buy more expensive brands

86
Q

What is Energy Density?

A

cals for a given weight/volume of food

> Higher energy density– a lot of cals for a low weight/volume [ex. white pasta, bread, rice]
Lower energy density— few cals for a low weight/volume [ex. fruit, veggies, whole grains]

87
Q

What are 3 disease risks associated w/ excess body fat?

A

> Type 2 diabetes
Heart disease
Hypertension
–
Respiratory problems, e.g. sleep apnea (disrupted sleep)
Increased risk of breast, colon, prostate cancer

88
Q

What is Body Mass Index (BMI)? Does it apply to the individual?

A

BMI = kg/m2
does not measure body fat
>Applies to large groups of people, not the individual

89
Q

What are 2 impt methods for assessing body composition?

A 
>underwater weighing (gold standard!)
>skin-fold thickness
--
>Bioelectric Impedance Analysis
>Dilution Methods
90
Q

What is Visceral Fat?

A 
INTERIOR FAT
>>Fat surrounding organ (btwn muscle and organ)
>Central Obesity!! 
>Poses health risks
>Tight stomach, protruding belly
91
Q

What is Subcutaneous Fat?

A

> Fat btwn mscl and skin
No health risks
»butt and thigh fat

92
Q

What is the realtionship btwn waist circumference and disease risk?

A

as waist size increases, disease risk increases

93
Q

What is the set point theory?

A

The weight at which the body resists weight change
>can increase w/ long term overeating
>can decrease w/ long term physical activity

94
Q

What is satiety?

A

the feeling of fullness and satisfaction
>Hunger– physiological response (real)
>Appetite– psychological response (perceived)

95
Q

What is leptin’s (hormone) role in regulating body fat (long-term)?

A

> Weight LOSS leads to LESS leptin → stimulates hunger = increased energy intake, and decreases energy expenditure

> Weight GAIN leads to MORE leptin → suppresses appetite = decreased energy intake, and increases energy expenditure

96
Q

What is Ghrelin’s (hormone) role in regulating energy balance (short-term)?

A

stomach, stimulates desire to eat

97
Q

What is CCK’s (hormone) role in regulating energy balance (short-term)?

A

small intestine, suppresses appetite

98
Q

[NOT TESTED] What factors contribute to obesity?

A

> Thrifty Metabolism— efficient at storing fat/energy
Adaptive thermogenesis– decreased energy expenditure
Low brown adipose tissue– fat tissue w/ high mitochondria content

99
Q

What is obesity? What 3 qualities does one need for treatment?

A

> chronic disease– leads to other illnesses
**better success w/ cancer treatment

> For treatment: one should be OVERWEIGHT, have RISK FACTORS for chronic diseases, be MOTIVATED

100
Q

What is the best diet composition for weight management?

A

> Nutrient composition short-term doesn’t matter
>Eat less!
>Compliance is key– [taste, cost, convenience impt!]

Olive oil– health benefits and satiety

101
Q

Why do you lose weight on low-carb diets? What is major issue w/ this diet?

A

> Lose weight bc you eat less, since carbs are in so many foods
Not healthy long-term if skimping on plant foods

102
Q

What are 4 Components of a Healthy Weight Loss Program?

A

> CTRL OF ENERGY (reduce calories!)
SLOW WEIGHT LOSS: 1-2lbs/wk
(EXERCISE) Increase in energy expenditure– to maintain w8 loss
CHANGE IN BEHAVIOR

**(flynn) Food improves health

103
Q

What are some components of a Fad Diet? Why do they work?

A 
>Promise of fast weight loss
>Selling a product
>Eating behaviors not changed
--
>Limit nutrients/food groups or rituals
>Testimonials from “famous” ppl
>Critical of science community

> > Work bc ppl eat less

104
Q

What is the major danger associated w/ EDs?

A

EDs have highest mortality rate of any mental illness

> Mortality rate associated w/ anorexia 12x higher than death rate of ALL causes of deaths for females 15-24rys old

105
Q

What are some complications associated w/ Anorexia?

A

> Bradycardia—heart rate slows, systems shut off
Hypothermia—body doesn’t heat itself to conserve energy
Ostopenia/Osteoporosis—lack of Ca2++ in diet

106
Q

How did we get info about anorexia?

A

> self starvation studies with healthy young men

>Showed the body starts to misfire, brain starts thinking it’s healthy and normal

107
Q

What are some complications associated w/ Bulimia Nervosa?

A

Mouth sores and dental erosion

-dentist often 1st to diagnose

108
Q

What are some complications associated w/ Binge Eating?

A 
>obesity
>diabetes
>weight related hypertension
--
>Abnormal lipid profile
109
Q

What is the cycle of an ED?

A

Obsessive Thinking and Compulsive Food Rituals → Reduced stomach size and early satiety → Mscl loss leads to stomach protrusion → Bloating and fluid retention secondary to maturation → fears of fatness reinforced → body image distortion worsens → increased fixation on refusing food and weight loss

110
Q

How are ED treated?

A

Multi-disciplinary treatment (medical, psychiatric, nutrition, psychotherapeutic)

> Medical—stability of serum electrolytes, heart fxn, bone health
Psychiatric—treatment of co-existing mood disorders
Nutritional—weight restoration, normalization of eating habits, improve body image
Psycho therapeutic—family therapy, CBT/DBT, acceptance commitment therapy

111
Q

What are 5 Levels of Care for an ED?

A

> Inpatient Hospitalization (24hr care)—patient is medically unstable, has poor motivation for recovery
Residential Treatment
Day Treatment
Intensive Outpatient
Outpatient—insurance and patient dependent

112
Q

What is cost of treatment for an ED?

A

EXPENSIVE! CAN BE OVER 100k, undercovered by insurance

113
Q

What are some Nutritional Management Treatment Goals associated w/ EDs?

A 
>Weight restoration
>Normalization of eating behavior
>Improving body image/body acceptance
--
>Elimination or redxn of symptom use 
>Promoting healthy physical activity when appropriate
>Independent meal planning
>Shopping
>Food prep
114
Q

What is Re-Feeding Syndrome?

A

A METABOLIC COMPLICATION that occurs when nutritional support is given to severely malnourished patients.

Metabolism shifts from catabolic to anabolic state.
**The quick shift from catabolic to anabolic can cause cardiac arrhythmias and possible death

Insulin released on carb intake causes cellular uptake of K, Mg, Phosphorous (P).
**Possible heart failure due to electrolyte and fluid shifts that strain the heart

115
Q

How can we prevention Re-Feeding Snydrome?

A

> Replenish Electrolytes first
Start low, and advance slow!
»Be careful with carbs

116
Q

Are vitamins essential or non-essential?

A

ESSENTIAL

>Body cannot synthesize

117
Q

What do vitamins do?

A

Promote growth and health maintenance

118
Q

What are water soluble vitamins? Bioavailability?

A

B vitamins and Vit C
>Easy to absorb (Don’t req fat) but may require transport molecules or specific molecules in GI tract
>Can excrete, so dont worry about high abspt

119
Q

What are fat soluble vitamins? Bioavailability?

A

A, D, E, and K

>Require fat for abspt

120
Q

What are risks associated w/ Fortified Foods?

A

> Unregulated industry

>Vitamins can build up to toxic lvls

121
Q

What are risks associated w/ Dietary Supplements?

A

> Widely abused and promoted
Fat-soluble vitamins can accumulate in fat tissues to toxic lvls
U.S. food supply contains all necessary vitamins
»Can’t replace phytonutrients or benefit of varied diet

122
Q

What is Bioavailability of Vitamins?

A

> Vits must be absorbed by body in order to preform their fxns
Mostly absorbed in small intestine
Some absorbed in inactive provitamin forms that must be converted into active forms by the body

123
Q

What is the primary fxn of B vitamins?

A

> Co-enzyme—Combines w/ an enzyme to push fwd chem rxns, esp energy metabolism
Don’t supply energy, only help release energy through co-enzyme process

124
Q

Most nutrient dense to least? Food sources of b-vitamins?

A

frozen produce > fresh/local > canned

> Many B-vitamins are in fruits and veggies

125
Q

What are major fxns of Thiamin (Vit B1)? Dietary sources?

A

> Assist in carb metabolism (need for pyruvate → acetyl CoA)
Health of nervous system

> Animal foods (pork and dairy)

126
Q

What are 2 deficiencies of thiamin?

A

Deficiency can cause:

> Nervous system abnormalities, e.g. tingling, loss of feeling

  • Beriberi disease
  • Wernicke-Korsakoff Syndrome (alcoholics)

> Problems w/ energy metabolism

127
Q

What are major fxns of Riboflavin?

A

> Coenzyme

  • “FAD,” part of citric acid cycle–breakdown of fatty acids
  • “FMN” (and FAD) = electron carrier in ETC
128
Q

(NOT TESTED) How can riboflavin be destroyed?

A

Heat or exposure to light. Milk-clear glass bottle is BAD

129
Q

What are dietary sources of Riboflavin?

A

Animal foods (Pork, beef, milk)

130
Q

What is deficiency of Riboflavin?

A

Ariboflavinosis—Inflammation of lips, mouth, tongue

-Rare in US

131
Q

What are major fxns of Niacin?

A

Coenzyme– NAD (Glycolysis, citric acid cycle) and NADP (electron acceptance)

132
Q

What are dietary sources of Niacin?

A

Animal foods (chicken)

133
Q

Can Niacin be synthesized by the body?

A

Can be synthesized from essential AA tryptophan (if diet is adequate in tryptophan)

134
Q

What is deficiency of Niacin?

A

Pellagra

*4 D’s: dermatitis, diarrhea, and dementia and eventually death

135
Q

What is toxicity of Niacin?

A

Niacin supplements can lower blood triglycerides, but may result in:

  • Elevated BP
  • Cardiac arrhythmia
  • Elevated blood sugar
  • Impaired liver fxn
136
Q

What are major fxns of Biotin?

A

co-enzyme in energy metabolism
>synthesis of glucose and fatty acids
>metabolism of certain amino acids

137
Q

What can destroy biotin?

A

Avidin in raw eggs

138
Q

What are dietary sources of Biotin? Deficiency?

A 
Animals foods (liver, egg yolks, yogurt) and NUTS
-Deficiency is uncommon
139
Q

What is Vit B6 (Pyridoxine)?

A

Group of compounds, all form pyridoxal phosphate (coenzyme)

140
Q

What are major fxns of Vit B6 (Pyridoxine)? Dietary sources?

A

> Protein metabolism
AA metabolism (deamination)
Neurotransmitter synthesis

> Animal foods, Nuts and seeds

141
Q

What is deficiency of Vit B6?

A

Deficiency may result in ANEMIA due to impaired hemoglobin synthesis and neurotransmitter issues

142
Q

What is toxicity of Vit B6?

A

Only supplements can cause toxicity

-Can cause irreversible nerve damage

143
Q

What are major fxns of Folate? Dietary sources?

A

Coenzyme needed for DNA SYNTHESIS and metabolism of some AAs

> PLANT FOODS (lentils, seeds & nuts, fortified or enriched grain products)

144
Q

What is role of folate deficiency during pregnancy?

A

Neural tube defects are associated w/ folate deficiency during pregnancy
-Fortification of food

145
Q

What is overall risk of low folate intake? Deficiency?

A

increased risk of heart disease due to increase in homocysteine (AA metabolism)

> Deficiency can lead to macrocytic anemia

  • Cells unable to divide properly (magloblast) → macrocyte
  • Early warning sign for B12 deficiency
146
Q

What can excess folate consumption cause?

A

> Excess folate intake (supplement) can mask a B12 deficiency
If B12 is low, folate can’t be activated → RBC division is impaired → macrocytic anemia
You can take supplements of (activated) folate to correct macrocytic anemia ⇒ BUT you will still be B12-deficient

147
Q

What is Homocystine? How to lower lvls?

A

Unstable intermediate w/ oxidative potential in AA metabolism of Methionine
>High lvs in blood increase risk of CVD
>Can lower lvls w/ Folate or Vit B12 (convert to methionine) and Vit B6 (covert to cysteine)

148
Q

What are major fxns of Vit B12? Dietary sources?

A

Required for metabolism (activation) of folate and fatty acids and to maintain insulting layer of myelin surrounding nerves

> Animal foods

149
Q

What is deficiency of Vit B12?

A

Pernicious anemia—immature red blood cells

> B12 is recycled w/ bile in the liver, so it can take years for deficiency to develop
Deficiency typically caused by poor absorption rather than low intake alone
B12 deficiency causes activated folate deficiency

150
Q

How is B12 absorbed? How is abspt related to deficiency?

A

> Stomach acid helps release “intrinsic factor,” transport protein needed for abspt of B12 across membrane of small intestine
Deficiency is typically caused by poor absorption rather than by low intake alone

151
Q

What are major fxns of Vit C?

A

> Antioxidant—Neutralizes free radicals
Helps maintain immune system
Prodxn of collagen

152
Q

What is deficiency of Vit C?

A

Scurvy—bleeding gums, fatigue, poor wound healing

153
Q

What is Vit C’s role in common cold?

A

No correlation to cold

>Placebo effect

154
Q

What are dietary sources of Vit C?

A

FRUITS (Oranges, strawberries, tomato)

155
Q

(NOT TESTED) How can Vit C be destroyed?

A

O2, light, heat, contact with copper/iron cookware

NUTRITION (10 decks)

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