Exam 2 - Lecs 1-6 Flashcards

(155 cards)

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
What determines proportion of AAs in AA pool?
AA composition of the diet
26
What organ can excess protein consumption damage and why?
Kidneys bc we don't store protein, we excrete it
27
**What are some fxns of protein in the body?**
>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
28
What is US and global impact of protein deficiency?
Not a problem in US but major cause of early mortality globally
29
What is Protein-Energy Malnutrition (PEM) and 2 types?
>Range of protein deficiency conditions | >>Kwashiorkor and Marasmus
30
What is Kwashiorkor?
PURE protein deficiency | >Characterized by swollen belly
31
What is Marasmus?
energy AND protein deficiency >Depletion of fat stores >Wasting of mscl
32
Diets that contain animal protein can result in what?
consuming protein in excess of need
33
What are consequences of excess protein consumption over long periods of time?
>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)
34
**Why might red meat be related to an increased risk of chronic diseases?**
>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)
35
What is the implication of excess Nitrogen in the urine (N out > N in)?
Means you're burning up body tissue (protein is seen as N in urine)
36
What is the implication of N in > N out?
Indicates tissue growth
37
How much protein do adults require by bodyweight?
0.8g/kg bodyweight | >Assumption: not excess body fat
38
When do we need more protein?
during periods of growth, pregnancy, and lactation
39
Do we need protein supplements?
>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
40
What is protein complementation?
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
41
Why are we eating more as a population?
Portion Distortion – portions are larger = more cals
42
How is body weight assessed on popul'n lvl?
BMI = Weight in kg/ height in m2 | >Tells whether overweight [BMI 25 – 29.9] or obese [BMI 30+]
43
Issues with BMI measurement?
>Does not measure fat | >Not useful for individuals but for popul’n measures
44
What is energy balance?
energy consumed equals energy expenditure
45
What constitutes an individual's total energy expenditure?
Basal metabolic rate (BMR), physical activity, Thermic effect of food (TEF)
46
What's Basal metabolic rate (BMR)?
energy you need to run your body, equals 60-75% of energy expenditure >Varies by size, body composition, age, gender
47
What are 2 types physical activity?
>Daily, e.g. chores, walking, normal activity | >Strucutred, e.g. sports, gym
48
What's the Thermic effect of food (TEF), aka diet-induced thermogenesis? What is Non-exercise activity thermogenesis (NEAT)?
>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
49
When are body energy stores used or built?
>Weight loss = stores are used | >Weight gain= stores are built
50
**Extra protein is stored as what?**
FAT! >Not stored as mscl or AA but as fat! >>>>(converted to fatty acids and stored in adipose tissue)
51
What is the Hunger-Obesity Paradox?
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
52
Define food insecure
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
53
What are reasons for the Hunger-Obesity Paradox?
>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)
54
What is passive overconsumption?
>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)
55
What are eating disorders?
Diagnostic and Statistical Manual (DSM) IV: >Anorexia Nervosa (AN) >Bulimia Nervosa (BN) >Eating Disorder Not Otherwise Specified (EDNOS) >>>Binge Eating Disorder (BED)
56
About how many women struggle w/ an eating disorder or disordered eating in the U.S.?
1 in 5 women
57
What is DSM-IV diagnostic criterion for Anorexia Nervosa (AN)?
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
58
What are the 2 AN subtypes?
>Restricting types | >Binge-eating/purging type
59
Restricting Type
(AN subtype) | During current episode of AN, no regular binge eating or purging behavior
60
Binge-eating/purging type
(AN subtype) During current episode of AN, regular binge eating or purging >DIFFERENTIATED from bulimia bc of presence of a body weight
61
What is DSM-V diagnostic criterion for Anorexia Nervosa (AN)?
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
62
**CHANGES in diagnostic criterion for Anorexia Nervosa (AN) from DSM-IV to DSM-V?**
ELIMINATES objective weight criterion (specificity of below 85% ideal body weight), amenorrhea, and use of the word “refusal”
63
What is DSM-IV diagnostic criterion for Bulimia Nervosa (BN)?
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
What are the 2 BN subtypes?
>Purging type | >Non-purging type
65
Purging type
(BN subtype) | self-induced vomiting, laxative abuse, diuretic abuse
66
Non-purging type
(BN subtype) | Fasting, over-exercise
67
What is DSM-V diagnostic criterion for BN?
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
**CHANGES in diagnostic criterion for BN from DSM-IV to DSM-V?**
>Reduced frequency of symptom use to 1x/week vs. 2x/wk ----- My own observation: >In (B), Changes "compulsive behavior" to "compensatory behavior"
69
What is DSM-V diagnostic criterion for Binge-Eating Disorder (BED)?
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
What is The Binge Cycle?
Binge → feel better → feel bad/guilty → want to feel better → binge again → cycles
71
**CHANGES in diagnostic criterion for BED from DSM-IV to DSM-V?**
BED became its own separate category
72
**CHANGES in diagnostic criterion for EDNOS from DSM-IV to DSM-V?**
>Eliminated as a category >Development of OSFED (other specified feeding and eating disorder) >Development of UFED (unspecified feeding and eating disorder)
73
What is OSFED (other specified feeding and eating disorder)?
>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
What is UFED (unspecified feeding and eating disorder)?
Individuals uncategorized as OSFED or w/ insufficient info to make a diagnosis
75
Purging disorder
recurrent purging behavior to influence shape or weight w/o prior bingeing
76
Night eating syndrome
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
What are some risk factors for EDs?
>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
What are high-risk popul'ns for EDs?
>Athletes [Female Athlete Triad] >Bariatric (weight loss surgery) candidates >Adolescents
79
Female Athlete Triad
disordered eating, amenorrhea, bone loss | >Drop in estrogen + lack kcals = osteoporosis
80
Orthorexia Nervosa
>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
**Dangers of EDs**
EDs have highest mortality rate of any mental illness!!!
82
Complications of EDs
>AN – bradycardia, orthostasis, hypothermia >BN – bradycardia, orthostatis, dry skin >BED – diabetes/pre-diabetes, obesity, altered hormone secretion
83
**What is Hunger-Obesity Paradox?** Reasons for it?
food insecurity increases risk of obesity >Overeating when food is available >Ppl may become more efficient at storing fat (survival)! >Erratic eating
84
What helps with weight control?
Meal planning
85
What makes us choose food? How does this relate to income?
Taste, cost, convenience | >When ppl increase income, they typically don’t change food choices – only buy more expensive brands
86
What is Energy Density?
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
What are 3 disease risks associated w/ excess body fat?
>Type 2 diabetes >Heart disease >Hypertension -- >Respiratory problems, e.g. sleep apnea (disrupted sleep) >Increased risk of breast, colon, prostate cancer
88
What is Body Mass Index (BMI)? Does it apply to the individual?
BMI = kg/m2 does not measure body fat >Applies to large groups of people, not the individual
89
What are 2 impt methods for assessing body composition?
``` >underwater weighing (gold standard!) >skin-fold thickness -- >Bioelectric Impedance Analysis >Dilution Methods ```
90
**What is Visceral Fat?**
``` INTERIOR FAT >>Fat surrounding organ (btwn muscle and organ) >Central Obesity!! >Poses health risks >Tight stomach, protruding belly ```
91
What is Subcutaneous Fat?
>Fat btwn mscl and skin >No health risks >>>butt and thigh fat
92
What is the realtionship btwn waist circumference and disease risk?
as waist size increases, disease risk increases
93
What is the set point theory?
The weight at which the body resists weight change >can increase w/ long term overeating >can decrease w/ long term physical activity
94
What is satiety?
the feeling of fullness and satisfaction >Hunger-- physiological response (real) >Appetite-- psychological response (perceived)
95
What is leptin's (hormone) role in regulating body fat (long-term)?
>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
What is Ghrelin's (hormone) role in regulating energy balance (short-term)?
stomach, stimulates desire to eat
97
What is CCK's (hormone) role in regulating energy balance (short-term)?
small intestine, suppresses appetite
98
[NOT TESTED] What factors contribute to obesity?
>Thrifty Metabolism--- efficient at storing fat/energy >Adaptive thermogenesis-- decreased energy expenditure >Low brown adipose tissue-- fat tissue w/ high mitochondria content
99
What is obesity? What 3 qualities does one need for treatment?
>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
What is the best diet composition for weight management?
>Nutrient composition short-term doesn’t matter >>Eat less! >>Compliance is key-- [taste, cost, convenience impt!] Olive oil-- health benefits and satiety
101
Why do you lose weight on low-carb diets? What is major issue w/ this diet?
>Lose weight bc you eat less, since carbs are in so many foods >Not healthy long-term if skimping on plant foods
102
What are 4 Components of a Healthy Weight Loss Program?
>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
What are some components of a Fad Diet? Why do they work?
``` >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
What is the major danger associated w/ EDs?
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
What are some complications associated w/ Anorexia?
>Bradycardia---heart rate slows, systems shut off >Hypothermia---body doesn’t heat itself to conserve energy >Ostopenia/Osteoporosis---lack of Ca2++ in diet
106
How did we get info about anorexia?
>self starvation studies with healthy young men | >Showed the body starts to misfire, brain starts thinking it's healthy and normal
107
What are some complications associated w/ Bulimia Nervosa?
Mouth sores and dental erosion | -dentist often 1st to diagnose
108
What are some complications associated w/ Binge Eating?
``` >obesity >diabetes >weight related hypertension -- >Abnormal lipid profile ```
109
What is the cycle of an ED?
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
**How are ED treated?**
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
What are 5 Levels of Care for an ED?
>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
What is cost of treatment for an ED?
EXPENSIVE! CAN BE OVER 100k, undercovered by insurance
113
What are some Nutritional Management Treatment Goals associated w/ EDs?
``` >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
**What is Re-Feeding Syndrome?**
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
How can we prevention Re-Feeding Snydrome?
>Replenish Electrolytes first >Start low, and advance slow! >>>Be careful with carbs
116
Are vitamins essential or non-essential?
ESSENTIAL | >Body cannot synthesize
117
What do vitamins do?
Promote growth and health maintenance
118
What are water soluble vitamins? Bioavailability?
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
What are fat soluble vitamins? Bioavailability?
A, D, E, and K | >Require fat for abspt
120
What are risks associated w/ Fortified Foods?
>Unregulated industry | >Vitamins can build up to toxic lvls
121
What are risks associated w/ Dietary Supplements?
>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
What is Bioavailability of Vitamins?
>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
What is the primary fxn of B vitamins?
>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
Most nutrient dense to least? Food sources of b-vitamins?
frozen produce > fresh/local > canned >Many B-vitamins are in fruits and veggies
125
What are major fxns of Thiamin (Vit B1)? Dietary sources?
>Assist in carb metabolism (need for pyruvate → acetyl CoA) >Health of nervous system >Animal foods (pork and dairy)
126
What are 2 deficiencies of thiamin?
Deficiency can cause: >Nervous system abnormalities, e.g. tingling, loss of feeling - Beriberi disease - Wernicke-Korsakoff Syndrome (alcoholics) >Problems w/ energy metabolism
127
What are major fxns of Riboflavin?
>Coenzyme - "FAD," part of citric acid cycle--breakdown of fatty acids - "FMN" (and FAD) = electron carrier in ETC
128
(NOT TESTED) How can riboflavin be destroyed?
Heat or exposure to light. Milk-clear glass bottle is BAD
129
What are dietary sources of Riboflavin?
Animal foods (Pork, beef, milk)
130
What is deficiency of Riboflavin?
Ariboflavinosis---Inflammation of lips, mouth, tongue | -Rare in US
131
What are major fxns of Niacin?
Coenzyme-- NAD (Glycolysis, citric acid cycle) and NADP (electron acceptance)
132
What are dietary sources of Niacin?
Animal foods (chicken)
133
Can Niacin be synthesized by the body?
Can be synthesized from essential AA tryptophan (if diet is adequate in tryptophan)
134
**What is deficiency of Niacin?**
Pellagra | *4 D's: dermatitis, diarrhea, and dementia and eventually death
135
What is toxicity of Niacin?
Niacin supplements can lower blood triglycerides, but may result in: - Elevated BP - Cardiac arrhythmia - Elevated blood sugar - Impaired liver fxn
136
What are major fxns of Biotin?
co-enzyme in energy metabolism >synthesis of glucose and fatty acids >metabolism of certain amino acids
137
What can destroy biotin?
Avidin in raw eggs
138
What are dietary sources of Biotin? Deficiency?
``` Animals foods (liver, egg yolks, yogurt) and NUTS -Deficiency is uncommon ```
139
What is Vit B6 (Pyridoxine)?
Group of compounds, all form pyridoxal phosphate (coenzyme)
140
**What are major fxns of Vit B6 (Pyridoxine)? Dietary sources?**
>Protein metabolism >AA metabolism (deamination) >Neurotransmitter synthesis >Animal foods, Nuts and seeds
141
What is deficiency of Vit B6?
Deficiency may result in ANEMIA due to impaired hemoglobin synthesis and neurotransmitter issues
142
What is toxicity of Vit B6?
Only supplements can cause toxicity | -Can cause irreversible nerve damage
143
What are major fxns of Folate? Dietary sources?
Coenzyme needed for DNA SYNTHESIS and metabolism of some AAs >PLANT FOODS (lentils, seeds & nuts, fortified or enriched grain products)
144
What is role of folate deficiency during pregnancy?
Neural tube defects are associated w/ folate deficiency during pregnancy -Fortification of food
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What is overall risk of low folate intake? Deficiency?
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
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**What can excess folate consumption cause?**
>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
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What is Homocystine? How to lower lvls?
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)
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What are major fxns of Vit B12? Dietary sources?
Required for metabolism (activation) of folate and fatty acids and to maintain insulting layer of myelin surrounding nerves >Animal foods
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What is deficiency of Vit B12?
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
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How is B12 absorbed? How is abspt related to deficiency?
>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
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What are major fxns of Vit C?
>Antioxidant---Neutralizes free radicals >Helps maintain immune system >Prodxn of collagen
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What is deficiency of Vit C?
Scurvy---bleeding gums, fatigue, poor wound healing
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What is Vit C's role in common cold?
No correlation to cold | >Placebo effect
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What are dietary sources of Vit C?
FRUITS (Oranges, strawberries, tomato)
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(NOT TESTED) How can Vit C be destroyed?
O2, light, heat, contact with copper/iron cookware