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NUTR 120 > CHOs, Protein, Energy > Flashcards

CHOs, Protein, Energy Flashcards

1
Q

Carbohydrates contain

A

carbon, hydrogen, oxygen

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2
Q

Common monosaccharides

A

glucose
fructose
galactose

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3
Q

common disaccharides and enzyme needed to cleave them

A

maltose (2 glucoses) - maltase
sucrose (glucose and fructose) - sucrase
lactose (glucose and galactose) - lactase

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4
Q

Hydrolysis rxn definition

A

need water to cleave disaccharide

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5
Q

Condensation rxn definition

A

releases water to make a disaccharide

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6
Q

fatty acids with ____ solidify first if we start lowering the temperature

A

least double bonds

- think of extremophile membranes: lots of 2x bonds to keep them liquid at low temperatures

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7
Q

Simple sugars are?

A

monosaccharides and disaccharides

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8
Q

Oligosaccharides

A

3-10 monosaccharides

ex, prebiotics - encourage healthy bacterial growth in large intestine

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9
Q

Polysaccharides

A

> 10 monosaccharides

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10
Q

complex carbohydrates

A

non-fibre polysaccharides

STARCH

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11
Q

glycogen vs starch

A

glycogen is storage form of glucose in animals and humans and starch is the plant version

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12
Q

Carbohydrate sources

A

make up 45-65% of our diet
found in:
grains
vegetables (carrots, corn, peas, potatoes *starch)
fruit (most contain simple sugars, bananas have starch)
milk and alternatives (milk *lactose, legumes *soy)
VIRTUALLY NONE IN MEAT AND ALTERNATIVES

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13
Q

Which place in the world has most kcal coming from carbohydrates?

A

Africa: >80% – Casava vegetable

The caribbean is next with ~65%

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14
Q

DRI for fibre

A

14g / 1000kcal intake / day

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15
Q

Pattern of carbohydrate intake in NA

A

last 120 yrs
inc animal protein, inc fat and dec carbohydrates
BUT inc in refined carbos (white flour and sugar) and dec the good carbos (which retains fibre from original product)

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16
Q

CHO digestion

A
  1. mouth: salivary amylase begins starch breakdown into maltose, speed of eating determines how much breakdown occurs
  2. stomach: HCl denatures amylase
  3. small intestine: CHO enters as maltose, sucrose, lactose, and starch
    - pancreatic amylase breaks starch into maltose
    - maltase, sucrase, lactase break down their disaccharides
    - ends with 4 glucose, 1 fructose, 1 galactose
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17
Q

CHO absorption

A

monosaccharides absorb through mucosa into HPC via portal vein, into liver for filtering

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18
Q

Monosaccharide metabolism in the liver

- what does it provide?

A

galactose and fructose get converted to glucose:

  • provides kcal for liver
  • liver stores extra as glycogen
  • liver converts needed to one of 11 non-essential AA
  • any more excess converts to fat (VLDL)
  • glucose needed sent into blood to inc BS
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19
Q

Glucose uses in blood

A
  • energy/fuel for most body cells (brain, CNS, RBCs)

- stored as muscle glycogen (energy when contracting)

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20
Q

Glucose basic facts

A
  • very few food sources of JUST glucose
  • not essential
  • primary energy source for brain, CNS, RBCs, kidney cortex
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21
Q

insulin release occurs when?

A

after a meal, glucose released into blood, triggers insulin inc as BS increases
- pancreas releases insulin: anabolic hormone, allows for glycogen production, use of glucose and fat production

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22
Q

Effects of insulin release

A
  • facilitates uptake of glucose from blood to cells: once glucose is uptaken in cell, cell releases insulin
  • stimulates glycogen production
  • returns BS to normal basal levels
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23
Q

Basal blood glucose levels

A

4.5 - 5.5 mmol

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24
Q

What happens when BS drop?

A

hunger pangs

  • insulin levels to drop, glucagon levels inc in pancreas
  • glucagon metabolizes glycogen to glucose, released into blood
  • blood glucose rises and hunger response temporarily curbed
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25
Q

2019 food guide iterations showed which nutrient needs not met?

A

K, Ca, D

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26
Q

type 2 diabetes global levels

A

highest rates (inc quickest) in china, india, USA
can cause blindness, kidney disease, CHD risk inc (67% die from CHD, vs ~30% for av person)
- amputation possible

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27
Q

Diabetes stats overtime (1958 to 2015)

A

1958: .98% of people had diabetes ~1.6 million
2015: 7.3% of people have diabetes ~23.4 million
places with greatest jump in prosperity had greatest climb as toxic food enviro inc (bc people can now afford to eat out instead of making/growing own food)

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28
Q

Type 1 mellitus (diabetes)

A
  • pancreas cannot make effective insulin
  • genetic disposition
  • early viral infections associated: pancreatic insulin producing B cells get infected - autoimmune disorder)
  • ~5% have this
  • must take insulin
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29
Q

Type 2 mellitus

A
  • body cells become resistant to influence of insulin
  • correlated with obesity and inactivity (90% overlap)
  • can be genetic, most diet tho
  • early treatment - diet change and activity inc (inc sensitivity to insulin)
  • eventually, pancreas will wear out and need to take insulin
  • makes up 95% of diabetes cases
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30
Q

Glucose tolerance

A

measure of persons ability to remove excess blood glucose following a meal
- range of numbers from normal to mellitus

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31
Q

glucose tolerance test

A
  • give glucose drink to fasted person
  • take blood samples over 2-3 hours
  • blood glucose will inc as its absorbed from GI
  • body should respond as pancreas makes insulin
  • hopefully BS spikes then drops/levels out
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32
Q

glucose tolerance curve of a normal person vs someone with mellitus

A

normal: fasted BS ~5 mmol. ~30 min after drink, jumps to 7.5mmol, then begins to drop. At 1 hour, ~6, after 2 hours back to 5 mmol
mellitus: fasted BS ~7.5 mmol. ~30 min after drink, jumps to ~12 mmol, and keeps rising. At 1 hour, ~15 mmol. After 2 hours back to ~10 mmol.

> 10 mmol, glucose starts to appear in urine (renal threshold)

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33
Q

Doctors are looking for what during a glucose tolerance test?

A
  • higher fasted blood glucose level
  • higher blood glucose peak attained
  • highest point is later than in a normal person (delayed peak)
  • blood glucose levels stay higher for longer
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34
Q

Diabetes symptoms

A

thirsty, hungry, having to pee constantly

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35
Q

glycemic response to foods with fibre vs refined foods

A

in refined CHOs, higher and quicker peak of glucose levels in blood, then drops off

with fibre, gradual peak that keeps for longer

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36
Q

Fructose basics

A
  • fruit sugar
  • less cariogenic than sucrose (caries cavities)
  • in 1970 0% used, in 2020 33% all sugar intake
  • coincides with inc in obesity and type 2 mellitus
  • sweetener in cereals, ketchup, pop, syrups, candy
  • most americans over 2 yrs old have >62 lbs of high fructose corn syrup (HFCS)/yr which is ~130 kcal/day
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37
Q

is HFCS contributing to the obesity epidemic?

A
  • body does not stimulate insulin secretion to HFCS or enhance leptin production (full feeling, no satiety cue to stop eating)
  • stimulates liver fat synthesis and boosts blood TGs (inc CHD risk)
  • humans have never consumed current amnt of HFCS
  • just 1 daily 16 oz bottle pop adds to 20 lb weight gain in 1 year
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38
Q

Sucrose basics

A

glucose and fructose
table sugar
isolated from sugar beet/cane

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39
Q

sucrose myths: blamed for… (12)

- which are true?

A
  • dental carries (TRUE)
  • glucose intolerance
  • insulin resistance
  • behavioural hyperactivity
  • malabsorption syndromes
  • kidney disease
  • diabetes type 2 (CORRELATED)
  • lipidemias (inc TG and LDL, dec HDL) (CORRELATED)
  • CHD risk inc
  • obesity (CORRELATED)
  • food allergies
  • carcinogenicity
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40
Q

Do sugars cause obesity? *facts

A
  • low fat trend removed cals from fat and made them up with excess sugars so total cal intake had more sugar
  • overall kcal/day increased in general tho
  • kcal from drinks is not detected in same way as food so we won’t get full - inc cal and we still eat after that
  • foods with simple sugars and refined carbos are less filling than foods rich in complexes (starch) and fibre
  • refined sugars have no nutrient value other than 4 kcal/g so empty kcal
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41
Q

Her recommendations about sugar?

A

have low kcal beverage in smaller vols

select nutrient dense options over cal dense

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42
Q

metabolic syndrome symptoms

A
  • abdominal obesity
  • elevated fasting glucose levels inc
  • TG inc
  • dec HDL
  • inc BP

only need 3/5 of these to be diagnosed
inc CHD risk
in last 30 years, more rates of this and has a dietary connection to inc intake of refined CHO and sugars

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43
Q

what can reduce chance of metabolic syndrome

A

eat more fruits and vegetables
less juice
inc fibre

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44
Q

Added sugar recommendations over the years

A

2005 DRI - <25% total kcal *too much: ~31 tsps
WHO - <10% total kcal ~12.5 tsps
EWCFG - make foods to dec sugar
2009 AHA - women have 25g/day ~6 tsps (<100kcal)
men have 37.5g/day ~9 tsps (~150kcal)

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45
Q

timmy hoe’s 430g chocolate muffin has how many tsps of added sugar?

A

10 tsps

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46
Q

Lactose basics

A

disaccharide of glucose and galactose
milk sugar
relative sweetness of 0.2, sucrose is 1 (aspartate is 200-300)
all infants and kids have lactase, as we get older most ppl lose ability to make lactase (intolerance)

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47
Q

lactase deficiency

A

most adults cannot break down lactose bc we can’t make lactase (gradual dec 4 yrs old to 16 yrs old)

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48
Q

lactose intolerance

A

symptoms associated with lactase deficiency

MILK SUGAR INTOLERANT

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49
Q

Issues with undigested lactose (i.e. why do you get a stomach ache?)

A
  • enters SI as disaccharide, attracts lots of water (bloating)
  • enters LI and bacterial enzymes ferment lactose producing water, methane and carbon dioxide (gassy)
  • fermentation causes diarrhea with all extra water (not able to be absorbed by colon)
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50
Q

milk allergy

A

MILK PROTEIN causes immune response

  • milk protein leaks out of SI and into blood via mucosa
  • blood mounts immune response (antibodies, can lead to anaphylaxis)
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51
Q

Digestible carbohydrates

A
  • simples (monos and di’s)
  • oligos (raffinose, stachyose, verbascose - prebiotics, common thickener agent)
  • starch (complex)
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52
Q

Indigestible carbohydrates

A
  • resistant starch (legumes, oats - soft when warm, solid when cool - resist amylase ex, cooked white rice and potatoes)
  • dietary fibre (soluble and insoluble) *PLANT materials
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53
Q

soluble fibre

A
  • inside of fruit
    apples, pears, any pulp, oatmeal, psyllium, citric anything
    pectin and gums
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54
Q

insoluble fibre

A
  • outside (skin) of fruit/veg, psyllium

cellulose, hemicellulose, lignin (strawberry seeds)

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55
Q

what does soluble fibre do inside the colon

A

viscous - gel forming

- digesta enters LI and bacteria ferment it (make methane, hydrogen gas) into acetate, propionate and butyrate

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56
Q

Acetate

A
  • 2C
  • enter HPS via portal vein
  • offers minimal cal
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57
Q

Propionate

A
  • 3C

- goes to liver by HPS and stops cholesterol synthesis

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58
Q

Butyrate

A
  • 4C
  • preferred energy source of colon cells
  • potential risk reductor of colorectal cancer
59
Q

the more soluble fibre intake…

A

slowe glucose risk = fuller for longer and less BP spike and drop
- recommended for diabetes

60
Q

what does insoluble fibre do inside the colon?

A
  • digesta is like a scrubbing pad for dishes: tight network, not viscous – resists fermentation, minimal amount happens
  • some production of gases and the 3 short chain FA
  • most comes out in feces, keesp us regular
61
Q

How does soluble fibre dec risk of colorectal cancer

A
  • production of propionate
  • stimulates healthy microbial growth and reduces pathogen growth (overcrowds it)
  • lowers pH (favourable since dec ammonium - prevents damage to colon cells)
62
Q

how does insoluble fibre dec risk of colorectal cancer

A
  • bc of bulking effect, dilutes colonic contents (more gets to intestines, and more toxins are kept in the bulk, not absorbed)
  • provides surface for absorption of colonic contents
  • dec transit time in body which inc regularity (less time for something bad to get absorbed)
  • altered bile metabolism: bile carried to LI helps to reduce amnt that bad bacteria can turn bile to secondary bile acids cancer promoter
63
Q

part of a piece of fruit thats fibre

A
  • bran (outside) : insoluble fibre
  • aleurone layer (inside bran) : vit B and iron
  • germ (seed inside) : vit B and E, iron, MUFA and PUFA
  • endosperm (inside) : whats left after refining (milling). Starch and protein
64
Q

Fibre and blood cholesterol levels

A

soluble fibre dec TC (effectiveness depends on intial TC levels: threshold effect - start with higher TC levels, better results)

  • does this by binding bile acid and chol, taking it out
  • constant fermentation in LI causes propionyl production which shuts cholesterol synthesis down (3:0)
65
Q

fibres key role in weight loss and management

A
  • inc in satiety
  • dec rate of food leaving stomach = delayed gastric emptying = less hungry
  • takes longer to eat (good bc takes 20min to actually feel full)

generally, inc fibre diet means dec fat

66
Q

dietary fibre intake recommendations

NA need to ____ their fibre intake

A

now we have 12-15g/day

  • 1990 FG says we should have most CHO intake as complex with emphasis on whole grains and fruits/veg
  • 2002 DRI AI is ~14g/1000cal which means NA need to DOUBLE fibre intake!
67
Q

Best fibre sources

A
  • legumes and chickpeas
68
Q

Protein basics

A
  • found in every living cell
  • made of AA, 9/20 are essential
  • AA linked by peptide bonds
  • 16% nitrogen by weight as all AA contain amines
69
Q

Protein (g) =

A

Nintake (g) x 6.25

70
Q

Amino acid basics

A

1 carbon bonded to a hydrogen, carboxylate, amino and R side chain group
ex, glycine - CH3
methionine - CH2CH2SCH3

71
Q

Methionine sources

A

high in grains

low in legumes

72
Q

Aspartame and nutrasweet get their low cal sweetner from?

A

Phenylalanine

73
Q

Phenylketonuria (PKU)

A
  • can’t digest Phe
  • shouldn’t have aspartame: Phe will accumulate in blood and cause CNS/brain damage
    Normally, Phe is metabolized to Tyr, but in people with PKU, that rxn is blocked - Phe builds up and becomes phenylketones which is toxic to the brain
74
Q

Protein structure

A
  • many AA linked linearly together via peptide bonds
  • each formation of a peptide bond releases an H2O
  • will form shapes within that linear bond bc of R groups (hydrophobic pockets, positive/negative charge) *alpha helices and B sheets
75
Q

final 3D shape of protein predicted by?

A

way AA are linked together (linear form)

76
Q

structure determines ____

A

Function

77
Q

Insulin structure

A

has 2 interacting peptides that form disulfide bridges which holds its shape
“peptide hormone”

78
Q

Structure function relationship

A
  • in many animals, certain structures are conserved b/n spp (ex insulin) so structure must be important: denaturing the structure stops the function
  • altering the AA sequence can change function of protein dramatically: Sickle cell anemia (Hb has 1 AA changed which means RBC has dec O2 carrying ability)
79
Q

Most at risk group for inadequate protein levels

A

men and women above 70

80
Q

Most common protein sources

A
  • grains, dairy, meat, poultry, pulses/nuts, veggies *cruciferous ones like broccoli or cauliflower, eggs and fruit only ~1%
81
Q

Why we do we need protein

A
  • regulate body processes (hormones *insulin/glucagon, enzymes, neurotransmitters, fluid balance, acid/base balance)
  • growth and repair of tissues (muscles; collagen, actin, myosin) *turn over of tissues and organs
  • immune defense (antibodies)
  • transportation (Hb, transferrin *Fe)
82
Q

protein digestion

A

starts in stomach

  • HCl denatures proteins to ruin function
  • pepsin cleaves peptide bonds, breaks pro into small bits

then in SI

  • pancreas secretes trypsinogen and chymotrypsinogen
  • SI secretes intestinal enterokinase to activate trypsinogen into trypsin
  • trypsin activates intestinal pre-peptidases into peptidases and chymotrypsinogen into chymotrypsin
  • chymotrypsin and trypsin break down dietary peptides for various peptidases to cleave AAs off 1 by 1
83
Q

protein absorption

A
  • pro broken into AA and di and tripeptides via peptidases in SI absorb into portal vein, then into liver (HPS)
  • **most of what we absorb are di and tri’s
84
Q

AA uses in liver

A
  • synthesize into needed proteins
  • immediately used for kcal
  • converted into glycogen or fat stores in adipose (VLDL)
  • released into blood (rest)

WE DO NOT STORE AA THEMSELVES!

85
Q

overall scheme of AA metabolism

A
  • synthesis of body proteins (enzymes, antibodies, lean body mass)
    or
  • breakdown (deamination) to free ammonium ion and remaining C skeleton. Ammonium in liver turned into urea, enters renal system of kidneys, excreted as urine
86
Q

C skeleton uses

A
  • glucose synthesis *body forced to use AA for making glucose via gluconeogenesis
  • energy source (enters krebs cycle)
  • fat synthesis (what happens to any extras! Stored as fat)
87
Q

Protein quality determinants

A
  • digestibility
  • types of AA within
  • proportion of AA in relation to ideal protein source (which has all 9 essential AA ex, human milk protein, chicken eggs)

So good quality pro is fully digested and absorbed, has all essential AAs in proportions needed by body

  • most animal proteins are 90-99% digested
  • plants 70-90% digested but legumes >90% ex. soybeans
88
Q

Adult AA reference intake mg AA / g protein

- Lys, Met and Cys

A

lysine: 51
methionine and cysteine: 25
- so an animal egg has 70 Lys, and 57 Met and Cys
- a pinto bean has 69 Lys and 21 Met and Cys

89
Q

dietary AA called?

AA made from protein turn over called?

A

exogenous AA and endogeneous AA

90
Q

Ex of combining complementary proteins

A
  • grains and legumes good with each other since grains high in Met and Cys and legumes high in Lys
  • good meal has: grains, some legumes, some seeds and nuts, a milk product = lactovegetarian
  • if add an egg onto this = lactovovegetarian
  • can add fish onto this = pescativegetarian
91
Q

Proteins of animal origin are low in __ AA

A

NONE

- have all 9 essential AA

92
Q

Proteins of plant original are low in __ AA

A

at least one

  • grains: limiting AA is Lys
  • legumes: limiting AA is Met and Cys
93
Q

Potential benefits of a plant centred diet?

A
  • healthy, low-cost alternative
  • vegetarians: lower body weight, dec cases of obesity, diabetes, cardiovascular disease, high BP, some cancers
  • lower body weight bc of dec overall kcal intake (since inc fibre intake = inc satiety for longer)
  • lower chronic disease risk bc of inc fibre = dec in body weight, as well fats in plants are lower in sat fats and chol
  • also higher in grains, legumes, fruits, vegetables (so antioxidants, fibre, minerals and vitamins)
94
Q

Which nutrients are at risk of insufficient levels in a plant based diet?

A
  • protein, vit B12, calcium, vit D, iron, zinc, omega 3 FA
95
Q

N-balance =

A

N(in) - N(out)

  • for adults maintaining weight, = 0
  • for ppl gaining lean body mass or repairing tissues (growth, pregnacy, athletic training) = +ve
  • for ppl losing weight/protein (diet, wasting, disease, severe burns!!) = -ve
96
Q

DRI protein levels

A
  • AMDR = 10-35% kcal
    RDA = 0.8g pro / kg of body weight / day for adults 19+
    (this is for non athletes)
    babies need most protein
97
Q

Protein trends

A
  • canadians get ~15% kcal from pro
  • in NA, often 1.5-2.5 x more than needed
  • dieters and elderly at risk of inadequate pro intake
98
Q

Determining protein needed =

A

own weight in lb / 2.2 to get kg
then, __ kg • 0.8
= ___ g protein in one day

99
Q

Do athletes need more protein

A

YES

  • endurance athletes need 1.2-1.4 g/kg weight /day
  • power athletes need 1.2-1.7 g/kg weight /day
100
Q

If Jane is not an athlete, and is 60kg, intaking 2000 kcal/day with 15% of that coming from protein, how much protein is she having in one day? Should she increase or decrease her protein intake?

A

60kg • 2.2 = 132 lb
2000 kcal • 0.15 = 300kcal
300 kcal ÷ 4 g pro/kcal = 75 g protein /day
UNITS: ___ g protein / kg of body weight
so 75g protein ÷ 60 kg = 1.25 g protein / kg weight / day

she needs to decrease the amount of protein she gets

101
Q

AA supplements

A

has absorption and transport issues that:

  • limit protein synthesis (outcompetes other essential AA, saturate transporters with 1 AA)
  • limit neurotransmitters synthesis since they are peptide based (blood brain barrier transporters also saturated, insufficient in other types)
  • N retention dec since body can retain more N via di and tripeptides vs individual AA
  • expensive, taste terrible, cause GI distress
  • better and easier to get AA from food
102
Q

Is too much protein bad

A
  • inc overall kcal intake
  • high protein foods usually high sat fat
  • in Ca loss in urine
  • overworked/damaged kidneys converting ammonium to urea to urine (but if otherwise healthy, this not an issue)
  • cancer: link b/n red/deli meats and colorectal cancer rates inc (why moderation, variety, and dilution so important)
103
Q

Ebalance =

A

Eintake - Eutilization
if +ve, gain weight
if -ve, lose weight

104
Q

Total energy expenditure =

A

TEE = basal needs + activity + thermogenesis
basal needs ~55-70%, inc for sedentary ppl
activity ~15-30%, inc for active ppl
thermogenesis ~5-10%

105
Q

Basal energy expenditure

A

BEE
amnt of kcal needed to sustain basic life processes
- men burn more (more lean body mass), larger body = burn more, younger ppl burn more

106
Q

Basal metabolic rate

A

BMR

  • measure of O2 use and CO2 release at rest
  • generally carried out right after waking but before getting up
  • measured via calorimeter (ventilated hood) either directly (amnt of body heat released) or indirectly (O2 and CO2)
107
Q

BMR estimates for men and women

A
  • 1.0kcal/kg/hr for men

- 0.9kcal/kg/hr for women

108
Q

resting metabolic rate

A

RMR
same as REE
- often measured instead since its more practical
- wake up at home, drive into lab, get tested same way
- Harris Benedict equation used
- will be 10-20% higher than BMR

109
Q

Lean body mass

A

all non-fat components in body

  • organs, tissues, bone, fluids – anything that is metabolically active
  • inc overall LBM = inc kcal burned
110
Q

obesity causes BMR how

A

as overall fat inc, overall LBM inc so BMR inc bc…

  • inc in skeletal muscle to support weight
  • inc in organ size (GI tract, heart)
  • inc in # of fat cells
  • inc in vascularization
111
Q

BMR or RMR response to injury or illness

-burn, bad infection (peritonitis), fracture, diet/partial starvation, total starvation

A

Start at 100% of BMR/RMR
Burn: dramatic peak, then drop. Almost 200% peak
Bad infection: less dramatic peak and drop. ~150%
Fracture: minimal peak and drop. ~125%
Diet: bit of a steady decline as metabolism dec. ~80%
Total starvation: dramatic decline as less important functions begin to shut off (ex, GI tract) ~25%

112
Q

Thermogenesis occurs in response to

A
  • stress
  • cold exposure (shivering)
  • drugs and medications (caffeine, nicotine, alcohol)
  • food (thermic effect of food or DIT)

stress and cold exposure = adaptive thermogenesis

113
Q

Why does metabolism increase with food intake?

“thermic effect of food”

A
  • digestive processes (hormones, enzymes, motility)
  • absorption via active transporter
  • causes inc in biosynthesis of glycogen, fat, non-essential fa
114
Q

energy intake recommendations: what is used to measure how much energy we need?

A

RDA is too general, and if we use an EAR some people will lose and some will gain weight
- use EER: estimated energy requirement

115
Q

EER

A
  • disadv: uses reference adult which isn’t representative
  • different for men and women
  • will be given PA value in Q
116
Q

1 Kg = ____ lb

A

2.2 lb

117
Q

1 inch = ___ m

A

(2.54 cm) so 0.0254 m

118
Q

EER equation of men over 19 years old

A

EER = 662 - (9.53 • age) + PA • [(15.91 • weight in kg) + (539.6 • height in m)]

119
Q

EER equation of women over 19 years old

A

EER = 354 - (6.91 • age) + PA • [(9.36 • weight in kg) + 726 • height in m)]

120
Q

healthy body weight

A
  • life insurance
  • very controversial, as a person’s health should be assessed individually and in person, by a professional health person, and taking many different factors into consideration
121
Q

BMI =

A

weight in kg ÷ (height in cm)²

122
Q

BMI values

A

≤ 18.4 is underweight (women can lose period; anemia, bone density dec, have digestive disorders)
18.5 - 24.9 is normal weight
25.0 - 29.9 is overweight
≥ 30 is obese

123
Q

BMI benefits

A
  • accurate health predictor (and future morbidity)
  • widely used measure of health risk w under/over weight
  • compares well with body fat measures: fat fold, bioelectric impedance, underwater weighing
124
Q

BMI limitations

A
  • intended for adults only
  • never used for pregnant/lactating women
  • lots of special considerations
  • doesn’t adress body fat distribution: visceral fat is worse
125
Q

Waist Circumference: visceral fat cutoff levels for men and women (where risk for health problems inc)

A

men - ≥ 102 cm or 40 in around

women - ≥ 88cm or 35 in around

126
Q

special considerations BMI does not account for (6)

A
  • kids and adolescents (growth charts)
  • young adults ≥ 18 not at full growth (men)
  • muscular athletes/adults (BMI can’t tell fat from lean body mass –– body composition)
  • thicc ppl (fit and heavy set)
  • ethnic/racial groups differ in body composition
  • older adults ≥ 65 have height dec and weight stays the same so inaccurate reading
127
Q

BMI error margins for men and women

A

women: +/- 160
men: +/- 200

128
Q

Health risks associated with obesity and being overweight? (11)

A
  • Cardiovasc diseases: CHD, ischemic stroke
  • insulin resistance leading to type 2 mellitus
  • dyslipidemia (lots of lipids in blood leads to inc LDL/TG, dec HDL)
  • hypertension
  • osteoarthritis
  • inc # and types of cancer
  • gall bladder disease
  • obstructive sleep apnea and respiratory issues
  • psychosocial problems
  • functional limitations bc of carrying excess weight
  • impaired fertility
129
Q

Cancer risk increases as weight increases why? (3)

A
  • more estrogen released from adipose tissue (fat) that acts on receptors in tissues causing rapid proliferation (cell turn over)
  • inflammatory markers inc causing inc proliferation
  • as insulin resistance inc, pancreas releases more insulin which builds up in blood and causes inc cell proliferation
130
Q

Why do people not follow recommended dietary intake?

A
  1. ambivalence/lack of concern/ignorance is bliss
    - pleasure and enjoyment of food (taste)
    - leisure/personal choice (“can’t tell me what to do”)
    - culture/tradition (cooking for other ppl, they don’t want to eat anything else)
    - priorities (Maslow’s Hierarchy)
    - misinformation and myths (under-education)
  2. parental disconnect with children’s weight and health risks
    - parents think kids are normal weight when really over/under *normal curve has shifted right
131
Q

Some calls to action about obesity rise

A
  • British government targeted obesity in 2008 by bringing back home-ec, encouraging cooking at home, and bringing in nutrition team to answer phone calls (questions, recipes..)
  • CDPAC (chronic disease prevention alliance of canada) in 2010 targeted schools/community centres and identifying overweight in infants and kids (BMI like), trying to inc availability/affordability of nutritious foods, and protecting kids from marketing of foods and beverages
132
Q

____% of attempts to lose weight via diets fail to produce long term health weight

A

95%

133
Q

Yo-Yo Dieting Effects

A

-weight cycling causes dec in metabolism because your body thinks you are starving so you actually end up gaining more weight than you would have normally if you hadn’t dieted

134
Q

Causes of diets (Why do we diet)?

What does dieting cause?

A
  • NA culture: attention is misdirected at weight loss instead of being healthy via changing lifestyle and eating habits
  • Dieting will dec BMR and also dec self-esteem
135
Q

Recommendation if your BMI ≥ 25, your waist circumference is increasing, triglyceride (cholesterol) levels are inc, blood pressure is inc, and blood glucose is inc?

A

5-10% weight loss

136
Q

Health weight loss steps for long term weight management

A
  1. have sensibile, balanced diet you enjoy that incorporates all 4 fg to ensure fibre is high, fat is lowish, and protein is adequate (look at directive statements)
  2. eat less overall portion control - dec overall kcal
  3. enjoy regular activity to prevent LBM loss (to build some too), will burn more kcal
137
Q

Diet blueprint to attain and maintain healthy weight (7)

A
  1. have a kcal deficit (less food and inc exercise)
  2. must be adequate in ALL nutrients (fibre, minerals, vitamins – veg, fruit, whole grains, lean meat)
  3. should have high satiety value
  4. should be adaptable for family meals and eating out
  5. must have reasonable cost: learn how to do it yourself
  6. person needs patience since lose ≥ 1-2lb/week, won’t be maintainable
  7. need people to teach, support and result in changing eating habits
138
Q

Effects that predict weight control success (6)

A
  1. high social class (correlated with inc education)
  2. no family history of obesity
  3. social support
  4. physical activity
  5. behavioural self-control (eat slower, have planned meal times, don’t eat after supper, some ppl are told to keep a record of meals)
  6. coping abilities *cognitive restructuring
139
Q

self worth ≠ ____

A

weight loss

140
Q

Fad/popular diets (2)

A

Crash diets and low CHO/high protein and fat diets

141
Q

Crash Diets

A
  • after last normal meal, body will use glycogen stores to keep RBCs, kidneys, etc supplied with glucose (fuels body until next meal)
  • 12-15 hours after that meal, liver glycogen is depleted, so protein from muscles begin to break down via gluconeogenesis into glucose for RBCs, kidneys..
  • over the next 2-3 days, will have a massive LBM loss (protein, water, electrolytes like Na, K, Cl) *this is where the “weight loss” comes from
  • over the next 7-10 days, body will gradually shift into starving mode i.e. Ketosis will occur: fat is still used at 9kcal/g but some will be broken down into Ketones to fuel parts of brain; still have same LBM breakdown (lessened rate tho).*BMR decreases too to conserve energy – unnecessary body processes shut down. *hard to exercise here too
142
Q

End result of crash diets?

A
  • loss of fat, LBM, reduced BMR, ability to exercise

- weight will return once starting eating normally again

143
Q

Low CHO/high protein and fat diets

A

(assuming this is a weight loss diet)

  • similar change in metabolism as fasting (BMR dec)
  • counterintuitive because even though you’re consuming protein/fat, the CHO overall decreases, so not enough glucose to feed RBCs, etc, and gluconeogenesis turns LBM into glucose
144
Q

How much CHO do we need minimum to spare body protein breakdown

A

≥ 100g CHO/day

  • the DRI of 45-65% IS AROUND 200-300G OF CHO
  • want high fibre CHO!

NUTR 120 (4 decks)

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