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Flashcards in Nutrition 1 Deck (40)

What are the essential amino acids?

Essential fatty acids?

Essential amino acids

Essential fatty acids


What is Dietary Reference Intake (DRI)?

Dietary Reference Intake (DRI) : defined as intake meeting nutrient requirements in 97.5% of population of specific age and gender, ie, two standard deviations above the mean requirement.

Schematic of normal distribution of nutrient requirements for a population, area under the curve to the left of arrow indicates coverage of population by DRI


Describe the primary energy sources calorie content:

lipids/dietary fats

What are the current national dietary recommendations?

- primary energy sources carbohydrates ( 4 kcal/g),

lipids or dietary fats (9 kcal/g),

protein ( 4 kcal/g)

- additional energy source is alcohol ( 7 kcal/g)
current national dietary recommendations:
less than 30% kcal from fat ( less than 10% saturated fats, less than 1% trans fats)

15% kcal from protein

55-60% kcal from carbohydrate

Carbohydrate, fat and protein comprise the essential macronutrients


A male patient has been admitted with severe inflammatory bowel disease and significant weight loss. His nutritional requirements include an increase in protein intake to 2.5 g/kg body weight (current recommendation for adults is approx 0.8 g/kg/day), and decrease in calories from fat to 20% of total intake. Patient current weight is 60 kg and energy intake prescription is 2400 kcal/day.

How many calories will be derived from protein? Proportion of total intake?

How many grams of fat will be provided?

How many grams of carbohydrate will be provided?

How many calories will be derived from protein? Proportion of total intake? 600g (25%)

How many grams of fat will be provided? 53.3 g

How many grams of carbohydrate will be provided? 330 g


What is the definition of energy requirement?

amount of food energy needed to balance energy expenditure in order to maintain body size, body composition and a level of necessary and desirable physical activity consistent with long-term good health.

This includes the energy needed for optimal growth and development of children, for deposition of tissues during pregnancy and for production of milk during lactation.


Define calorimetry.
Define indirect calorimetry.

Upon combustion (cellular respiration), based upon its chemical structure each substrate (eg, carbohydrate, fat) produces a set amount of CO2 and energy. How many kcal/mol do glucose and fat produce?

Calorimetry – measurement of heat produced in physical reactions

Indirect calorimetry – calculation of heat produced from measuring CO2 production and O2 consumption.

Glucose produces 671 kcal per mole

Fat produces 2390 kcal per mole


What is the respiratory quotient (RQ) and what does it give you an estimate of?

What would an RQ of .70 indicate? An RQ of 1?

The ratio of CO2 produced to O2 consumed (VCO2/VO2) is called the respiratory quotient (RQ) and gives you an estimate of the relative mix of fuels burned, eg, a RQ of 0.70 indicates that fat was the only fuel burned during the measurement period while RQ of 1.00 is all glucose (RQ greater 1.00 suggests excess glucose is being stored as in after eating)


What is basal or metabolic rate? How is it measured?

Basal or resting metabolic rate – amount of energy required for maintenance of functions essential for life while the body is at rest (eg, respiration, cardiac functions, maintenance of muscle tone).

Measured by indirect calorimetry.


Define joule and calorie. What is the conversion between the two?

1 joule (J) is the amount of mechanical energy required to displace a mass of 1 kg through a distance of 1 meter with an acceleration of 1 meter per second
(1 J = 1 kg x 1 m2 x 1 sec2).

1 calorie is the amount of heat required to raise 1 gram of water 1 degree centigrade. Typically used as 1000 calories or 1 kilocalorie (kcal).

The conversion factors between joules and kilocalories are: 1 kcal = 4.184 kJ, or conversely, 1 kJ = 0.239 kcal.


What are some components of daily energy expenditure in weight stable adults and special stages of growth?

Weight stable adults
basal metabolic rate (resting metabolic rate) 60-70%
dietary-induced thermogenesis (thermic effect of food) 10%
physical activity (non-BMR, non-DIT expenditure) 20-30%

Special stages of growth
growth (tissue development & energy in new tissue)
pregnancy (maternal & fetal tissue deposition)
lactation (milk production & energy in milk)


Describe how the following stages contribute to energy requirements at various points in the life-cycle:

Growth (and energy cost of growth) during first 3 months of life, 12 months, second year...


Growth: energy cost of Growth has 2 components: 1) energy needed to synthesize growing tissues and 2) energy deposited in those tissues

Energy cost of growth is 35% of total energy requirement during the first 3 months of age, falls to 5% at 12 months & 3% in the second year, remains 1 to 2% until mid-adolescence, negligible in the late teens onward

Pregnancy: extra energy needed for growth of fetus, placenta and various maternal tissues, such as the uterus, breasts and fat stores, as well as for changes in maternal metabolism and the increase in maternal effort at rest and during physical activity.

Lactation: energy cost of lactation has 2 components: 1) energy content of milk secreted and 2) energy required to produce milk


Describe the components of the basal metabolic rate (or resting metabolic rate).

What are the most metabolically active organs?

How much BMR does skeletal muscle comprise? Why?

Within cells, what is more BMR energy expended in?

How does this change in exercise?

Over 60% of BMR in healthy adults from heart (most metabolically active), kidneys, liver and brain

Skeletal muscle, although low relative metabolic activity at rest, comprises over 25% of total BMR because of sheer volume of tissue

Within cells, most BMR energy expended in macromolecule turnover, ion transport, and regulatory cycling of intermediary metabolites

In exercise sig. redistribution of that E expenditure.
as exercise increases, muscle metabolic rate or proportion of expenditure increases dramatically


Describe whether the following constitute decreases or increases in BMR:

Down Syndrome
Parkinson's disease
Anorexia nervosa
Starvation state
Very low-calorie diets
Hypermetabolic state (burns, sepsis)

Decreases in BMR (per kg of fat-free mass) can occur:
- hypothyroidism
- anorexia nervosa
- Down syndrome
- very-low-calorie diets
- starvation states

Increases in BMR can also be observed:
- hyperthyroidism
- Parkinson’s disease
- asthma
- hypermetabolic state – eg, burns, sepsis


True or False?
1. Overweight and obese individuals have relatively low metabolic rates.

2. Low metabolism contributes significantly to obese individuals excess weight gain.

3. There are diets available to increase a person’s metabolic rate thereby inducing weight loss.

4. A person’s metabolic rate decreases during caloric restriction inhibiting the rate of weight loss.

True or False?
Overweight and obese individuals have relatively low metabolic rates. -False

Low metabolism contributes significantly to obese individuals excess weight gain. (False- In healthy individuals, there is always some variation in parameters of metabolism. There is about a 7-9% normal variation in BMR per kg fat-free mass. However, relatively low BMR does not lead to increased weight gain in most adult populations – White US adults, African-American women, Nigerian adults or Jamaican adults.
In only one population – the Pima Indians of Arizona – has relatively low BMR been associated with increased weight gain.)

There are diets available to increase a person’s metabolic rate thereby inducing weight loss. (False)

A person’s metabolic rate decreases during caloric restriction inhibiting the rate of weight loss. (True)


Explain why the following statement is false:

Overweight and obese individuals have relatively low metabolic rates.

basal metabolic rate comprised of organ mass and tissue (fat mass rel. inert metabolically)

2 people.. one 400 pounds, one 200 pounds and same fat free mass (organ mass, muscle mass, then have same metabolic rate…) per unit weight… 400 pound has lots of extra fat mass adding to weight so now denometer gets much bigger so per kg/mass they have lower metabolic weight but not bc of slower metabolism its due to extra weight from fat tissue


What is the only way to increase metabolic rate?

( cant increase metabolism except short term w caffeine..)

not long term adaptation. only way to increase metabolic weight is add more fat-free mass)

Except for short-term increases in metabolism associated with ingestion of caffeine or ephedrine, diets cannot increase one’s metabolic rate. Increasing one’s fat-free mass (ie, metabolically active tissue) through muscle-building exercise will increase metabolic rate proportionally. Metabolism naturally slows gradually in aging as cellular metabolism slows down.


How is the relationship between basal metabolic rate and fat free mass represented on a graph?

Where is anorexia on this graph?

Relationship between basal metabolic rate & fat-free mass is linear and consistent across a wide range of body sizes.

Slide 12, 13

Basal metabolism is suppressed in situations of severe caloric restriction – such as anorexia nervosa, very-low-calorie diets or semi-starvation….
Slide 22


Describe the two mechanisms by which basal metabolic rate does decrease.

Describe the Minnesota Study during WWII.

Basal metabolic rate does decrease during severe caloric restriction through two mechanisms: 1) loss of fat-free mass (metabolically active tissue) and 2) adaptive down-regulation of BMR

The Minnesota Study during World War II illustrated the effect of 6 months of semi-starvation on male “volunteers”

BMR was decreased by 631 kcal/day – one-third of which was due to loss of fat-free mass and two-thirds due to unspecified down-regulation (decreased heart rate, decreased blood cell production, slowed respiration)

Upon refeeding, BMR normalized per unit fat-free mass quickly


In a semi-starvation state and in refeeding is one is negative or positive or equilibrium nitrogen balance?

negative nitrogen balance throughout semi-starvation period, positive during refeeding


A 30-year-old man has been fasting for religious reasons for several days. His blood glucose level is now about 60% of normal, but he does not feel lightheaded because his brain has reduced its need for serum glucose by using which of the following sources as an alternate energy source?

a. Apoprotein B
b. Beta-carotene
c. Beta-hydroxybutyrate
d. C reactive protein
e. Coenzyme A



In an overnight fast or simple 2 day fast describe the breakdown of energy utilization.

In normal overnight fast or simple 1-day fast this is the breakdown of energy utilization.

Body proteins are normally turning over and the catabolized proteins yield amino acids that can be used in gluconeogenesis – this is normal process.

So, for a 24-hour fast you see here that about 75 g protein are used for fuel after conversion to glucose, about 160 g of adipose tissue is broken down and used for fuel (1080 kcal from fatty acids) – a portion is converted to ketones and the rest straight fatty acids.

Glycogen provides the remainder along with glucose derived from gluconeogenesis (180g - 720 kcal).

In the urine of normal and short fasted individuals we see between 5-10 g of urea/d – normal turnover and utilization of proteins and relatively little ketone bodies.

Most important message from this graph is that individuals normally breakdown a mixture of proteins, adipose tissue and glycogen for fuel utilization.


How does the body change after prolonged fast (5-6 weeks)?

Metabolic rate? Protein breakdown? Glucose? Brain? What do tissues use for fuel?

After a prolonged fast, there are a few things to observe. Metabolic rate decreases (adaptation to fasting), protein breakdown slows dramatically, use of glucose for fuel decreases except in those tissues that have absolute requirement (RBC & lens & some nerve tissue), brain adapts to using ketones (can cross blood brain barrier), other tissues rely almost exclusively on fatty acids for fuel. Thus body protein is spared as much as possible.


What is the correlation between BMI and body fat?

R= . 85

Body mass index is highly correlated with adiposity in most populations. BMI can be misleading for some individuals.

ethnic and racial diff in proportions of lean to fat at any given BMI

SA indian higher proportion of body fat

BMI imperfect. in some groups not a good measure of metabolic health


What are the consequences of low levels of body fat?

High levels of body fat?

consequences of low levels body fat
amenorrhea, cold intolerance, excessive use of body protein stores for energy

consequences of high levels of body fat
type 2 diabetes
pretty much every organ system is affected….


Define the following terms in regards to protein energy malnutrition (PEM).


Stunting - chronic, relatively mild PEM; defined as greater or equal to 2 standard deviations below the mean height-for-age in children

Underweight – result of acute mild PEM; defined in adults as BMI less than 18.5

Wasting - sign of acute, severe PEM; defined as greater than or equal to 2 standard deviations below mean weight-for-height


Describe Marasmus and Kwashiorkor.

Wasting - sign of acute, severe PEM; defined as
greater or equal to 2 standard deviations below mean weight-for-height

Marasmus - severe wasting ( less than 60% expected weight) with marked loss of subcutaneous fat and skeletal muscle

Kwashiorkor - wasting with edema and impaired renal function (60-80% expected weight) - skin and hair color changes often present; fatty liver which does not progress to cirrhosis


In what clinical context are we most likely to see PEM in the US?

hypermetabolic states (burns, infection); anorexia nervosa; chronic kidney disease/dialysis; elderly; poorly managed post-bariatric surgery


Describe lipids and dietary fats.

Which types are hydrophobic/hydrophilic?
What do dietary lipids include?

Compounds soluble in organic solvents, such as acetone, ether or chloroform.

Vary widely in size, polarity and function: hydrophobic triglycerides & sterol esters to more water-soluble phospholipids

Dietary lipids include cholesterol and phytosterols, triglycerides (majority of lipids consumed by humans, primary source of fat-derived E, 3 fatty acids esterified to glycerol)


Describe saturated fatty acids (SFA)

Double bonds/single bonds?
State at room temperature?

No double bonds
(ex: palmitic acid, stearic acid)

Fats high in SFA tend to be solid at room temperature

Associated with hypercholesterolemia - recommended intake less than 7% total caloric intake

Mechanism by which plasma cholesterol raised by SFA not clearly elucidated - may be decreased catabolism of LDL


Which type of fat is in high concentration in animal and dairy fats?

palm and coconut oils?

olive and canola oils?

saturated fatty acids

saturated fatty acids

olive and canola- MUFA


Describe mono-unsaturated fatty acids (MUFA):

Describe the structure (How many C's? What type of bonds?
What is it found in?

How is it associated with increased plasma LDL or decreased HDL concentrations?

- Must be at least 12 carbons long, contain a double bond at the n-9 position.

- Example: Oleic acid (C18:1, n-9 cis) CH3(CH2)7CH=CH(CH2)7COOH
- Found in high concentration - olive & canola oils

- Not associated with increased plasma LDL or decreased HDL concentrations!!


Describe Polyunsaturated Fatty Acids (PUFA).

What are the essential fatty acids?

In what state are oils high in PUFA at room temp?

How are they associated with LDL and HDL?

Fatty acids with double bonds at the n-3 or n-6 positions cannot be synthesized by humans

Essential fatty acids: Linoleic acid, alpha-Linolenic acid

Oils high in PUFA generally liquid at room temp

Associated with lower serum LDL concentrations (especially n-3) – but also can lower HDL


Which fatty acids have an impact on LDL and HDL? Describe.

Which are associated with hypercholesterolemia?

poly unsaturated fatty acids- Associated with lower serum LDL concentrations (especially n-3) - but also can lower HDL

monounsaturated fatty acids- Not associated with hypercholesterolemia or decreased HDL

saturated fatty acids- Associated with hypercholesterolemia


Describe trans fatty acids.

How do they affect LDL/HDL?

Typically man-made; added to vegetable oils to increase viscosity – used in margarine and commercially-produced baked goods (currently make up 2-3% of fats in US diet)

Increase LDL & lowers HDL

Mechanism for raising plasma cholesterol not known

Hydrogenation turns liquid oils to solid fats

Reduces the rotational mobility of the fatty acyl chain

Associated with increased LDL levels, CHD and atherosclerosis

- to the same degree or more than saturated fats


What substances have omega-6-fatty acids?

What type of development do they aid in?

How do they affect people at risk for CVD? Those not at risk?

- Omega-6 fatty acids found in corn, safflower & soybean oils; omega-3 fatty acids found in oily fish

- Omega-3 fatty acids – eicosapentaenoic acid EPA (C20:5) and docosahexaenoic acid (DHA) (C22:6) derivatives of linolenic acid; found to be important for structure and function of membranes in retina & CNS

- Oils high in PUFA liquid at room temperature

- Associated with lower plasma LDL concentrations

Likely critical for neural and retinal tissue development
Have been shown to reduce CVD risk in people at high risk –
decrease risk of arrhythmias (sudden cardiac death)
decrease plasma triglyceride levels
decrease growth rate of atherosclerotic plaques
Multiple large-scale population-based clinical trials have shown no evidence for lowered CVD risk in non-high risk individuals

Preterm infants may be vulnerable to omega-3 deficiency because of immature desaturase and elongase enzyme activities & low fat stores


Describe essential fatty acid deficiency.

Classic signs of EFA deficiency: reduced growth rates, scaly dermatitis with increased loss of water, male and female infertility, depressed inflammatory responses; kidney abnormalities, abnormal liver mitochondria, decrease capillary resistance, increased fragility of erythrocyes and reduced contractility of cardia muscle

EFA deficiency is rare in humans

Can result from very low fat diets – approx. 10-20% of calories coming from fat (eg, Ornish diet)


What causes lipid peroxidation?

What results?

What is produced? Clinical manifestations?

Oxidative stress (normal byproduct of cellular & extracellular metabolic activity) induces lipid peroxidation of cell membranes

Results in decrease in membrane fluidity & increased permeability to cations, loss of enzyme & receptor activity, impacts membrane secretory activity

Oxidation of membrane cholesterol produces oxysterols or cholesterol oxides, implicated in atherosclerosis.


Describe soluble fibers.

Describe their roles?
How do they affect insulin?
What might they simulate?

Dietary sources?

Soluble fibers, ie, water soluble, includes pectins and gums; fermented
in colon into gas and by-products

Implicated in cholesterol lowering
act as bile-acid sequestering agent
reduce rate of insulin rise by slowing CHO absorption thereby slowing hepatic cholesterol synthesis
stimulate production of short-chain fatty acids in gut which are then absorbed by portal circulation and inhibit cholesterol synthesis

Dietary sources: legumes, oats, some fruits, some vegetables, nuts


Describe insoluble fibers.

What is included?

How do they affect cholesterol?
Dietary sources?

Insoluble fibers include cellulose and lignans; less impact on lowering cholesterol levels

Dietary sources: whole grains, wheat bran, some vegetables, potato skins


What benefits might high fiber diets maintained for a long term yield?

High fiber diets maintained for long term believed to reduce the incidence of colon cancer; proposed mechanisms include 1) bulking action of fiber speeds transit through the colon reducing absorption of adverse chemicals and 2) fiber adsorbs carcinogenic agents