Transcript MacronutI

Thomas O. Henderson, Ph. D.
Professor Emeritus
Dept. of Biochemistry &
Molecular Genetics
• Office: 321 CMW
• Phone: 6-5978
• email: [email protected]
Macronutrients
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Lecture 2
Carbohydrates & Fiber
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Lecture 3
Fats (Lipids)
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Lecture 4
Proteins
From MMWR 53, No. 4; February 6, 2004
Macronutrients I
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Overview
Carbohydrates
Fiber
2002 IOM-FNB Guidelines for
Macronutrients
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Goal of new recommendation
“to
meet the body’s daily energy and
nutritional
needs while minimizing risks for chronic disease.”
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Guidelines set for macronutrients:
carbohydrates, fats, proteins
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For first time, DRI’s set for dietary fiber and
essential fatty acids (n-3 & n-6)
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Guidelines set for exercise
Acceptable Macronutrient
Distribution Range (AMDR)
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AMDR just another way of stating the % of calories
from a given class of macronutrient
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2002 recs adults ≥19 years:
% of daily calories
Carbohydrates
45 - 65
Fats
20 - 35%
Proteins
10 - 35%
 ≤25%
of total calories from “added sugar”
AMDR (continued)
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Recommendations more flexible than in past
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Ranges set so that total dietary intake would be of
breadth and quality to insure intake of essential
nutrients (i.e., vitamins & minerals)
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Diets very low in either carbs or fat likely to be
deficient in one or more essential nutrient
AMDR (continued)
When fat intakes are low and carb intake is high:
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HDL is reduced
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ratio of plasma cholesterol:HDL increased
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plasma triacylglycerol (TAG) increased
These all consistent with increased risk of coronary
heart disease (CHD; CAD)
AMDR (continued)
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When fat intakes are high, people gain weight
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Can exacerbate health of persons already
susceptible to obesity, particularly risk of CHD
and Type II diabetes
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High fat diets usually associated with increased
intake of saturated fatty acids
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The latter, in turn, can increase LDL levels and
thereby increase risk of CHD
All Fatty Acids are NOT Equal!
If fat intake is at high end of 20 -35% range,
one would be well advised to
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limit intake of cholesterol and
saturated and trans fatty acids
replace them with monounsaturated and
polyunsaturated fatty acids
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Carbohydrates
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2002 IOM-FNB report set RDA for intake of
digestible carbohydrate
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for ages 1 - >70, 130 g/d recommended
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175 & 210 g/d for lactating and pregnant women,
respectively
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for 0 - 6 months, AI set at 60 g/d
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for 7 - 12 months, AI set at 95 g/d
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RDA (& AI) for carbs based on minimum amount
needed to provide glucose for brain function
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Most of us regularly exceed RDA
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AMDR set at 45 - 65% of calories/day
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No more than 25% of calories/day from “added
sugars”
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Emphasis should be on obtaining bulk of daily
carbs from fruits, vegetables, and minimally
processed whole grains and whole grain
products
Major Sources of Carbohydrates
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disaccharides (sucrose, lactose)
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starch (amylose & amylopectin)
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minor, variable amounts of glycogen (in meats),
maltose, trehalose (mushrooms), raffinose
(legumes)
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very little monosaccharide in natural diet
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increased amounts of added fructose (highfructose corn syrup or solids)
Forms of Starch
Amylose
Amylopectin
Cellulose
(NOT a form
of starch)
On a Food Label, Sugars Include:
brown sugar
invert sugar
corn sweetener
lactose
corn syrup
maltose
fructose
molasses
fruit juice concentrate
raw sugar
glucose (dextrose)
[table] sugar (sucrose)
high-fructose corn syrup
syrup
honey
Consequences of chronic elevation in
concentration of hexoses in blood
2 possible consequences are
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enzymatic formation of sugar alcohols
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nonenzymatic glycosylation (“glycation”) of
proteins
 Both
of these associated with long term
pathologies of nerves, blood vessels, kidneys,
and lens as found in diabetes and galactosemia
Sugar Alcohols
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Aldose reductase and polyol dehydrogenase
involved
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Isozymes of aldose reductase found in most
tissues
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Especially high in Schwann cells of peripheral
nerves, kidney papillae, and lens epithelium
Ways in which sugar alcohols cause cell damage
and pathologies not known
However, since they do not diffuse out of cells very
readily, they can cause cell damage by cellular
swelling associated with osmosis
The enzymatic reactions are reversible so that
favored direction is determined by
substrate/product concentrations (i. e., “mass
action”)
Protein glycosylation (glycation)
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nonenzymatic process
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get advanced glycosylation product
formation (“AGE products”) with proteins
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quite possible that glycosylation of DNA
occurs also
An estimate of how well a diabetic patient has
controlled her/his hyperglycemia over past 5-6
weeks can be made by measuring extent of
hemoglobin glycosylation (HbA1c)
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Recall - RBC hemoglobin has lifespan of
~120 days
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Shorter or more recent periods can be
estimated by measuring albumin
glycosylation
Galactose Metabolism
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By far major source of galactose in human diet is
in form of lactose
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Major source of lactose is milk and milk products
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Major organ involved in galactose metabolism is
liver
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There are several inborn errors involving
metabolism of galactose
Lactase deficiency (aka Hypolactasia)
(lactose or milk intolerence)
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In most mammals, including the great majority of humans,
lactase activity disappears after weaning or at the latest
during adolescence.
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In the case of humans, especially true for Southeast
Asians and Africans.
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About 70% of African-Americans, >80% of Chinese and
>70% of Mexicans are lactose intolerant
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In contrast, lactase deficiency uncommon in Northwest
Europeans such as Scandinavians (~3% of Danes)
2 types of galactosemia are caused by
deficiency or absence of:
D-galactose 1-P uridyltransferase
and
galactokinase
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The first more common (prevalence = 1 in 70,000) than
second (prevalence = 1 in 1 x 105) and has far greater
clinical importance in terms of associated pathologies,
especially in homozygotes
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In Illinois the incidence of the first defect is ~1 in 30,000
live births
Definitions:
Incidence = 1 in n live births
Prevalence = 1 in n people
The pathologies associated with defective Dgalactose 1-P uridyl transferase include:
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severe mental retardation, hepatomegaly,
cataracts, and non-specific morphological
changes in the CNS
In Illinois, all newborns are screened for
galactosemia
Affected infants MUST be placed on a galactosefree (i. e., milk-free) diet immediately to prevent
irreversible damage
Fructose Metabolism
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Major sources of fructose in diet are fruits, honey,
sucrose and, now, in form of high fructose corn
syrup or solids as an added sweetener in soft
drinks, candy, etc.
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Fructose -in one form or another- may account for
30 - 60% of total dietary carbohydrates for some
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Major organ involved in fructose metabolism is the
liver
There are two (rare) inherited diseases of
fructose metabolism
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Essential fructosuria - caused by deficiency in
fructokinase and leads to transitory elevation of
blood fructose level and to fructosuria (fructose in
the urine)
Fructose intolerance - MUCH MORE SERIOUS
EFFECTS similar to those associated with
galactosemia - caused by a defect in fructose-1-P
aldolase (aldolase B)
In fructose intolerance fructose and its sources
(sucrose!) must be eliminated from diet
Essential Fructosuria
Fructose Intolerance
“Baby Bottle” Caries
“Baby Bottle” Caries.
Rampant caries due to use of sugar-sweetened
beverages in nursing bottle as a pacifier
From Nutrition in Clinical Dentistry, 3/ed, 1989, A. E. Nizel and A. S. Papas (W. B.
Saunders), Fig. 3-7, p. 46.
Glycemic Index (GI)
Glycemic index of a carbohydrate defined as
incremental area under blood glucose response
curve of a 50g carbohydrate portion of a test food
expressed as a percentage of the response to the
same amount of carbohydrate from a standard
food (usually glucose or white bread) taken by the
same subject.
 An
abbreviated table of GI’s found on
of Macronutrient I handout
p. 8
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In general, carbohydrate-containing foods such as
whole grains, legumes, fruits, vegetables have low
GI’s
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Amylose form of starch has lower GI than
amylopectin
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Broadly speaking about grain products, the greater
the processing, the higher the GI
Factor Influencing GI
Number of factors influence GI besides amount or type of
carbohydrate in a meal.
In a multi-component food or meal, these include:
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amount & type of carbohydrate
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nature of starch
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presence or absence of fat, protein, fiber
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how food was prepared
 Table of factors influencing GI found on p. 8 of
Macronutrient I handout
Diabetes Care 27, Supplement 1,
pp. S36 - S46, January 2004
American Diabetes Society issued Position Statement
entitled “Evidence-Based Nutrition Principles and
Recommendations for the Treatment and Prevention of
Diabetes and Related Complications”
The panel concluded, “If there are long term
effects
(of carbohydrate intake) on glycemia and
serum lipids,
these effects appear to be modest.”
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Their position is that recommendations on intake of
carbohydrates (and monounsaturated fat)
should be
individualized for each diabetic patient
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Dietary Fiber
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Defined as nondigestible carbohydrates & lignin
intrinsic and intact in plants
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Functional fiber defined as isolated nondigestible
carbohydrates that have been shown to have
beneficial effects in humans
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Total fiber: dietary fiber + functional fiber
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AI 38g/d for men ages 14 - 50 y;
for women ages 19 - 50 y
 Tables
25g/d
for Total Fiber DRI (AI) and sources of fiber
on p. 9, Macronutrient I handout
Viscous Fiber
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Some types of fiber form highly viscous solutions
(viscous fiber)
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Viscous fibers delay gastric emptying of ingested
foods into small intestine
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This produces sensation of fullness
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Delayed gastric emptying also results in reduced
postprandial blood glucose levels
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Intake of even moderate amounts of viscous
fiber is associated with lowering plasma
cholesterol levels
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They apparently interfere with absorption of
dietary fat and cholesterol and enterohepatic
circulation of bile acids and cholesterol
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Viscous fibers includes pectins, various gums,
mixed-linkage -glycans, psyllium, agar, and
carrageenan
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Oat bran, barley, legumes and various
vegetables are good sources of viscous fiber
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Isolated fibers or fiber sources that are not
viscous (e.g., cellulose, corn and wheat bran)
rarely found to lower plasma cholesterol levels