Friday, September 5
• Discuss the science background for our topic
IPHY 3700 Writing Process Map
Our Research Questions
Do low-carbohydrate diets offer a metabolic
advantage for weight loss?
Do low-carbohydrate diets cause significant changes
in markers of cardiovascular health?
Low-carbohydrate diets and weight loss: Conflicting study findings
Golay et al. (1996): No significant difference in
weight loss between subjects on a 1,000 kcal/day
high-carbohydrate diet (45% of total calorie
intake) versus subjects on an isocaloric lowcarbohydrate diet (15% of total calorie intake)
Samaha et al. (2003): Subjects on a lowcarbohydrate (Atkins) diet lost significantly more
weight than subjects on a conventional highcarbohydrate diet
Low-carbohydrate diets: Effects on weight and blood lipids
Shortcomings of Previous Studies
1. In all of the longer studies (6 months and beyond), subjects
lived in their communities and attempted to follow instructions
for their assigned diets. The subjects self-reported their food
intake.
2. Some of the studies included nutrition education and exercise
programs, which can be considered extraneous variables.
3. In studies on low-carbohydrate diets and cardiovascular
health, researchers have not controlled for the confounding
effects of weight loss.
4. Researchers have not designed their studies to definitively
determine the mechanisms by which low-carbohydrate diets
cause weight loss and changes in blood lipids. For example, the
question of whether the diets afford a “metabolic advantage”
(substantial weight loss despite energy balance or positive
energy dynamics) has not been answered conclusively.
5. No study to date has exceeded 1 year.
If low-carbohydrate diets do indeed cause greater weight loss,
the underlying mechanisms might involve . . .
1. Ketogenesis, which involves the diet-induced production and
excretion of fat- derived molecules called ketones.
2. Thermogenesis, which involves an increase in energy
expenditure associated with the thermic effect of food (TEF).
3. Increased satiety, which involves the diet-induced reduction of
hunger and calorie intake. The underlying mechanism might be
psychological, physiological, or both.
4. Water loss, due to the breakdown and use of glycogen.
5. Muscle wasting, due to protein degradation associated with
gluconeogenesis.
Ketogenesis
-When dietary carbohydrate intake
decreases, insulin levels decrease. In
response, free fatty acids (FFA) are released
from adipose tissue into the bloodstream.
FFAs are mobilized (transported) to the
muscles and liver.
-In muscle, FFAs can be used for ATP
production. In addition, the muscles can use
proteins and glycogen as energy sources.
-In the liver, FFAs are converted into ketone
bodies, which are transported in the blood to
the brain, where they can be used for ATP
production. The liver can also break down its
glycogen stores to form glucose, which is
transported to the brain.
-When the body's carbohydrate stores fall to
extremely low levels, glucose can be
produced through gluconeogenesis.
- What is the "metabolic advantage" theory
of weight and fat loss?
Diet-induced Thermogenesis
The thermic effect of food (TEF) is the increase in energy expenditure that occurs as
a result of eating. In other words, it's the energy cost of chewing, digesting,
absorbing, and storing food energy in the body. TEF is commonly calculated as a
percentage of calories ingested.
Macronutrient
Thermic Effect
Fat
~4% to 15%
Carbohydrate
~5 to 15%
Protein
~20 to 35%
Readings: Halton and Hu (2004), Eisenstein et al. (2002), Johnston et al.
(2002), Luscombe et al. (2003)
Evidence for the Thermogenic Hypothesis:
Johnston et al. (2002)
Objective: To measure the thermic effect of a high-protein meal
Subjects: 10 healthy, normal-weight women
Design: Randomized, cross-over
Meals
1. High-CHO: 50% complex carbohydrate, 10% simple sugar, 15%
protein and 25% fat
2. High-protein: 30% complex carbohydrate, 10% simple sugar,
30% protein and 30% fat
Procedure
For 2.5 hours following a breakfast, lunch, and dinner meal,
resting energy expenditure (REE) was measured and compared
to baseline values, in order to calculate TEF.
Johnston et al.’s Results
The thermic effect was significantly greater for
the high-protein meal versus the highcarbohydrate meal at breakfast and dinner.
Evidence against the Thermogenic Hypothesis: Luscombe et al. (2002)
Objective: To determine the effects of energy restriction and a high-protein diet on body weight,
resting energy expenditure (REE), and TEF
Subjects: 36 obese hyperinsulinemic men (n = 10) and women (n = 26)
Design and Procedure
Baseline (week 0): Subjects were randomly assigned either to a low-protein or high-protein
diet; REE and TEF were measured in subjects after eating a low-protein meal or a high-protein
meal
Week 0 to week 12: Energy intake of the two diets was restricted by ~30% relative to energy
expenditure
Week 12 to week 16: Energy intake of the two diets was balanced (with energy expenditure).
Week 16: Body weight, REE, and TEF were measured in subjects after eating a low-protein
meal or a high-protein meal
ER = energy restricted; EB = energy balanced
Luscombe et al.’s Results for Body Weight
Luscombe et al.’s Results for REE and TEE
Low-Protein Diet
High-Protein Diet
Week 0
7782
7890
Week 16
7002
7240
Change
-780
-650
Week 0
7.1
9.1
Week 16
7.8
8.6
Change
.69
-.56
REE (kj/day)
TEF (% energy intake)
Key Findings
1. REE was significantly lower at week 16 than at week 0 for subjects on both diets; thus, the 12-week period of
calorie restriction and weight loss significantly slowed resting metabolism. However, there was no significant
difference in the amount of change across the two groups; thus, there was no effect of diet composition on REE.
2. At week 0, the TEF after a high-protein (HP) test meal (9.1%) was significantly greater than that for a lowprotein (LP) test meal (7.1%), although the difference was small.
3. At week 16, there was no statistically significant difference between the TEF values.
4. Over the 16-week period, the change in TEF was not statistically significant for either the LP or HP group; thus,
there was no effect of diet composition on TEF.
Latner & Schwartz (1999) : Evidence for Satiating Effects of Protein
Objective: To determine the effects of dietary protein on satiety and food intake
Subjects: 12 normal-weight women
Meals
1. High-protein lunch (450 kcals): 71.5% P, 9.5% C, 19.2% F
2. High-carbohydrate lunch (450 kcals): 0% P, 99% C, 0% F
3. Combined lunch (450 kcals): 35.7% P, 55.1% C, 9.6% F
Design and Procedure
On three separate occasions, subjects consumed one of the three lunch meals in
liquid form. Between 4.5 to 4.75 hours later, subjects consumed a buffet-style dinner
meal. Outcome measures included the caloric value of each subject’s dinner and the
subject’s responses to a questionnaire designed to assess feelings of hunger and
satiety.
Latner & Schwartz’s (1999) Results
A Metabolic Disadvantage of Low-carbohydrate Diets?
1. Do low-carbohydrate diets cause excessive water loss?
Theory: One gram of carbohydrate is stored in the body with 3-4 grams
of water. So when carbohydrate stores are lowered and not replenished
through the diet, water is lost from the body.
Supporting research: Yang & Van Itallie, 1976
Opposing research: Rabast et al., 1981
2. Do low-carbohydrate diets cause excessive muscle loss?
Theory: When carbohydrate stores are lowered and not replenished
through the diet, the body produces glucose through gluconeogenesis.
A substrate for gluconeogenesis is protein, which can be taken (wasted)
from muscle tissue.
Supporting research: Rabast et al., 1981
Opposing research: Volek et al., 2002
Mechanisms Relating Insulin Resistance and Dyslipidemia: Part 1
Liver
Fat Cells
Insulin-resistant fat cells release
large amounts of free fatty acids into
FFA
the circulation. These FFAs are
taken up by the liver, which uses them
to form triglycerides.
IR
X
Slide source: Lipids Online Slide Library (http://www.lipidsonline.org)
Mechanisms Relating Insulin Resistance and Dyslipidemia: Part 2
Fat Cells
Liver
IR X
to the production of apolipoprotein
(apo) B and very low density
FFA
 TG
 Apo B
 VLDL
Increased levels of triglycerides lead
lipoprotein (VLDL). The release of
VLDL into the blood contributes to
VLDL
the development of LDL-cholesterol.
Insulin
Slide source: Lipids Online Slide Library (http://www.lipidsonline.org)
Atherosclerosis
1. A once-normal arterial wall (coronary
artery) can be damaged through various
mechanisms.
2. Formation of a fatty streak: LDL-C
builds up under the endothelial lining. LDLC is oxidized by free radicals. In response,
cells of the immune system (macrophages)
are mobilized to the area.
3. Formation of stable plaques: The plaque
can be pushed into the lumen by thickening
of smooth muscle cells.
4. Vulnerable plaques: Stable plaques can
disintegrate and rupture, forming thrombi,
or blood clots, which can block blood flow
through the coronary arteries.