Do low-carbohydrate diets afford a metabolic advantage that causes more weight loss than that which...

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Do low-carbohydrate diets afford a metabolic advantage that causes more weight loss than that which occurs in individuals on conventional, high- carbohydrate, calorie-cutting diets? Our Research Question

Transcript of Do low-carbohydrate diets afford a metabolic advantage that causes more weight loss than that which...

Page 1: Do low-carbohydrate diets afford a metabolic advantage that causes more weight loss than that which occurs in individuals on conventional, high-carbohydrate,

Do low-carbohydrate diets afford a metabolic advantage that causes more weight loss than that which occurs in individuals on conventional, high-carbohydrate, calorie-cutting diets?

Our Research Question

Page 2: Do low-carbohydrate diets afford a metabolic advantage that causes more weight loss than that which occurs in individuals on conventional, high-carbohydrate,

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 low-carbohydrate diet (15% of total calorie intake)

Samaha et al. (2003): Subjects on a low-carbohydrate (Atkins) diet lost significantly more weight than subjects on a conventional high-carbohydrate diet

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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.

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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?

Readings: McDonald, 1996

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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)

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Evidence for the Thermogenic Hypothesis: Johnston et al. (2002)

Objective: To measure the thermic effect of a high-protein mealSubjects: 10 healthy, normal-weight womenDesign: Randomized, cross-over

Meals1. 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

ProcedureFor 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.

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Johnston et al.’s Results

The thermic effect was significantly greater for the high-protein meal versus the high-carbohydrate meal at breakfast and dinner.

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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

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Luscombe et al.’s Results for Body Weight

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Luscombe et al.’s Results for REE and TEE

Low-Protein Diet High-Protein Diet

REE (kj/day)

Week 0 7782 7890

Week 16 7002 7240

Change -780 -650

TEF (% energy intake)

Week 0 7.1 9.1

Week 16 7.8 8.6

Change .69 -.56

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 low-protein (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.

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Latner & Schwartz (1999) : Evidence for Satiating Effects of Protein

Objective: To determine the effects of dietary protein on satiety and food intakeSubjects: 12 normal-weight women

Meals1. High-protein lunch (450 kcals): 71.5% P, 9.5% C, 19.2% F2. High-carbohydrate lunch (450 kcals): 0% P, 99% C, 0% F3. Combined lunch (450 kcals): 35.7% P, 55.1% C, 9.6% F

Design and ProcedureOn 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.

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Latner & Schwartz’s (1999) Results

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deGraaf et al. (1992): Evidence against Satiating Effects of Protein

Objective: To determine the 3 macronutrients differ in their effects on satiety

Subjects: 29 normal-weight women

Meals: 10 550-mL liquid breakfasts-- A control meal contained only 8 kcals-- The remaining 9 meals varied by macronutrient composition and energy level, as

follows:

Design and Procedure

On different days, each subject consumed all 10 preload meals. Subjects then recorded their voluntary food intake for the rest of the day.

Low-energy (100 kcal)

Moderate-energy (250 kcal)

High-energy (400 kcal)

High-carbohydrate (99% CHO)

Low-energy/High-CHO

Moderate-energy/High-CHO

High-energy/High-CHO

High-protein(70% protein)

Low-energy/High-protein

Moderate-energy/High-protein

High-energy/High-protein

High-fat (92% fat)

Low-energy/High-fat

Moderate-energy/High-fat

High-energy/High-fat

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deGraaf et al.’s Results

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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, 1976Opposing 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