SCIENTIFIC SUPPORT FOR NATURALLY LEAN MATRIX
Prepared by: Robert Thoburn
Date: 02/15/2003
“Promotes a negative fat balance” and related claims
In order to lose body fat you must achieve a negative fat balance. This means that you are ‘burning’ (oxidizing) more fat than you are storing on your body. When a negative fat balance is maintained over time, we see progressive loss of body fat.
Any intervention (e.g., exercise, ingestion of thermogenic substances) that stimulates the burning of fat (i.e., stimulates fat-burning metabolism) can therefore also be said to promote a negative fat balance. As a corollary, any intervention which has been shown to cause fat loss must be capable of promoting a negative fat balance.
Evodia rutaecarpa: Kobayashi et al. (2001) examined the anti-obesity effects of the major alkaloid of Evodia, evodiamine, and Evodia fruit extracts, in male mice and male rats.
The evodiamine diet contained 0.03% evodiamine. In the rat experiment, a high-fat diet (30% fat) was used to accelerate body fat gain. Mice were fed a diet lower in fat, as they had an aversion to the 30% fat diet. The Evodia fruit extract diet was prepared to provide 1.35% extract and 0.02% evodiamine.
Results: Body weight increased more slowly in the high-fat Evodia diet group when compared with the animals fed a high-fat diet only (control). Both groups consumed the same number of calories.
The authors found evidence that the anti-obesity effects of Evodia were associated with enhanced breakdown of body fat (lipolysis) and greater thermogenesis. This may be attributed to vanilloid receptor stimulation by evodiamine, as found for capsaicin.
It was proposed the evodiamine promotes both heat loss and heat generation, thereby accelerating loss of food energy and preventing body fat gain.
REFERENCES
Kobayashi Y, Nakano Y, Kizaki M et al. (2001). Capsaicin-like anti-obese activities of Evodiamine from Fruits of Evodia rutaecarpa, a vanilloid receptor agonist. Planta Med, 67: 628.
Caffeine (from Guarana and Green Tea):
Dulloo et al. (1989) found that a single dose of 100 mg caffeine (~ 1 small cup of coffee) increased metabolic rate by 3-4% over a period of 2.5 hours.
Measurements of energy expenditure in a room respiration chamber indicated that when the same dose was given every 2 hours for 12 hours, metabolic rate increased by about 10 %. Other groups have found comparable results.
Acheson et al. (1980) also observed an increase in the burning of fat (fatty acid oxidation). This appeared to be mediated by an increased lipolysis leading to higher free fatty acid levels in the blood.
In a double-blind placebo-controlled study in moderate habitual coffee drinkers, Astrup et al. (1989) found increases in energy expenditure of 38.5, 30.1 and 136 kJ/h with 100, 200, 400 mg caffeine ingestion respectively. These effects were positively correlated to plasma caffeine response. In contrast, no significant correlations were found for plasma responses of theophylline and theobromine.
“On the basis of data from the literature, a single oral dose of >= 100 mg caffeine is required to produce a thermogenic response sustainable for >= 1-2 h, and a stimulatory effect of caffeine per se on 24-h EE under respiratory chamber conditions has only been reported with dosages of 600-1000 mg caffeine/d (Dulloo et al., 1989; Bracco et al., 1995).”
It is suggested that most people develop caffeine tolerance due to a decrease in the inhibitory effect on adenosine. However, in the study of Dulloo et al. (1989) habitual caffeine intake of the subjects was 250–500 mg/d. In the study of Astrup et al. (1989) habitual intake of caffeine was 100–200 mg/d. Although a certain degree of tolerance to the thermogenic effect of caffeine may have been developed, these results suggest that a substantial effect remains during moderate daily caffeine consumption.
REFERENCES
Acheson KJ, Zahorska-Markiewicz B, Pittet Ph, Anantharaman K & Jéquier E (1980) Caffeine and coffee. Their influence on metabolic rate and substrate utilization in normal weight and obese individuals. Am J Clin Nutr, 33: 989–997.
Astrup A, Toubro S, Cannon S, Hein P, Breum L & Madsen J (1989) Caffeine: a double-blind placebo-controlled study of its thermogenic metabolic and cardiovascular effects in healthy volunteers. Am J Clin Nutr, 51: 759–767.
Bracco D, Ferrarra JM, Arnaud MJ, Jequier E, Schutz Y (1995). Effects of caffeine on energy metabolism, heart rate, and methylxanthine metabolism in lean and obese women. Am J Physiol, 269: E671-E678.
Dulloo AG, Geissler CA, Horton T, Collins A & Miller DS (1989) Normal caffeine consumption: influence on thermogenesis and daily energy expenditure in lean and obese human volunteers. Am J Clin Nutr, 49: 44–50.
Hoffman BB, Chang H, Dall’Aglio E, Reaven GM (1986). Desensitization of adenosine receptor-mediated inhibition of lipolysis. J Clin Invest, 78: 185-190.
Moser GH, Schrader J, Deussen A (1989). Turnover of adenosine in plasma of human and dog blood. Am J Physiol, 256: C799-C806.
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