[Space]

A lot of people post about fat burners on this forum so I thought I would make a post about scientific studies behind the effectiveness of fat burners.

OTC FAT BURNERS

The only OTC fat burner that has been scientifically studied is the EC stack and a lot of people are unclear on the effectiveness of the EC stack.

Before I go into the studies of EC's effectiveness I would like to say that EC is the most effective OTC fat burner. This may be debated but even if I am wrong in this respect, no OTC fat burner could possibly claim to be twice as effective as EC and as these studies show even twice the effectiveness of EC is substantially less than most people expect from a fat burner.

EC'S EFFECTIVENESS FOR WEIGHT LOSS

Ephedrine and Caffeine administered at 25/200 mgs respectively at a max dosage of 75/600 has been attributed to 35 pounds or 16 Kg of weight loss in obese individuals on a medically supervised diet over 24 weeks compared to 22 pounds or 10 Kg of weight loss for individuals on a placebo over 24 weeks. The net weight loss associated with EC is 0.5 pounds or 0.245 Kg a week.

APPETITE SUPPRESSION AND THERMOGENESIS

So it's clear that EC works. But why does it work? Is it due to thermogenesis or appetite suppression? Studies have shown that fat loss associated with EC is 75% due to appetite suppression and 25% due to thermogenesis. This is a significant finding because many fat burners have no appetite supression properties and appetite suppression accounts for the majority of weight loss.

THERMOGENIC CALORIC EXPENDITURE

How significant is the thermogenic effect of EC then? This is greatly over estimated by many. Astrup et al. (1986) conducted a metabolic study of 5 healthy subjects to gauge the calorie expenditure associated with EC at normal dosage. Their findings were EC is associated with 184 calories in a 24 hour period or a 10% increase in basal metabolic rate. To put this into perspective 15 minutes of cardio on a treadmill at 14 kmh accounts for 250 calories and 2 slices of buttered bread accounts for 201 calories. You need a net calorie deficit of 3500 calories to lose 1 pound or 7700 to lose 1 Kg.

CONCLUSION

These figures are all the findings of peer reviewed studies on weight loss. While it's clear fat burners such as EC work, they are of especially limited effectiveness unless a person's diet is adequate to suit their goals and administering a thermogenic to compensate for a cheat meal is clearly inadequate unless 2 slices of buttered bread is your idea of a cheat!

[edwards]

good find. any chance you could post links to the studies? that would make it a better find.

[Space]

A concise review on the therapeutics of obesity.

Pharmacology of thermogenic drugs

The effect of chronic ephedrine treatment on substrate utilization, the sympathoadrenal activity, and energy expenditure during glucose-induced thermogenesis in man.

These are the references to each boldface statement respectively, though you need Pub Med access to read the discussion sections of each study.

[dsade]

Lipolysis and thermogenesis is also not the only pathway to reducing bodyfat. A lot depends on rate of energy formation (mitochondrial activation) as well as preferred fuel (glucose vs. fats) .

Still, good post that should be read by people that think fat burners are magic.

[Hank Vangut]

another good excerpt on this subject.....

FOOD: THE ULTIMATE BODY TRANSFORMATION TOOL
Let me be perfectly honest with you: nothing can affect body composition as
fast and as drastically as the food you eat, not even drugs! Let’s talk fat loss
for example, a substance like synthetic T3 (e.g. cytomel) or T4 (e.g.
synthroid) can boost metabolism and daily energy expenditure by around
10%. If you are anywhere between 175 and 225lbs we’re talking about 200-
300 calories per day which is basically the amount of calories in ½ cup of
rice measured dry or of a bagel. When we consider that your average fast
food hamburger can provide anywhere from 750 to 1000 calorie and that an
hour of cardio will “burn” an average of 450 to 500 calories; it’s quite easy
to see how simply controlling our food intake can have a huge impact on
how our body looks.

[Mulletsoldier]

All great info, however: You do not mention cAMP modulation, satiation pathways, preventing the synthesis and/or accumulation of FAs and TGs (in addition to their hydrolyzation), regulation of lipid binding genes (PPAR Family), controlling rate-limitation of mitochondrial oxidation, nor do you mention anti-gluccocorticoidal pathways; all important pathways in respects to the synthesis and accumulation of lipids.

Your analysis may have been somewhat premature as well:

2. Godard MP, Johnson BA, Richmond SR. Body composition and hormonal adaptations associated with forskolin consumption in overweight and obese men. Obes Res. 2005 Aug;13(8):1335-43.

7. Kuriyan R, Raj T, Srinivas SK, et al. Effect of Caralluma fimbriata extract on appetite, food intake and anthropometry in adult Indian men and women. Appetite. 2007 May;48(3):338-44.

In reality, any OTC which modulates noradrenergic/monoaminergic Catecholamines has the potential for adipose mitigation - to claim two ingredients are the pinnacle is somewhat short-sighted. As I mentioned above, there are an unfathomable amount of pathways through which we can mitigate adipose storage; far more than simply thermogenesis and lipolysis.

[Mulletsoldier]

L-DOPA mediated fat loss anyone? I can't believe I forgot to mention GH modulation and its lipolytic effect.

Low-Dose Growth Hormone Treatment with Diet Restriction Accelerates Body Fat Loss, Exerts Anabolic Effect and Improves Growth Hormone Secretory Dysfunction in Obese Adults

Kyung Rae Kim et al.

Horm Res 1999;51:78-84 (DOI: 10.1159/000023319)

Growth hormone (GH) can induce an accelerated lipolysis. Impaired secretion of GH in obesity results in the consequent loss of the lipolytic effect of GH. Dietary restriction as a basic treatment for obesity is complicated by poor compliance, protein catabolism, and slow rates or weight loss. GH has an anabolic effect by increasing insulin-like growth factor (IGF)-I. We investigated the effects of GH treatment and dietary restriction on lipolytic and anabolic actions, as well as the consequent changes in insulin and GH secretion in obesity. 24 obese subjects (22 women and 2 men; 22-46 years old) were fed a diet of 25 kcal/kg ideal body weight (IBW) with 1.2 g protein/kg IBW daily and were treated with recombinant human GH (n = 12, 0.18 U/kg IBW/week) or placebo (n = 12, vehicle injection) in a 12-week randomized, double-blind and placebo-controlled trial. GH treatment caused a 1.6-fold increase in the fraction of body weight lost as fat and a greater loss of visceral fat area than placebo treatment (35.3 vs. 28.5%, p < 0.05). In the placebo group, there was a loss in lean body mass (-2.62 ± 1.51 kg) and a negative nitrogen balance (-4.52 ± 3.51 g/day). By contrast, the GH group increased in lean body mass (1.13 ± 1.04 kg) and had a positive nitrogen balance (1.81 ± 2.06 g/day). GH injections caused a 1.6-fold increase in IGF-I, despite caloric restriction. GH response to L-dopa stimulation was blunted in all subjects and it was increased after treatment in both groups. GH treatment did not induce a further increase in insulin levels during an oral glucose tolerance test (OGTT) but significantly decreased free fatty acid (FFA) levels during OGTT. The decrease in FFA area under the curve during OGTT was positively correlated with visceral fat loss. This study demonstrates that in obese subjects given a hypocaloric diet, GH accelerates body fat loss, exerts anabolic effects and improves GH secretion. These findings suggest a possible therapeutic role of low-dose GH with caloric restriction for obesity.

[Space]

Originally Posted by Mulletsoldier

In reality, any OTC which modulates noradrenergic/monoaminergic Catecholamines has the potential for adipose mitigation - to claim two ingredients are the pinnacle is somewhat short-sighted. As I mentioned above, there are an unfathomable amount of pathways through which we can mitigate adipose storage; far more than simply thermogenesis and lipolysis.

Physiology aside randomised controlled trails have only shown 0.5 pounds of weight loss per a week in conjunction with proper diet.

I would also stand by the comment that EC is the pinnacle of OTC fat burners. The only OTC fat burner that compares is Yohimbine, which has no appetite suppression component hence will be much less effective in people who don't strictly adhere to diet.

Yohimbine also does not share the same consensus in the scientific literature as does EC. There are many studies attributing no weight loss to Yohimbine.

[1ArmMan]

Thanks for the information.

I just started an EC cycle. Hopefully it does the same for me as it did for the people in the test

[Mulletsoldier]

Originally Posted by Space

Physiology aside randomised controlled trails have only shown 0.5 pounds of weight loss per a week in conjunction with proper diet.

I would also stand by the comment that EC is the pinnacle of OTC fat burners. The only OTC fat burner that compares is Yohimbine, which has no appetite suppression component hence will be much less effective in people who don't strictly adhere to diet.

Yohimbine also does not share the same consensus in the scientific literature as does EC. There are many studies attributing no weight loss to Yohimbine.

Physiology cannot be put aside because dietary trials are notoriously fickle - diet and portion control, as well as careful monitoring of training programs necessarily remove much of the validity from strictly weight monitoring trials. As a result - and contradictory to your assertion - physiological assays are a necessary component to examining the feasibility of any ingredient.

However, that aside, I have seen clinical trials on the topic of HIIT vs., moderate cardiovascular training exhibit much higher than 0.5/week losses.

As well, I can pull up more L-DOPA/Dopamine related clinical trials; if you wish to see them.

[Mulletsoldier]

As well, absolute decreases in adiposity are cumulative and seen over time, whereas you seem to be judging by an incredibly acute rubric - that is, the degradative effects of the EC stack (increased blood pressure, disruption of NREM/REM patterns [which in itself can contribute to increased cortisol:estradiol:testosterone ratio, increased cortisol release and myriad other effects], cardiac over exertion and so on) can stall or completely impede fat loss over time.

Stimulant-based fat burners are not the pinnacle, IMO, when viewed from an aggregate lens.

[dsade]

Originally Posted by Mulletsoldier

L-DOPA mediated fat loss anyone? I can't believe I forgot to mention GH modulation and its lipolytic effect.

Low-Dose Growth Hormone Treatment with Diet Restriction Accelerates Body Fat Loss, Exerts Anabolic Effect and Improves Growth Hormone Secretory Dysfunction in Obese Adults

Kyung Rae Kim et al.

Horm Res 1999;51:78-84 (DOI: 10.1159/000023319)

Growth hormone (GH) can induce an accelerated lipolysis. Impaired secretion of GH in obesity results in the consequent loss of the lipolytic effect of GH. Dietary restriction as a basic treatment for obesity is complicated by poor compliance, protein catabolism, and slow rates or weight loss. GH has an anabolic effect by increasing insulin-like growth factor (IGF)-I. We investigated the effects of GH treatment and dietary restriction on lipolytic and anabolic actions, as well as the consequent changes in insulin and GH secretion in obesity. 24 obese subjects (22 women and 2 men; 22-46 years old) were fed a diet of 25 kcal/kg ideal body weight (IBW) with 1.2 g protein/kg IBW daily and were treated with recombinant human GH (n = 12, 0.18 U/kg IBW/week) or placebo (n = 12, vehicle injection) in a 12-week randomized, double-blind and placebo-controlled trial. GH treatment caused a 1.6-fold increase in the fraction of body weight lost as fat and a greater loss of visceral fat area than placebo treatment (35.3 vs. 28.5%, p < 0.05). In the placebo group, there was a loss in lean body mass (-2.62 ± 1.51 kg) and a negative nitrogen balance (-4.52 ± 3.51 g/day). By contrast, the GH group increased in lean body mass (1.13 ± 1.04 kg) and had a positive nitrogen balance (1.81 ± 2.06 g/day). GH injections caused a 1.6-fold increase in IGF-I, despite caloric restriction. GH response to L-dopa stimulation was blunted in all subjects and it was increased after treatment in both groups. GH treatment did not induce a further increase in insulin levels during an oral glucose tolerance test (OGTT) but significantly decreased free fatty acid (FFA) levels during OGTT. The decrease in FFA area under the curve during OGTT was positively correlated with visceral fat loss. This study demonstrates that in obese subjects given a hypocaloric diet, GH accelerates body fat loss, exerts anabolic effects and improves GH secretion. These findings suggest a possible therapeutic role of low-dose GH with caloric restriction for obesity.

Centralized control of adipostat and energy usage rate is one of the more neglected aspects (so far in the industry) of fatloss. We did a good job of enhancing it with HEAT Stack, through the actions of Alpha-Yohimbine...hoping to be able to bring it back soon in an enhanced version.

[Mulletsoldier]

Originally Posted by dsade

Centralized control of adipostat and energy usage rate is one of the more neglected aspects (so far in the industry) of fatloss. We did a good job of enhancing it with HEAT Stack, through the actions of Alpha-Yohimbine...hoping to be able to bring it back soon in an enhanced version.

Agreed; more attention needs to be payed to preferential energy use, and qualitative energy expenditure. Not just "how much", but "which cells" should be the operative question [re: expending energy].

As well, I would like to see more AMPk modulators out there!

[luclyluciano]

I always new that fat burners without appetite suppres