I-Force Dexaprine Ingredient Write-Up.

Figure 1: I-Force Nutrition's
newest fat burner Dexaprine

Just received an email from the marketing guys @I-Force Nutrition informing me that "Dexaprine is finally here...". Well, to be honest, I had not been waiting for it, but the email intrigued me and I would like to give you a brief rundown on the ingredients, which are "guaranteed to give you more energy, increased appetite suppression, and insane mood enhancement than you have ever experienced!" - I don't know about you, but I think I have heard similar claims before ;-)

Ok, here we go: One bottle of Dexaprine, which is 39.99 (pre-order offer @ I-Force webshop) has 60 servings (serving size 1 capsule) of the "thermogenic powerhouse" (I love these advertisment guys) @ 600mg of the following ingredients

• Thermophoric Amine Mood Enhancing Complex,
  which is basically just synephrine (from citrus aurantium) + geranamine (which is also known as 1,3-dimethylamylamine, 4-methyl-2-hexylamine, or as I-Force has it on the label 1,3-dimethylpentylamine)
  
• Extended Release Energy Complex,
  which is a combination of caffeine and theophylline, with the latter having identical beneficial (stimulant, beta receptor agonism, etc.) as well as detrimental (e.g. temporary insulin resistance in muscle tissue, cf. Colnes. 2010, adrenal problems due to long term (over-)use etc.) effects on perceived energy and weight loss, but a longer half-life, which is even prolonged by the concomittant admistration of caffeine (Jonkman. 1991)
  
• Anabolic Protein Synthesis Enhancing Complex,of which I think that it is completely mislabeled, because it is a combination of the two diiodo-L-Thyronines (also known as T2s), 3,3'-T2 and 3,5-T2, of which I have already written in a paper for a German BodyBuilding and fitness magazine (click here for Google-translation) that their impact on metabolic rate (in non-hypothyroid individuals) is probably negligible and would - according to the mice studies that are presently available - require much higher doses than those present in current "thyroid stimulating" products to up-regulate UCP significantly above "normal" levels.

So, overall this does leave us with a probably relatively long lasting stimulant that will enable you to work harder and thus burn more calories and subsequently more fat. Not bad, but nothing new or even revolutionary here.

On a side note: As it is quite often the case in the supplement industry, Dexaprine is deliberately named to sound similar to a potent drug, the synthetic amphetamine Dexedrine (has up to 15 mg dextro-Amphetamin per cap). This practice is about as shabby as calling a product XYZ-"drol". The latter, i.e. the "drols", have incidentally been banned by bodybuilding.com - good idea, guys ;-)

Protein's Effects on Gene Expression: Higher Protein Lower Carbohydrate Diet Spares Gylcogen, Lowers Insulin and Reduces Lipogenesis

High protein diets have become the "gold standard" within the fitness community. On the countless bodybuilding, fitness and weight loss related bulletin boards on the Internet, athletes, gymrats and even overweight house-wives report outstanding benefits of a higher than normal protein intake on weight gain and/or fat loss. French scientists (Stepien. 2011) have now taken a closer look at the mechanism behind these success stories and found a strong (epi)genetic component (for an introduction to epigenetics, I recommend listening to Dr Rouse's interview series on Carl Lenore's Super Human Radio).

 Figure 1: Effect of high protein diet on genes regulating lipogenesis [lipo = fat; genesis = production] in the liver (Stepien. 2011)

Stepien et al. fed 80 male winstar rats either a normal or a high protein (50% protein) diet for 1,3,6 or 14 days and evaluated the mRNA levels [indicators of how active these genes are] of genes "involved in carbohydrate and lipid metabolism", energy expenditure (EE) and substrate oxidation, as well as liver glycogen, plasma glucose and hormones. What they observed stands in line with the positive anecdotal evidence you will find if you google muscle gain or fat loss "success stories":

    In liver, HP feeding 1) decreased mRNA encoding glycolysis enzymes (GK, L-PK) and lipogenesis enzymes(ACC, FAS), 2) increased mRNA encoding gluconeogenesis enzymes (PEPCK), 3) first lowered, then restored mRNA encoding glycogen synthesis enzyme (GS), 4) did not change mRNA encoding b-oxidation enzymes (CPT1, ACOX1, bHAD).

So, interestingly, with the exception of the 1st day of the experiment (where the increase in protein intake resulted in a short-term increase in fat oxidation), fat oxidation was stable (cf. 4) The "fat burning" effect, which is often ascribed to high protein diets, thus is not existent - or let's say its not a direct one, but a result of the synergy of other genetic and metabolic adaptations and the calorie restriction all weight loss regimens have in common.

Figure 2: Postprandial macronutrient balance as assessed during a 4 h period after the intake of a calibrated meal consisting of 4 g of an adequate diet.  (Stepien. 2011)

Here is where the insulin lowering effect, the reduced hepatic glucose uptake and the reduction in lipogenesis (cf. fig. 1) come into play. Combined with an overall increase in postprandial energy expenditure (observed only under long term high protein feeding conditions, cf. fig 2, HP14) and a slight but significant increase in the percentage of fat (LOX, fig. 2) that is used to fuel these demands, these genetic and metabolic adaption (most prominently the lower insulin levels and the reduction in lipogenesis) are the most probable mechanisms to explain the reduced fat gains and increases in fat loss on high protein weight gain and weight loss diets, respectively.

Want to Burn More Fat During Your Cardio Training? Eat Low Carb Before Workout!

Modulation of substrate utilization is the key to effective weight loss. For years we have been told that "training in the zone" (referring to a specific heart rate) would do the trick - recent research does yet suggest otherwise: High Intensity Interval Training (HIIT) has been shown to be at least as effective in burning off unwanted body fat, as the longstanding "gold standard", Low Intensity Steady State (LISS) in the "fat burning zone".

Researchers from the Department of Exercise Science and Sports Studies at Springfield College, Springfield, MA, USA, have now found that apart from the type of exercise you chose to perform, the nutrition, especially in the hours before working out, determines whether you will predominantly burn fat or carbs to sustain the workout.

In their study (Gregory. 2011), Gregory et al. compared the metabolic responses of a group of 8 "active, pre-menopausal" women to a 30 minute exercise regimen performed after either a low carbohydrate (LC: 392 kcal @ 15% carbohydrate, 68% fat, and 18% protein) or a low fat (LF: 396 kcal @ 78% carbohydrate, 7% fat, and 15% protein) meal. Respiratory gas exchange (RER), blood glucose (G), insulin (IN), triglycerides (TG), and free fatty acids (FFA) were measured. While "no significant differences existed between test meals for fasting blood measurements", the post-exercise results showed significant differences:

Postexercise (PE) FFA (mEq·L-1) levels were significantly greater following LC [1.1 (0.3) vs. 0.5 (0.3)]. PE TG (mg·dL-1) levels were significantly greater following LC [152.0 (53.1) vs. 114.4 (40.9)]. RER was significantly lower at all time points following LC compared to LF.

With the respiratory gas exchange being a measure of the relative contribution of fatty acids to fulfill the exercise-induced energy demand (Chessex. 1995), the researchers rightly conclude "ingestion of a single LC meal resulted in greater lipid oxidation at rest and during exercise as compared to a single LF meal." But, let's be honest - did you expect anything else?

Low Dose Caffeine Ameliorates Catabolic Effects and Increases AMPK and PPAR Expression During Reduced Food Intake in Mice

Caffeine, "the mother of all stimulants", has lately developed a bad reputation. Stress, Cortisol, Adrenal Fatique, Insulin Resistance etc. are only the most recognized buzzwords occurring within the context of caffeine consumption. A very recent paper (Shermann. 2011) coming from scientists from the University of Jerusalem draws a wholly different picture.

Shermann et al. investigated the effect of caffeine consumption (3.5 mg/kg/day or 7 mg/kg/day) on circadian rhythms and expression of disease and metabolic markers in mice under two distinct dietary conditions over a period of sixteen weeks. When the rats were fed an ad libitum diet (meaning they could consume as much food as they wanted), ...

caffeine reduced the average daily mRNA levels of certain disease and inflammatory markers, such as liver alpha fetoprotein (Afp), C-reactive protein (Crp), jejunum alanine aminotransferase (Alt), growth arrest and DNA damage 45β (Gadd45β), Interleukin 1α (Il-1α), Il-1β mRNA and serum plasminogen activator inhibitor 1 (PAI-1).

For those of you who still want to shed some pounds of fat, it may yet be even more interesting to read that "caffeine supplementation led to decreased expression of catabolic factors under RF". With the RF = restricted feeding condition being comparable to what is known as "intermittent fasting" in the fitness community, this finding is highly significant.

Figure 1: Metabolic markers PPAR-Gamma (above) and PPAR-Alpha (below) in mice fed an ad libitum (AL) or a restricted diet (RF) (Shermann. 2011)

This is particularly valid given the fact that there was a highly significant increase in PPAR-Gamma, PPAR-Alpha (cf. figure 1) and AMPK (not shown) activities in the group receiving "high dose" (7mg/kg; for humans this would equal a pretty low dose of about 0.6mg/kg) caffeine. Both, peroxisome proliferator activated receptor (PPAR), as well as AMPK are regarded as master metabolic regulators that have been implicated in the physiology of fat loss. A moderate caffeine consumption, i.e. about one cup of coffee, in the course of an intermittent fast, may thus well spare muscle protein and burn body fat, at the same time.

Burn Additional 27 kcal with 6mg/kg Caffeine Pre-Workout

Caffeine is the cornerstone of almost each and every fat-burner on the market. But how effective is it in raising your energy expenditure? A study (Astorino. 2011) conducted at the Department of Kinesiology of the California State University provides an answer: Not very effective.

Astorino et al. had 14 strength-trained men who were regular caffeine consumers perform a strength workout with either 6mg/kg (thanks to Ezhan who pointed me to a type here. It's 6mg not 0.6 as it said before) caffeine or placebo supplement pre-workout. What they found was that

Caffeine intake increased total energy expenditure by 15% (P<0.05), but the additional calories burned was minimal (+27 kcal).

Well, I suppose this is about the amount of calories of a small carrot and not really what you would expect from a fat burner.

Calcium + Vitamin D for Breakfast Increase Dietarily Induced Thermogenesis and Fatty Acid Oxidation

Ever since the first studies suggested beneficial effects of dairy on weight loss, there have been a lot of trials that investigated the role of (supplemental) calcium in these contexts (mostly with discouraging results). A very recent study by Wendy and Soares (Wendy. 2011) took a very similar approach, but added vitamin D to the equation.

In their study, the scientists fed their 11 subjects (aged (mean ± SEM) 54 ± 1.2 y and BMI 31 ± 2.4 kg/m) a meal that was either high (HCT) or low (LCT) in vitamin D and calcium and measured diet induced thermogenesis (DIT), fat oxidation rates (FOR), serum leptin, subjective feelings of hunger/satiety hourly over a period of 8 hours. The results were far from earth-shattering; they could however solve the mystery of why most people find it easier to lose weight on a diet that is generally rich in dairy and calcium + vitamin D rich foods:

HCT resulted in lesser suppression of ΔFOR (p=0.02) and a significantly greater DIT (p=0.01). Further, the buffet to dinner interval was prolonged (p=0. 083) and reported 24h energy intake following this trial was significantly reduced (p=0.017). ∆leptin following HCT but not LCT was negatively related to 24 h fat intake (r = - 0.81, p=0.016).

So, the underlying mechanism is actually threefold and much different from the commonly heard hypothesis that dietary caclium would "bind fat in the intestine" and thus reduce caloric intake:

1. greater postprandial fat oxidation
2. significantly greater thermogenesis
3. beneficial effect on leptin and thus decrease in hunger

What else would you want? If there was not the issue with lactose intolerance, eating as much dairy as possible could actually become a general recommendation for everyone who intends to lose weight and/or improve body composition

Hydroxycitrate (HCA) for Weight Loss - Revisited

The hype around hydroxycitrate (HCA) as a remedy for obesity and general weight problems has long abated. Nevertheless, in a recent review (Onakpoya. 2010), scientists from the Peninsula Medical School at the University of Exeter reexamine past studies and come to the (surprising?) conclusion that

The evidence from RCTs suggests that Garcinia extracts/HCA generate weight loss on the short term. However, the magnitude of this effect is small, is no longer statistically significant when only rigorous RCTs are considered, and its clinical relevance seems questionable.

So, although the data from the study shows that there is a minor improvement in weight loss in the supplemented groups (cf. fig. 1, below)

Figure 1: Forest plot of comparison showing the effect of hydroxycitrate on body weight. The vertical line represents no difference in weight loss between HCA and placebo. (Onakpoya. 2010)

buying a pure HCA supplement for weight loss purposes is probably not worth it. There are certainly better fat-burners out there.