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Recommended for:
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Weight loss & slimming
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How does it work?
The primary active ingredients are 7-keto DHEA and guggulsterones. The ingredients have been available in separate products but not in one single product before.
The basic premise behind this product is that it speeds-up lipogenesis - the process by which your body uses fat to create energy in the absence of carbohydrates. To achieve this the body needs to sustain high cAMP and T3 levels, which are natural body chemicals that trigger the process or burning fat. The difference here is that the body is being fooled into doing this at elevated levels before it has burned all available carbohydrates, and then continuing to do so. The result is basically imitating something that would normally take over 60 minutes of intense exercise to trigger, and ongoing exercise to maintain. It's an experience that is only really achieved by extreme athletes who are able to get past what is know in athletics as 'hitting the wall'. Past 'the wall' is the trigger point at which lipogenesis kick-in and high level fat-burn occurs.
For a much more detailed look into how it works, see "Detailed description of how it works" at the bottom of the page.
How should I use it?
Hot-Rox provides an easy way to achieve an impossible feat for most. However, the effect is enhanced further when taken in combination with exercise - which we strongly recommend to get the most out of this powerful product.
What it contains
The horsepower that fuels Hot-Rox is comprised of two novel compounds and their synergists. The big daddy, which is also the real magic behind our formula, is called A7-E™. A7-E was designed from scratch by Bill Roberts and is best described as a tricked out, supercharged version of 7-keto DHEA.
A7-E is completely new to the industry; it has a patent filed on it; and it's so powerful on its own as a fat-loss agent that there's no contest when compared to anything else that's currently on the market. A7-E launches us right smack dab in the middle of a new fat-loss era!
It also utilizes compounds in the formula that elevate mood and suppress hunger, especially for carbohydrates. To do this, included is ample amounts of acetyl-L-tyrosine and 5-hydroxy-L-tryptophan to maximize brain levels of norepinephrine, dopamine, and serotonin, all of which tend to decrease while following a calorie-restricted diet.
Maintaining high levels of norepinephrine, dopamine, and serotonin will not only elevate mood and suppress appetite, but also:
- Decrease fat storage.
- Stimulate oxygen consumption.
- Increase resting energy expenditure.
- Decrease insulin levels.
Additional information:
- 110 Capsules.
- Manufacturer: Biotest.
Detailed description of how it works
Rapid Fat Loss: A Mission of 2 Tasks
The first thing to understand about fat loss is that almost everyone has the science backward. They hope that by burning energy, say on a Stairmaster, it will somehow suck the fat right out of their blurred abs or other problem areas. This simply isn't true. There is no pipeline through which muscle can pull fat from adipocytes. There must be ample supplies of fatty acids in the bloodstream to use as fuel or the muscle burns itself!
People also hope that cutting calories will guarantee fat loss. This also isn't true. Again, energy-burning or energy deficits won't suck fat from the fat cells. The energy can and often will come from glycogen or muscle protein. And most important, caloric reduction slows the metabolism and can actually interfere with fat release!
Once this occurs, you're in a physiological nightmare… a state that not only makes it nearly impossible to lose any additional body fat, but you also begin to lose muscle mass as well, leaving you skinny-fat.
Triggering lipolysis is the crucial first step, but you must also support the burn. If not, it's perfectly plausible to stimulate lipolysis only to have the fat redistributed back into adipocytes. What a waste of time!
If your goal is to get as lean as possible while maintaining or even gaining muscle mass, in addition to managing caloric intake, you must successfully accomplish two and only two critical tasks. Everything else is subordinate to these:
1) Support rapid lipolysis (fat release) while simultaneously minimizing lipogenesis (fat creation).
2) Keep the TCA* cycle primed for maximum, aerobic-metabolic burn.
*Note: The TCA (tricarboxylic acid) cycle is also known as the Krebs cycle or aerobic metabolism.
TASK 1: Release the Fat Hounds!
Lipolysis Up, Lipogenesis Down
Simply put, the goal here is to get fat cells to release fat (lipolysis) faster than they create fat from dietary calories (lipogenesis).
If you want to induce lipolysis, you have to increase cAMP (cyclic adenosine monophosphate). Cyclic AMP is responsible for triggering the cellular processes for lipid metabolism. In other words, it's the chief gatekeeper for stimulating lipolysis and slowing lipogenesis.
Ramping up cAMP within fat cells activates protein kinase, which in turn activates hormone-sensitive lipase, the enzyme that breaks down the fat in adipocytes. This causes fatty acids and glycerol to be released into the bloodstream.
High sensitivity to hormone-sensitive lipase depends upon ample thyroid hormone being present. If T3 levels are low, lipase activity won't increase as it should. In contrast, increased cAMP in combination with high T3 levels will send lipolysis rates through the roof.
Cyclic AMP can be stimulated directly by increasing adenylate-cyclase activity. Adrenergic compounds (endogenous or exogenous) can also indirectly increase cAMP by activating adenylate cyclase when binding beta receptors. The adrenoreceptor route, as mentioned before, has its limitations.
Additionally, both increased cAMP and high T3 levels decrease lipoprotein lipase activity, which is an enzyme responsible for lipogenesis. So in addition to stimulating lipolysis, cAMP and T3, as a team, put the kibosh on lipogenesis as well.
This double-whammy effect that cAMP and T3 deliver is very powerful, priming the body for the burn.
TASK 2: Prime the TCA Cycle
Ignition and Burn
When lipolysis outraces lipogenesis and releases fatty acids into the blood, they diffuse into all cells of the body to be used as fuel.
Upon entering a cell, fatty acids are actively transported, via carnitine acyltransferase, into mitochondria, which act as cellular power plants. Once in the mitochondria, the fatty acid is converted into fatty acid-CoA. Next, the fatty acid-CoA is broken down further, two carbons at a time, into acetyl-CoA. This is the "fat" that fuels aerobic metabolism through the TCA (tricarboxylic acid) cycle. In other words, when you think of burning off body fat, the "fat" being consumed is actually acetyl-CoA.
This is when T3 plays another huge role. T3 produces thermogenic malic enzyme, which is the intermediary required to produce oxaloacetate. And oxaloacetate, in combination with acetyl-CoA, fuels the TCA cycle. For maximum thermogenesis, via the TCA cycle, oxaloacetate needs to be present in ample amounts or the entire process falls apart.
This is a weak link in the TCA cycle and requires exogenous support through nutritional means if you want to maintain continuous and rapid fat loss. (Just how you do that through nutritional means is something I'll go over later.)
Additionally, T3 increases UCP3 uncoupling protein, which can have profound effects on fat loss. In fat cells, uncoupling dramatically increases lipolysis. And in other tissues, like in muscle, uncoupling increases metabolic rate, thus supporting the burn. The net effect is faster fat release from adipocytes, followed by faster fat burning due to an overall-increased metabolic rate.
The Whole Fat-Loss Enchilada
Bottom line, if you ramp up and sustain high cAMP and T3 levels, you've done all that's required for maximum, continual fat metabolism. In essence, you've achieved what's tantamount to
thermogenic nuclear war.
(Managing food intake is, of course, also required; hopefully that's obvious.)
So how do we formulate a supplement that sustains non-beta-receptor-mediated cAMP and increased T3 levels without causing down-regulation?
Well, we have the answer. Specifically, we've developed a series of compounds that when combined, produces a more profound effect than our greatest expectations. In fact, at this point, we can't imagine anything better.
The horsepower that fuels HOT-ROX is comprised of two novel compounds and their synergists. The big daddy, which is also the real magic behind our formula, is called A7-E™. A7-E was designed from scratch by Bill Roberts and is best described as a tricked out, supercharged version of 7-keto DHEA.
A7-E is completely new to the industry; it has a patent filed on it; and it's so powerful on its own as a fat-loss agent that there's no contest when compared to anything else that's currently on the market. A7-E launches us right smack dab in the middle of a new fat-loss era!
A7-E™: Rev Up and Potentiate Thyroid Activities
The most challenging task was finding a way to boost T3 levels without suppressing TSH. From the scientific literature, there are two compounds that when taken together in relatively high dosages, would do the trick nicely: 7-keto DHEA supported by guggulsterones.
7-Keto DHEA has been shown to increase T3 in humans by as much as 30% (200 mg/day) without suppressing TSH! Additionally, and to a much greater degree, 7-keto DHEA increases thermogenic malic enzyme. Remember, malic enzyme is the compound responsible for producing oxaloacetate, which fuels the TCA cycle.
Guggulsterones, on the other hand, increase the peripheral conversion of T4 into T3, making it the ideal complement to 7-keto DHEA. Increasing the peripheral conversion of T3 is very important because the thyroid only produces 20% of the body's T3. Most of the remaining 80% is derived from T4 through a conversion process that occurs in various target tissues, like skeletal muscle, for example.
On the surface, 7-keto DHEA and guggulsterones appear to be great choices for the HOT-ROX formula. Unfortunately, however, both have inherent problems which needed fixing if we were to achieve the desired magnitude of effect. In other words, we wanted to improve the wow factor by a bunch.
In essence, the bioavailability of 7-keto DHEA isn't high enough and its active life is far too short. Furthermore, of the entire family of androst-5-ene compounds researched, 7-keto DHEA didn't show the best performance when converting into the active species androst-5-ene-3,7,17-triol (A5-T). And since A5-T is the compound that elicits profound thermogenic actions, why not use the androst-5-ene derivative that shows the greatest conversion rate?
The superior choice is androst-5-ene-7-one-3,17-diol (A7-D), which has 3x better conversion into the active A5-T. So A7-D is our top choice for the job. And to improve both bioavailability and length of active life, Bill engineered A7-D into a carbonate ester, called androst-5-ene-7-one-3,17-diethylcarbonate, or A7-E.
A7-E, due to its superior rate of conversion into A5-T, its longer active life, and its increased bioavailability, represents a quantum leap beyond 7-keto DHEA, making it a real powerhouse for fat loss.
With its enhanced molecular design, A7-E is the premier fat-loss compound of our time. In and of itself, it's a very powerful and effective fat-loss agent. But we didn't stop there…
We wanted a synergist for A7-E. All of our research pointed to one obvious candidate -- guggulsterone -- because it increases the peripheral conversion of T4 into T3, further supporting the actions of A7-E. The problem, however, is guggulsterones are not available in a pure state. They're found in a plant called Commiphora mukul, which contains only small amounts of guggulsterone Z and E.
Unfortunately, a good Commiphora mukul extract is only 2.5% active, and that alone makes using an herbal extract unfeasible. Additionally, it's very difficult to get consistent raw material, making accurate dosing literally impossible. And if these weren't big enough problems, there are other constituents in the plant material that cause rather severe allergic reactions in a significant portion of the population.
Our only solution was to produce 100% pure guggulsterones, preferably with a 2:1 ratio between Z and E. And that's just what we did. We included two parts purified guggulsterone Z to one part purified guggulsterone E in our HOT-ROX formula.
So to recap, A7-E has the incredible ability to stimulate the production of T3 and thermogenic malic enzyme; and pure guggulsterones further enhance (synergize) these activities by facilitating the peripheral conversion of T4 into T3.
SCLAREMAX™: The King of Cyclic AMP
The second novel compound in HOT-ROX is called Sclaremax. Sclaremax is a diterpenoidal lactone found in a plant called Salvia sclarea. It's known to be an extremely potent adenylate cyclase activator, very similar to that of the diterpene derivative, forskolin. In fact, cyclic AMP assays indicate Sclaremax either equals or exceeds the actions of forskolin, but with a much longer active life.
Additionally, like forskolin, Sclaremax stimulates adenylate cyclase independently of beta-2 receptors, which means it has no limitations because it won't down-regulate and it has a higher maximal effect. In other words, the more you take, the greater the effect -- day after day after day…
So Sclaremax essentially mimics or acts like TSH -- activating adenylate cyclase in the membrane of thyroid cells, which in turn elevates cyclic AMP and eventually leads to thyroid hormones being released. It may also enhance the cyclic AMP response to TSH in thyroid cells as well.
And because Sclaremax produces an accumulation of cyclic AMP, it will also increase nitrogen retention. This means that it will help preserve or even build lean-body mass (muscle) while increasing lipolysis.
Another huge bonus in comparison to ephedra and other beta agonists is that Sclaremax doesn't interact with beta-1 adrenoreceptors and over stimulate cardiac tissue or raise blood pressure. In fact, Sclaremax, in very high doses, exhibits a vasodilatory effect and slightly decreases blood pressure.
Some other benefits of Sclaremax include its antithrombotic and antidepressant effects, as well as its stimulating effect on luteinizing hormone, via cyclic AMP, resulting in the production of additional Testosterone (in males).
To synergize the effects of Sclaremax, we included the methylxanthine caffeine. Caffeine is a potent competitive inhibitor of phosphodiesterase enzyme, which is responsible for the inactivation of cyclic AMP.
In comparison to caffeine, Sclaremax increases the formation of cyclic AMP, whereas caffeine acts to prevent its degradation. In other words, caffeine potentiates the effects of Sclaremax, thus increasing the magnitude of cyclic AMP accumulation.
And since Sclaremax and caffeine increase cyclic AMP, but via different mechanisms and not through the beta receptor, a combination produces a powerful, synergistic effect on lipolysis.
So you can see that, even though A7-E, Sclaremax, guggulsterones, and caffeine have discrete roles in the fat-loss process, they also potentiate one another's activities, making the combination extremely powerful.
