FASTIN Ingredients

Fastin’s proprietary formula includes the following:

• R-Beta-methylphenylethylamine HCL – this amazing compound is the active isomer of MPEA much like 1R, 25 Norephedrine was of PPA years ago. This compound stimulates norepinephrine unlike any other and leads to appetite suppression, energy, and ultimate fat loss.

• Methylphenylethylamine tartrate – this is the racemic version of MPEA bound to tartaric acid, which keeps the molecule stable. This compound is found in Hi-Tech’s line and is a rising star of the fat loss industry.

• N-methyl-phenylethylamine – is another isolated amine from acacia rigidula that is both for stimulating fat burning and energizing effects. This is t
the Nmethyl derivative of the compound B-Phenylethylamine. This is a very potent compound for all who lack a chemistry degree.

• Methylsynephrine – is phenolic B-Phenylethylamine found in Acacia Rigidula and some cacti, which produces considerable nervous system stimulation (CNS). With Hi-Tech’s research over the past five years on Acacia Rigidula (as Thermo-Rx®), we have identified and isolated several key phenylethylamine alkaloids. The newest of which is methylsynephrine. The alkaloids from the acacia rigidula are biologically and physiologically similar to those found in ephedra, and possess properties that are shared
with ephedra alkaloids. Scientifically, this is in part due to the similarities in pharmacokinetics and pharmacodynamics. The most obvious similarity is that acacia alkaloids, like the ephedra alkaloids, readily pass into the brain. The main factor governing the transfer of small molecules into the central nervous system is lipophilicity. The distribution of drugs and/or compounds into the CNS from the blood is unique, because functional barriers are present that restrict entry of drugs into this critical site. One reason for this is that the brain capillary endothelial cells have continuous tight junctions;
therefore, drug penetration into the brain depends on transcellular rather than paracellular transport between cells. The unique characteristics of percipaillary gilial cells also contribute to the blood-brain barrier. At the choroids plexus, a similar blood-cerebrospinal fluid (CSF) barrier is present, except that it is epithelila cells that are joined by tight junctions rather than endothelial cells. As a result, the lipid solubility of the nonionized and unbound species of the drug is an important determinant of its uptake by the brain; the more lipophilic it is, the more likely it is to cross the blood-brain
barrier. This situation is used in drugs design to alter the brain distribution, which is the case with drugs like amphetamine, phentermine, and benzphetamine. As you can see from the comparison of the structures of ephedrine, norephedrine, and methylsynephrine they all possess the b-methyl substituent of the aliphatic sidechain, which is characteristic of ephedrine and its congeners, as well as methylsynephrine, thus further increasing
lipophilicity.

What is a suitable substitute for ephedra? How about another beta agonist?

Methylsynephrine is just the answer that the industry has been waiting on for years! The sympathetic nervous system is involved in the regulation of energy. Therefore, pharmacological manipulation of the system offers a mechanism of targeting a reduction in excess body fat stores. Many betaadrenergic agonists are known to increase muscle mass while concurrently decreasing fat mass. Prolonged treatment with sympathomimetic compounds reduces energy intake and increases energy expenditure. The beta 2&3
receptors appear to be responsible for the lipolytic and thermogenic effects of
adrenergic agents, while interaction with beta-1 and to a much lesser extent,
beta-2 control cardiac effects. Accordingly, the ideal fat loss compound would
be one identical to acacia rigidula and especially methylsynephrine. Until now, there has never been a beta-adrenergic compound like methylsynephrine that can stimulate lipolysis and increase resting metabolic rate like ephedra.

• Theobromine – is the primary methylxanthine found in products of the cocoa tree, Theobroma cocao. As a member of the methylxanthine family, it is thought to elevate levels of serotonin, the same action as the popular antidepressants. Theobromine has a lot of research that shows its extraordinary effects on fat loss, appetite suppression, and mobilization of fatty deposits. Theobromine acts as a mild diuretic and stimulant, which creates a synergistic effect with caffeine.

• Phenylethylamine HCL – this amazing compound is probably the cleanest stimulant ever researched, and it is naturally present in human fluids and tissues. Although categorized as a stimulant, it has the remarkable ability to simulate the central nervous system without causing nervousness or the jittery feeling. Phenylethylamine is found in chocolate and is responsible for its effects on mood, appetite, and sense of well-being. Until recent discoveries, PEA, or phenylethylamine, was rapidly destroyed within the body. If included with novel delivery systems, phenylethylamine HCL is provided “safe transport” and this metabolic fate is avoided and pharmacological activity becomes extremely apparent. This catecholamine precursor is responsible for elevating the metabolic rate and promoting a sense of satiety.

Phenylethylamine acts on alpha-receptors in the brain, as do norepinephrine and certain prescription anti-obesity drugs. It is also believed to cause the release of dopamine in the pleasure sensing areas of the brain. Phenylethylamine HCL has a close chemical relationship to pharmaceutical stimulants, because it is the “backbone” of many pharmaceutical compounds.

• Yohimbine HCL – has been shown in many clinical trials to effectively block alpha 2 adrenoreceptors. These studies have found that yohimbine increases the amount of non-esterfied fatty acids (NEFA’s) a product of lipolysis (the breakdown of fat), in the blood-stream for both lean and overweight subjects. There are a number of feedback mechanisms that prevent the release of norepinephrine (NE), one of the body’s primary lipolytic hormones. When NE is released, such as when taking methylsynephrine and
acacia rigidula, it stimulates both the alpha and beta adrenoreceptors. Stimulation of the beta adrenoreceptors has the opposite effect, preventing the release of NE and lipolysis. Yohimbine prevents this negative feedback mechanism, and works in a synergistic fashion with the other components to increase NE and lipolysis. There are a number of reasons why alpha-2 inhibition is specifically useful. First, while the beta-adrenergic system
primarily controls lipolysis during periods of intense activity, during rest, which makes up most of our day, the alpha-adrenergic system is in control. Also, “stubborn fat” areas – usually the abdominal area in men and the glutofemoral area in women – contain a higher ratio of alpha-2 receptors, making yohimbine particularly effective in these areas (whereas other drugs that increase NE may be somewhat counterproductive). Finally, alpha-2
blockade increases blood flow in adipose tissue, which prevents fat from being retained in the area.

• Synephrine HCL – is a drug used primarily in fat loss, although the effectiveness is minimal in Fastin. It is very popular and has been used as an alternative to ephedrine (a substance with a history of controversy). Synephrine is derived primarily form the fruit of a small citrus tree.

• Caffeine Anhydrous USP – acts as a stimulant and thermogenic in humans, and is commonly taken to boost energy or mental concentration. It will stimulate the central nervous system and the metabolism. Once metabolized, caffeine can increase lipolysis in the body. Caffeine may also increase the effectiveness of other substances such as ephedrine or yohimbe, and was incredibly popular in the commonly used ECA stack (ephedrine, caffeine, and aspirin).