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The best supplements in the world

I am a sport Scientist, who has designed a revolutionary range of products, to go into development soon. I have only used doseages that have been shown to be effective in clinical trials (unlike other companies).

Here is my fat burning formula - what do you think? - Personally (and I know I'm biassed here) I think that give the ingredients, this formula will have drug-like effects. It is far superior to anything from Muscletech, twinlab or any other company.

to be taken 3x per day, each dose containing"

HCA (Garnicia carbinogia derived hydroxycitric acid)
(1556mg standardized to 60% HCA, providing (936mg)

HCSX (Hydroxycitric acid) – (of the SUPER CITRIMAX variety)
(1556mg standardized to 60% HCA, providing (936mg)

NBC (Niacin bound chromium)



(of active epigallocatchin gallate)

YOHIMBINE (standardization varies between 25-75%
10mg (of active yohimbine alkaloid)

100mg (after standardization)

(standardized to 75% gymnema acid) 50mg (providing 33mg gymnema acid)

White willow (standardized to 75% salacin)
(Providing 40mg salacin after standardization)




APHANIZOMENON FLOS-AQUAE (AFA) Standardised to contain appropriate amounts of 2-phenylethylamine (PEA)


L-Phenylalanine 1000mg


What do you think guys? - I have other formulas for ATP synthesis, a gaining meal, a ketogenic diet meal and a bedtime protein. - The beauty is that the "special" ergogenic ingredients will be in capsules, to be taken with the base protein powder/ meal replacement powder - meaning you can add tham to any protein/meal replacement r just take them on their own.

I would appreciate any feedback
I would think u should test it before you even bring about hypothesis of how effective you might think it will be.

Evidence, proof etc
would think u should test it before you even bring about hypothesis of how effective you might think it will be.

Evidence, proof etc

-Yeah, it's going into development next week - The factory is getting the raw materials, with up to 100 test batches to be made in the next 6 months.

I already know that the product will be very effextive, as the doseages mimmick that of real world trials. I'll give you an example:

: Diabetes Obes Metab. 2004 May;6(3):171-80. Related Articles, Links

Effects of a natural extract of (-)-hydroxycitric acid (HCA-SX) and a combination of HCA-SX plus niacin-bound chromium and Gymnema sylvestre extract on weight loss.

Preuss HG, Bagchi D, Bagchi M, Rao CV, Dey DK, Satyanarayana S.

Department of Physiology and Biophysics, Georgetown University Medical Center, Georgetown, Washington, DC 20057, USA. [email protected]

AIM: The efficacy of optimal doses of highly bioavailable (-)-hydroxycitric acid (HCA-SX) alone and in combination with niacin-bound chromium (NBC) and a standardized Gymnema sylvestre extract (GSE) on weight loss in moderately obese subjects was evaluated by monitoring changes in body weight, body mass index (BMI), appetite, lipid profiles, serum leptin and excretion of urinary fat metabolites. HCA-SX has been shown to reduce appetite, inhibit fat synthesis and decrease body weight without stimulating the central nervous system. NBC has demonstrated its ability to maintain healthy insulin levels, while GSE has been shown to regulate weight loss and blood sugar levels. METHODS: A randomized, double-blind, placebo-controlled human study was conducted in Elluru, India for 8 weeks in 60 moderately obese subjects (ages 21-50, BMI >26 kg/m(2)). Subjects were randomly divided into three groups. Group A was administered HCA-SX 4667 mg, group B was administered a combination of HCA-SX 4667 mg, NBC 4 mg and GSE 400 mg, while group C was given placebo daily in three equally divided doses 30-60 min before meals. All subjects received a 2000 kcal diet/day and participated in supervised walking. RESULTS: At the end of 8 weeks, body weight and BMI decreased by 5-6% in both groups A and B. Food intake, total cholesterol, low-density lipoproteins, triglycerides and serum leptin levels were significantly reduced in both groups, while high-density lipoprotein levels and excretion of urinary fat metabolites increased in both groups. A marginal or non-significant effect was observed in all parameters in group C. CONCLUSION: The present study shows that optimal doses of HCA-SX and, to a greater degree, the combination of HCA-SX, NBC and GSE can serve as an effective and safe weight-loss formula that can facilitate a reduction in excess body weight and BMI, while promoting healthy blood lipid levels.
split endz said:
SELEGELINE 3.33 mg ??? Do you mean Selegiline (deprenyl) ? I hope not. If not, what is Selegeline ?

Sorry, my bad - looks very unprofessional. I cut and pasted the wrong version of the formula (strike selegeline). I did mean deprenyl selegeline - yes this is a drug. This is for my own useage, as if I was to use the formula myself, I would add some deprenyl. SEE BELOW:

Autopsy studies have shown that while deprenyl increases dopamine levels in Parkinson patient brains by only 40-70%, deprenyl increases PEA levels 1300 - 3500%! INCREDIBLE!

Deprenyl is a drug that was discovered around 1964-65 by Dr. Joseph Knoll and colleagues. It was originally developed as a “psychic energizer,” designed to integrate some amphetamine-like brain effects with antidepressant effects. Also known as L-deprenyl, (-)-deprenyl, and selegiline, deprenyl has been intensively researched over the past 36 years - many hundreds of research papers on deprenyl have been published. Knoll has stated that deprenyl “ an exceptionally lucky modification of PEA [phenylethylamine], an endogenous ... member of the family to which also the transmitters noradrenaline and dopamine belong.” Deprenyl has shown a unique and exciting pharmacologic/clinical profile. It is the only potent, selective MAO-B inhibitor in medical use.Deprenyl is a “catecholamine activity enhancer.” Deprenyl has been shown to protect nerve cells against a wide (and growing) number of neurotoxins. Deprenyl has also been shown to be a “neuroprotection/ neurorescue agent” when nerve cells are exposed to damaging or stressful conditions.
Deprenyl (Selegiline, Jumex, Eldepryl, Movergan), a close structural relative of phenylethylamine (PEA), is a drug with a unique pharmacological spectrum. Whereas PEA and its long-lasting variants, the amphetamines, are mixed-acting stimulants of the sympathetic system in the brain, they primarily enhance the impulse propagation generated release of catecholamines (catecholamine activity enhancer, CAE, effect) and displace catecholamines in higher concentration (catecholamine releasing effect). (-)Deprenyl is the first CAE substance in clinical use devoid of catecholamine releasing activity. (-)Deprenyl is a highly potent and selective, irreversible inhibitor of B-type monoamine oxidase (MAO), a predominantly glial enzyme in the brain. The activity of this enzyme significantly increases with age. (-)Deprenyl, the first selective inhibitor of MAO-B described in the literature, has become a universally used research tool for selectively blocking B-type MAO and is still the only selective MAO-B inhibitor in world wide clinical use. In contrast to MAO inhibitors which strongly potentiate the catecholamine releasing effect of tyramine, (-)deprenyl inhibits it and is free of the 'cheese effect', which makes it a safe drug. Because its lack of the catecholamine releasing activity deprenyl is devoid of amphetamine like dependence capacity.
By 1971 Knoll had shown that deprenyl was a unique kind of MAO inhibitor - a selective MAO-B inhibitor, without the “cheese effect.” To fully appreciate what this means, some technical background is necessary.
Some of the most important neurotransmitters in the brain are the monoamine transmitters: serotonin, dopamine and noradrenalin. After being secreted into the synaptic gap, where one neuron connects to another, many to the transmitter molecules are reabsorbed by the secreting neuron and then disposed of by enzymes called “monoamine oxidases” (MAO). This prevents excessive levels of transmitters from accumulating in the synaptic gap and “over-amping” the brain. However, with aging MAO activity significantly increases in the human brain, often to the point of severely depressing necessary levels of monoamine transmitters. In the 1950s the first antidepressant drugs to be developed were MAO inhibitors.
By 1968, further research had shown that there were two types of MAO-A and B. It is primarily intestinal MAO-A that digests incoming tyramine. Most of the MAO inhibitors that have been used clinically inhibit both MAO-A and MAO-B, however deprenyl has the unique ability to prevent tyramine from getting into noradrenalin-using nerve calls, and it’s only when tyramine enters noradrenalin nerve cells that control arterial blood pressure that it triggers the “cheese effect.” Deprenyl thus has a dual “safety lock” in preventing the “cheese effect,” making it far safer than other MAO inhibitors. At doses over 20-30 mg/day, however, deprenyl does start to significantly inhibit MAO-A

“CHEESE EFFECT”: When most MAO inhibitors are used in people consuming a diet rich in a substance called “tyramine,” a dangerous, even fatal, high blood pressure crisis can be triggered. Tyramine is found in many foods, including aged cheeses, some wines, beans, yeast products, chicken liver and pickled herring, to name just a few.

MAO-B breaks down dopamine and the “traceamine” phenylethylamine (PEA). At doses of 10 mg + per day deprenyl will inhibit MAO-B about 90%. MAO-B inhibition can significantly increase synaptic dopamine levels.

Deprenyl (and its “cousin”, PEA) are “catecholamine activity enhancers”.
Catecholamines refers to the inter-related neurotransmitters dopamine, noradrenalin, and adrenalin. Catecholamines are the transmitters for key activating brain circuits - the mesolimbic-cortical circuit and the locus coeruleus. The neurons of the mesolimbic-cortical circuit and locus coeruleus project from the brain stem, through the mid-brain, to the cerebral cortex. They help to maintain focus, concentration, alertness and effortful attention. Dopamine is also the transmitter for a brainstem circuit - the nigrostriatal tract - which connects the substantia nigra and the striatum, a nerve tract that helps control bodily movement and which partially dies off and malfunctions in Parkinson’s disease.
When an electrical impulse travels down the length of a neuron - from the receiving dendrite, through the cell body, and down the transmitting axon - it triggers the release of packets of neurotransmitters into the synaptic gap. These transmitters hook onto receptors of the next neuron, triggering an electrical impulse which then travels down that neuron, causing yet another transmitter release. What Knoll and colleagues discovered through their highly technical experiments is that deprenyl and PEA act to more efficiently couple the release of neurotransmitters to the electrical impulse that triggers their release.
In other words, deprenyl (and PEA) cause a larger release of transmitters in response to a given electrical impulse. It’s like “turning up the volume” on catecholamine nerve cell activity. And this may be clinically very useful in various contexts - such as Parkinson’s disease and Alzheimer’s disease, where the nigrostriatal tract and mesolimbic-cortical circuits under-function, as well as in depression, where they may be under-activity of both dopamine and noradrenalin neurons.
Knoll’s research also indicates that after sexual maturity the activity of the catecholamine nervous system gradually declines, and that the rate of decline determines the rate at which a person or animal ages.
Knoll therefore believes that deprenyl's catecholamine activity enhancers effect explains its anti-aging benefit. Knoll also believes that deprenyl's catecholamine activity enhancer activity is independent of its MAO-B inhibition effect, because in rats he has shown catecholamine activity enhancer effect at doses considerably lower than that needed to achieve MAO-B inhibition.
Knoll’s work indicates that PEA is also a catecholamine activity enhancer substance. (16) PEA is a trace amine made in the brain that modulates (enhances) the activity of dopamine/noradrenalin neurons. (16,21) Autopsy studies have shown that while deprenyl increases dopamine levels in Parkinson patient brains by only 40-70%, deprenyl increases PEA levels 1300 - 3500%! PEA is the preferred substrate for MAO-B, the MAO that deprenyl inhibits. Paterson and colleagues have shown that PEA has an extremely rapid turnover due to its rapid and continuous breakdown by MAO-B. (21) Thus deprenyl's catecholamine activity enhancer activity has a dual mode of action. At low, non-MAO-B inhibiting doses, deprenyl has a direct catecholamine activity enhancer activity.
At higher, MAO-B inhibiting doses, deprenyl creates an additional catecholamine activity enhancer effect, due to the huge increases in brain PEA levels that deprenyl causes, PEA also being a catecholamine activity enhancer substance. Many authors have pointed out the probable dopamine neuron activity enhancing effect of PEA in Parkinson patients taking deprenyl.
Knoll’s discovery of PEA’s catecholamine activity enhancer effect now explains this PEA dopamine-enhancing effect

Maintenance on (-)deprenyl selectively enhances superoxide dismutase (SOD) and catalase activity in the striatum and protects the nigrostriatal dopaminergic neurons from selective neurotoxins (6-hydroxydopamine, MPTP, DSP- Maintenance of an animal on deprenyl prevents the characteristic age-related morphological changes in the neuromelanin granules of the neurocytes in the substantia nigra. Many other protective effects of (-)deprenyl, denoted as 'neuroprotective', 'trophiclike neurorescue', 'apoptosis reducing', etc, have been described. All the protective actions of (-)deprenyl are thought to be primarily related to the CAE effect of the drug. All in all, (-)deprenyl increases the activity of the nigrostriatal dopaminergic system and slows its age-related decline. Maintenance of male rats on (-)deprenyl delays the age-related loss of their capacity to ejaculate, slows the age-related decline of their learning capacity and prolongs their life. Parkinsonian patients on levodopa plus (-)deprenyl (10 mg daily) live significantly longer than those on levodopa alone. Parkinsonian patients maintained, after diagnosis, on (-)deprenyl, need levodopa significantly later than their placebo-treated peers. Maintenance on (-)deprenyl significantly improves the performance of patients with Alzheimer's disease. It is concluded that patients developing Parkinson's or Alzheimer's disease need to be treated daily with 10 mg (-)deprenyl from diagnosis until death, irrespective of other medication. Because of the peculiar pharmacological spectrum and safety of the drug it may be advisable to combat the age-related decline of the nigrostriatal dopaminergic neurons in man by taking 10-15 mg (-)deprenyl weekly during the postdevelopmental phase of life. Prophylactic (-)deprenyl medication may improve the quality of life in the latter decades, delaying the time of natural death and decreasing the susceptibility to age-related neurological diseases.

Effect of low-dose treatment with selegiline on dopamine transporter (DAT) expression and amphetamine-induced dopamine release in vivo
Itschak Lamensdorf1, Shai Porat2, Rabi Simantov2 and John P.M. Finberg*,1
1 Rappaport Faculty of Medicine, Technion, POB 9649, Haifa, Israel
2 Department of Molecular Genetics, Weizmann Institute of Science, Israel
*Correspondence to: John P.M. Finberg, Rappaport Faculty of Medicine, Technion, POB 9649, Haifa, Israel
1. Chronic treatment with low doses of the selective monoamine oxidase (MAO) type B inhibitors selegiline [(-)-deprenyl] and rasagiline, causes elevation in extracellular level of 3,4-dihydroxyphenylethylamine (dopamine) in the rat striatum in vivo (Lamensdorf et al., 1996). The present study was carried out to determine whether this effect of selegiline could be the result of an inhibition of the high-affinity dopamine neuronal transport process.
2. Changes in activity of the dopamine transporter (DAT) in vivo following selegiline treatment were evaluated indirectly by microdialysis technique in the rat, from the change in striatal dopamine extracellular concentration following systemic amphetamine administration (4 mg kg-1, i.p.). Striatal levels of the DAT molecule were determined by immunoblotting. Uptake of [3H]-dopamine was determined in synaptosomes from selegiline-treated animals.
3. Amphetamine-induced increase in striatal extracellular dopamine level was attenuated by one day and by chronic (21 days) treatment with selegiline (0.25 mg kg-1, s.c.).
4. Striatal levels of DAT were elevated after 1 and 21 days treatment with selegiline, but were not affected by clorgyline, rasagiline, nomifensine or amphetamine.
5. The increase in DAT expression, and attenuation of amphetamine-induced dopamine release, were not accompanied by a change in [3H]-dopamine uptake in synaptosomes of selegiline-treated animals.
6. The results suggest that a reversible inhibition of dopamine uptake occurs following chronic low dose selegiline treatment in vivo which may be mediated by an increase in endogenous MAO-B substrates such as 2-phenylethylamine, rather than by the inhibitor molecule or its metabolites. Increased DAT expression appears to be a special property of the selegiline molecule, since it occurs after one low dose of selegiline, and is not seen with other inhibitors of MAO-A or MAO-B. The new DAT molecules formed following selegiline treatment appear not to be functionally active.
Sustained antidepressant effect of PEA replacement
Sabelli H, Fink P, Fawcett J, Tom C
Rush University and the
Center for Creative Development,
Chicago, Illinois, USA.
J Neuropsychiatry Clin Neurosci 1996 Spring; 8(2):168-71

Phenylethylamine (PEA), an endogenous neuroamine, increases attention and activity in animals and has been shown to relieve depression in 60% of depressed patients. It has been proposed that PEA deficit may be the cause of a common form of depressive illness. Fourteen patients with major depressive episodes that responded to PEA treatment (10-60 mg orally per day, with 10 mg/day selegiline to prevent rapid PEA destruction) were reexamined 20 to 50 weeks later. The antidepressant response had been maintained in 12 patients. Effective dosage did not change with time. There were no apparent side effects. PEA produces sustained relief of depression in a significant number of patients, including some unresponsive to the standard treatments. PEA improves mood as rapidly as amphetamine but does not produce tolerance.

L-deprenyl (Selegiline) used in the treatment of Parkinson's and Alzheimer's disease also enhances longevity. Oxidized low density lipoprotein promotes atherosclerosis and is toxic to both vascular and neural tissue. The reported association between vascular dysfunction and neurodegenerative diseases prompted us to investigate the effect of l-deprenyl, a MAO-B inhibitor, on low density lipoprotein (LDL) oxidation. LDL was isolated from freshly collected blood and the kinetics of copper induced oxidation of LDL was monitored continuously by spectrophotometry. Oral administration (10 mg) or in vitro (2.8 to 84 microM) addition of l-deprenyl inhibited oxidation of LDL isolated from healthy men and post-menopausal women. This is the first report demonstrating that the antioxidant action of l-deprenyl may be antiatherogenic and cardioprotective. Such an action could contribute to reported extension of life span associated with long-term administration of the drug. In conjunction with inhibition of LDL oxidation, l-deprenyl is unique in that it demonstrates protective effects on both vascular and neuronal tissue. Prophylactic use of low doses of l-deprenyl may accord protection against vascular and neurodegenerative diseases associated with aging.
Great ingrediece list, I think I'll boil myself up a batch. Is it a suppository? lol Sounds like good shit, keep us posted on the trials, and hey if you ever need a guinee pig... I love freebes :evil:
StereOMaN said:
Great ingrediece list, I think I'll boil myself up a batch. Is it a suppository? lol Sounds like good shit, keep us posted on the trials, and hey if you ever need a guinee pig... I love freebes :evil:

Thanks for the positive response, I'll keep you posted. We'll have to see about the freebies lol!
I should mention that it is designed to be stacked with the ketogenic slim meal see below:

2 meals required for optimum daily doseages:




CHRONDROITIN SULPHATE (depolarized version) 600mg





DIINDOLYMETHANE (DIM) 200mg (50mg pure DIM)

PROBIOTICS Each serving to contain more than 1 billion bacteria




Magnesium 363mg

Zinc 7.5mg

AMINOGEN (proteolytic enzyme) 250mg

OKG 5g

FIBRE (ARABINOGALACTAN)- soluble prebiotic fibre 5.0g

FIBRE (GUAR GUM) Cyamopsis tetragonolobus 2.5g



GUGGALIPID/GUGGLESTERONE (type E&Z from the Commiphora Mukul plant) 38mg (after standardization)

7-KETO DHEA 100mg

5HTP (Hydroxytryptophan) 300mg

COLEUS FORSKOLI (standardized to 20% forskolin)
150mg (30mg forskolin)

CLA (10 cis- 12 trans isomer) 3g

MCTs 10g

TRIBULUS TERRESTRIS (30-45% steroidal saponins- furostanol)


GRAPE SEED EXTRACT (standardized to a procyanidolic value of greater than 95% or 95% polyphenols per dose.)
50mg (after standardization)



HORNY GOATS WEED (EPIMEDIUM) (alcohol extract containing icariin)

VITAMIN E (alpha tocopherol form) 200IU



MUCUNA PRURIENS (containing 15% L-Dopa) – inc. GH? (AKA Couhage, Cowhage, Cowitch, Kiwach). 700mg



- 20g WHEY 80cals


5g OKG 20 cals

10% CARBS 5g ARABINOGALACTAN soluble prebiotic

(20 cals)

2.5g GUAR GUM Cyamopsistetragonolobus -Hydrocolloid fibre
(10 cals)

(on a keto diet these do not count as carbs as they are non impact carbs)

36.7% FAT
3g CLA 27 cals

10g MCTs 83 cals
Interesting??? I'd love to see Macro or Ulter chime in on this.... could be QUITE and interesting thread!! :)
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