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Acetyl L Carnitine

One of the key uses of Acetyl l Carnitine supplement is for fatty acid oxidation helping users burn unwanted body fat. Fatty acids are one the key energy sources the body uses and oxidation is the process by which they're broken down to create energy. The fatty acids cannot penetrate the inner mitochondria membrane (where they are burned for energy), and the key role for L-Carnitine is to transport fatty acids across the mitochondria membrane to allow for oxidation of the fats.

Acetyl l Carnitine BENEFITS of according to published studies:
  • Acetyl l carnitine may improve mental fatigue in those who suffer from chronic fatigue syndrome.Patients with multiple sclerosis are helped by acetyl l carnitine, which reduces their fatigue.
  • In aging rats, chronic administration of acetyl l carnitine increases cholinergic synaptic transmission and consequently enhances learning capacity. The memory of aging rats is rejuvenated by giving them a combination of acetyl l carnitine and lipoic acid.
  • Acetyl l carnitine is a promising nutrient for those with diabetic neuropathy. >This nutrient could be helpful in chemotherapy induced peripheral neuropathy.
  • May reduce alcohol-induced cellular damage to organs.
  • May be helpful in geriatric patients with mild depression.
  • Acetyl l carnitine improves the function of mitochondria, the organelles within cells that are involved in energy production.
  • May be effective in the therapy of acute and early chronic Peyronie's disease.
  • May help individuals with degenerative cerebellar ataxia.
  • Acetyl l carnitine is suitable for clinical use in the reduction of neuronal death after peripheral nerve trauma.
  • May be helpful in those with Alzheimer's disease. Acetyl l carnitine protects against amyloid-beta neurotoxicity.As always, we strongly advise you do your own research and more importantly consult your own medical professional before commencing any use of this or any other dietary supplement This statement has not been evaluated by the FDA. This is not intended to diagnose, treat, cure or prevent any disease .
  • L Carnitine is derived from the lysine and methionine amino acids. It is mainly synthesized in the liver and the kidneys, and must be transported for use to other tissues in the body. It is found in highest concentration in tissues that use fatty acids as the main dietary fuel, such as the skeletal and cardiac muscles.


Assists removal of ammonia from central nervous system.

500mg PER DAY OR AS DIRECTEDAlpha-ketoglutaric (AKG) is an organic acid that is important for the proper metabolism of all essential amino acids and the transfer of cellular energy in the citric acid cycle. It is a precursor to glutamic acid, the non-essential amino acid involved in protein synthesis and the regulation of blood glucose levels. In combination with L-glutamate, AKG can reduce levels of ammonia formed in the brain, muscles and kidneys, as well as help balance the body’s nitrogen chemistry and prevent nitrogen excess in body tissues and fluids. Individuals with high protein intake, bacterial infections, or gastrointestinal dysbiosis may benefit from supplemental AKG to help balance ammonia levels and protect tissues.Alpha-ketoglutaric acid (a-KG) is a naturally-occurring chemical, formed primarily as part of the citric acid cycle inside cells. One of its most important functions is to detoxify ammonia from tissues of the central nervous system. In the brain and central nervous system, alpha-keto combines with ammonia to form glutamic acid and then glutamine. Glutamine crosses the brain-blood barrier and transports the ammonia out of the brain. Alpha-ketoglutaric also scavenges nitrogen released by the catabolism of amino acids, thereby balancing the body’s nitrogen chemistry and preventing nitrogen overload in body tissues and fluids.

As a result of excessive protein ingestion or poor amino acid metabolism, excess nitrogen and ammonia can accumulate in cell tissue. Bacterial infections and intestinal dysbiosis can also elevate ammonia levels in the body. High levels of ammonia or nitrogen in the body can deplete the supply of alpha-keto, allowing ammonia to reach toxic levels. The consequences of excess ammonia (hyperammonemia) may include headaches (migraine), fatigue, irritability, nausea, and diarrhea. Ammonia can attack lipid membranes such as the myelin sheath of neurons. Chronically elevated ammonia in brain tissues can lead to mental confusion and decreased cognitive abilities.

Individuals with high protein intake, problems in nitrogen detoxification or intestinal dysbiosis may benefit from supplemental alpha-ketoglutaric as a central nervous system detoxifier.

Other conditions associated with elevated ammonia levels include:
  • Autism Spectrum disorders
  • Excess aluminum exposure
  • Magnesium deficiency
  • Manganese deficiency
  • Liver disease (cirrhosis)
  • Reyes syndrome
  • Urea cycle dysfunctions
  • Exposure to toxic nitrogen chemicals such as amines, hydrazines, ammonium compounds
Other functions of alpha-ketoglutaric which may suffer as a result of depletion include:

Production of cellular energy via the chemical transfer of energy during the citric acid cycle. (Alpha-ketoglutaric has been found to be helpful in alleviating fatigue and increasing stamina.) Formation of carnitine, necessary for proper metabolism of fats. (Inadequate carnitine may result in elevated triglycerides.) Formation of a biologically active coenyzme form of vitamin B3.

Alpha Lipoic Acid (ALA)

Alpha Lipoic Acid serves as a coenzyme in the energy production process in the cells which can provide quick bursts of energy. Alpha Lipoic Acid is unique in that it is both water and fat soluble which allows it to enter all parts of the cell to neutralize free radicals. Alpha Lipoic Acid contributes to invigorating mental and physical energy and a reduction in muscle fatigue. Dr. Lester Packer, a leading researcher in the area of antioxidants and a professor of molecular and cell biology at the University of California at Berkeley says "Alpha-Lipoic acid could have far-reaching consequences in the search for prevention and therapy of chronic degenerative diseases such as diabetes and cardiovascular disease" .... "and because it’s the only antioxidant that can easily get into the brain, it could be useful in preventing damage from a stroke". Common uses for supplemental alpha Lipoic Acid:

Suggested dosage for R-Alpha Lipoic Acid is 100 mg two to three times daily. · · · · · · · · · · · · · · · · · May be useful in relieving syptoms of stomatopyrosis, or Burning Mouth Syndrome (BMS).Important for regulating aspects of the immune system, in particular immune cells called T-lymphocytes. Because both alpha lipoic acid and dihydrolipoic acid are antioxidants, their combined actions give them greater antioxidant potency than any natural antioxidant now known. Easily absorbed when taken orally and once inside cells is quickly converted to its most potent form, dihydrolipoic acid. Not only does it act as an antioxidant itself, it also stimulates production of glutathione (an antioxidant produced by the body), giving cells a double dose of antioxidant. Prevents tissue damage and death after a heart attack. Significantly increase survival in rats that have suffered a stroke if given before the stroke occurs. Recycles and enhances the effects of other antioxidants such as Vitamin E and Vitamin C. Inhibits Glycation which is responsible for accelerated tissue damage. Chelates (grabs) heavy metals and binds them reducing these oxidants from blood system. May help improve memory. May help reduce LDL (bad) blood cholesterol. Neutralizes free radicals. Unlike Vitamin C which is water soluble and Vitamin E which is fat soluble, alpha Lipoic Acid is both water and fat soluble which allows it to enter all parts of the cell to neutralize free radicals. Important for the production of energy inside the cell by utilizing sugar to produce energy contributing to mental and physical stamina. May help prevent the onset of type 2 diabetes. May play a role in controlling blood sugar. Currently used in Europe to treat peripheral nerve degeneration (neuropathy) resulting from diabetes.


Alcohol and AlcoholismJournal of the American Medical AssociationLe Dernier Verre (The Last GlassThe End of My Addictionintrathecally,Alcohol and AlcoholismJournal of Clinical Psychopharmacology.It is an agonist specific to mammalian but not fruit fly (Drosophila) GABAB receptor Its beneficial effects result from actions at spinal and supraspinal sites. Baclofen can also be used to treat hiccups. It has been shown to prevent rises in body temperature induced from the drug MDMA in rats. A very beneficial property of baclofen is that tolerance does not seem to occur to any significant degree in that baclofen retains its therapeutic anti-spasmodic effects even after many years of chronic use. spasticity.

and dependence potential. The modulation of the GABAB receptor is what produces baclofen's range of therapeutic properties.Baclofen has been shown to be as effective as diazepam in uncomplicated alcohol withdrawal syndrome An Italian study showed that it was effective in promoting alcohol abstinence in patients with severe liver cirrhosis. Baclofen. Ameisen believes, based on his own experience and other anecdotal evidence, that Baclofen acts on some mechanism within the brains of addicts to suppress cravings brought on by addiction to various substances such as alcohol, cocaine, and heroin.GHB which also has the same mechanism of action and also similar effects. However, there are some pharmacological differences in that baclofen appears to have reduced abuse , and by Roberta Agabio et al. who published another case in agitation, delirium, disorientation, fluctuation of consciousness, insomnia, inattention, memory impairments, perceptual disturbances, anxiety, depersonalization, OverdoseSymptoms of a baclofen overdose include vomiting, weakness, drowsiness, slow breathing, seizures, unusual pupil size, and coma.hypertonia, hyperthermia, formal thought disorder, psychosis, mania, mood disturbances, restlessness, and behavioral disturbances, tachycardia, seizures, tremors, autonomic dysfunction, hyperpyrexia, extreme muscle rigidity resembling neuroleptic malignant syndrome. Intrathecal administration is particularly used in patients with multiple sclerosis who have severe painful spasms which are not controllable by oral baclofen, or patients with spastic diplegia in whom management of spasticity is made easier by regular self-administering of the drug through its pump. Dr. William Bucknam, who published a case report in These pump systems are quite sophisticated and expensive, so careful patient selection is required. In about 5% of patients, the intrathecal route has no effect on the nervous system. Because of their placement just beneath the skin, baclofen pumps are notably vulnerable to infection at least, or at worst, to breakage which releases the whole of the baclofen supply into the body at onceDosageBaclofen therapy is usually started with an initial low dose of about 10 mg daily in divided doses and gradually titrated up in a stepwise fashion until symptomatic relief occurs. The usual maximum dose is 80 mg per dayWithdrawal syndromeDiscontinuation of baclofen can be associated with a withdrawal syndrome which resembles benzodiazepine withdrawal and alcohol withdrawal. Withdrawal symptoms are more likely if baclofen is used for long periods of time (more than a couple of months) and can occur from low or high doses. The severity of baclofen withdrawal depends on the rate at which baclofen is discontinued. Thus to minimise baclofen withdrawal symptoms the dose should be tapered down slowly when discontinuing baclofen therapy. Abrupt withdrawal is most likely to result in severe withdrawal symptoms. Acute withdrawal symptoms can be stopped by recommencing baclofen. Withdrawal symptoms may include auditory hallucinations, visual hallucinations, tactile hallucinations, delusions, confusion.

With pump administration, a test dose is given to assess the effect, and if successful a chronic intrathecal catheter is inserted and connected to a computer-controlled implanted pump. The reservoir in the pump can be replenished by injection.

(directly into the cerebral spinal fluid). Intrathecal administration is often preferred in spasticity patients, as very little of the oral dose actually reaches the spinal fluid. Recently, based on Ameisen's therapeutic model, some trials have been conducted in using Baclofen to treat cocaine addiction. While no final study has been released, people have said once they took Baclofen they felt their desire for cocaine plummet almost overnightThere is a report that baclofen has beneficial role in the management of reflux diseaseDescription of compoundBaclofen is a white (or off white) mostly odorless crystalline powder, with a molecular weight of 213.66 g/mol. It is slightly soluble in water, very slightly soluble in methanol, and insoluble in chloroform.PharmacokineticsThe drug is rapidly absorbed after oral administration and is widely distributed throughout the body. Biotransformation is low and the drug is predominantly excreted in the unchanged form by the kidneys.Routes of administrationBaclofen can be administered either orally or in English) to inform public opinion and physicians. Since his book has been released, hundreds of patients have been treated in academic centers and rapidly become "indifferent to alcohol".[ Also, clinical trials are finally being mounted as a result of public pressure, titled Ameisen, who currently is a visiting professor of medicine at State University of New York Downstate Medical Center, authored (JAMA). His therapeutic model was reproduced by that he successfully used Baclofen to completely suppress his own alcohol addiction. In his paper, he called for randomized trials of high-dose baclofen to be conducted to test the therapeutic model he had proposed. He renewed his call for clinical trials in the Baclofen is used for the treatment of spastic movement, especially in instances of spinal cord injury, spastic diplegia, multiple sclerosis, amyotrophic lateral sclerosis (Lou Gehrig's Disease) and trigeminal and glossopharyngeal neuralgias.Mechanism of actionBaclofen produces its effect via modulating the GABAB receptor, similar to the drug HistoryHistorically baclofen was designed to be a drug for epilepsy in the 1920s. The effect on epilepsy was disappointing but it was found that in certain patients spasticity decreased. Baclofen was and is still given orally with variable effects. In severely affected children, the oral dose is so high that side effects appear and the treatment loses its benefit. How and when baclofen came to be used in the spinal sac is not really clear but this is now an established method for the treatment of spasticity in many conditions.As a treatment for addictionsDr. Olivier Ameisen, a French-American associate professor of medicine and a cardiologist at Weill Cornell Medical College of Cornell University, reported in 2004 in the journal is a derivative of gamma-aminobutyric acid (GABA) primarily used to treat.


Have More Energy And Lose More Fat! 1. What is it and where does it come from? Caffeine is an alkaloid; of which there are numerous compounds such as the methylxanthines, with three distinguished compounds: caffeine, theophylline, and theobromine, found in guarana, kola nuts, coffee, tea, cocoa beans, mate and other plants. These compounds have different biochemical effects, and are present in different ratios in the different plant sources.

Caffeine is the most popular drug on the globe. It is a powerful stimulant to the Central Nervous System. Moderate use seems to be desireable by all, male and female; although excessive use can produce undesireable effects. Caffeine was discovered in 1820. In 1838, it was found that theine, a substance in tea, was identical to caffeine. Six or so caffeine containing plants are used more worldwide as a beverage than any other plants and herbal materials put together. The many caffeinated natural plants are are: Coffee, Tea, Kola, Cocoa, and Guarana. 2. What does it do and what scientific studies give evidence to support this? Caffeine is a power and energy accelerant! It's perfect to super energize your body for powerful workouts. This fast-acting substance delivers the right molecular structure to your energy systems for maximum energy and power output. Caffeine much like Ephedra acts to increase mental alertness and neurologically provide the surge you need to maximize your training. Not just a stimulant, this powerful substance reaches deep into the muscle cell to provide lasting power and delaying the onset of muscle fatigue.

So how does caffeine work to provide you with maximum energy support and increased endurance? Caffeine affects the CNS causing more alertness and allowing for more intense focus. The chemical structure of caffeine is very similar to that of adenine (a component of ATP, DNA, and cyclic AMP). Only the substituents are different. This helps explain caffeine's stimulating effects. It is really close to being an energy metabolite in and of itself! Because of the structural similarities, caffeine can slip right into adenosine receptors, keeping cyclic AMP active rather than it being broken down. When cyclic AMP breaks down, the body's energy supply decreases. Because caffeine fools the body into using enzymes to break it down instead, the cyclic AMP supply remains higher for longer. I bet you always wanted to know that. It increases the potency of aspirin or other analgestics. The majority of caffeine is produced in decaffeinating coffee. 3. Who needs it and are there any symptoms of deficiency? Well, this is an interesting question. Nobody really needs caffeine, but I once read an article that said if all of America were to stop drinking coffee or caffeine-containing soft drinks/beverages, productivity would fall by 70%. So, anyone who wants more alertness and a mental/physical boost could use a little caffeine safely. Anyone who doesn't want to drink coffee or soda could easily supplement their diets with an energy-enhancing supplement that contains caffeine. Deficiency is not an associated problem with caffeine because it is not an essential nutrient. 4. How much should be taken? Are there any side effects? Nonpregnant adults should limit their intake to about 250mg per day. Pregnant women should be even more conservative with their intake. Moderation in all caffeine containing products is the basic rule of thumb for the positive attributes without the undesireable effects of taking too much.


Mental processes like memory and attention are complex processes, so they cannot be addressed with a single pathway. At the same time, it is well-known that acetylcholine (Ach) is central to our mental function, and especially our ability to focus and to remember facts and verbal information. Acetylcholine is made in the nervous system from a B-vitamin-like raw material called choline which comes from lecithin. Lecithin, found in foods such as eggs, soybeans, peanuts, and liver, is the predominant source of choline in the human diet.Health Benefits of Choline Bitartrate.

Growing evidence now suggests that dietary choline is very important for the prevention of many pathologic conditions, and has been used as a dietary supplement for the purpose of treating or preventing several human diseases including arteriosclerosis and certain deficiencies of brain function and memory.Choline has also been shown to be essential for proper brain development in infants and children. In fact, supplementation of animal diets with choline or lecithin at particular times of brain development has been shown to permanently increase cognitive function. Lower levels of acetylcholine are associated with memory loss and learning difficulties that occur in aging brains. In one experiment, university students improved test scores after taking supplemental choline.


DMAE alleviates the behavioral problems and hyperactivity associated with Attention Deficit Disorder (ADD) [DMAE increases Attention Span, decreases Aggression, improves Learning ability and sometimes increases Intelligence in 70% of ADD patients].

DMAE increases Attention Span [after 6 weeks of DMAE supplementation students were able to concentrate at lectures better and were able to study and concentrate on exams better].

DMAE inhibits and reverses the Cross-Linking of proteins.

DMAE extends the lifespan of mice by 27-49%.

DMAE facilitates the removal of Lipofuscin from Neurons.

DMAE decreases the incidence and severity of Hangovers in people who consume excessive amounts of Alcohol [after 6 weeks of DMAE use subjects reported freedom from the depression or headaches associated with hangovers].

DMAE may improve Athletic Performance (by improving the body’s production of Energy) [anecdotal reports: many athletes report increased subjective feelings of Energy following DMAE supplementation].

DMAE increases the body's production of Energy and persons using DMAE subjectively report increases in their levels of Energy.

DMAE mildly stimulates the Central Nervous System (CNS).

Most people who use DMAE supplements report that after 3-4 weeks of DMAE use, they notice a continual mild stimulation of their CNS without side effects.

DMAE increases Alertness.

DMAE alleviates Anxiety [subjects administered 1,200 mg (1.2 gm) of DMAE per day for 5 days exhibited better control of anxious reactivity].

DMAE increases Assertiveness [after 6 weeks of DMAE supplementation subjects reported having a more outspoken personality].

DMAE reduces Apathy and increases Motivation in persons afflicted with Depression.

DMAE improves the Interhemispheric Flow of Information in the Corpus Callosum of the Brain (thereby improving Creativity and Verbal Fluency).

DMAE improves the behavior and Mental Function of children afflicted with Down’s Syndrome.

DMAE exerts favorable effects on those chronic Dyskinesias (including Tardive Dyskinesia) that occur as a result of long periods of use of Major Tranquilizers.

DMAE increases Intelligence (especially in children).

DMAE improves Learning and Memory.

DMAE decreases the accumulation of Lipofuscin within the Brain.

DMAE elevates Mood [after 6 weeks of DMAE supplementation, subjects reported more affable moods].

DMAE reduces the amount of Sleep required by about 1 hour per night [this effect noted after 6 weeks of DMAE use].

DMAE causes Dreams to become more lucid (vivid).

DMAE users experience a sounder Sleep [after 6 weeks subjects reported waking earlier and having a clearer mind upon waking].

DMAE increases daytime motivation and physical Energy in persons afflicted with Insomnia.

DMAE increases Willpower [after 6 weeks of DMAE use, subjects who previously were unable to stop smoking reported success].

DMAE removes Lipofuscin (age spots) from the skin.

DMAE increases Acetylcholine levels within the Brain:

Medical researchers have speculated that the means by which DMAE increases Brain Acetylcholine levels is by inhibiting Choline metabolism in peripheral tissues, thereby allowing free Choline to accumulate and subsequently enter the Brain where it is converted to Acetylcholine.

DMAE increases the content of Ribonucleic Acid (RNA) in the Brain [research - rats].

DMAE is a component of the chemical structure of Centrophenoxine.

DMAE increases the concentration of Choline in the bloodstream because it enhances the rate at which free Choline enters the blood from other tissues:

DMAE increases the levels of Choline in the brain due to DMAE’s superior ability to cross the Blood-Brain Barrier.

DMAE inhibits the metabolism of Choline in peripheral tissues (permitting "free" Choline to enter the Brain and stimulate the production of Acetylcholine) [research - mice].OVERVEIWDimethylamino Ethanol (DMAE), a natural amino alcohol found, in small amounts, in the brain, is considered a precursor of choline necessary for the brain to make acetylcholine.

Acetylcholine is a neurotransmitter in healthy nerve signal conduction and function. As a supplement, DMAE works with gingko biloba and other "smart nutrients".

DMAE is found in fish, salmon, and especially sardines. The human brain maintains a small amount of DMAE, which plays various crucial functions. DMAE protects the integrity of cell membranes, the deterioration of which can lead to premature aging.More DMAE factsDMAE is a mood elevator, counteracting depression and bad moods, and raising and improving cognitive functions like memory and concentration.

It may also treat autism, Alzheimer’s, ADHD, memory deficits, depression, and dementia. DMAE can even increase intelligence. These benefits result from DMAE’s role in manufacturing acetylcholine, a substance responsible for healthy mental functioning.

Physicians monitoring patients on DMAE have reported them to be more upbeat and exhibiting greater mental acuity. Those who regularly take DMAE have reported both sleeping more soundly and being more energetic when awake.

One DMAE benefits most promising benefits is that, by stopping the manufacture of arachidonic acid, which can lead to wrinkles and aging of the skin, DMAE promotes healthy skin. DMAE used to stop arachidonic acid production can be either taken internally as a nutritional supplement, or applied as a topical cream.

What to Watch Out ForWhile DMAE has no known toxicity, and is considered a very safe supplement, there is no RDA.

Those with epilepsy or seizure disorders, bipolar depression, or Parkinson’s disease and pregnant or nursing women should not use DMAE without their doctors’ approval.

The rare side effects of DMAE include gastro-intestinal problems, body odor, drowsiness, confusion, high blood pressure, moderate depression, and persistent irritability.(Recommended Daily Allowance) set for it (1 gram per day is a good starting point) . There are, however, some cautions for people with certain conditions.


Methylhexaneamine (Forthan, Forthane, Floradrene, Geranamine) or dimethylamylamine (DMAA) is a psychoactive drug and simple aliphatic amine used as a nasal decongestant, putatively via acting as a norepinephrine reuptake inhibitor (NRI) and/or norepinephrine releasing agent (NRA), as well as treatment for hypertrophied or hyperplasic oral tissues and as an active ingredient in party pills in New Zealand. Once trademarked under Forthane by Eli Lilly in 1971, the trademark has since expired, and so methylhexaneamine should not be confused with isoflurane, whose proprietary name in Australia is also Forthane. It is a vasoconstrictor, and can be administered by inhalation to the nasal mucosa to exert its effect. The trademark Geranamine is currently owned by Proviant Technologies. Methylhexaneamine is also a constituent of flower oil, sold as an integral component of nutritional supplements. Chemistry

Methylhexaneamine may be synthesized by reacting 4-methylhexan-2-one with hydroxylammonium chloride to give the oxime, followed by reduction via sodium in ethanol.

Uses Although intended by Eli Lilly to be used as a nasal decongestant, methylhexaneamine has been marketed by certain companies as a dietary supplement in combination with caffeine and other ingredients, under trade names such as Geranamine and Floradrene, to be used as an OTC thermogenic or general purpose stimulant. Geranamine itself has not been researched intensively, with its pharmacological profile not looked at since Eli Lilly filed its patent in 1944, stating that the stimulant effects on the CNS are less than that of amphetamine or ephedrine.

Methylhexaneamine is not FDA approved in its own right, although it is a component of geranium oil which is approved for use in foods, and so this has been used to justify claims that it should be classified as a dietary supplement rather than a pharmaceutical product. However while it may be technically correct to say that geranamine is a dietary supplement as it is a component of the oil from Pelargonium graveolens which is approved for use in foods, geranamine comprises only 0.66% of geranium oil, and pure synthetic geranamine is thus quite different from geranium oil.Use as a recreational drug.

In New Zealand, Methylhexanamine (under the name 1,3 dimethylamylamine or DMAA) is an emerging active ingredient of party pills, where it has replaced benzylpiperazine or BZP which has been illegal in that country since 2008. Serious adverse effects including headache, nausea, and stroke have been reported in recreational users of these products. In November 2009 the New Zealand government indicated that DMAA would be scheduled as a restricted substance. Doping in sports.

Methylhexanamine was implicated as a stimulant used by five Jamaican athletes in 2009. JADCO, the Jamaican anti-doping panel, was initially unable to determine whether it was prohibited by the rules, but subsequently decided to impose sanctions on some of the affected athletes on the grounds that the drug was similar in structure to the banned substance tuaminoheptane.


Hordenine (N,N-dimethyl-4-hydroxyphenylethylamine) is a phenylethylamine alkaloid with antibacterial and antibiotic properties. It stimulates the release of norepinephrine in mammals. It is produced in nature by several varieties of plants in the family Cactaceae and by some in Acacia. Occurrence in nature.

Sprouting Hordeum vulgare (barley) seeds contain hordenine as the main alkaloid in their roots.

Peyote (Lophophora williamsii), San Pedro cactus (Echinopsis pachanoi), and Peruvian Torch cactus (Echinopsis peruviana) all produce high levels of this compound. These cacti also produce high levels of mescaline and other phenylethylamine compounds.

Cacti in the genus Ariocarpus, Opuntia, Pereskia, and Coryphantha also produce these alkaloids, though not in high concentrations.

Aztekium also contains it.

". . .it has been shown that hordenine, N, N-Dimethyl-hydroxyphenylethylamine, exhibits an inhibitory action against at least 18 strains of penicillin resistant Staphylococcus bacteria."


Other names N-[4(2-Amino-4-hydroxy pteridin-6-ylmethylamino) benzoyl]-L(+)-glutamic acid; pteroyl-L-glutamic acid; Vitamin B9; Vitamin M; Folacin

Folate is necessary for the production and maintenance of new cells. This is especially important during periods of rapid cell division and growth such as infancy and pregnancy. Folate is needed to synthesize DNA bases (most notably thymine, but also purine bases) needed for DNA replication. Thus folate deficiency hinders DNA synthesis and cell division, affecting most notably bone marrow and cancer, both of which participate in rapid cell division. RNA transcription, and subsequent protein synthesis, are less effected by folate deficiency as the mRNA can be recycled and used again (as opposed to DNA synthesis where a new genomic copy must be created). Since folate deficiency limits cell division, erythropoiesis, production of red blood cells (RBCs) is hindered and leads to megaloblastic anemia which is characterized by large immature RBCs. This pathology results from persistently thwarted attempts at normal DNA replication, DNA repair, and cell division and produces abnormally large cells (megaloblasts) with abundant cytoplasm capable of RNA and protein synthesis but with clumping and fragmentation of nuclear chromatin. Some of these large cells, although immature, are released early from the marrow in an attempt to compensate for the anemia caused by lack of RBCs. [2] Both adults and children need folate to make normal RBCs and prevent anemia Deficiency of folate in pregnant women has been implicated in neural tube defects and so many cereals sold in developed countries are enriched with folate to avoid such complications.

In the form of a series of tetrahydrofolate (THF) compounds, folate derivatives are substrates in a number of single-carbon-transfer reactions, and also are involved in the synthesis of dTMP (2'-deoxythymidine-5'-phosphate) from dUMP (2'-deoxyuridine-5'-phosphate). It is a substrate for an important reaction that involves vitamin B12 and it is necessary for the synthesis of DNA, required for all dividing cells.

The pathway leading to the formation of tetrahydrofolate (FH4) begins when folate (F) is reduced to dihydrofolate (DHF) (FH2), which is then reduced to THF. Dihydrofolate reductase catalyses the last step. Vitamin B3 in the form of NADPH is a necessary cofactor for both steps of the synthesis.Methylene-THF

In other words: F → DHF2 → THF → CH2-THF Formyl-THF <--> Methynl-THF <.--> Methylene-THF --> Methyl-THFOverview of drugs that interfere with folate reactions A number of drugs interfere with the biosynthesis of folic acid and THF. Among them are the dihydrofolate reductase inhibitors such as trimethoprim, pyrimethamine and methotrexate; the sulfonamides (competitive inhibitors of para-aminobenzoic acid in the reactions of dihydropteroate synthetase). (CH2FH4) is formed from THF by the addition of methylene groups from one of three carbon donors: formaldehyde, serine, or glycine. Methyl tetrahydrofolate (CH3-THF) can be made from methylene-THF by reduction of the methylene group with NADPH. If is important to note that Vitamin B12 is the only acceptor of methyl-THF. There is also only one acceptor for methyl-B12 which is homocysteine in a reaction catalyzed by homocysteine methyltransferase. This is important because a defect in homocysteine methyltransferase or a defeciency of B12 can lead to a methyl-trap of THF and a subsequent deficiency. Thus, a deficiency in B12 can generate a large pool of methyl-THF that is unable to undergo reactions and will mimic folate deficiency. Another form of THF, formyl-THF or folinic acid) results from oxidation of methylene-THF or is formed from formate donating formyl group to THF. Finally, histidine can donate a single carbon to THF to form methenyl-THF.· · · 1998 RDAs for Folate.

Men Women
(19+) (19+) Pregnancy Breast feeding
400 µg 400 µg 600 µg 500 µg

1 µg of food folate = 0.6 µg folic acid from supplements and fortified foodsThe National Health and Nutrition Examination Survey (NHANES III 1988-91) and the Continuing Survey of Food Intakes by Individuals (1994-96 CSFII) indicated that most adults did not consume adequate folate. However, the folic acid fortification program in the United States has increased folic acid content of commonly eaten foods such as cereals and grains, and as a result diets of most adults now provide recommended amounts of folate equivalents. Folic Acid / Folate deficiency.

Human reproductionFolic acid is very important for all women who may become pregnant. Adequate folate intake during the periconceptional period, the time just before and just after a woman becomes pregnant, helps protect against a number of congenital malformations including neural tube defects Neural tube defects result in malformations of the spine (spina bifida), skull, and brain (anencephaly). The risk of neural tube defects is significantly reduced when supplemental folic acid is consumed in addition to a healthy diet prior to and during the first month following conception. Women who could become pregnant are advised to eat foods fortified with folic acid or take supplements in addition to eating folate-rich foods to reduce the risk of some serious birth defects. The most notable birth defects that occur from folate deficiency are neural tube defects. Taking 400 micrograms of synthetic folic acid daily from fortified foods and/or supplements has been suggested. The Recommended Dietary Allowance (RDA) for folate equivalents for pregnant women is 600-800 micrograms, twice the normal RDA of 400 micrograms for women who are not pregnant.

Recent research has shown that it is also very important for men who are planning on fathering children, reducing birth defect risksFolic acid supplements and masking of B12 deficiencyThere has been concern about the interaction between vitamin B12 and folic acid Folic acid supplements can correct the anemia associated with vitamin B12 deficiency. Unfortunately, folic acid will not correct changes in the nervous system that result from vitamin B12 deficiency. Permanent nerve damage could theoretically occur if vitamin B12 deficiency is not treated. Therefore, intake of supplemental folic acid should not exceed 1000 micrograms (1000 mcg or 1 mg) per day to prevent folic acid from masking symptoms of vitamin B12 deficiency. In fact, to date the evidence that such masking actually occurs is scarce, and there is no evidence that folic acid fortification in Canada or the US has increased the prevalence of vitamin B12 deficiency or its consequences.

However one recent study has demonstrated that high folic or folate levels when combined with low B12 levels are associated with significant cognitive impairment among the elderly. If the observed relationship for seniors between folic acid intake, B12 levels, and cognitive impairment is replicated and confirmed, this is likely to re-open the debate on folic acid fortification in food, even though public health policies tend generally to support the developmental needs of infants and children over slight risks to other population groups.

In any case, it is important for older adults to be aware of the relationship between folic acid and vitamin B12 because they are at greater risk of having a vitamin B12 deficiency. If you are 50 years of age or older, ask your physician to check your B12 status before you take a supplement that contains folic acid.Health risk of too much folic acidThe risk of toxicity from folic acid is low.[16] The Institute of Medicine has established a tolerable upper intake level (UL) for folate of 1 mg for adult men and women, and a UL of 800 µg for pregnant and lactating (breast-feeding) women less than 18 years of age. Supplemental folic acid should not exceed the UL to prevent folic acid from masking symptoms of vitamin B12 deficiency.

Research suggests high levels of folic acid can interfere with some antimalarial treatments.

A 10000-patient study at Tufts University in 2007 concluded that excess folic acid worsens the effects of B12 deficiency and in fact may affect the absorption of B12. Some current issues and controversies about folateDietary fortification of folic acidSince the discovery of the link between insufficient folic acid and neural tube defects (NTDs), governments and health organizations worldwide have made recommendations concerning folic acid supplementation for women intending to become pregnant. For example, the United States Public Health Service (see External links) recommends an extra 0.4 mg/day, which can be taken as a pill. However, many researchers believe that supplementation in this way can never work effectively enough since about half of all pregnancies in the U.S. are unplanned and not all women will comply with the recommendation.

This has led to the introduction in many countries of fortification, where folic acid is added to flour with the intention of everyone benefiting from the associated rise in blood folate levels. This is controversial, with issues having been raised concerning individual liberty, and the masking effect of folate fortification on pernicious anaemia (vitamin B12 deficiency). However, almost all American countries now fortify their flour, along with a number of Middle Eastern countries and Indonesia. Mongolia and a number of ex-Soviet republics are amongst those having widespread voluntary fortification; about five more countries (including Morocco, the first African country) have agreed but not yet implemented fortification. In the UK the Food Standards Agency has recommended fortification. To date, no EU country has yet mandated fortification.[23] Australia is considering fortification, but a period for comments ending 2006-07-31 attracted strong opposition from industry as well as academia.

Recent debate has emerged in the United Kingdom and Australia regarding the inclusion of folic acid in products such as bread and flour.

In the USA many grain products are fortified with folic acid.

In 1996, the United States Food and Drug Administration (FDA) published regulations requiring the addition of folic acid to enriched breads, cereals, flours, corn meals, pastas, rice, and other grain products.[27][28] This ruling took effect 1998-01-01, and was specifically targeted to reduce the risk of neural tube birth defects in newborns There are concerns that the amount of folate added is insufficient[2]. In October 2006, the Australian press claimed that U.S. regulations requiring fortification of grain products were being interpreted as disallowing fortification in non-grain products, specifically Vegemite (an Australian yeast extract containing folate). The FDA later said the report was inaccurate, and no ban or other action was being taken against Vegemite.

Since the folic acid fortification program took effect, fortified foods have become a major source of folic acid in the American diet. The Centers for Disease Control and Prevention in Atlanta, Georgia used data from 23 birth defect registries that cover about half of United States births and extrapolated their findings to the rest of the country. This data indicates that since the addition of folic acid in grain-based foods as mandated by the Food and Drug Administration, the rate of neural tube defects dropped by 25% in the United States.

Although folic acid does reduce the risk of birth defects, it is only one part of the picture and should not be considered a cure. Even women taking daily folic acid supplements have been known to have children with neural tube defects.Heart diseaseAdequate concentrations of folate, vitamin B12, or vitamin B6 may decrease the circulating level of homocysteine, an amino acid normally found in blood. There is evidence that an elevated homocysteine level is an independent risk factor for heart disease and stroke.[31] The evidence suggests that high levels of homocysteine may damage coronary arteries or make it easier for blood clotting cells called platelets to clump together and form a clot. However, there is currently no evidence available to suggest that lowering homocysteine with vitamins will reduce risk of heart disease. Clinical intervention trials are needed to determine whether supplementation with folic acid, vitamin B12 or vitamin B6 can lower the risk of developing coronary heart disease. The NORVIT trial suggests that folic acid supplementation may do more harm than good.

As of 2006, studies have shown that giving folic acid to reduce levels of homocysteine does not result in clinical benefit. One of these studies suggests that folic acid in combination with B12 may even increase some cardiovascular risks.

However a 2005 study found that 5 mg. of folate daily over a three-week period reduced pulse pressure by 4.7 mmHg. compared with a placebo, and concluded that[Folic acid is a safe and effective supplement that targets large artery stiffness and may prevent isolated systolic hypertension.

Also, as a result of new research, "heart experts" at Johns Hopkins Medical Center reported in March 2008 in favour of therapeutic folate, although they cautioned that it was premature for those at risk of heart attack to self-medicate.StrokeFolic acid appears to reduce the risk of stroke. The reviews indicate only that in some individuals the risk of stroke appears to be reduced, but a definite recommendation regarding supplementation beyond the current recommended daily allowance has not been established for stroke prevention. Observed stroke reduction is consistent with the reduction in pulse pressure produced by folate supplementation of 5 mg per day, since hypertension is a key risk factor for stroke.CancerThe association between folate and cancer appears to be complex It has been suggested that folate may help prevent cancer, as it is involved in the synthesis, repair, and functioning of DNA, and a deficiency of folate may result in damage to DNA that may lead to cancer. Some investigations have proposed that good levels of folic acid may be related to lower risk of esophagus, stomach and ovarian cancer, but benefices of folic acid against cancer may depend on when it is taken and on individual conditions. In addition folic acid may not be helpful, and could even be damaging, in people who already are suffering from cancer or from a precancerous condition. Conversely, it has been suggested that excess folate may promote tumor initiation. Diets high in folate are associated with decreased risk of colorectal cancer; some studies show an association which is stronger for folate from foods alone than for folate from foods and supplements, while other studies find that folate from supplements is more effective due to greater bioavailability and a 2007 randomized clinical trial found that folate supplements did not reduce the risk of colorectal adenomas.[45] A 2006 prospective study of 81,922 Swedish adults found that diets high in folate from foods, but not from supplements, were associated with a reduced risk of pancreatic cancer Most epidemiologic studies suggest that diets high in folate are associated with decreased risk of breast cancer, but results are not uniformly consistent: one large cancer screening trial reported a potential harmful effect of high folate intake on breast cancer risk, suggesting that routine folate supplementation should not be recommended as a breast cancer preventive but a 2007 Swedish prospective study found that a high folate intake was associated with a lower incidence of postmenopausal breast cancer. It is very difficult to affirm how each nutrient or nutrient combination affects a person’s risk of cancer. People whose diets are rich in vegetables and low in animal fat and meat have lower risks for some of the most frequent types of cancer. Taking a variety of healthful foods, with most of them coming from plant sources, is a better solution than taking vitaminic supplements. So the authorities are not really sure if this will work for cancer or not, (or the age at which it is safe to start taking folate supplements) but hopefully this will all become clear in the light of research now underway.AntifolatesFolate is important for cells and tissues that rapidly divide.

Cancer cells divide rapidly, and drugs that interfere with folate metabolism are used to treat cancer. The antifolate methotrexate is a drug often used to treat cancer because it inhibits the production of the active form of THF from the inactive dihydrofolate (DHF). Unfortunately, methotrexate can be toxic, producing side effects such as inflammation in the digestive tract that make it difficult to eat normally.Folinic acidDepressionSome evidence links low levels of folate with depression. There is some limited evidence from randomised controlled trials that using folic acid in addition to antidepressant medication may have benefits Researchers at the University of York and Hull York Medical School have confirmed a link between depression and low levels of folate in a research study involving 15,315 However, the evidence is probably too limited at present for this to be a routine treatment recommendation.Memory and mental agilityIn a 3-year trial on 818 people over the age of 50, short-term memory, mental agility and verbal fluency were all found to be better among people who took 800 micrograms of folic acid daily—twice the current RDA—than those who took placebo. The study was reported in The Lancet on 19 January 2007FertilityFolate is necessary for fertility in both men and women. In men, it contributes to spermatogenesis. In women, on the other hand, it contributes to oocyte maturation, implantation, placentation, in addition to the general effects of folic acid and pregnancy. Therefore, it is necessary to receive sufficient amounts through the diet, in order to avoid subfertility. Induction of acute renal failureFolic acid is used in extremely high doses to induce Acute renal failure in murine models. It should be noted that the dose reported below represents about 120 years of the recommended daily intake [0.4 mg for adults] in one application, an experiment irrelevant to human nutrition. The exact method through which folic acid induces kidney injury in such massive dose is unknown, however it is characterized by the appearance of folic acid crystals in renal tubules and acute tubular necrosis. This method of renal injury is also linked to increased expression of Tumor necrosis factor-alpha. The dose of folic acid used to induce renal injury is usually around 250mg of folic acid per kg of body weight. The folic acid is usually administered in a vehicle of 0.3mmol/L of sodium bicarbonate. , under the drug name leucovorin, is a form of folate (formyl-THF) that can help "rescue" or reverse the toxic effects of methotrexate Folinic acid is not the same as folic acid. Folic acid supplements have little established role in cancer chemotherapy.[53][54] There have been cases of severe adverse effects of accidental substitution of folic acid for folinic acid in patients receiving methotrexate cancer chemotherapy. It is important for anyone receiving methotrexate to follow medical advice on the use of folic or folinic acid supplements.

The supplement of folinic acid in patients undergoing methotrexate treatment is to give non rapidly dividing cells enough folate to maintain normal cell functions. The amount of folate given will be depleted by rapidly dividing cells (cancer) very fast and so will not negate the effects of methotrexate. Low dose methotrexate is used to treat a wide variety of non-cancerous diseases such as rheumatoid arthritis, lupus, scleroderma, psoriasis, asthma, sarcoidoisis, primary biliary cirrhosis, and inflammatory bowel disease Low doses of methotrexate can deplete folate stores and cause side effects that are similar to folate deficiency. Both high folate diets and supplemental folic acid may help reduce the toxic side effects of low dose methotrexate without decreasing its effectiveness.[56][57] Anyone taking low dose methotrexate for the health problems listed above should consult with a physician about the need for a folic acid supplement. While the role in folate as a cancer treatment is well established its long term effectiveness is diminished by cellular response. In response to decreased THF the cell begins to transcribe more DHF reductase, the enzyme that reduces DHF to THF. Because methotrexate is a competitive inhibitor of DHF reductase increased concentrations of DHF reductase can overcome the drugs inhibition.Recommended Daily Allowence (RDA) Biochemistry of DNA base and amino acid production DNA and cell division Biological roles of Folic Acid / folateFolic acid

GABA amino acid

GABA stands for gamma-aminobutyric acid, is the product of a biochemical decarboxylation reaction of glutamic acid by the vitamin pyridoxal, as well as from decarboxylase (GAD).GABA is required forGABA is required as an inhibitory neurotransmitter to block the transmission of an impulse from one cell to another in the central nervous system, which prevents over-firing of the nerve cells.

It is also used for brain metabolism and to treat both epilepsy and hypertension where it is thought to induce tranquility in individuals who have a high activity of manic behavior and acute agitation.

In combination with inositol and nicotinamide it helps with blocking anxiety and stress related impulses from reaching the motor centers of the brain.

Gamma-Aminobutyric Acid can be used to calm a person, much like tranquilizers, but without the possibility of addiction.Deficiency of GABAIt has been suggested that a shortage of GABA may cause panic attacks, since an intake of tranquilizers can increase the level of GABA in the body. GABA may also be effective in treating PMS in women.DosageThe dosage listed is .5gm , but be aware that this dosage is the minimum that you require per day, to ward off serious deficiency of this particular nutrient. In the therapeutic use of this nutrient, the dosage is usually increased considerably, but the toxicity level must be kept in mind.

Dosage has not been established, but it is interesting to note that some research suggests that the supplement Kava (kava is a herbal root used as a supplement) causes more GABA receptors to form in the brain. Toxicity and symptoms of high intakeToxic levels have not been established, but very high intake of GABA may cause anxiety, tingling of extremities, shortness of breath as well as a numb feeling around the mouth.Other interesting pointsIt is sometimes used as sexual a stimulant because of its relaxing capabilities, as well as with prostate problems, since it also assists with the release of sex hormones.


Glycine is a protein amino acid found in the protein of all life forms. It is the simplest amino acid in the body and the only protein amino acid that does not have chirality. Although most glycine is found in proteins, free glycine is found in body fluids as well as in plants. The normal diet contributes approximately 2 grams of glycine daily.

Glycine is not considered an essential amino acid, i. e., the cells in the body can synthesize sufficient amounts of glycine to meet physiological requirements. However, glycine is of major importance in the synthesis of proteins, peptides, purines, adenosine triphosphate (ATP), nucleic acids, porphyrins, hemoglobin, glutathione, creatine, bile salts, one-carbon fragments, glucose, glycogen, and L-serine and other amino acids. Glycine is also a neurotransmitter in the central nervous system (CNS). Glycine and gamma-aminobutyric acid (GABA) are the major inhibitory neurotransmitters in the CNS. Recently, a glycine-gated chloride channel has been identified in neurophils that can attenuate increases in intracellular calcium ions and diminish oxidant damage mediated by these white blood cells. Thus, glycine may be a novel antioxidant.

Glycine is also known as amino acetic acid, aminoethanolic acid, glycocoll, glycinium and sucre de gelatine. Its IUPAC abbreviation is Gly and its one-letter abbreviation, used when spelling out protein structures, is G. It is a neutral amino acid. Glycine is a solid water-soluble substance that has a sweetish taste.

Supplemental glycine may have antispastic activity. Very early findings suggest it may also have antipsychotic activity as well as antioxidant and anti-inflammatory activities.

In the CNS, there exist strychnine-sensitive glycine binding sites as well as strychnine-insensitive glycine binding sites. The strychnine-insensitive glycine-binding site is located on the NMDA receptor complex. The strychnine-sensitive glycine receptor complex is comprised of a chloride channel and is a member of the ligand-gated ion channel superfamily. The putative antispastic activity of supplemental glycine could be mediated by glycine's binding to strychnine-sensitive binding sites in the spinal cord. This would result in increased chloride conductance and consequent enhancement of inhibitory neurotransmission.

The ability of glycine to potentiate NMDA receptor-mediated neurotransmission raised the possibility of its use in the management of neuroleptic-resistant negative symptoms in schizophrenia.

Animal studies indicate that supplemental glycine protects against endotoxin-induced lethality, hypoxia-reperfusion injury after liver transplantation, and D-galactosamine-mediated liver injury. Neutrophils are thought to participate in these pathologic processes via invasion of tissue and releasing such reactive oxygen species as superoxide. In vitro studies have shown that neutrophils contain a glycine-gated chloride channel that can attenuate increases in intracellular calcium and diminsh neutrophil oxidant production. This research is ealy-stage, but suggests that supplementary glycine may turn out to be useful in processes where neutrophil infiltration contributes to toxicity, such as ARDS.

Following ingestion of glycine, the amino acid is absorbed from the small intestine via an active transport mechanism. From the small intestine, glycine is transported to the liver by means of the portal circulation where a portion enters into one of several metabolic pathways. Glycine not metabolized in the liver enters the systemic circulation and is distributed to various tissues in the body. Glycine readily crosses the blood-brain barrier.

Glycine may be indicated to help alleviate the symptoms of spasticity. An indication for potentiating some anti-convulsant drugs and preventing some seizures could emerge, as could an indication for its use in managing schizophrenia. Research in progress also suggests usefulness in some cancers. There is no evidence to support use of glycine as an ergogenic aid, and it is too early to say whether it can play any useful role in lipid metabolism. There are no well-designed clinical trials to support its use in benign prostate hypertrophy.

Glycine first attracted interest in the medical research community for its reputed ability to dampen reflex excitability in the CNS. A pilot study of its effects on severe chronic leg spasticity (most of the subjects were suffering from chronic multiple sclerosis) yielded improvement in spasticity and mobility of the lower limbs, rated at about 25% overall. The dose used was 1 gram daily for six months to a year. All patients noted some benefits, and no adverse events were recorded. Other researchers have since reported that glycine can potentiate some but not all anticonvulsant drugs in some animal models. It has also been shown to prevent some experimentally produced seizures.

The effects of oral glycine (200 mg/kg/day) were tested in two siblings suffering from 3-phosphoglycerate dehydrogenase deficiency, an inborn error of L-serine biosynthesis. A significant amount of glycine is made from L-serine. Among the features of this disorder are intractable seizures. L-serine in doses up to 500 mg/kg/day failed to control the seizures, but oral glycine completely stopped them, and electroencephalographic abnormalities resolved after six months of treatment.

High-dose glycine may be beneficial in the management of enduring negative symptoms of schizophrenia. Twenty-two treatment-resistant schizophrenic patients participated in a double-blind, placebo-controlled, six-week, crossover treatment trial with 0.8 grams per kilogram daily of glycine added to their ongoing antipsychotic medication. Glycine intake ranged from 40 to 90 grams daily. Only mild gastrointestinal side effects (nausea and vomiting) were reported in one patient taking glycine. Patients taking glycine experienced significantly diminished negative symptoms. Followup studies are planned.

Recent animal studies suggest that glycine may have some anti-cancer properties. In one recent study, 51 weeks of glycine supplementation did not stop early foci formation of cancer but reduced formation of small liver tumors by 23%, medium-sized tumors by 64% and large tumors by nearly 80% in rats given an agent that is a peroxisome proliferator and liver carcinogen.

In another recent study, dietary glycine inhibited B16 melanoma tumors in mice. Glycine-supplemented mice had tumors that were 50 to 70% smaller in size than those in controls. The protective mechanism in this case appeared to be inhibition of angiogenesis effected by suppressed endothelial-cell proliferation. Tumors in mice fed glycine had 70% fewer arteries than were present in the tumors of controls.

Whether very preliminary data suggesting some positive effects of glycine on lipid metabolism will be mirrored in human research remains to be seen.

Partly because glycine is a precursor of creatine, some have assumed that it might have some of the same ergogenic potential that has been claimed for creatine. This, so far, has not been demonstrated. Glycine is claimed to be beneficial for benign prostatic hypertrophy based on a dated clinical study that has never been confirmed.

Glycine supplementation is contraindicated in those hypersensitive to any component of the preparation. It is also contraindicated in those who are anuric (some glycine gets converted to ammonia).

Glycine supplementation should be avoided by pregnant women and nursing mothers. Because of some conversion of glycine to ammonia, those with hepatic impairment should avoid glycine supplementation unless prescribed.

Doses of 1 gram daily are very well tolerated. Mild gastrointestinal symptoms are infrequently noted. In one study doses of 90 grams daily were also well tolerated.

Antispastic drugs. Theoretically, supplemental glycine might have additive effects when used in conjunction with baclofen, diazepam, dantrolene sodium and tizanidine.

No other drug, nutritional supplement, food or herb interactions are known.

There are no reports of overdosage in humans. The majority of mice receiving 3 to 4.5 grams per kilogram by intravenous infusion experienced bradycardia, prolongation of the PQ interval, QRS duration and death.

Glycine is available in 500 milligram tablets and capsules. Those who supplement use up to 1 gram daily in divided doses. Doses used for management of schizophrenia have ranged from 40 to 90 grams daily.As always, we strongly advise you do your own research and more importantly consult your own medical professional before commencing any use of this or any other dietary supplement .This statement has not been evaluated by the FDA. This is not intended to diagnose, treat, cure or prevent any disease.



L-Dopa Info

L-Dopa (L-3,4-dihydroxyphenylalanine) is an amino acid that is formed in the liver and converted into dopamine in the brain. It is essential for integrated movement of individual muscle groups.

Dopamine apparently does not enter the brain from the blood, and is ineffective when it is medically administered. L-Dopa enters the brain through the blood and then it is converted into dopamine.

usage 250mg to 500mg per day best before bed What it is: L-Dopa is an amino acid, which converts to Dopamine. Dopamine is an essential component of our body and it is required for proper functioning of the brain.

What it does:
Although L-Dopa Extract is well known for its treatment of Parkinson's, there are many other benefits. L-Dopa Extract has been shown to significantly increase the body's natural production of human growth hormone (HGH). This is very important because increasing HGH has powerful Health benefits for both men and women.

The benefits to your body are: Mucuna Pruriens gives us an "All Natural" source of L-Dopa Extract. Because the L-Dopa is extracted from a natural plant source, our body actually absorbs and utilizes a higher percentage. The improved absorption means you experience better results with smaller servings.

Because the L-Dopa Extract is from an "All Natural" source, the L-Dopa extract has no side effects. With "Mucuna Pruriens" L-Dopa Extract, you have better absorption and no side effectsIt is recommended that you consult your professional health care provider before supplementing L-Dopa into your daily diet.


  • Nervous system support
  • Supports energy production
  • Critical for enzyme function
Magnesium is a mineral that is critical for energy production and metabolism, muscle contraction, nerve impulse transmission and bone mineralization. It is required cofactor for an estimated 300 enzymes. Among the reactions catalyzed by these enzymes are fatty acid synthesis, protein synthesis and glucose metabolism. Magnesium status is also important for regulation of calcium balance through its effects on the parathyroid gland.A Dietary Supplement Suggested UseAs a dietary supplement, take .5 gm with or between meals.


Phenylalanine is an essential amino acid (building block for proteins in the body). It is essential to human health but cannot be manufactured by the body. For this reason, phenylalanine must be obtained from food. It is available in three chemical forms, including L-phenylalanine (the natural form of phenylalanine found in proteins throughout the body), D-phenylalanine (a mirror image of L-phenylalanine that is synthesized in a laboratory), and DL-phenylalanine, a combination of the previous two forms. The body converts phenylalanine into tyrosine, another amino acid essential for making proteins, brain chemicals including dopamine and norepinephrine, and thyroid hormones. Symptoms of phenylalanine deficiency include confusion, lack of energy, depression, decreased alertness, decreased memory, and diminished appetite. On the other hand, a rare metabolic disorder called phenylketonuria (PKU) occurs in people who are missing an enzyme that is needed to properly metabolize phenylalanine, causing high levels of phenylalanine in the body. Symptoms of PKU, which tend to appear between 3 and 6 months of age, include eczema, developmental delay, an abnormally small head, and hyperactivity. If it is not treated before 3 weeks of age, PKU can cause severe, irreversible mental retardation. In the United States, newborns are tested for PKU during the first 48 - 72 hours of life. People with PKU must eat a phenylalanine-restricted, tyrosine-supplemented diet to have optimum brain development and growth. Rarely, over-restriction of phenylalanine in the diet can lead to deficiency of this amino acid, with the same symptoms described above.


Chronic pain:
Although results of clinical studies have not been entirely consistent, preliminary evidence suggests that D-phenylalanine may help reduce chronic pain associated with certain health conditions, such as multiple sclerosis (MS) and fibromyalgia, by stimulating nerve pathways in the brain that control pain. Some scientists, for example, report that they have observed enhanced pain relief when D-phenylalanine is used together with prescription painkillers, including opiates. Other clinical studies have found D-phenylalanine to be no more effective than placebo in reducing pain. Further research is needed to determine the safety and effectiveness of this amino acid for pain.

Parkinson's disease:
One animal study suggests that D-phenylalanine may improve rigidity, walking disabilities, speech difficulties, and depression associated with Parkinson's disease. It is not clear whether these results translate into a possible treatment for people with this disease, however. Further studies in people are necessary before supplementation with this amino acid can be recommended for individuals with Parkinson's disease.

Clinical evidence suggests that combining L-phenylalanine (oral and topical) with UVA radiation for people with vitiligo, a condition characterized by irregular depigmentation (loss of color) or white patches of skin. L-phenylalanine may lead to some darkening or repigmentation of the whitened areas, particularly on the face. Although preliminary clinical information suggests that it is safe when used under appropriate medical guidance and supervision of a health care professional, more research is needed to assess potential side effects of this treatment approach.

Some clinical evidence suggests that phenylalanine may be effective as part of a comprehensive therapy for depression. Individuals have reported improvement in mood when taking phenylalanine. This is thought to be due to enhanced production of brain chemicals, such as dopamine and norepinephrine. More research is needed in this area.Dietary Sources:L-phenylalanine is found in most foods that contain protein such as beef, poultry, pork, fish, milk, yogurt, eggs, cheese, soy products (including soy protein isolate, soybean flour, and tofu), and certain nuts and seeds. The artificial sweetener aspartame is also high in phenylalanine.

Name: S-Adenosyl-L-methionine(SAMe)Synonyms:

SAM-e is an amino acid derivative that has been clinically proven to benefit brain and joint function. SAMe is a molecule produced constantly by all living cells. It is a good nutrition for the liver,can prevent alcohol, drugs and the liver-cell injury; has remarkable preventive effects on chronic active hepatitis, and other factors caused liver injury,heart disease, cancer and so on.. SAMe has been found to be as effective as pharmaceutical treatments for arthritis and major depression as well. Found in all living cells, SAM-e is also called "activated" methionine (an essential amino acid) since it is formed by the combining of ATP with methionine. SAM-e has undergone dozens of trials involving thousands of patients. Researchers studying the beneficial effects of SAM-e have indentified the following benefits :

(3S)-5'-[(3-Amino-3-carboxylatopropyl)methylsulphonio]-5'-deoxyadenosine; SAMJoint Strenght.

SAM-e supports the production of healthy connective tissue through transulfuration. In this process, critical components of connective tissue, including glucosamine and the chondroitin sulfates, are sulfated by SAM-e.

Brain Metabolism:
SAM-e methylation reactions are involved in the synthesis of neurotransmitters such as L-dopa, dopamine and related hormones, epinephrine and phosphatidylcholine (a component of Lecithin).

Methylation of DNA appears to be important in the suppression of errors in DNA replication. Demethylation of DNA is considered a contributor to the aging process. Proper methylation through substances such as SAM-e positively influence longevity.

SAM-e metabolism supports the synthesis of glutathione (GSH) and glutathione-dependent enzymes (glutathione peroxidase and glutathione-S-transferase), which are substances important for liver function.

Take 400mg per day on an empty stomach, or as directed by your qualified health consultant.


Synephrine (or oxedrine) is a drug aimed at encouraging fat loss. While its effectiveness is widely debated, synephrine has gained significant popularity as an alternative to ephedrine, a related substance which has been made illegal or restricted in many countries due to concerns about potential problems with heart disease risk Synephrine is derived primarily from the fruit of Citrus aurantium, a relatively small citrus tree, of which several of its more common names include Bitter Orange, Sour Orange, and Zhi shi.
  • Claims
  • Burns fat
  • Increases energy levels
  • Increases metabolism
  • Promotes weight loss
  • Synephrine is not neosynephrine
There has been some confusion surrounding synephrine and phenylephrine (neosynephrine), one of its positional isomers. The chemicals are similar in structure; the only difference is the location of the aromatic hydroxyl group. In synephrine, the hydroxyl is at the para position, whereas, in neosynephrine, it is at the meta position. Each compound has differing biological properties.

Phenylephrine acts primarily on alpha1 adrenergic receptors, so it has mainly vasoconstricting actions.

Synephrine's pharmacology has not been thoroughly studied. Some comparisons with octopamine have been performed There is some evidence that it may act at.

Associated risks:
Many diet products such as Stacker 2 contain synephrine along with caffeine. Some reports have indicated that such diet pills cause numerous harmful effects. The Mayo Clinic published a report that suggested a link between Stacker 2 pills and increased risk of ischemic stroke, increased blood pressure, and cardiac infarcts.

Synephrine can also cause arrhythmias. It is similar to ephedrine and can therefore show similar symptoms.

What can tryptophan do for you?

What is tryptophan?Preventing Niacin DeficiencyTryptophan has two important functions. First, a small amount of the tryptophan we get in our diet (about 3%) is converted into niacin (vitamin B3) by the liver. This conversion can help prevent the symptoms associated with niacin deficiency when dietary intake of this vitamin is low. Raising Serotonin LevelsSecond, tryptophan serves as a precursor for serotonin, a neurotransmitter that helps the body regulate appetite, sleep patterns, and mood. Because of its ability to raise serotonin levels, tryptophan has been used therapeutically in the treatment of a variety of conditions, most notably insomnia, depression, and anxiety. Deficiency Symptoms.

As an essential amino acid, dietary deficiency of tryptophan may cause the symptoms characteristic of protein deficiency, which include weight loss and impaired growth in infants and children.

When accompanied by dietary niacin deficiency, lack of tryptophan in the diet may also cause pellagra, the classic niacin deficiency disease that is characterized by the "4 Ds" - dermatitis, diarrhea, dementia, and death. This condition is very rare in the United States, however, and cannot occur simply because of a tryptophan deficiency.

Dietary deficiency of tryptophan may lead to low levels of serotonin. Low serotonin levels are associated with depression, anxiety, irritability, impatience, impulsiveness, inability to concentrate, weight gain, overeating, carbohydrate cravings, poor dream recall, and insomnia. Toxicity Symptoms.

High dietary intake of tryptophan from food sources is not known to cause any symptoms of toxicity. In addition, tryptophan has been given therapeutically, as a prescription medicine or dietary supplement, in doses exceeding five grams per day with no report of adverse effects.

However, in 1989, the use of dietary supplements containing tryptophan was blamed for the development of a serious condition called eosinophilia-myalgia syndrome (EMS), which caused severe muscle and joint pain, high fever, weakness, swelling of the arms and legs, and shortness of breath in more than a thousand people. In addition, more than 30 deaths were attributed to EMS caused by tryptophan supplements.

Many experts believe that the EMS was caused by a contaminant that was found in one batch of tryptophan sold by one manufacturer and occurred in only a small number of susceptible individuals. However, the United States Food and Drug Administration, the agency responsible for overseeing the dietary supplement industry, remained convinced that high doses of tryptophan were categorically unsafe. Since 1989, tryptophan has not been available as a dietary supplement in the United States.

To date, a Tolerable Upper Intake Level (TUL) for tryptophan has not yet been established by the Institute of Medicine at the National Academy of Sciences. Factors that Affect Function.

Vitamin B6 is necessary for the conversion of tryptophan to both niacin and serotonin. Consequently, a dietary deficiency of vitamin B6 may result in low serotonin levels and/or impaired conversion of tryptophan to niacin.

In addition, several dietary, lifestyle, and health factors reduce the conversion of tryptophan to serotonin, including cigarette smoking, high sugar intake, alcohol abuse, excessive consumption of protein, hypoglycemia and diabetes. Drug-Nutrient Interactions.

People taking the anti-depressant medications known as selective serotonin reuptake inhibitors (SSRIs) (including Prozac, Paxil, and Zoloft) should consult a physician before taking any other supplement or medication that also increases the amount of, or the effect of, serotonin, in the body. Nutrient Interactions

Vitamin B6, vitamin C, folic acid and magnesium are necessary for the metabolization of tryptophan. In addition, tyrosine and phenylalanine compete with tryptophan for absorption. Because of this, some healthcare practitioners believe that food sources of tryptophan do not cause a significant enough increase in blood levels of tryptophan to produce therapeutic results, and that tryptophan must, therefore, be taken as a supplement to increase its blood levels. Form in Dietary Supplements

Until 1989, tryptophan supplementation was standard practice in many countries around the world - including the United States - to treat insomnia, depression, and anxiety.

In the summer and fall of 1989, hundreds of people taking tryptophan supplements in the U.S. began to report the development of serious side effects including muscle and joint pain, high fever, weakness, swelling of the arms and legs, and shortness of breath, a constellation of symptoms that later became known as eosiniphilia-myalgia syndrome (EMS).

Upon investigation, it was discovered that nearly all of the cases of EMS could be traced back to a contaminant found in one batch of tryptophan produced by a Japanese manufacturer called Showa Denko K.K.

While all manufacturers of supplemental tryptophan synthesized this amino acid through a fementation process using bacteria, several months before the outbreak of EMS, Showa Denko K.K. had altered its process to make it more efficient and was apparently unaware that a toxic contaminant was being produced.

The United States Food and Drug Administration took immediate steps to limit the availability of tryptophan, and since 1989 this amino acid has not been sold as a dietary supplement. Tryptophan is still available, however, for use in the manufacture of infant formulas and entereral and parenteral (intravenous) nutritional supplements prescribed by physicians.

A few years ago, a new tryptophan-like supplement emerged in the U.S. marketplace. This supplement is called 5-hydroxytryptophan or 5-HTP. 5-HTP has been used in much the same way as tryptophan for the treatment of depression and insomnia, and for weight loss.

The reason is simple: the body ordinarily takes tryptophan and converts it into 5-HTP, and then takes the 5-HTP and converts it into serotonin. By taking 5-HTP, a person is taking a compound that is actually one step closer to serotonin than tryptophan.

In its most recent 2005 public health recommendations for amino acids (published as the Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients), National Academies Press, 2005), the National Academy of Sciences (NAS) established a general principle for tryptophan intake. The NAS recommended that all individuals 1 year of age or greater consume 7 milligrams of tryptophan for every 1 gram of food protein. Here is how that recommendation would look for each age and gender group, assuming RDA-level protein intake for each group: ·Children 1-3 years: 91 mg of tryptophan · · · · · · Females 14 years and older: 322 mg of tryptophan As always, we strongly advise you do your own research and more importantly consult your own medical professional before commencing any use of this or any other dietary supplement .This statement has not been evaluated by the FDA. This is not intended to diagnose, treat, cure or prevent any diseaseFemales 9-13 years: 238 mg of tryptophan Males 19 years and older: 392 mg of tryptophan Males 14-18 years: 364 mg of tryptophan Males 9-13 years: 238 mg of tryptophan Children 4-8 years: 133 mg of tryptophan Tryptophan is one of the 10 essential amino acids that the body uses to synthesize the proteins it needs. It's well-known for its role in the production of nervous system messengers, especially those related to relaxation, restfulness, and sleep. What is the function of tryptophan?Insomnia Poor dream recall Overeating and/or carbohydrate cravings Slow growth in children Weight gain or unexplained weight loss Inability to concentrate Impulsiveness Impatience Irritability Anxiety Depression Elevate your mood What events can indicate a need for more tryptophan?Help you sleep better Help regulate your appetite

Tyrosine amino acid

Tyrosine was first isolated from casein in 1849 and is abundant in insulin as well as the enzyme papain and can be synthesized from the amino acid phenylalanine in the body.It is a precursor of the neurotransmitters epinephrine, norepinephrine and dopamine, all of them extremely important in the brain and transmits nerve impulses and prevents depression. Dopamine is also vital to mental function and seems to play a role in sex driveTyrosine required forThe action of this amino acid in brain functions is clear with its link to dopamine as well as norepinephrine, but it is also helpful in suppressing the appetite and reducing body fat, production of skin and hair pigment, the proper functioning of the thyroid as well as the pituitary and adrenal gland.

It is used for stress reduction and may be beneficial in narcolepsy, fatigue, anxiety, depression, allergies, headaches as well as drug withdrawal. In a study, using soldiers, tyrosine proved effective in alleviating stress and keeping them more alert.Deficiency of nutrientTyrosine, a parent amino acid for skin, hair, and eye pigments and is involved in syndromes, known generally as oculocutaneous albinism, that are characterized by the failure to form melanin pigments, resulting in partial or complete albinism.

It is also the precursor amino acid for the thyroid gland hormone thyroxin, and a defect in this may result in hypothyroidism - an enlargement of the thyroid gland (goiter), severe growth failure, and retardation of central nervous system development.

A deficiency may also have symptoms of low blood pressure, low body temperature (including cold hands and feet) and "restless leg syndrome".DosageThe dosage listed is the Recommended Daily Allowance (RDA), but be aware that this dosage is the minimum that you require per day, to ward off serious deficiency of this particular nutrient. In the therapeutic use of this nutrient, the dosage is usually increased considerably, but the toxicity level must be kept in mind.

Dosage levels are not confirmed but some experiments have been performed with people taking up to 5 - 7 grams per day, with no confirmed toxic levels, but people taking MAO inhibitors, who suffer from high blood pressure and have problems with skin cancer should not take supplementation of L-tyrosine, and should aim to limit their intake of food sources high in this nutrient. Best used withIf taking a tyrosine supplement it is best to take it at bedtime, or with a high carbohydrate meal to prevent competition of absorption with other amino acids. Folic acid, copper and vitamin B6 is a good combination to have with this nutrient to maximize absorption and effectiveness.Other interesting pointsTyrosine and tryptophan have with been used with some success in the treatment of cocaine abuse and in another study it was combined with the antidepressant Imipramine to treat chronic cocaine abuse where it was reported that the combination blocked the cocaine high and prevented the severe depression that accompanies withdrawal.Food sources of tyrosineMeat, dairy, eggs as well as almonds, avocados and bananas are good sources of this nutrient.As always, we strongly advise you do your own research and more importantly consult your own medical professional before commencing any use of this or any other dietary supplement .This statement has not been evaluated by the FDA. This is not intended to diagnose, treat, cure or prevent any disease.

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