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WEIGHT LOSS & APPETITE SUPPRESSION

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.

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.

ABOUT B.C.A.A’s

B.C.A.A ‘s are amino acid and are not only essential amino acids but is also a branched-chain found in high concentration in the muscles. l BCAA's are L-Valine ,l-leucine and L-Isoleucine.

B.C.A.A ‘s can not be made by the body, and must be acquired through food or dietary supplements.What does it do and what scientific studies give evidence to support this?
It has a stimulating effect and is needed for muscle metabolism, repair and growth of tissue and maintaining the nitrogen balance in the body.

Since it is a branched-chain amino acid, it can be used as an energy source in the muscles, and in doing so preserves the use of glucose.Who needs it and what are some symptoms of deficiency?B.C.A.A,s are essential amino acids. Therefore, everyone needs BCAA’s to maintain basic health.How much should be taken? Are there any side effects?BCAA’s should be dosed at two parts L-Valine for every two parts L-Leucine and for every one part of L-Isoleucine. This product takes the guess work out and is ready to go .RDA to 5gm per day.

No side effects have been reported, BCAA is generally considered to be safe for healthy persons.

Consult your physician before using any dietary supplement.

BERBERINE hcl

Berberine and Diabetes:
A collaboration between Chinese, Korean, and Australian scientists at Sydney's Garvan Institute indicates berberine could be helpful. They say "Our studies in animal models of diabetes show that berberine acts in part by activating an enzyme in the muscle and liver that is involved in improving sensitivity of the tissue to insulin. This in turn helps lower blood sugar levels. In addition, it seems berberine can help reduce body weight". "Berberine has been used for decades, if not centuries, with few reported side effects. Given the limitations of existing medicines we are excited to have evidence that berberine may be a helpful new treatment for type 2 diabetes; however, despite its widespread use in traditional medicine practices, it will still have to be evaluated properly following the defined clinical trials process", said Professor James, head of the Garvan's Diabetes & Obesity Research Program and co-author of the Diabetes paper.

Berberine, blood sugar, cholesterol, and blood pressure:
Berberine may be helpful in maintaining healthy blood sugar and cholesterol levels in those with type 2 diabetes. Dr. Guang Ning, of Shanghai Jiao Tong University School of Medicine in Shanghai and colleagues randomized 116 diabetes patients to receive one gram of berberine daily or placebo for 3 months. Average hemoglobin A1C -- a measure of long-term blood sugar control -- dropped from 7.5 percent to 6.6 percent in those taking berberine supplements. Patients taking berberine also showed significant reductions in total and "bad" LDL cholesterol. Blood pressure also fell in patients taking berberine. Patients on berberine lost 2.3 kilograms (5.1 pounds), on average, compared to 1.3 kilograms (2.9 pounds) for the placebo group. Patients taking berberine were more likely to have a side effect of constipation, and two patients in the berberine group had their dosage reduced for this reason. Journal of Clinical Endocrinology and Metabolism, July 2008.

Berberine Research Update:
Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells. Mol Cancer Ther. 2006 Feb;5(2):296-308. Department of Dermatology, University of Alabama at Birmingham, Volker Hall 557, 1670 University Boulevard, Birmingham, AL Berberine, a naturally occurring isoquinoline alkaloid, has been shown to possess anti-inflammatory and antitumor properties in some in vitro systems. Here, we report that in vitro treatment of androgen-insensitive (DU145 and PC-3) and androgen-sensitive (LNCaP) prostate cancer cells with berberine inhibited cell proliferation and induced cell death in a dose-dependent and time-dependent manner. The effectiveness of berberine in checking the growth of androgen-insensitive, as well as androgen-sensitive, prostate cancer cells without affecting the growth of normal prostate epithelial cells indicates that it may be a promising candidate for prostate cancer therapy.

Antimicrobial activity of berberine alone and in combination with ampicillin or oxacillin against methicillin-resistant Staphylococcus aureus.
J Med Food. 2005 Winter;8(4):

454-61.
Department of Food and Nutrition,
Kunsan National University,
Kunsan.

Methicillin-resistant Staphylococcus aureus (MRSA) bacteria have been responsible for substantial morbidity and mortality in hospitals because they usually have multidrug resistance. Some natural products are candidates as new antibiotic substances. In the present study, we investigated the antimicrobial activity of berberine, the main antibacterial substance of Coptidis rhizoma (Coptis chinensis Franch) and Phellodendri cortex (Phellodendron amurense Ruprecht), against clinical isolates of MRSA, and the effects of berberine on the adhesion to MRSA and intracellular invasion into human gingival fibroblasts (HGFs). Berberine showed antimicrobial activity against all tested strains of MRSA. These results suggest that berberine may have antimicrobial activity and the potential to restore the effectiveness of beta-lactam antibiotics against MRSA, and inhibit the MRSA adhesion and intracellular invasion in HGFs.

Hepatobiliary excretion of berberine:
Drug Metab Dispos. 2004 Apr;32(4):405-12.

To investigate the detailed pharmacokinetics of berberine and its mechanisms of hepatobiliary excretion, an in vivo microdialysis coupled with high-performance liquid chromatography was performed. In the control group, rats received berberine alone; in the drug-treated group, 10 min before berberine administration, the rats were injected with cyclosporin A (CsA), a P-glycoprotein (P-gp) inhibitor; quinidine, both organic cation transport (OCT) and P-gp inhibitors; SKF-525A (proadifen), a cytochrome P450 inhibitor; and probenecid to inhibit the glucuronidation. The results indicate that berberine displays a linear pharmacokinetic phenomenon in the dosage range from 10 to 20 mg kg(-1), since a proportional increase in the area under the concentration-time curve (AUC) of berberine was observed in this dosage range. Moreover, berberine was processed through hepatobiliary excretion against a concentration gradient based on the bile-to-blood distribution ratio (AUC(bile)/AUC(blood)); the active berberine efflux might be affected by P-gp and OCT since coadministration of berberine and CsA or quinidine at the same dosage of 10 mg kg(-1) significantly decreased the berberine amount in bile. In addition, berberine was metabolized in the liver with phase I demethylation and phase II glucuronidation, as identified by liquid chromatography/tandem mass spectrometry. Also, the phase I metabolism of berberine was partially reduced by SKF-525A treatment, but the phase II glucuronidation of berberine was not obviously affected by probenecid under the present study design.

Cytotoxic effects of Coptis chinensis and Epimedium sagittatum extracts and their major constituents (berberine, coptisine and icariin) on hepatoma and leukemia cell growth.

Clin Exp Pharmacol Physiol. 2004 Jan-Feb;31(1-2):65-9.

The present study was conducted to evaluate the cytotoxic effects of Coptis chinensis and Epimedium sagittatum extracts and their major constituents on hepatoma and leukemia cells in vitro. Four human liver cancer cell lines, namely HepG2, Hep3B, SK-Hep1 and PLC/PRF/5, and four leukemia cell lines, namely K562, U937, P3H1 and Raji, were used in the present study. Of the two crude drugs, Coptis chinensis exhibited the strongest activity against SK-Hep1 and Raji cell lines. Icariin (the major compound of E. sagittatum) showed no inhibition of either the hepatoma or leukemia cell lines. The results of the present study suggest that the Coptis chinensis extract and its major constituents berberine and coptisine possess active antihepatoma and anti leukemia activities.

Effect of berberine on regression of pressure-overload induced cardiac hypertrophy in rats.
Am J Chin Med. 2002;30(4):589-99.

Berberine is the basic chemical component of a Chinese herb, Coptis chinensis Franch (coptis), considered to be useful in treating some diseases of the cardiovascular system, such as hypertension and chronic heart failure (CHF). In this study, we investigate the inhibitory effect of berberine on experimental cardiac hypertrophy, which is regarded as a risk factor of CHF and other heart diseases. Forty-two male SD rats were divided into four groups: age-matched control, aortic banding model, berberine-treated group and captopril-treated group. Cardiac hypertrophy was induced by suprarenal abdominal aorta constriction (banding). The drugs were orally administered for 8 weeks starting from 4 weeks after surgery at dosage of berberine 10 mg/kg and captopril 50 mg/kg. Blood pressure (BP) was measured four times during the period of the experiment, and hemodynamic parameters, cardiac index, cell size of left ventricular myocardium and total protein of left ventricular tissue were detected 8 weeks after treatment with drugs. The data from the present study showed that: The BP of the aorta banded rats was increased compared with those of the normal and the age-matched control rats, and berberine showed no significant effect on it. After 8 weeks of treatment with berberine, the elevated left ventricular end diastolic pressure (LVEDP) was slightly decreased compared with the aortic banded rats. Meanwhile, the maximum rates of contraction and relaxation (+/- dp/dtmax) was increased and the time to reach the point of maximum rate from beginning of contraction (t-dp/dt) was shortened, indicating that the functions of heart, both contraction and relaxation, were improved. Cardiac growth was inhibited by treatment with berberine. Both whole heart and left ventricular weight were notably decreased compared with the banded rats. The cell size of left ventricular myocardium was significantly reduced and the total protein of left ventricular tissue was slightly down-regulated by treatment with berberine. These data suggest that berberine can improve abnormal cardiac function and can prevent the development of left ventricular hypertrophy induced by pressure-overload. This indicates that it may have therapeutic potential in the treatment of CHF.

Efficacy and safety of berberine for congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.
Am J Cardiol. 2003 Jul 15;92(2):173-6.

This study was designed to assess the efficacy and safety of berberine for chronic congestive heart failure. One hundred fifty-six patients with CHF and >90 ventricular premature complexes (VPCs) and/or nonsustained ventricular tachycardia (VT) on 24-hour Holter monitoring were randomly divided into 2 groups. All patients were given conventional therapy for congestive heart failure, consisting of angiotensin-converting enzyme inhibitors, digoxin, diuretics, and nitrates. Patients in the treatment group (n = 79) were also given berberine 1.2 to 2.0 g/day. The remaining 77 patients were given placebo. Symptoms, a 6-minute walk test, left ventricular (LV) ejection fraction (EF), frequency and complexity of VPCs, and quality of life were assessed after 8 weeks of treatment and during a mean 24-month follow-up. After treatment with berberine, there was a significantly greater increase in LVEF, exercise capacity, improvement of the dyspnea-fatigue index, and a decrease of frequency and complexity of VPCs compared with the control group. There was a significant decrease in mortality in the berberine -treated patients during long-term follow-up (7 patients receiving treatment died vs 13 on placebo). Proarrhythmia was not observed, and there were no apparent side effects. Thus, berberine improved quality of life and decreased VPCs and mortality in patients with congestive heart failure.

Effect of berberine on bone mineral density in SAMP6 as a senile osteoporosis model.
Biol Pharm Bull. 2003 Jan;26(1):110-1.

The effects of berberine in senescence accelerated mice P6 (SAMP6) were investigated to learn whether the alkaloid affects bone mineral density (BMD). Oral administration of berberine (10 mg/kg/d) to male and female mice for 22 weeks resulted in an increase in BMD in both sexes. A decreased concentration of deoxypyridinoline (Dpd) in urine was only observed in female mice. There was no effect on body or tibia weight or on the concentration of procollagen type I carboxyterminal extension peptide (PICP) in serum.

A comparative study on the anti-inflammatory, antinociceptive and antipyretic effects of isoquinoline alkaloids from the roots of Turkish Berberis species.

Life Sci. 2002 Dec 27;72(6):645-57. Roots and barks of various Berberis species are used as folk remedy for the treatment of various inflammatory diseases such as lumbago, rheumatism and to reduce fever. Six isoquinoline alkaloids namely berberine, berbamine, palmatine, oxyacanthine, magnoflorine, and columbamine were isolated as the main components of alkaloidal fraction from the roots of Turkish Berberis species and effects were studied using various in vivo models in mice. All alkaloids inhibited inflammations in varying degrees, among them berberine, berbamine and palmatine were shown to possess significant and dose-dependent inhibitory activity against serotonin-induced hind paw oedema both on oral and topical applications and acetic acid-induced increase in vascular permeability on oral administration. Moreover, these three alkaloids were also shown to possess dose-dependent antinociceptive activity, which assessed by using the model based on the inhibition of p-benzoquinone-induced writhing movements as well as antipyretic activity on FCA-induced increased rectal temperature on subacute administration. However, all alkaloids induced gastric lesions in varying degrees.

Inhibitory effects of berberine on IK1, IK, and HERG channels of cardiac myocytes.

Acta Pharmacol Sin. 2001 Feb;22(2):125-31.
To study the effects of berberine on inward rectifier potassium current (IK1) and outward delayed rectifier potassium current (IK) of guinea pig ventricular myocytes, and on human ether-a-go-go related gene (HERG) channel expressed in Xenopus oocytes. Berberine prolonged action potential duration (APD) and inhibited IK1 and IK in a concentration-dependent manner. Berberine 100 micromol/L increased APD90 from (450 +\- 48) ms to (888 +\- 90) ms, and inhibited IK1 by 65 %. Berberine 50 micromol/L inhibited IK by 57 %, IKtail by 53 %. Berberine produced a voltage-dependent block on IK that increased with stronger depolarization, and once all channels were activated, there was no further block at positive potentials. Berberine blocked the HERG channels potently with an IC50 value of approximately 75 micromol/L. This block was voltage-dependent, suggesting that it probably bind to either open or inactivated HERG channels. Berberine prolonged APD and possessed blocking effect on IK1, IK, and HERG channel expressed in Xenopus oocytes. The antiarrhythmic mechanism of berberine is related to its inhibitory effects on IK1, IK, and HERG channel.

Cardiovascular actions of berberine.
Cardiovasc Drug Rev. 2001 Fall;19(3):234-44.

Berberine, is an alkaloid from Hydrastis canadensis L., Chinese herb Huanglian, and many other plants. It is widely used in traditional Chinese medicine as an antimicrobial in the treatment of dysentery and infectious diarrhea. This manuscript describes cardiovascular effects of berberine and its derivatives, tetrahydroberberine and 8-oxoberberine. Berberine has positive inotropic, negative chronotropic, antiarrhythmic, and vasodilator properties. Both derivatives of berberine have antiarrhythmic activity. Some cardiovascular effects of berberine and its derivatives are attributed to the blockade of K+ channels (delayed rectifier and K(ATP)) and stimulation of Na+ -Ca(2+) exchanger. Berberine has been shown to prolong the duration of ventricular action potential. Its vasodilator activity has been attributed to multiple cellular mechanisms. The cardiovascular effects of berberine suggest its possible clinical usefulness in the treatment of arrhythmias and/or heart failure.

BETA ALANINE

With literally hundreds of different supplements available and so many that are based on bogus claims and ridiculous hype, it's a challenge to find even one that delivers results. If you've rummaged through the garbage of the supplement scrap heap, you know how difficult it is to find solid science or real-world proof.

Beta-alanine:
The science behind beta-alanine makes sense and it works. In reading this article, you will understand how beta-alanine works. You will also learn how to maximize its use and how it can help you safely work out much harder and longer. Used properly, beta-alanine can take your training and results to new levels, helping you set personal records and add lean mass. First lets start with some basic background information on beta-alanine.

is an exception. This supplement actually lives up to its claim: beta-alanine efficacy is backed by major university, peer-reviewed studies performed on humans, not the typical cell or rat studies upon which many supplement manufacturers generally base claims. Background On Beta-Alanine Although only recently brought to the forefront, beta-alanine was discovered over 100 years ago. Also known as 3-aminopropanoic acid, it is a non-essential amino acid and is the only naturally occurring beta-amino acid. Not to be confused with alanine, beta- alanine is classified as a non-proteinogenic amino acid as it is not used in the building of proteins.

The greatest natural dietary sources of beta-alanine are believed to be obtained through ingesting the beta-alanine containing dipeptides: carnosine, anserine and balenine, rather than directly ingesting beta-alanine. These dipeptides are commonly found in protein rich foods such as chicken, beef, pork and fish.

However, obtaining beta-alanine through these dipeptides is not the only way, as our bodies can synthesize it in the liver from the catabolism of pyrimidine nucleotides which are broken down into uracil and thymine and then metabolized into beta-alanine and B-aminoisobutyrate. Of course, it can also be ingested through direct supplementation which is the focus of this article.

Recently, researchers began studying beta-alanine and examining its effects on exercise performance and lean body mass. We owe a great deal of credit and respect to the scientists who are in the trenches doing the work and publishing the research on beta-alanine.

If it wasn't for them, great supplements like beta-alanine and creatine might never have seen the light of day. Their ongoing research has revealed how to properly use these compounds and how to safely and effectively maximize their benefits.

One of the key scientists pioneering the performance research on beta-alanine is Dr. Roger Harris. His name may or may not sound familiar, but it should, as he is the same man that brought creatine to the bodybuilding world with his groundbreaking study in 1992.

It looks like the good doctor has found another juggernaut of a supplement in beta-alanine. However, he is not alone. In the last two years, highly respected research scientist Dr. Jeffrey Stout has been in a frenzy publishing and compiling research on beta-alanine and doesn't look to be slowing down any time soon. Other notable researchers who have been publishing research on beta-alanine include Dr. Tallon, Dr. Hill and Dr. Kim.

How Can Beta-Alanine Benefit Me?
Below is a list of the benefits of beta-alanine. But before we go on to explain how beta-alanine works, you must first understand what's going on in our body's during exercise that limits our gains and muscular performance.

Benefits of Beta-Alanine as supported by Scientific Studies:
  • Boosts explosive muscular strength and power output.
  • Increases muscle mass.
  • Boosts muscular anaerobic endurance.
  • Increases aerobic endurance.
  • Increases exercise capacity so you can train harder and longer.
What Stops Us From Reaching Our Full Potential In Making Strength, Endurance And Muscle Mass Gains? When we exercise, especially when it's high intensity exercise, our bodies accumulate a large amount of hydrogen ions (H+), causing our muscles' pH to drop (become more acidic). This process is occurring whether you feel a burn or not.

The breakdown of ATP and the subsequent rise in H+ concentrations occur in all of our energy systems but H+ buildup is most prevalent in an energy system called glycolysis, which also produces lactic acid. At physiological pH, lactic acid dissociates H+ and is the primary source of released H+ ions during exercise, causing pH to drop.

It is the released H+ from lactic acid that causes muscular performance problems, not the leftover lactate ions as many incorrectly believe. While lactic acid is the primary source of released H+, it is not the only source. H+ ions are also being released at a rapid rate when you break down the high energy compound ATP during exercise. With the presence of many sources during energy production releasing H+, pH drops quickly.

As our muscles pH quickly drops, so does their ability to contract forcibly and maintain a high level of performance throughout your workout session. Not being able to perform and maintain forceful muscular contractions and push your body to the limit during your workout session, seriously hampers your ability to maximally overload your muscles and force new muscle gains.

In a nutshell, H+ causes your muscles pH to drop, in turn decreasing your strength and causing you to fatigue faster. These limitations stop you from adequately overloading your muscles and forcing NEW muscle gains.

Strength, Endurance And Muscle Mass?
To understand how beta-alanine works to fight the drop in pH within our muscle, you must first understand how carnosine works. The reason being is, beta-alanine's performance benefits are not direct but realized through its ability to boost the synthesis of carnosine. Background On Carnosine The Russian scientist Gulewitsch was the first to identify carnosine in 1900. Eleven years later, he would discover and identify its constituent amino acids, beta-alanine and histidine. Seven years later, Barger and Tutin and Baumann and Ingvaldsen confirmed Gulewitsch's findings. However, it wasn't until 1938 that the first research on carnosine and its effects on muscle buffering were published.

Carnosine is a naturally occurring di-peptide that is found in both type 1 and type 2 muscle fibers, but is in significantly higher concentrations in type 2 fibers. Type 2 muscle fibers are primarily used in high intensity strength workouts and are most responsive to muscular growth.

How Does Carnosine Work?
There are a handful of ways carnosine is thought to impact performance but its most studied function, and the focus of this article, is its role as an intracellular buffer. Carnosine helps stabilize muscular pH by soaking up hydrogen ions (H+) that are released at an accelerated rate during exercise.

Our bodies work to keep our pH in balance by utilizing various buffering systems. Buffers largely work by soaking up H+ to maintain optimal pH balance, which we need to function most effectively. As mentioned above, our muscles function best in a specific pH range. When pH drops below that range, so does muscular performance. By helping to keep us in a more optimal pH range, our muscles can continue to contract forcibly for a longer time.

There are a handful of buffering systems that work in our bodies. Some maintain pH in extra cellular fluids (ECF) outside of the cell, while others perform their duties in intracellular fluids (ICF) inside the cell and some perform in both.

Our focus in this article is on exercise performance and, as mentioned above, the primary source of H+ released during exercise is from lactic acid and ATP breakdown. Take a guess where this breakdown and release of H+ is occurring?

If you guessed inside our muscles or intracellular, you would be correct. As a result, the first line of defense in absorbing the H+ is going to be the cell from intracellular buffers such as carnosine, not from extra cellular buffers.

Aside from carnosine being just where we need it, buffering H+ inside our cells, it has additional, unique attributes that make it really shine. Carnosine is unique; in that, other natural buffering systems our bodies use are also used in many other cellular reactions aside from buffering, watering down much of their buffering abilities.

However, what makes carnosine really exciting, is that by supplementing with extra beta-alanine, we can specifically and dramatically increase carnosine levels.

How much, you ask?
Researchers have shown that when supplementing with beta-alanine for just 4 weeks, we can increase our carnosine concentration by 42-65%. Longer beta-alanine studies going up to 10-12 weeks, show carnosine concentrations increased up to 80%. This is a tremendous increase in an already powerful intracellular buffer.

It is this large increase in buffering capacity within our muscles that is largely responsible for the strength, lean body mass, power and muscular endurance gains that researchers are seeing from beta-alanine studies.

Summary:
By boosting carnosine concentrations, with beta-alanine, our type 2 muscle fibers can soak up more H+ and stay in an optimal pH range. By keeping our type 2 muscle fibers in an optimal pH range, they are better able to maintain maximal strength and endurance throughout your workout session and bring on new muscle gains.

Dosage and Use:
The best time to take Beta-Alanine is before your workout and if you only take 500mg (.5gm daily then that is definitely the time you want to take it. If you don’t workout everyday, you should still take at least one capsule sometime during the day. If you are taking more than 500mg daily, as in a 15 week cycle, then spread out the capsules you take throughout the day as much as possible, with one dosage always being before your workout, if you workout on that day.

Caffeine

Have More Energy And Lose More Fat!

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. You can provide yourself with the intracellular high-octane fuel for optimum energy system efficiency straight.

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.

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.

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.

Carnitine (vitamin Bt)

Carnitine and lysine. Carnitine is the generic term for a number of compounds that include L-carnitine, L-acetylcarnitine, acetyl-L-carnitine, and L-propionyl carnitine. Carnitine can be synthesised within the body from lysine or methionine. As with all amino acids used directly in the metabolism, carnitine exists in the left-handed form. This isomer is expressed as L-carnitine, as it is usually marketed. Carnitine is eaten in the diet in red meats and dairy products, including breast milk, and is also made in the body from breaking down muscle protein and converting it to carnitine.

Carnitine is a nutrient responsible for the transport of long-chain fatty acids into the energy-producing centers of the cells (known as the mitochondria). Carnitine plays a critical role in metabolizing a number of other important substances as well, which helps to explain why it holds promise for so many disorders. Carnitine transports fats into the mitochondria, the cellular powerhouse, where these fats are converted into an energy source for the body. Our heart and skeletal muscle tissue rely on fat utilization as a source of energy, and also to spare glycogen. Carnitine helps the body convert fatty acids into energy, which is used primarily for muscular activities throughout the body. The body produces carnitine in the liver and kidneys and stores it in the skeletal muscles, heart, brain, and sperm. Carnitine can also act as an antioxidant and appears to play a role in maintaining the health of nerves and protecting the liver and kidneys from the toxicity of drugs. is a non-essential amino acid produced in the liver, brain and the kidneys from the essential amino acids methionine.

Carnitine (vitamin Bt) functions, uses, and health benefits

Carnitine helps transport fatty acids to the powerhouse of the cell. Fatty acids are the main fuel source for heart and skeletal muscle. Long-chain fatty acids require l-carnitine to transport them across the inner membranes of the mitochondria, wherein their metabolism produces bioenergy. L-carnitine can remove short-chain and medium-chain fatty acids from the mitochondria in order to maintain coenzyme A levels in these organelles. L-Carnitine also facilitates the metabolism of carbohydrates and enhances the rate of oxidative phosphorylation. L-Carnitine works synergistically with CO-Q10, an antioxidant and energy co-factor that is found in the inner membrane of the mitochondria.

Carnitine plays a critical role in metabolizing a number of other important substances as well, which helps to explain why it holds promise for so many disorders. Carnitine mediates the transport of medium/long-chain fatty acids across mitochondrial membranes, facilitating their oxidation with subsequent energy production. Carnitine may have neuroprotective effects. This means that the strong antioxidant properties of acetyl-L-carnitine may help to prevent oxidative damage to nerve cells that are important for brain functioning.

The strongest evidence for the use of supplemental L-carnitine may be in the management of cardiac ischemia and peripheral arterial disease. It may also more generally be indicated for cardioprotection. It lowers triglyceride levels and increases levels of HDL-cholesterol in some. It is used with some benefit in those with primary and secondary carnitine deficiency syndromes. There is less evidence to support arguments that carnitine is indicated in liver, kidney and immune disorders or in diabetes and Alzheimer's disease.

Carnitine is used for a small percentage of people who are at risk of liver damage from AEDs and is used for children with multiple seizure types who are taking multiple AEDs.

Carnitine is used in emergency situations where there is liver damage caused by valproate, or in cases of valproate overdose. It is used in rare diseases involving problems of the transport of carnitine into the mitochondria.

L-carnitine has been marketed as a weight loss supplement, because the primary function of carnitine in human cells is to burn fat as a source of energy. Carnitine supplementation may actually help increase energy, burn fat more efficiently and may improve heart and liver health all at the same time.

Carnitine is recommended as a daily supplement to help maintain blood lipid profile and promote fatty acid utilization within heart muscle. People who take l-carnitine supplements soon after suffering a heart attack may be less likely to suffer a subsequent heart attack, die of heart disease, experience chest pain and abnormal heart rhythms, or develop congestive heart failure. Some studies have shown Carnitine may reduce the pain and complications of lack of oxygen to the heart and improve exercise tolerance in people with existing heart disease.

The function of carnitine is to help the body use stored fat as fuel. Carnitine is helpful for improving exercise performance. Supplementation with carnitine has been said to enhance lipid oxidation, increase VO2max and decrease the accumulation of lactic acid during exercise.

Carnitine reduces the incidence of angina and cardiac arrythmias as well as reduces the need for anti-angina and anti-arrythmic medications.

Acetyl-L-carnitine may be indicated for use in cases of mild Alzheimer's disease, dementia, Down's syndrome, recovery from stroke and for the management of various neuropathies.

Carnitine (vitamin Bt) dosage, intake, recommended daily allowance (RDA)

Carnitine is not an essential amino acid and, since it is not a vitamin or a mineral, no RDA or dietary reference intake (DRI) values have been established. The L-isomer of carnitine (L-carnitine) is the only physiologically useful form of carnitine. Recommended doses of l-carnitine supplements vary depending on the health condition being treated. The normal recommended dose appears to be 500 milligrams (MG) to 1,000 mg per day. Then gradually work up to 2 to 4 grams (2,000 to 4,000 mg) per day. Typical doses of supplemental acetyl-L-carnitine are between 500 mgs to 2 gms daily in divided doses. Doses of 2 to 6 grams per day are typically recommended for cardiovascular, sports performance and weight loss benefits. Infant formulas (including total parenteral nutrition solutions) that do not contain carnitine should be supplemented with carnitine to the levels found in human milk, 11.3 mg/L (70 mmol/L).

Sources of carnitine

Dietary sources of carnitine include foods of animal origin, such as meat and dairy products. Red meat (particularly lamb) and dairy products are the primary sources of carnitine. Carnitine can also be found in fish, poultry, tempeh (fermented soybeans), wheat, asparagus, avocados, and peanut butter. Cereals, fruits, and vegetables contain little or no carnitine. Carnitine can be manufactured in the body provided the requisite vitamins and minerals are also present. A typical Western diet supplies about 100mg of carnitine per day. It is found mostly in red meats and dairy products. Plant foods are not good sources of carnitine. In general, healthy adults do not require dietary carnitine as carnitine stores are replenished through endogenous synthesis from lysine and methionine in the liver and kidneys.

Carnitine deficiency

There are two types of carnitine deficiency, primary and secondary. In both primary and secondary carnintine deficiencies, increased dietary intake and supplements of carnitine can be beneficial. Although the exact mechanism is unknown, it is thought that flooding the body with high concentrations of carnitine assures that some carnitine are able to get into the cells. Carnitine deficiency occurs as a primary genetic defect of carnitine transport and secondary to a variety of genetic and acquired disorders. A person with primary carnitine deficiency has very low levels of carnitine in the blood due to a faulty carnitine transporter which prevents carnitine from getting into the cells where it is needed. The secondary form of carntine deficiency can arise secondary to metalobic disorders in the mitochondria. Blockage of metabolic pathways in the mitochondria leads to a build-up of acyl compounds. Infants are particularly susceptible to carnitine depletion, because the demands of tissue accretion associated with rapid growth exceed the ability of the infant to synthesize carnitine.

Carnitine overdose, toxicity, side effects

There have been no reports of toxicity from L-carnitine overdosage. The oral LD50 of L-carnitine in mice is 19.2 grams per kilogram. D-carnitine supplements should be avoided as they interfere with the natural form of L-carnitine and may produce undesirable side effects. L-carnitine supplementation may cause mild gastrointestinal symptoms, including nausea, vomiting, abdominal cramps and diarrhea. Adverse effects may include transient nausea, vomiting, abdominal cramps and diarrhea. Less frequent reactions may include body odour or gastrointestinal symptoms. Other rare side effects include increased appetite, body odor, and rash.

CARNOSINE

There are a handful of ways carnosine is thought to impact performance but its most studied function, and the focus of this article, is its role as an intracellular buffer. Carnosine helps stabilize muscular pH by soaking up hydrogen ions (H+) that are released at an accelerated rate during exercise.

Our bodies work to keep our pH in balance by utilizing various buffering systems. Buffers largely work by soaking up H+ to maintain optimal pH balance, which we need to function most effectively. As mentioned above, our muscles function best in a specific pH range. When pH drops below that range, so does muscular performance. By helping to keep us in a more optimal pH range, our muscles can continue to contract forcibly for a longer time.

There are a handful of buffering systems that work in our bodies. Some maintain pH in extra cellular fluids (ECF) outside of the cell, while others perform their duties in intracellular fluids (ICF) inside the cell and some perform in both.

Our focus in this article is on exercise performance and, as mentioned above, the primary source of H+ released during exercise is from lactic acid and ATP breakdown. Take a guess where this breakdown and release of H+ is occurring?

If you guessed inside our muscles or intracellular, you would be correct. As a result, the first line of defense in absorbing the H+ is going to be the cell from intracellular buffers such as carnosine, not from extra cellular buffers.

Aside from carnosine being just where we need it, buffering H+ inside our cells, it has additional, unique attributes that make it really shine. Carnosine is unique; in that, other natural buffering systems our bodies use are also used in many other cellular reactions aside from buffering, watering down much of their buffering abilities.

However, what makes carnosine really exciting, is that by supplementing with extra beta-alanine, we can specifically and dramatically increase carnosine levels.

How much, you ask?
Researchers have shown that when supplementing with beta-alanine for just 4 weeks, we can increase our carnosine concentration by 42-65%. Longer beta-alanine studies going up to 10-12 weeks, show carnosine concentrations increased up to 80%. This is a tremendous increase in an already powerful intracellular buffer.

CLA

What is it and where does it come from?
Conjugated Linoleic Acid (CLA), is a naturally occurring free fatty acid found mainly in meat and dairy products, in small amounts. CLA was discovered by accident in 1978 by Michael W. Pariza at the University of Wisconsin while looking for mutagen formations in meat during cooking.

CLA is research proven to build muscle, reduce body fat, and induce an optimum cellular environment for improved health!

CLA occurs naturally in foods such as milk, cheese, beef, and lamb as well as many processed foods. One processed food in particular that's high in CLA is Cheez Wiz. But getting enough CLA from your diet for the preferred benefit would require considerable intake of these types of foods. This is not only impractical, but would also have a seriously negative impact on your metabolism due to the high caloric penalty you would pay.

What does it do and what scientific studies give evidence to support this?
Since this research has surfaced, a more economical and efficient way to get the required CLA has been devised. Through advanced lipid technology, a CLA synthesizing process allows for precision intake through premeasured softgel capsules. This allows for precise CLA intake at determined time intervals without the high calorie food consumption. Not only has CLA been shown to increase muscle mass while reducing body fat, studies have also shown remarkable anti-catabolic, antioxidant, and immune enhancement benefits. All this from a structured lipid. A designer fat if you would.

For many years, performance nutrition experts basically dismissed fats, assuming they didn't have any useful role in nutrition. Instead, experts focused on the protein-sparing and energy-producing effects of carbohydrates, and studied how amino acids and various proteins might affect nitrogen retention, anabolism, and catabolism. Perhaps "inquiring minds" were influenced by the mass media's "all-fat-is-bad" campaign. But now the scales are tipping toward the contrary. Nutritional geniuses like The Zone author, Dr. Barry Sears have shown us how fatty acids are not only essential for proper health but also how the proper use of such compounds may have numerous positive effects. Dr. Sears is certain that fatty acids directly influence the body's growth-promoting hormones.

Although all the intricacies of CLA are not fully understood, it is widely accepted in the research community that CLA counterbalances the negative effects of linoleic acid and regulates fat and protein metabolism in animals. Pariza, director of the Food Research Institute at the University of Wisconsin said, "A growing body of data indicates that CLA is a newly recognized nutrient that functions to regulate energy retention and metabolism." CLA can best be described as a Growth Factor.

Food intake efficiency! CLA has been shown in animal studies to increase growth rate through increased feed efficiency. In controlled studies, animals that had their diets supplemented with CLA increased their body protein (muscle tissue) while at the same time, had a significant decrease in body fat. This all occurred in the CLA supplemented animals while their food intake was decreased. Their lean mass increased even though they were eating less! This indicates that CLA increases feed efficiency and also points to a potent nutrient repartitioning effect.

This significant change in body composition can also be attributed in part to CLA's effect on immune function. CLA has been shown to inhibit the lean tissue wasting caused by high levels of these cytokines.

Actual human studies are on the way with anticipation of similar outcomes. CLA may be the most significant bodybuilding nutrient discovered in this decade. With anti-catabolic effects rivaling even the strongest pharmaceutical compounds, CLA is a naturally occurring nutrient with the ability to help you pack on lean muscle, reduce body fat and at the same time possesses health promoting properties.

Who needs it and what are some symptoms of deficiency?
To the athlete looking to add more muscle and drop body fat, CLA is a unique discovery that will make accomplishing this feat easier and faster, all the while having positive effects on immune function and antioxidant status.

How much should be taken? Are there any side effects?
CLA is typically found in capsules or softgels between potencies between 600mg and 1000mg. All preliminary evidence shows that CLA is nontoxic and safe at recommended dosages.
While this is powder RDA’s remain the same .

DIMETHYLAMYLAMINE

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.

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.

HORDENINE

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."

Orlistat

Use caution with: obstructed bile duct, impaired liver function, and pancreatic disease DosageAt the standard prescription dose of 120 mg three times daily before meals, orlistat prevents approximately 30% of dietary fat from being absorbed Pregnancy and breastfeeding Reduced gallbladder function (e.g. after cholecystectomy) Hypersensitivity to Orlistat Malabsorption Orlistat also known as tetrahydrolipstatin—is a drug designed to treat obesity. Its primary function is preventing the absorption of fats from the human diet, thereby reducing caloric intake. It is intended for use in conjunction with a physician-supervised reduced-calorie diet.

Orlistat is the saturated derivative of lipstatin—a potent natural inhibitor of pancreatic lipases isolated from the bacterium Streptomyces toxytricini. However, due to simplicity and stability, orlistat rather than lipstatin was developed into Pharmacology.

Orlistat works by inhibiting gastrointestinal lipase, an enzyme that breaks down triglycerides in the intestine. Without this enzyme, triglycerides from the diet are prevented from being hydrolyzed into absorbable free fatty acids and are excreted undigested. Only trace amounts of orlistat are absorbed systemically; the primary effect is local lipase inhibition within the GI tract after an oral dose. The primary route of elimination is through the feces.

At the standard prescription dose of 120 mg three times daily before meals, orlistat prevents approximately 30% of dietary fat from being absorbed. Higher doses do not produce more potent effectsEfficacyThe amount of weight loss achieved with orlistat varies. In one-year clinical trials, between 35.5% and 54.8% of subjects achieved a 5% or greater decrease in body mass, although not all of this mass was necessarily fat. Between 16.4% and 24.8% achieved at least a 10% decrease in body mass. After orlistat was stopped, a significant number of subjects regained weight—up to 35% of the weight they had lost. The incidence of type 2 diabetes in an obese population over four years is decreased with orlistat ( 6.2% ) compared to placebo ( 9.0% ) Side effectsThe primary side effects of the drug are gastrointestinal-related, and include steatorrhea—that is, oily, loose stools; because orlistat blocks some of the dietary fat from being absorbed, the fat is excreted unchanged in the feaces—, fecal incontinence, frequent or urgent bowel movements, and flatulence. GlaxoSmithKline recommends that alli users be cautious of the possible side effects until they "have a sense of any treatment effects". To minimize these effects, foods with high fat content should be avoided; the manufacturer advises consumers to follow a low-fat, reduced-calorie diet. Oily stools and flatulence can be controlled by reducing the dietary fat content to somewhere in the region of 15 grams per meal.

According to Roche, side effects are most severe when beginning therapy and may decrease in frequency with time; this is supported by the results of the XENDOS study, which found that only 36% of people had gastrointestinal adverse effects during their fourth year of taking orlistat, whereas 91% of study subjects had experienced at least one GI-related side effect during the first year of treatment. It has also been suggested that the decrease in side effects over time may be associated with long-term compliance with a low-fat diet. Long-termDespite a higher incidence of breast cancer amongst those taking orlistat in early, pooled clinical trial data—the analysis of which delayed FDA review of orlistat—a two-year study published in 1999 found similar rates between orlistat and placebo (0.54 versus 0.51%), and evidence that tumors predated treatment in 3 of the 4 participants who had them. There is evidence from an in vitro study to suggest that the introduction of specific varied preparations containing orlistat, namely the concurrent administration of orlistat and the monoclonal antibody trastuzumab, can actually induce cell death in breast cancer cells and block their growth.

A 2006 animal study linked orlistat with aberrant crypt foci (ACF), lesions found in the colon which are believed to be one of the earliest precursors of colon cancer. PrecautionsAbsorption of fat-soluble vitamins and other fat-soluble nutrients is inhibited by the use of orlistat. A multivitamin tablet containing vitamins A, D, E, K, and beta-carotene should be taken once a day, at bedtime, when using orlistatInteractionsOrlistat may reduce plasma levels of ciclosporin (also known as "cyclosporin" or "cyclosporine", trade names Sandimmune, Gengraf, Neoral, etc.), an immunosuppressive drug frequently used to prevent transplant rejection; the two drugs should therefore not be administered concomitantly Orlistat can also impair absorption of the antiarrhythmic amiodarone.

Rimonabant

Rimonabant (also known as SR141716, Acomplia, Bethin, Monaslim, Remonabent, Riobant, Slimona, Rimoslim, and Zimulti,Riomont) is an anorectic anti-obesity drug. It is an inverse agonist for the cannabinoid receptor CB1. Its main avenue of effect is reduction in appetite.

Rimonabant was the first selective CB1 receptor blocker to be approved for use anywhere in the world. In Europe, it was indicated for use in conjunction with diet and exercise for patients with a body mass index greater than 30 kg/m², or patients with a BMI greater than 27 kg/m² with associated risk factors, such as type 2 diabetes.

IT STARTED with a joint. Back in the 1960s, psychologists studying the effects of cannabis on short-term memory noticed the subjects couldn't keep their hands off the free marshmallows. What the researchers were seeing was confirmation of a well-known side effect of smoking cannabis - intense hunger pangs known as the munchies.

Fast-forward 40 years, and scientists are talking about the munchies again, albeit in a different way. Early next year, the French pharmaceutical company Sanofi-Aventis will start selling a drug designed to induce the "anti-munchies". Rimonabant taps into the same brain circuits as cannabis, but instead of turning them on, it turns them off. If what has been made public from the clinical trials is anything to go by, Rimonabant has almost miraculous powers, helping people to control their appetites and banish many of the metabolic problems associated with being too fat.

And that's not all. Rimonabant could possibly be a quit-smoking aid and might even be useful in treating alcoholism and other addictions. No wonder many industry analysts are backing it to become the first blockbuster drug of the 21st century.

But some are yet to be convinced. They agree that the available results look promising, but point out that there has been only one peer-reviewed article from the clinical trials. And although the drug's reported side effects are minor, nothing is known about potential long-term effects.

In 1988, researchers at the St Louis University School of Medicine in Missouri discovered the active ingredient of cannabis exerts its effects by binding to specific receptors in the brain. These cannabinoid receptors, or CB1s, turned out to be part of a network throughout the brain and body whose main role is to damp down the activity of other signalling systems.

Researchers have discovered that this "endocannabinoid" system is involved in all kinds of functions, including memory, nausea, pain, reproduction and immunity. It also plays a part in appetite and fat storage.

The details are unclear, but animal studies suggest that cannabis-like molecules produced in the body bind to CB1 receptors on neurons in the hypothalamus, the brain's main control centre for food intake. In doing so, the molecules inhibit other signals that tell us not to eat, and make us feel hungry. Rimonabant blocks CB1 receptors, which appears to reduce the hunger.

In the 1990s, Sanofi-Avenist - then Sanofi-Synthelabo - recruited 6600 overweight or obese people into four clinical trials to test Rimonabant and another 6500 volunteers in smoking cessation trials. All four obesity trials are complete. Sanofi-Avenist has published only one set of results, in the April 16 issue this year of The Lancet, from the halfway point of a two-year European study of 1507 volunteers.

All the volunteers were put on a calorie-restricted diet and an exercise program, plus a daily dose of either a placebo or a low or high dose (5 or 20 milligrams) of Rimonabant. Those on the placebo shed an average of 1.8 kilograms and saw their waists shrink by 2.4 centimetres. But those on a high dose of Rimonabant lost an average of 6.6 kilograms and reduced their waist size by 6.5 centimetres. More than two-thirds of this group had lost 5 per cent or more of their body weight.

And there was a big drop in the proportion who had "metabolic syndrome" - a cluster of symptoms associated with obesity, including lipid imbalance, high blood pressure and insulin resistance, which can lead to heart disease and diabetes. The number with the syndrome fell from about 42 per cent to 20 per cent in the high-dose group, compared with a fall from 40 to 31 per cent in the placebo group.

The researchers who analysed the results, led by Luc Van Gaal of Antwerp University Hospital in Belgium, found the improvements in metabolic benefit were better than could be expected from the weight loss alone.

As for the smoking cessation trials, so far the company has only released the results of a 10-week trial involving 787 people, but these look promising.

Sanofi-Aventis submitted its results to the US Food and Drug Administration and the European Medicines Agency earlier this year. If it gets the go-ahead, Rimonabant will sell as Acomplia. The investment bank JP Morgan predicts sales will reach 5 billion a year by 2010.

Curiously, however, Sanofi-Aventis does not intend to market Rimonabant for weight loss or smoking cessation, preferring to cast it as a heart medication on the back of the cardiovascular benefits of curbing metabolic syndrome and giving up cigarettes. This could make good business sense, since US health insurance companies rarely pay for anti-obesity drugs but will cover cardiovascular medication. And the regulatory agencies tend to be extra critical of weight-loss medications.All the volunteers were put on a calorie-restricted diet and an exercise program, plus a daily dose of either a placebo or a low or high dose (5 or 20 milligrams) of Rimonabant. Those on the placebo shed an average of 1.8 kilograms and saw their waists shrink by 2.4 centimetres. But those on a high dose of Rimonabant lost an average of 6.6 kilograms and reduced their waist size by 6.5 centimetres. More than two-thirds of this group had lost 5 per cent or more of their body weight.

And there was a big drop in the proportion who had "metabolic syndrome" - a cluster of symptoms associated with obesity, including lipid imbalance, high blood pressure and insulin resistance, which can lead to heart disease and diabetes. The number with the syndrome fell from about 42 per cent to 20 per cent in the high-dose group, compared with a fall from 40 to 31 per cent in the placebo group.

The researchers who analysed the results, led by Luc Van Gaal of Antwerp University Hospital in Belgium, found the improvements in metabolic benefit were better than could be expected from the weight loss alone.

As for the smoking cessation trials, so far the company has only released the results of a 10-week trial involving 787 people, but these look promising.

Sanofi-Aventis submitted its results to the US Food and Drug Administration and the European Medicines Agency earlier this year. If it gets the go-ahead, Rimonabant will sell as Acomplia. The investment bank JP Morgan predicts sales will reach 5 billion a year by 2010.

Curiously, however, Sanofi-Aventis does not intend to market Rimonabant for weight loss or smoking cessation, preferring to cast it as a heart medication on the back of the cardiovascular benefits of curbing metabolic syndrome and giving up cigarettes. This could make good business sense, since US health insurance companies rarely pay for anti-obesity drugs but will cover cardiovascular medication. And the regulatory agencies tend to be extra critical of weight-loss medications.New Scientistexcitotoxicity, it can be theorized that Rimonabant promotes the development of neurodegenerative diseases of the central nervous system such as Multiple sclerosis, Alzheimer's disease, Amyotrophic lateral sclerosis (ALS), Parkinson's disease, and Huntington's disease in persons that are susceptible. The reported development of previously clinically-silent multiple sclerosis in one patient taking Rimonabant suggests that any patients with an underlying neurological condition should not take Rimonabant, given the neuroprotective role of the endocannabinoid system in many experimental paradigms of neurological disease.Side-effectsPress reports suggest that side-effects occur stronger and more commonly than shown by the manufacturer in their clinical studies. Reports of depression are frequent. This is deemed to result from the drug's being active in the central nervous system, an area of human physiology so complex that the effects of a drug are extremely difficult to predict or anticipate.

Because the drug has the opposite effects of cannabinoid receptor agonists such as tetrahydrocannabinol (THC, one of the substances found in marijuana), which is neuroprotective against Other usesSmoking cessationRimonabant may also be found to be effective in assisting some smokers to quit smoking. Sanofi-Aventis is currently conducting studies to determine the possible value of rimonabant in smoking-cessation therapy. The Studies with Rimonabant and Tobacco Use (STRATUS) Program involves more than 6,000 subjects.

STRATUS is designed to explore two smoking-related therapies:
first, to use rimonabant directly to aid in smoking cessation; second, to help prevent weight gain in former smokers. Initial results apparently suggest that rimonabant is effective for both uses. However, the FDA has explicitly stated to Sanofi-Aventis that, without additional studies, rimonabant cannot be approved in the United States for smoking cessation therapy. According to Cochrane review in 2007 Rimonabant "may increase the odds of quitting approximately 1(1/2)-fold"AddictionRimonabant reduced resumption of cocaine-seeking responses triggered by two of the three most common triggers of relapse in humans, priming and cues. It may also reduce ethanol- and opiate-seeking behaviorMemoryTetrahydrocannabinol(THC) is known to impair short-term memory. It was therefore hypothesised that Rimonabant may improve short-term memory. Indeed in animal studies it significantly improved the performance of rats to encode information in the short-term memoryBlockade of Cannabis effectsRimonabant blocks the psychoactive and some of the cardiovascular effects of Δ9-Tetrahydrocannabinol (THC) in humans without affecting the pharmacokineticsDosageTake 20mg (1 capsule) per day.

Sibutramine

Pregnant and lactating women (relative C.I.) Side effectsFrequently encountered side effects are: dry mouth, paradoxically increased appetite, nausea, strange taste in the mouth, upset stomach, constipation, trouble sleeping, dizziness, drowsiness, menstrual cramps/pain, headache, flushing, or joint/muscle pain.

Sibutramine can substantially increase blood pressure and pulse in some patients. Therefore all patients treated with sibutramine should have regular monitoring of blood pressure and pulse.

The following side effects are infrequent but serious and require immediate medical attention: cardiac arrhythmias, paresthesia, mental/mood changes (e.g., excitement, restlessness, confusion, depression, rare thoughts of suicide).

Symptoms that require urgent medical attention are seizures, problems urinating, abnormal bruising or bleeding, melena, hematemesis, jaundice, fever and rigors, chest pain, hemiplegia, abnormal vision, dyspnea and edema.

Currently, no case of pulmonary hypertension has been noted, although related compounds (such as Fen-Phen) have shown this rare but clinically significant problem.InteractionsSibutramine has a number of clinically significant interactions. The concomitant use of sibutramine and monoamine oxidase inhibitors (MAOIs, such as selegiline) is not indicated, as it may increase the risk of serotonin syndrome, a somewhat rare but serious adverse drug reaction. Sibutramine should not be taken less than two weeks after stopping or before starting use of an MAOI. Taking both sibutramine and certain medications used in the treatment of migraines—such as ergolines and triptans—, as well as opioids, may also increase the risk for serotonin syndrome, as may the use of more than one serotonin reuptake inhibitor at the same time.

The concomitant use of sibutramine and drugs which inhibit CYP3A4, such as ketoconazole and erythromycin, may increase plasma levels of sibutramine.[5] Sibutramine does not affect the efficacy of hormonal contraception. Dosage10 mg once daily (usually in the morning), if this proves insufficient the dose may be increased to 15 mg daily after 4 weeks.Pheochromocytoma Enlargement of the prostate gland with urinary retention (relative C.I.) Seizure disorders Closed angle glaucoma Hyperthyroidism (overactive thyroid gland) Stroke or transient ischemic attack (TIA) Existing damage on heart valves, coronary heart disease, congestive heart failure, serious arrhythmias, previous myocardial infarction Existing pulmonary hypertension Hypertension that is not sufficiently controlled (caution in controlled hypertension) Concomitant treatment with a MAO inhibitor, antidepressant or other centrally active drugs, particularly other anoretics Patients below 18 years of age Hypersensitivity to the drug Patients with a history of or a predisposition to drug or alcohol abuse Psychiatric conditions as bulimia nervosa, anorexia nervosa, serious depression or preexisting mania Sibutramine (trade name Meridia in the U.S. and Canada, Ectiva in South Africa, Reductil in Europe and most other countries), usually as sibutramine hydrochloride monohydrate, is an orally administered agent for the treatment of obesity, as an appetite suppressant. It is a centrally-acting serotonin-norepinephrine reuptake inhibitor structurally related to amphetamines, although its mechanism of action is distinct. PharmacokineticsSibutramine is well absorbed from the GI tract (77%), but undergoes considerable first-pass metabolism, reducing its bioavailability. The drug itself reaches its peak plasma level after 1 hour and has also a half-life of 1 hour. Sibutramine is metabolized by cytochrome P450 isozyme CYP3A4 into two pharmacologically-active primary and secondary amines (called active metabolites 1 and 2) with half-lives of 14 and 16 hours, respectively. Peak plasma concentrations of active metabolites 1 and 2 are reached after three to four hours. The following metabolic pathway mainly results in two inactive conjugated and hydroxylated metabolites (called metabolites 5 and 6). Metabolites 5 and 6 are mainly excreted in the urine.PharmacodynamicsSibutramine is a neurotransmitter reuptake inhibitor that reduces the reuptake of serotonin (by 53%), norepinephrine (by 54%), and dopamine (by 16%), thereby increasing the levels of these substances in synaptic clefts and helping enhance satiety; the serotonergic action, in particular, is thought to influence appetite. Older anorectic agents such as amphetamine and fenfluramine force the release of these neurotransmitters rather than affecting their reuptake.

Despite having a mechanism of action similar to tricyclic antidepressants, sibutramine has failed to demonstrate antidepressant properties in animal studies.

It was approved by the U.S. Food and Drug Administration (FDA) in November 1997for the treatment of obesity.

SYNEPHRINE

ContraindicationsSibutramine is contraindicated in:

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.

Taurine Powder

Taurine is an amino acid believed to play an important role in many areas of the body including the brain and nervous system. Some researchers hold that Taurine can be a beneficial dietary supplement for persons with bipolar disorder (manic depression).
  • Benefits
  • Works as an ion and pH buffer in the heart, skeletal muscles and central nervous system.
  • Taurine is instrumental in preventing loss of potassium from heart muscle.
  • Aids in the digestion of fat, soluble vitamins, and the management of cholesterol levels.
  • Aids electrolyte balance and proper utilization of sodium, potassium, calcium and magnesium.

    • Improves cell volumization.
    • Improves anabolic processes.
    • Boosts protein synthesis.
    • Maintains glucose uptake.
    • Makes muscles appear larger.
    • May help prevent cataracts.
    • Taurine works synergistically with any form of Creatine.
    • Boosts cardiac output in those suffering from congestive heart failure or cardiomyopathy.
May help control epileptic seizures, uncontrollable facial twitches, and motor tics.

DESCRIPTION:
Taurine is a nonprotein amino acid. It is an end product of L-cysteine metabolism and the principal free intracellular amino acid in many tissues of humans and other animal species. Taurine is present in high amounts in the brain, retina, myocardium, skeletal and smooth muscle, platelets and neutrophils. It is classified as a conditionally essential amino acid because it is necessary to be supplied in the diet of infants for normal retinal and brain development.

Research of taurine was greatly stimulated by the finding that it is an essential nutrient for cats. Taurine deficiency in cats can result in a variety of clinical abnormalities, including central retinal degeneration, dilated cardiomyopathy and platelet function abnormalities. Shortly after the discovery that dietary taurine deficiency leads to retinal degeneration in cats, it was observed that infants who were fed formulas lacking taurine had lower plasma levels of this amino acid than did infants fed human milk. Further, it was discovered that children receiving total parenteral nutrition not containing taurine had abnormal electroretinograms, as well as low plasma taurine levels. Taurine has been added to most human infant formulas since the mid-1980s.

Taurine is produced in the body from L-cysteine. The first reaction in the pathway is the formation of cysteine sulfinic acid. Cysteine sulfinic acid (CSA) is converted to hypotaurine via the enzyme CSA-decarboxylase, and taurine is formed from hypotaurine. Cats have low activity of CSA-decarboxylase. Dietary taurine mainly comes from animal food. Taurine is present in very low levels in plant foods. Taurine is found in seaweeds.

The most understood role of taurine in humans is its involvement in the formation of taurine bile acid conjugates in the liver, which are essential for micelle formation and fat absorption. Taurine is involved in the pre-and post-natal development of the central nervous system and visual system, although the details of its involvement in these processes are unclear. Taurine also has antioxidant and membrane-stabilizing activities. Much remains to be learned about the role of taurine in human physiology.

Taurine is different from most biological amino acids in a few particulars. It is a sulfonic acid rather than a carboxylic acid; it is a beta-amino acid rather than an alpha-amino acid and it does not have a chiral center. Taurine is also known as 2-aminoethane sulfonic acid. Its molecular formula is C2H7NO3 S, and its molecular weight is 215.15 daltons.ACTIONSTaurine has antioxidant activity. It has putative hypocholesterolemic, hypotensive, antiatherogenic and detoxifying activities. It may also have steatorrhea-reducing activity in those with cystic fibrosis and has putative antidiabetic, inotropic and antiseizure activities.

The major antioxidant activity of taurine derives from its ability to scavenge the reactive oxygen species hypochlorite, which is generated in neutrophils during respiratory-burst activity of these cells. Taurine reacts with excess hypochlorite produced in the process of phagocytosis to form the relatively harmless N-chlorotaurine. N-chlorotaurine is then reduced to taurine and chloride. This activity may protect against collateral tissue damage that can occur from the respiratory burst of neutrophils. Taurine may also suppress peroxidation of membrane lipoproteins by other reactive oxygen species. It is thought that this effect is not due to taurine's scavenging of these reactive oxygen species, but rather to taurine's membrane-stabilizing activity, which confers greater resistance to the membrane lipoproteins against lipid peroxidation.

Taurine has been demonstrated to reduce cholesterol levels in animals, but results in humans have been contradictory. The hypocholesterolemic effect of taurine in animals is thought to be due, in large part, to the stimulation of bile acid synthesis and enhancement of cholesterol 7 alpha-hydroxylase activity. Taurine has been found to have antiatherogenic activity in animals, but there is less evidence that it does in humans. The antiatherogenic activity of taurine in animals is thought to be due, in large part, to its hypocholesterolemic activity.

Taurine has been found to normalize blood pressure in spontaneous hypertensive rats, and there is some evidence from human studies that it also has hypotensive activity in hypertensive, but not normotensive, individuals. It is speculated that the hypotensive effect of taurine may result from the normalization of increased sympathetic activity in hypertensive individuals.

Taurine has been found to ameliorate bleomycin-induced lung fibrosis in hamsters and also to ameliorate the side effects of some nitrogen mustards. It is thought that the possible antioxidant and membrane-stabilizing activities of taurine may account for these detoxifying actions.

Some studies have shown decreased steatorrhea in cystic fibrosis patients receiving taurine. It is thought that the mechanism of this effect is taurine's stimulation of bile acid formation resulting in increased fat absorption in these individuals.

Again in animals, but not in humans, taurine has been found to have antidiabetic activity. The mechanism of this effect is unclear. It is thought that taurine may decrease insulin resistance.

Cats who are deficient in taurine develop dilated cardiomyopathy and congestive heart failure. Taurine has an inotropic effect when given to these animals. Some studies suggest that taurine has an inotropic effect in humans with congestive heart failure. The mechanism of this possible effect is unclear. It is thought that taurine may modulate the calcium current.

The mechanism of taurine's putative antiseizure activity is unknown.

PHARMACOKINETICS:
Following ingestion, taurine is absorbed from the small intestine via the beta-amino acid or taurine transport system, a sodium- and chloride-dependent carrier system that serves gamma-aminobutyric acid and beta-alanine, as well as taurine. This carrier system is located in the apical membrane of intestinal mucosa cells. Taurine is transported to the liver via the portal circulation, where much of it forms conjugates with bile acids. Taurocholate, the bile salt conjugate of taurine and cholic acid, is the principal conjugate formed via the action of the enzyme choloyl-CoA N-acyltransferase. The taurine conjugates are excreted via the biliary route. Taurine that is not conjugated in the liver is distributed via the systemic circulation to various tissues in the body. Taurine is not usually completely reabsorbed from the kidneys, and some fraction of an ingested dose of taurine is excreted in the urine.

INDICATIONS AND USAGE:
Taurine may be helpful in some with congestive heart failure and hypertension. It has demonstrated some antiatherogenic effects in both animal and human studies. There is the suggestion, mostly from animal data, that taurine might improve glucose tolerance and protect against some toxins. Some older studies suggest it might have some antiseizure activity. There is preliminary evidence that it might be helpful in some with cystic fibrosis.

RESEARCH SUMMARY:
In a study of 24 subjects with congestive heart failure, administration of 2 grams of taurine, twice a day, resulted in clinical improvement in 19 patients. Roentgenographic data helped confirm the improvement. These positive results were subsequently confirmed in a double-blind, randomized, crossover, placebo-controlled study in which taurine was added to conventional treatment for a four-week period. Compared with placebo, taurine produced significant improvement as evaluated by a number of measures, including chest films. In still another study, supplemental taurine, but not coenzyme Q10, was said to have significant benefit in patients with congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. This was a double-blind study using 3 grams of taurine daily.

Taurine has demonstrated hypotensive effects in some animal studies. In humans, it has lowered blood pressure in borderline hypertensive patients using 6 grams of taurine daily for seven days. Lipid-lowering effects have been seen in animals, but human data are few and contradictory. There is some preliminary evidence from one small study that 0.4 to 1.6 grams of taurine daily for eight days inhibited platelet aggregation in a dose-dependent manner. Supplementation with 1.5 grams of taurine daily decreased platelet aggregation in subjects with type 1 diabetes. Insulin sensitivity was significantly improved by taurine supplementation in a rat model of spontaneous type 2 diabetes. Serum cholesterol and triacylglycerol were decreased in the supplemented animals. Taurine was also effective in another animal model of insulin resistance.

Taurine has exerted some detoxifying effects in animal experiments. It helped prevent bleomycin-induced lung injury and fibrosis in mice. It also appeared to have protective effects, as measured by changes in memory and lipid peroxidation levels in the brain, in rats exposed to ozone. Additionally, it has inhibited ethanol-induced elevation of plasma acetaldehyde in other animal studies. In one of these, it prevented the development of ethanol-induced hypertension in rats.

In some older studies, taurine demonstrated some preliminary ability to suppress some epileptic seizures. Follow-up is needed.

Finally, taurine was shown to be of benefit in a study of 22 Canadian children with cystic fibrosis and documented steatorrhea. They were given taurine (30 mg/kg/day) and placebo during separate six-month periods. Severity of fat malabsorption was significantly reduced in most of the subjects, especially in those with the most severe steatorrhea. A more recent study, however, failed to note these benefits, but significant differences in the two study groups may account for this discrepancy. A second study by the Canadian group showed positive effects of taurine on fat absorption in cystic fibrosis patients. Again, those with the greatest malabsorption at baseline seemed to benefit the most.

CONTRAINDICATIONS:
Taurine is contraindicated in those hypersensitive to any component of a taurine-containing nutritional supplement.

PRECAUTIONS:
Pregnant women and nursing mothers should avoid taurine supplements unless recommended by their physicians. Those with congestive heart failure should only use taurine under medical supervision.

ADVERSE REACTIONS:
No reports of adverse reactions.

DRUGS:
In animal studies, taurine was found to ameliorate the pulmonary side effects (pulmonary fibrosis) of bleomycin.

DOSAGE AND ADMINISTRATION:
Doses are variable and range from 500 mg to 3 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.

TETRADECYLTHIOACETIC ACID (TTA)

A PPAR Antagonist And Effective Fat Loss Agent!TTA assists your.

In simplest terms, Tetradecylthioacetic Acid (TTA) is a fatty acid that can help burn body-fat.
  • Can be cost effectively incorporated into fat loss, lean bulking, or body recomposition regimens.
  • Contains 99.99% pure pharmasuetical Tetradecylthioacetic Acid (TTA). TTA is commonly used to help aid in fat loss and body recomposition.
  • TTA is stimulant free & can be used as a stand alone, or can be combined with other fat loss products. fat loss endeavors on multiple levels.
Not only will it release fat from your fat stores, but it will increase your body’s efficiency at burning fat. It does this by increasing both the "mini-furnaces" present in the cell that are responsible for burning fat, and by increasing the fat burning enzymes that assist these furnaces. It also increases fat usage by promoting the proteins in the cell responsible for "wasting" energy. On top of these remarkable fat burning effects, it promotes general health by boosting the immune system, improving blood flow, exerting anti-inflammatory effects and promoting healthy cholesterol.

MORE INFORMATIONTTA is a PPAR antagonist.
PPAR stands for Peroxisome proliferator-activated receptors.

PPAR's are a group of transcription factors (proteins that transcribe genetic information from DNA to RNA) that play key roles in cell development, glucose metabolism, and metabolism of carbohydrates, lipids, and proteins.

There are different types of PPAR's, but TTA relates to PPAR-alpha.TTA also helps increase mitochondrial activity, which in itself provides numerous benefits. Mitochondria proteins function mainly to produce ATP (ATP transports chemical energy within cells for metabolism).By enhancing mitochondria protein function, the body burns more fuel, which translates into fat loss. The more fat that someone is carrying, the more inhibition of mitochondrial function they generally have.

TTA also enhances mitochondrial oxidative capacity.

TTA also helps in reducing free fatty acids and triglyceride levels.

Directions:
As a dietary supplement, take 250mg (quarter gm) 4 times per day , approximately 30 minutes prior to meals. To assess individual tolerance, it is suggested that individuals begin usage with 500mg per day and increase dosage by 250mg every 3 days until a maximum of 100mg (1 gm). If cramping is experienced, maintain or lower dosage accordingly.

Warnings:
Keep out of reach of children. The product is not to be used by individuals under 18 years of age or by women that may be pregnant or nursing. Always consult a physician prior to using any dietary supplements.

There is a strong link between insulin resistance and the reduction of glucose oxidization in the mitochondria and the subsequent build up for glycolysis byproducts. The liver is the main site in which fatty acids are burnt as energy or stored dependant upon calorie intake and energy expenditure. When in a fasting state, the body generally switches from using carbohydrate and fats as an energy source to mainly fat. Fatty acids are released from adipocytes (the cells that primarily compose adipose tissue). These fatty acids are then either restored in adipocytes, go to cardiac and skeletal muscle to be burned as energy, or are broken down through beta oxidization to form ketones. PPAR-alpha mediates the genes that control fatty acid uptake, beta oxidization, and gamma oxidization which are upregulated when in a fasting state. Therefore, with TTA being a PPAR-alpha antagonist, it activates these receptors allowing you to receive these benefits while in a fed state as well. PPAR-alpha also helps inhibit triglyceride hydrolysis, which further enhances lipid oxidization.

L - TYROSINE DESCRIPTION

L-tyrosine is a protein amino acid. It is classified as a conditionally essential amino acid.

Under most circumstances, the body can synthesize sufficient L-tyrosine, principally from L-phenylalanine, to meet its physiological demands. However, there are conditions where the body requires a dietary source of the amino acid for its physiological demands. For example, L-tyrosine is an essential amino acid for those with phenylketonuria. L-tyrosine is found in proteins of all life forms. Dietary sources of L-tyrosine are principally derived from animal and vegetable proteins. Vegetables and juices contain small amounts of the free amino acid. The free amino acid is also found in fermented foods such as yogurt .

In addition to being involved in protein synthesis, L-tyrosine is a precursor for the synthesis of the catecholamines epinephrine, norepinephrine and dopamine, the thyroid hormones thyroxine and triiodothyronine, and the pigment melanin.

L-tyrosine is also known as beta- (para-hydroxyphenyl) alanine, alpha-amino-para-hydroxyhydrocinnamic acid and (S)- alpha-amino-4-hydroxybenzenepropanoic acid. It is abbreviated as either Tyr of by its one-letter abbreviation Y. The molecular formula of L-tyrosine is C9H10NO3, and its molecular weight is 181.19 daltons. L-tyrosine is an aromatic amino acid ACTIONSL-tyrosine has putative antidepressant activity.

MECHANISM OF ACTION:
The mechanism of L-tyrosine's putative antidepressant activity may be accounted for by the precursor role of L-tyrosine in the synthesis of the neurotransmitters norepinephrine and dopamine. Elevated brain norepinephrine and dopamine levels are thought to be associated with antidepressant effects.

PHARMACOKINETICS:
Following ingestion, L-tyrosine is absorbed from the small intestine by a sodium-dependent active transport process. L-tyrosine is transported from the small intestine to the liver via the portal circulation. In the liver, L-tyrosine is involved in a number of biochemical reactions, including protein synthesis and oxidative catabolic reactions. L-tyrosine that is not metabolized in the liver is distributed via the systemic circulation to the various tissues of the body.

INDICATIONS AND USAGE:
Results are mixed, but largely negative, with respect to claims that tyrosine is an effective antidepressant. Claims that it can alleviate some of the mental and physical symptoms of environmental stress are based on preliminary evidence. Further claims that tyrosine is useful in narcolepsy and attention deficit disorder have been refuted by some studies. Another study found that tyrosine supplementation did not improve neuropsychological performance in subjects with phenylketonuria. Claims that tyrosine is helpful in alleviating symptoms of premenstrual syndrome (PMS) and drug withdrawal are largely anecdotal and unconfirmed. There is no evidence tyrosine has any effect on dementia, Alzheimer's disease or Parkinson's disease.

RESEARCH SUMMARY:
Two small, early studies suggested that tyrosine might have useful antidepressant effects. A subsequent follow-up with more subjects and conducted in a randomized, double-blind fashion failed to find any significant antidepressant activity, compared with placebo, in subjects with major depression. The dose used was 100 mg/kg/day of tyrosine for four weeks.

One study has concluded that tyrosine can protect against some forms of environmental stress. Subjects were given a 100 mg/kg dose of tyrosine and then exposed for 4.5 hours to cold and hypoxia in this double-blind, placebo-controlled crossover study. Tyrosine was reported to significantly decrease adverse symptoms, including mood and performance impairment. Follow-up is needed.

In another double-blind, placebo-controlled trial, tyrosine had no significant effect on subjects with narcolepsy and associated cataplexy. Dose used was 9 grams daily for four weeks. Similarly, tyrosine failed to produce lasting, significant improvement in subjects with attention deficit disorder. In this small, open study, tyrosine seemed to improve this condition after two weeks of supplementation, but this improvement was not sustained.

Recently, tyrosine was tested to see if it could improve the neuropsychological test performances of individuals with phenylketonuria. This was a randomized, double-blind, placebo-controlled crossover study. Maximum dosage used was 100 to 150 mg/kg/day. The supplementation increased plasma tyrosine concentrations. Higher tyrosine levels correlated at baseline with improved performance on the neuropsychological tests, yet higher concentrations achieved through supplementation in this trial did not enhance test scores.

CONTRAINDICATIONSL:
Tyrosine is contraindicated in those with the inborn errors of metabolism alkaptonuria and tyrosinemia type I and type II. It is also contraindicated in those taking non-selective monoamine oxidase (MAO) inhibitors. L-tyrosine is contraindicated in those hypersensitive to any component of an L-tyrosine-containing supplement.

PRECAUTIONS:
Pregnant women and nursing mothers should avoid supplementation with L-tyrosine.

Those with hypertension should exercise caution in the use of L-tyrosine.

Those with melanoma should avoid L-tyrosine supplements.

ADVERSE REACTIONSL:
Tyrosine is generally well tolerated. There are some reports of those taking supplemental L-tyrosine experiencing insomnia and nervousness.

DRUGS:
Non-selective MAO inhibitors.

DOSAGE AND ADMINISTRATION:
Those who use supplemental L-tyrosine typically take 500 to 1500 mg 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 including phenelzine sulfate, tranylcypromine sulfate and pargyline HC1 — Concomitant use of L-tyrosine and non-selective MAO inhibitors may cause hypertension..

USNIC ACID

L-Valine

L-valine is a branched-chain essential amino acid (BCAA) that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. Valine is one of three branched-chain amino acids (the others are leucine and isoleucine) that enhance energy, increase endurance, and aid in muscle tissue recovery and repair. This group also lowers elevated blood sugar levels and increases growth hormone production. Supplemental valine should always be combined with isoleucine and leucine at a respective milligram ratio of 2:1:2. It is an essential amino acid found in proteins; important for optimal growth in infants and for growth in children and nitrogen balance in adults. The lack of L-valine may influence the growth of body, cause neuropathic obstacle, anaemia. It has wide applications in the field of pharmaceutical and food industry.

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