GABA: New Treatment To Improve Recovery After Stroke

Can adjusting the levels of the amino acid GABA improve post-stroke recovery? Results are positive in this animal study, which has led to new hope for stroke patients.

Stroke is a leading cause of death worldwide. And even if the stroke victim survives, the disturbance in the brain’s blood supply—the stroke—can cause brain damage. While some people can and do make a near-complete recovery, many are left with disabilities such as the inability to understand or to speak, or the inability to move limbs on one side of the body.

This damage is often so severe that one third of stroke survivors are confined to nursing homes or institutions.

A Clarkson, B Huang, et al, researchers at the Department of Neurology, The David Geffen School of Medicine at UCLA, LA, USA, hoped to improve post-stroke recovery with drugs. They knew that, depending on the severity of the brain damage, the brain can repair itself after a stroke. The neurons in the brain re-map cognitive functions using non-damaged brain tissue.

The amino acid GABA is critical for this re-mapping process in the brain. GABA is the main neurotransmitter, which means it transmits the signals within the brain. GABA is actually synthesized in the brain, from the amino acid glutamate.

In this animal study, the researchers wanted to examine the brain’s ability to re-map if GABA levels were adjusted.

GABA studied in stroke trial

In this animal study, the researchers analyzed data from post-stroke mice. Stroke caused an increase in extrasynaptic GABA transmission. But when the GABA levels were decreased, the brains showed earlier, and more robust, motor recovery.

The researchers reported that timing is crucial when adjusting GABA levels. It can actually cause more brain damage if done too early. With the mice, the researchers found that delaying treatment until 3 days after stroke improved recovery.

The researchers concluded that targeting GABA helps the brain re-map its neural pathways, which enhances motor recovery. Targeting GABA is therefore a possible treatment in post-stroke recovery.

My personal experience with GABA

I love taking a GABA supplement and the benefits it proposes. It enhances my cognitive function and ensures that my brain is in optimal health. This study is more supporting evidence that brain supplements can be life changing to people all across the globe. If you’re looking for a high quality GABA supplement, look no further than Powdercity. Out of all the other vendors, I find them to be the highest quality, best price and fastest shipping. Their GABA can be found here: and is offered in 100g, 250g, and 1kg quantities!




Amino Acid Taurine Prevents Diabetic Kidney Disease

More evidence on the preventive effect of the amino acid taurine. S Lin, J Yang et al, from Shenyang Agricultural University, China, published some great news for diabetics. They developed an animal study to test the preventive effect of taurine on the kidney disease known as diabetic nephropathy. This may be the light at the end of the tunnel for many diabetics.

Taurine is known to have some preventive effects on type 2 diabetes and its complications, but can it also prevent the kidney disease diabetic nephropathy? Rates of type 2 diabetes have risen over the past few decades, just as obesity rates have increased. This is no coincidence, as obesity is one of the main risk factors for developing diabetes.

Diabetic nephropathy is caused by longstanding diabetes. It’s a disease of the blood vessels in the kidneys. It’s one of the most difficult diabetic complications to treat, and can lead to chronic renal failure. Kidney dialysis is often the only possible treatment, and even then diabetic patients are 17 times more likely to die of renal failure than non-diabetic patients.

Preventing the kidney disease diabetic nephropathy is therefore a very urgent issue.

Can the amino acid taurine prevent diabetic kidney disease?

The amino acid taurine is the building block of all the other amino acids. It’s the most abundant amino acid in our bodies, and has some preventive and even curative effects on diabetes. The researchers in this trial tested its effects on diabetic rats.

One hundred and ten rats were given various concentrations of taurine for the ten week trial, and their blood was tested for blood glucose, cholesterol, and lipid metabolism.

High blood glucose results in many diabetic complications, as nerve endings and small blood vessels are damaged.  Taurine was shown to decrease blood glucose.

Lipid metabolism disorder is another complication of diabetes. Great news: results indicated that taurine significantly decreased blood fat, and improved lipid metabolism.

The preventive effects of taurine were proven in this trial. Blood glucose was decreased, lipid metabolism improved, and kidney function increased. This gives very positive hopes for taurine to be used in more treatments for diabetes.


Amino Acid: Glutamate in Stroke Treatment

Preventing brain damage after stroke is the primary goal for stroke treatment. Understanding the balance of brain chemicals—which include amino acids like glutamate (salt/ester of glutamic acid)—can help scientists develop new, successful treatments for stroke. 

Stroke is the second leading cause of death worldwide. This dangerous condition occurs when the supply of blood to the brain is disturbed. With ischemic strokes, blood supply is decreased (possibly by a blood clot), and rapidly leads to loss of brain function. Stroke can lead to permanent brain damage, when the neurons in the brain are destroyed.

Neurons are nerve cells which transmit information in our central nervous system, which includes our brain. Neuroprotection is the name for treatments which prevent, or slow, the progression of stroke by preventing the loss of neurons. It is also used to treat other central nervous system disorders, including neurodegenerative diseases, traumatic brain injury, and spinal cord injury.

Dr. Myron Ginsberg published an interesting review on ischemic stroke in Neuropharmacology. Dr. Ginsberg, from the Department of Neurology, University of Miami Miller School of Medicine, in Miami, Florida, covered many experimental neuroprotective treatments, including glutamate antagonism.

The role of glutamate role in treatment for stroke

The amino acid glutamate—sometimes known as or associated with glutamic acid—is one of our brain’s our main excitatory neurotransmitters. Glutamate is involved in cognitive functions such as learning and memory.  But with stroke, excess glutamate can accumulate in the brain. This allows calcium ions to enter the cells. This process is called excitotoxicity, and it causes neuron damage and brain cell death.

Glutamate and other excitatory amino acids interact with receptor-classes, such as N-methyl-D-aspartate (NMDA). Animal studies suggest that treatments which block NMDA receptors could be successful in preventing brain damage after stroke, but only with very early administration. Human trials have not yet been completed.

As further research continues into the role of neurotransmitting amino acids and stroke, it’s possible that a successful neuroprotective treatment using glutamate could be developed.


How Does Methionine Affect Bone Fractures?

According to previous studies, an elevated level of the protein amino acid homocysteine (in a condition called hyperhomocysteinemia) can hinder fracture healing. Because the essential amino acid methionine is a precursor of homocysteine and an important component in the biosynthesis of cysteine, researchers at the University of Saarland in Germany investigated if excess levels of methionine would also affect rate of bone repair.

Methionine also plays a key part in the biosynthesis of carnitine, taurine, lecithin, phosphatidylcholine and other phospholipids. An error in the conversion of methionine can lead to atherosclerosis, when fatty materials accumulate on artery walls and can cause inflammation.

For the experiment, researchers Joerg Holstein et al. divided 25 mice into two groups. One group received a diet high in methionine while the other group received a control diet that was equivalent in calories. Three weeks after methionine supplementation, the researchers anesthetized the mice using ketamine and xylazine.

They then fractured the right femur of each mouse. Four weeks after fracture, the researchers analyzed the healing process using histomorphometry and biomechanical testing. Blood samples were also taken to determine level of serum homocysteine.

The effect of amino acid methionine on bone healing

At the end of the study, Holstein, et al., found an increased level of homocysteine in the methionine group when compared to the control. Results from biomechanical testing showed no significant difference between the groups in bending stiffness of the healed bones. Results from histomorphometry analyses also did not show any significant difference between the two groups in size or tissue composition of the callus.

Based on these findings, the researchers conclude that excess methionine intake does not have a significant effect on bone repair in mice.

They further suggest that hyperhomocysteinemia does not pose a risk for inhibited fracture healing and that dietary methionine may even help regulate osteoblasts, cells that are responsible for bone formation.

They believe that additional testing will reveal the role methionine plays in bone healing.


Arginine for Inflammation and Erectile Dysfunction

For men, arginine may pose as almost a miracle amino acid for inflammation and erectile dysfunction, but one should be wary that arginine combined with other amino acids, protein, and lifestyle changes are more likely the answer.

Arginine, has been getting a lot of attention for it can be an amazing anti-aging amino acid. It also may be useful for graying hair, loss of hair, heart disease, preventing heart failure, and possibly inflammation.

This is where pieces of the arginine amino acid puzzle starts to thicken.  Inflammation and erectile dysfunction are two problems often linked together as exemplified by the article “Reduction of Inflammation Improves Endothelial Function and ED” whereby “minimizing infection and inflammation throughout the body, including avoiding fat accumulation, should improve both vascular and erectile health.”

The link may be attributed to arginine being needed by the body to make nitric oxide.

Because nitric oxide is crucial for maintaining healthy blood pressure, it also helps prevent atherosclerosis, and plays a role in modulating immune system function. In addition, nitric oxide regulates several processes in the body, including fat and glucose metabolism.

Researchers found that inhibiting nitric oxide production was associated with fat gain while stimulating nitric oxide secretion was correlated with enhanced lipolysis, or fat breakdown, according to research published in the September 2006 issue of the Journal of Nutritional Biochemistry.

The best part about nitric oxide is that it is readily available on a sunny day.

Is Nitric Oxide the Cure for Inflammation and ED?

There is some strong evidence that indicates nitric oxide may help both inflammation and ED. In the study, “Role of Nitric Oxide in Inflammatory Diseases” they concluded NO (nitric oxide) inhibitors “represent important therapeutic advance in the management of inflammatory diseases”.

Additionally, the amino acid L-arginine stimulates nitric oxide, which releases “growth hormone, insulin, and other substances in the body.” Prescription drugs also may contribute to maintain the nitric oxide in the body, which can also help prevent erectile dysfunction.

In conclusion, when it comes to adults, and particularly men of industrialized countries, the issue may not be so much about consuming enough protein and amino acids, the concern might be to see the bigger picture and rooting out the problem of inflammation and erectile dysfunction, instead of just ‘curing’ this challenge with a quick fix. Certainly stress is one factor, lack of sleep another, but also being mindful of our diets and exercise.


Phenylalanine amino acid: Importance of PKU Screening in Newborn Babies

In the United States a heel stick test (using a needle prick on the baby’s heel for a small blood sample) is done at the ripe old age of 3 days old to test for Phenylketonuria (PKU) and other disorders. PKU is a metabolic disorder that shows up when the gene is inherited from both parents of the newborn, which is an enzyme deficiency that is needed for proper metabolism of the amino acid phenylalanine.

People with PKU must avoid foods that contain phenylalanine altogether from birth, however, in order to survive since side effects can include pigmentation loss in the skin/eyes/hair, a “mousy” odor, muscles pains and aches, seizures, and mental retardation.

Newborn screening and phenylalanine-restricted diets for PKU patients

Phenylalanine is an essential amino acid that is in foods, including proteins like meats, dairy products, beans, eggs, tofu, nuts, and many others, including aspartame (the sugar substitute in diet soda). An “essential” amino acid means that the body cannot produce this amino acid on its own so it must be gotten from food. Aminos phenylalanine and tyrosine are both associated with PKU and are tested for in all newborn babies at clinics and hospitals.

According to the American Academy of Family Physicians, it is Dr. Richard Koch from the University of Southern California School of Medicine in Los Angeles, California, who promotes that repeat testing should occur in any child that tests positive for PKU. The amino acid phenylalanine in foods should be avoided and a special diet should begin from birth so as to prevent mental retardation.

Koch says, “Occasionally, cases of PKU are missed by newborn screening. Thus, a repeat PKU test should be performed in an infant who exhibits slow development.”

Phenlyketonuria (PKU) is a recessive defect in the enzyme phenylalanine hydroxylase

Koch discusses the enzyme deficiency: “Phenylketonuria (PKU) is caused by an autosomal recessive defect in the enzyme phenylalanine hydroxylase, which is required for converting phenylalanine to tyrosine. (Five percent of natural protein is composed of phenylalanine.)”

PKU is caused by a mutation that is located on chromosome 12, although the specific type of mutation may vary, which results in severity that is variable among those with the PKU disorder. Phenylalanine containing foods should be avoided in all of these cases. Of course, normal people who do not have PKU need phenylalanine and should have a diet consisting of enough proteins to provide this essential amino acid.


Phenylalanine for Pain Relief and Other Health Benefits

Phenylalanine is an essential amino acid, in which “essential” means you must get it through your diet or supplementation since your body cannot produce it on its own. Phenylalanine also is known as nature’s pain reliever. 

Interestingly, Phenylalanine is used in psychotropic drugs such as morphine, codeine, papaverine, and even mescaline because it is such an effective pain reliever.

Phenylalanine: How is it used in the body as a pain reliever?

Phenylalanine is one of the three aromatic amino acids, which include the other two, Tyrosine and Tryptophan. Phenylalanine is also the precursor for Tyrosine, and like Tyrosine, Phenylalanine is the precursor in the human body of catecholamines, which include dopamine, epinephrine, norepinephrine, and tryamine.

Dr. Winston Greene at DC Nutrition explains what catecholamines are and why we need phenylalanine, and how much: “Phenylalanine is a precursor of the neurotransmitters called catecholamines, which are adrenalin-like substances. … is highly concentrated in the human brain and plasma. … and requires biopterin, iron, niacin, vitamin B6, copper and vitamin C. An average adult ingests 5 g of phenylalanine per day and may optimally need up to 8 g daily.”

Phenylalanine essential amino acid comes from food and levels affect pain relief

You can get Phenylalanine from protein foods such as beef, chicken, fish, eggs, dairy products, and wheat germ. Dr. Greene shows that not only is this amino acid good as a pain reliever, but also that it is low in people who ingest caffeine. Interestingly, depressed people often seek out stimulants like caffeine drinks as a “pick me up” but may be doing themselves further harm since Dr. Greene says they’d found that “about 10 percent of depressed patients have low plasma Phenylalanine, and phenylalanine is an effective treatment in these cases.”

When someone gets an infection, however, Phenylalanine levels increase in the body to help aid any pain that might be associated with it, again acting as nature’s pain reliever. This amino is used in “premenstrual syndrome and Parkinson’s may enhance the effects of acupuncture and electric transcutaneous nerve stimulation (TENS). Phenylalanine and tyrosine, like L-dopa, produce a catecholamine effect. Phenylalanine is better absorbed than tyrosine and may cause fewer headaches.”

The bottom line is that Phenylalanine can be a great natural source for pain relief for numerous problems from infection to PMS to diseases such as Parkinsons. The health benefits are numerous, but always be sure to check with your doctor prior to any supplementation or changes to your diet when working to include this amazing amino acid for pain relief.


Acetyl-L-Carnitine: Grade-A Energy Producer

Acetyl-L-Carnitine (also called N-Acetyl-L-Carnitine) is one of the body’s basic building blocks, an amino acid that is involved in the production of energy, good heart and brain function, muscle movement, the metabolism of cells and many other bodily processes.

The body is capable of converting Acetyl-L-Carnitine into the closely related L-Carnitine, a substance that turns body fat into energy. It is also able to convert in the other direction. Your body makes both of these substances in the liver and kidneys, and they are packed away for future use at various sites around the body: in skeletal muscles, brain, heart and sperm, for instance. L-Carnitine, which sometimes is less available as a nutrient than Acetyl-L-Carnitine, is very important in the body, and having a more accessible version around helps with basic bodily function.

As a supplement, this amino acid reacts on the mitochondria in the cells of the human body. Because they are so vitally involved in the production of energy, boosting their production may lend an overall increase to physical and mental health.

Acetyl-L-Carnitine also has great potential as a treatment of many forms of disease. When taken in greater amounts than normally produced in the body, according to the Internet Drug Index, it has shown itself possibly effective against a wide variety of symptoms. It might be beneficial in loss of cognitive function and loss of memory in the elderly (such as those resulting from Alzheimer’s Disease or dimentia), for instance, as well as helping to rehabilitate stroke victims. It may also help with diabetes-induced nerve pain, male infertility and age-related testosterone issues.

Overall, this vital amino acid is very important to the body’s proper function, and when used in larger doses, may even provide a preventative against many symptoms of age and poor health. To read more about Acetyl-L-Carnitine, head to Dr. Weil’s Vitamin Library.

Can Lowering Homocysteine via Vitamin B Improve Cognitive Impairment?

As we age it’s common for cognitive functions to decline due to the increased rate of brain atrophy. According to previous studies, the amino acid homocysteine increases with age and is a marker for cognitive impairment, brain atrophy and dementia. High levels of homocysteine has also been associated with cardiovascular disease.

Because plasma concentrations of homocysteine can be reduced by dietary intake of B vitamins, researchers at the University of Oxford in England set out to test whether vitamin B supplementation would slow the rate of brain atrophy in elderly participants with mild cognitive impairment.

For the randomized, double-blind experiment, researchers David Smith et al. recruited 646 participants over the age of 70 who had mild cognitive impairment. The subjects were split into two groups and were either treated over the course of 24 months with high doses of folic acid (0.8 mg/d), vitamin B12 (0.5 mg/d) and vitamin B6 (20 mg/d), while the control group was treated with placebo.

Adherence to treatment was determined by measuring plasma vitamins and counting returned tablets. MRI scans were done at the start and end of the trial on a subset of the participants to assess the rate of atrophy.

The effect of vitamin B and homocysteine levels on brain atrophy in the elderly

Of the 168 participants that took part in the MRI scan, brain atrophy was found to be 0.76% per year in the vitamin B group and 1.08% per year in the placebo group. The trial supported the notion that homocysteine levels was associated with rate of atrophy.

They found that the rate of atrophy in participants with homocysteine levels greater than 13 µmol/L was reduced by 53% for the vitamin B group. Cognitive test scores were also shown to be higher for participants with lower rate of atrophy. Based on these results, Smith, et al., conclude that increased rate of brain atrophy in elderly individuals with mild cognitive impairment can be slowed by vitamin B intake.

Since Alzheimer’s disease, the most common form of dementia, starts with mild cognitive impairment, the researchers believe additional studies should be conducted to determine whether vitamin Bs will delay development of the disease.


Can threonine-encoding alleles reduce triglyceride levels?

High levels of triglycerides and triglyceride-rich lipoproteins are significant risk factors for cardiovascular diseases. Prevention plans to lower risk include reducing dietary total and saturated fat, but since lifestyle and genetics also play significant roles in developing heart diseases, researchers at the University of Minnesota examined the genetic variations in fatty acid binding proteins and lipid metabolism. Fatty acid binding protein 2 (FABP2) relates absorption and transportation of long chain fatty acids in the intestine. At codon 54 of FABP2, a DNA variation occurs where amino acid alanine is substituted with threonine in the protein. 

This allele of threonine at codon 54 (Thr54) can transport a greater amount of fatty acids than alanine, across the intestine into the plasma. Recent studies have found that the threonine allele have higher fasting plasma triglycerides than alanine variants.

Researchers Steven McColley, Angeliki Georgopoulos, Lindsay Young, Mindy Kurzer, Bruce Redmon and Susan Raatz hypothesize that a high-fat diet would reduce triglyceride-rich lipoproteins (TRL) and the threonine-encoding allele (Thr54) would respond by changing the transportation rate. Lipoproteins are the biochemical compounds containing both proteins and lipids that help transport fat inside and outside cells. One of their main functions is to emulsify fat molecules.

The effect of threonine-encoding alleles on triglyceride-rich lipoproteins

For the crossover study, the researchers used 16 healthy postmenopausal women as participants. The participants would undergo three different 8-week isoenergetic diet treatments: high fat, low fat, and low fat plus n-3 fatty acids.

The high fat treatment consisted of a diet where 40% of energy consumed is fat, the low fat treatment consisted of a diet where 20% of energy consumed is fat, and the low-fat plus n-3 fatty acids consisted of a diet where 20% of energy consumed is fat plus 3% as omega-3 fatty acids.

The treatments were assigned in a random order with a regular diet given 6-12 weeks between conditions. Blood samples were collected throughout the process to evaluate triglyceride levels and DNA analysis.

After assessing the data, researchers McColley et al. found that carriers of the Thr54 allele had significantly lower plasma triglycerides, chylomicron triglycerides, very low density lipoprotein and chylomicron remnant triglycerides after taking part in a high-fat diet. Participants with the Ala54 allele (alanine) did not demonstrate significant changes from baseline with any of the diets.