Friday, January 19, 2007

Patient Excitotoxins

This post (incomplete-to be updated) serves as a reminder for family meal planning, Patient supplement, environmental and diet NO-NOs:

_________BAD__________________________
Dopamine boosters

L-Theanine, Green Tea

Nicotine


_________BAD__________________________
Glutamate boosters

MSG - monosodium L-glutamate, (Seen as ingredient NATURAL FLAVORS in processed foods) Hydrolyzed Protein Sodium Caseinate or Calcium Caseinate, Autolyzed Yeast or Yeast Extract, Gelatin, Hydrolyzed Oat Flour

aspartame (nutrasweet),
candy, glutamic acid, glutamine, aspartate, and cysteine.
Mercury and aluminum trigger glutamate release.

hypoglycemia, or low calorie/starvation conditions stimulate release of glutamate and reduce the ability to remove excess levels of glutamate from the brain. Excess glutamate reduces glutathione levels - antioxidants found in the body which protect neurons from damage. Reduced Glutatione leads to the death of additional neurons.

Food Item
Free Glutamic
(mg/100g)
Free Aspartic
(mg/100g)
Tomato
140.0
35.0
Fresh tomato juice
260.0
60.0
Processed tomato juice
230.0
60.0
Grapefruit, white meat
11.5
87.1
Grapefruit juice
18.6
130.0
Orange juice
21.0
89.0
Nectarine, fruit
9.0
200.0
Peach juice
32.0
212.0
Plum, yellow fruit
7.9
185.0
Prunes (California)
14.4
185.5
Prunes, dry
18.6
518.4
Grape, red Malaga
184.0
12
Grape juice
258.0
16.8
Strawberry
44.4
60.1
Potato
102.0
-
Broccoli
176.0
40.0
Parmesan Cheese
1,200.0
-
Gruyere Cheese
1,050.0
60.0
Mushroom (Psalliota campestris)
180.0
30.0
(1.)

Food Item
Bound Glutamate
(mg/100g)
Parmesan Cheese
9,847
Eggs
1,583
Chicken
3,309
Duck
3,636
Beef
2,846
Pork
2,325
Cod
2,101
Mackerel
2,382
Salmon
2,216
Peas
5,583
Corn
1,765
(1.)

Food Item
Glutamate
(mg/g N)
Aspartate
(mg/g N)
Potato
639
775
Sweet Potato
541
825
Beet
946
1,131
Apple
700
1,300
Apricot
372
1,300
Avocado
769
1,413
Banana
575
656
Fig
600
1,500
Orange
760
880
Pear
540
2,800
Strawberry
920
1,400
(1.)


(1.) http://www.autismanswer.com/articles/yasko/approach_to_reversing.html

--gjh

Thursday, January 18, 2007

PRODH Deficiency

Patient had extra 100mg of L-Theanine today and within 90 minutes had elevated paranoia and panic. I've read that L-Theanine increases dopamine levels. Now when you read this genetic explanation, this entire blog/Patient history seems to parallel the information in the article.

The link below may be the genetic explanation for what may be happening with this Patient. The description of problematic neurotransmitters and the cause of the imbalance of glutamate and dopamine seems to match our findings with foods, supplements, drugs and behaviors of Patient history.

(1.) http://www.innovations-report.com/html/reports/life_sciences/report-52499.html

"Disruption of gene interaction linked to schizophrenia

Results of studies with laboratory model of PRODH deficiency demonstrate the role of COMT in compensating for overactive dopamine signaling, according to St. Jude

Disruption of the normal interaction between the genes PRODH and COMT contributes directly to major symptoms of schizophrenia by upsetting the balance of the brain chemicals glutamate and dopamine, according to a group of investigators that includes a scientist now at St. Jude Children’s Research Hospital.

The investigators developed a model of schizophrenia that provides a way to study and understand how the loss of both PRODH and COMT gene activity contributes to the symptoms of schizophrenia.

The insights they gained into the disease with this model are important because the loss of the PRODH gene causes the imbalance in the levels of both glutamate and dopamine; and this imbalance contributes directly to the symptoms of schizophrenia, according to Stanislav Zakharenko, MD, PhD, an assistant member of the Department of Developmental Neurobiology at St. Jude.

The team investigated the roles of PRODH and COMT because these genes are located in the q11 region of human chromosome 22. Previous work by other scientists showed that a mutation in this region--the 22q11 microdeletion--is one of the major risk factors for developing schizophrenia.

The study’s findings linked changes seen at the molecular level directly to symptoms of schizophrenia seen in humans, said Zakharenko, who is a co-author of a report on this work that appears in the November 15 issue of Nature Neuroscience. The work was completed by Zakharenko and his colleagues at Columbia University (New York), Rockefeller University (New York) and the University of Utrecht (the Netherlands). Zakharenko is continuing his work on the molecular causes of schizophrenia at St. Jude.

The key finding in the current study was that the models of PRODH deficiency had increased COMT activity in the frontal cortex of the brain. "This might reflect a response to the increased dopamine activity caused by PRODH deficiency," Zakharenko said. "And it shows that when PRODH is lost, the additional loss of COMT due to the 22q11 mutation may worsen the symptoms of schizophrenia by allowing dopamine levels to rise." The prefrontal cortex is the part of the brain involved in complex cognitive functioning (e.g., thinking and reasoning).

In the same issue of Nature Neuroscience, another group of investigators reports that their study of adolescents with the 22q11 deletion showed that low activity of COMT is a risk factor for loss of volume of the part of the brain called the prefrontal cortex; and that this same mutation also puts adolescents at risk for developing psychotic symptoms.

Using their model of schizophrenia, Zakharenko and collegues first discovered that the loss of PRODH function directly causes hyperactivity of nerves that use glutamate to signal other nerves in the brain. Next, they found that disruption of PRODH gene activity causes the upregulation of the COMT gene, which encodes for the enzyme that breaks down dopamine. Upregulation is the increase in the rate at which a gene is decoded so the protein it codes for can be manufactured by the cell.

Prior research had already shown that PRODH makes an enzyme that breaks down proline, an amino acid that mimics the action of glutamate on most nerves in the brain. When PRODH activity is low, proline levels are high, creating an excess of excitatory activity leading to overall hypersensitivity of nerve cells to stimulation that might contribute to some schizophrenia symptoms. "Our model of schizophrenia was particularly useful because it lacked only a part of PRODH gene, so the level of proline rose to approximately that seen in individuals with schizophrenia," Zakharenko said.

Although dopamine and glutamate systems were suspected to contribute separately to the development of schizophrenia, researchers had not found a clear connection between them, according to Zakharenko. However, the present study clearly shows this connection. Specifically, when PRODH activity is low, proline levels are high, and there is excess in dopamine activity, he said. The subsequent increase in COMT compensates for the increased release of this dopamine caused by PRODH deficiency. "This finding shows why loss of COMT activity is linked to symptoms of schizophrenia," Zakharenko said.

The study also showed why patients with schizophrenia who also have the 22q11 microdeletion are especially disadvantaged. "COMT upregulation appears to be a response that brings the level of dopamine signaling back to normal," Zakharenko said. "So patients with the 22q11 microdeletion are unable to compensate for their PRODH deficiency by upregulating COMT."

The team further showed that PRODH deficiency increased the release of glutamate at synapses formed by CA3 and CA1 neurons in the part of the brain called the hippocampus. These synapses are routinely used as models of specific types of brain activity responsible for learning and memory. A synapse is the gap between an incoming nerve and its target cell across that gap. Signals pass from one cell on one side of the gap to another cell on the other side. The increased release of excitatory chemicals glutamate and proline due to PRODH deficiency inhibited the ability of the synapse to undergo a change called long-term potentiation (LTP)--a long-lasting strengthening in the connection between two nerve cells. LTP is an important step in forming memories, and disruption of this process interferes with the ability to store information.

Another study using the PRODH-deficiency model showed that the drug D-amphetamine causes exaggerated movement similar to that caused by amphetamine in humans with schizophrenia, according to the researchers. A PRODH deficiency caused lab models to have problems remembering how to respond to an audible tone in a way that was previously learned.

"These observations showed that lack of regulation of glutamate levels due to loss of PRODH function contributed to learning difficulties similar to those found in schizophrenia," Zakharenko said.

Moreover, the researchers showed that PRODH deficiency caused a reduction in the levels of three proteins that, in combination, are associated with dopamine function in the frontal cortex. Because these proteins cooperate with COMT to regulate the overall dopamine activity, the microdeletion 22q11 is likely to contribute to schizophrenia symptoms by eliminating PRODH. "This finding is further evidence that PRODH and COMT interact to control dopamine levels and further explains why the 22q11 microdeletion is associated with schizophrenia," Zakharenko said.

Finally, the investigators used the drug D-amphetamine to stimulate release of dopamine, while blocking COMT activity with a drug called tolcapone. Blocking COMT activity significantly increased the effect of D-amphetamine in PRODH-deficient models, proving that disruption of COMT disrupts the brain’s ability to rein in dopamine activity.

"This genetic model offers a way to make additional predictions about how specific gene defects in addition to PRODH and COMT deletions contribute to the development of schizophrenia in patients with 22q11 microdeletions," said Zakharenko. "Further studies using this model will likely help to answer many more questions about this disease."

Other authors of the study include Joseph A. Gogos, Maria Karayiorgou, Marta Paterlini, Wen-Sung Lai, Jie Qin, Hui Zhang, Jun Mukai, David Sulzer, Paul Pavlidis and Steven A. Siegelbaum (Columbia University and Rockefeller University) and Koen G.C. Westphal and Berend Olivier (University of Utrecht)." (1.)

--gjh

Tuesday, January 16, 2007

Balancing mood with L-Theanine

L-Theanine information

Increasing L-Theanine from 100mg to 200mg today. Asked Patient to take one 100mg with AM meal and one 100mg with PM meal. The effects take approximately 30 minutes.

L-Theanine creates alert relaxation (non-drowsy) and stimulates production of Alpha brain waves, creating a deep state of relaxation similar to a massage or hot bath. Also plays a role in production of GABA.

(Updated 1-18-07) And unfortunately for this Patient it also appears to significantly increase Dopamine levels which elevates the SZ symptoms. Theanine is placed on hold in the supplement line up now.

CHANGED TO AVOID from ON HOLD 2-5-07

--gjh

Monday, January 15, 2007

Patient Update January 15, 2007

Patient reported January 14th that taste buds started working (normal flavors) the day the L-Carnosine was reduced to 250mg.

Additional L-Carnosine info:

Study that showed "Acceleration of metabolism of stress-related substances by L-carnosine."

--gjh

Wednesday, January 10, 2007

Patient Update January 10, 2007

Patient has been on Am and PM 475mg Kavinace daily for second week, first week PM only daily. Dizziness under control. Keeping the routine and the schedule on track is supportive for controlling the dizziness. Exercise on treadmill is daily for 10-15 minutes.

Minimum required exercise is 3 times a week for generating new brain cells. Challenging those cells with new learning and socialization helps integrate them permanently.

During the past week, 1,000 mg L-Carnosine (500mg am / 500mg pm) was taken and Patient had elevated levels of paranoia. L-Carnosine is said to have support affect on serotonin and dopamine. In the past, this Patient had elevated paranoia while on antidepressents. The 1,000mg has been reduced to 250mg once in AM for the next week. The intention was to have 500mg in AM, not 1,000mg which the Patient self administered. If paranoia reduces on the 250mg L-Carnosine, it will remain, otherwise it will be dropped to 100mg or eliminated. (update 1-13-07: Patient reported on 1-12-07 having difficulty exhaling, having tight chest - during the week long period of 1,000mg and this symptom is no longer present on 250mg after one day.)

L-Theanine 100mg has also been taken during the past week and will continue once in AM daily with regular supplements. (UPDATE 2-24-2007 Theanine caused elevated dopamine levels and paranoia so we have discontinued Theanine for this Patient.)

Sorry for the long delay in posting updates. Daily progress checks have been handled by phone over the period without posts. The progress has been consistent, slow, and positive. Mood appears to be improving. Still, there are good days and bad days for paranoia symptoms, but especially elevated over the past week on large 1,000 mg L-Carnosine-now reduced.

--gjh

Sunday, December 24, 2006

Patient Update December 24, 2006

Exciting Information... Finally located a company that may be able to
help us at www.neurorelief.com. They seem to understand the need for
testing and addressing deficiencies and food allergies.

Food Allergy Testing Link http://www.neurorelief.com/index.php?option=com_content&task=view&id=241&Itemid=46

Basic Info http://www.neurorelief.com/index.php?option=com_content&task=section&id=7&Itemid=49

We will definitely be contacting them regarding getting Patient's levels tested and devising a more targeted therapy.

note: important supplements: L-Theanine, Taurine, L-Carnosine

--gjh - very excited!

Patient Update December 23, 2006

SW reported Patient doing well in AM.

Phone call with Patient at 6PM revealed morning dizziness, dizziness after lunch. 2 Neuro Optimizer pills taken at lunch, 1 at dinner, 1 before bed. (Discontinued, see below)

Family members living with Patient aren't interested in tracking progress and have decided to not contribute to the record, despite repeated
requests. Therefor, each update posted is information gathered as a
result of a phone call with Patient. Relying on the information provided by the Patient only is not providing an accurate record on some days.

Neuro Optimizer contains Acetyl L-Carnitine, which has warnings for seizure prone individuals. For this reason, we may need to halt Neuro Optimizer if the dizziness continues. (UPDATE 2-24-2007 Neuro Optimizer has been discontinued for this Patient due to elevated levels of paranoia AND seizure possibly caused by L-Carnatine in the combined supplement. Negative effects were seen within 48 hours or less, tested twice.)

I will likely introduce some testing of the Taurine blends found at neurorelief.com and I have new found hope we will eventually get something in the protocol that stabilizes the Patient.

--gjh

Patient Update December 22, 2006

Patient started Dr. recommended Neuro Optimizer supplement. Took two with evening meal.

Tuesday, December 19, 2006

Patient Update December 19th 2006

Patient sounded alert and normal (7:40PM) and started conversation. Reported dizziness after getting out of bed. Exercised in AM. Turkey and Cheese sandwhich. Pumpkin pie today after lunch. Had spaghetti for dinner

--gjh.

Monday, December 18, 2006

Patient Update December 18th 2006

Spoke to at 9:00 PM, Patient sounded very tired, alertness increased slightly during 30 minute conversation. Family reported psychosis in the early evening which included voices and banging on something. Patient reported having cereal in morning, banana, spaghetti for dinner.

--gjh

Sunday, December 17, 2006

Patient Update December 17th 2006

Patient felt light-headed shortly after consuming decaf coffee with a small amount of sugar.

Patient reported voices in walls, concern about some vehicles in the early evening.

Patient Update December 16th

Patient experienced minor paranoia at 4:45pm. Patient had not eaten anything since noon.

Saturday, December 16, 2006

Patient Update December 15, 2006

Patient experienced minor psychosis late afternoon and revealed that a candy bar had been eaten an hour before. Discussed with Patient the possibility of sugar metabolism problem and requested elimination of unnecessary, excessive sugar.

Neurologist conference called at 4PM. Decision was made to schedule Endocrinologist before starting any new seizure medication. Family has observed Patient has been seizure free, with no complaints of dizziness.

Decision was made to include DMG supplement in protocol. Patient has been visiting family, away from home for past 4 days in effort to reduce stress factors of psychosis.

Endocrinologist will be consulted Monday regarding appointment.

--gjh

Friday, December 15, 2006

Dimethylglycine (DMG) links

http://www.autismwebsite.com/ARI/newsletter/dmg1.htm

(to be udated later)

Hyperthyroidism

This link has information of what to look for in blood tests to see presence of hyperthyroidism:

http://www.emedicine.com/NEURO/topic371.htm

Supplements and Epilepsy

Check this link out when more time is available.
Touches on supplements and nutrients recommended for seizures.
Also states the following:
"About 10 to 20% of epilepsy patients do not respond to drug therapy and may require surgery."

http://www.vitacost.com/science/hn/Concern/Epilepsy.htm#Condition-Symptoms

Thursday, December 14, 2006

Magnesium and the Brain

"Magnesium Calms the Brain
People don't need to become severely deficient in magnesium for the brain to become hyperactive. A new study confirms earlier reports that a marginal magnesium intake overexcites the brain's neurons and results in less coherence--creating cacaphony rather than symphony--according to electroencephalogram (EEG) measurements. During half of the six-month study, 13 women consumed 115 milligrams of magnesium daily--or about 40 percent of the Recommended Dietary Allowance (RDA). During the other half, they got 315 mg daily--a little more than the 280 mg recommended for women. After only six weeks on the marginal intake, EEG readings showed significant differences in brain function.

"Magnesium is the fourth most abundant element in the brain and is essential in regulating central nervous system excitability. Clinical studies of people severely deficient in this essential element have reported epilepsy-type convulsions, dizziness and muscle tremors or twitching as well as many psychological symptoms, including irritability, anxiety, confusion, depression, apathy, loss of appetite and insomnia. While the marginal intake in this study did not produce such severe symptoms, it did hype brain activity.

"This is the first experimental study in which magnesium intakes were tightly controlled and EEG measurements were analyzed by computer so they could be statistically compared. Good sources of magnesium include whole grains, nuts, peanut butter, cottonseed, peanut and soybean flours, green leafy vegetables and spices. It's better to get magnesium from foods rather than supplements because high doses have a laxative effect--the body's way of preventing toxic levels."
http://www.ars.usda.gov/is/np/fnrb/fnrb1095.htm

Sugar Cravings

"When any carbohydrate is eaten, it is broken down into glucose by the body and is known as blood sugar. Insulin is a hormone secreted by the pancreas that takes the glucose from the blood and brings it into the body’s cells where it can be used for energy. However, if there is too much glucose in the blood from eating too many refined carbohydrates, then the body’s cells can stop responding to the insulin. This is called carbohydrate intolerance or insulin resistance.

"The problem does not stop there, because the glucose can not get into the cells for energy and the cells essentially starve. This has profound effects on the body, especially the brain, whose only source of energy is glucose. If the brain is not getting the necessary energy, it signals the body to crave more dietary carbohydrates. This begins a vicious cycle of low energy, sugar cravings, and increased consumption of dietary carbohydrates.

"But poor nutrition is not the only cause of this cycle. Chronic stress is also responsible. When the body is under continued stress, the stress hormone cortisol is continually produced. One of cortisol’s effects is to increase insulin production. This produces the same effect as eating too many carbohydrates.

"Carbohydrate intolerance can directly lead to obesity, diabetes, heart disease or stroke. But the good news is that the vicious cycle of carbohydrate intolerance can be broken through dietary and stress management."
http://carolinanewswire.com/news/News.cgi?database=columns.db&command=viewone&id=258&op=t

Tuesday, December 12, 2006

Patient will see Dr. Margolis on Thursday.

Supplements for Seizure Control

Here's a post I found regarding Diet and Supplements for Seizure control. - (UPDATE) we HAVE changed our nutri-supplement protocol for dealing with seizures, we are still researching and making adjustments but, at this time we feel strongly that Kavinace was instrumental in controlling seizures for Patient.

The Post...

"
THE PROGRAM
Vitamins & Supplements prescribed by a Nutritionist MD
Eliminated Food Allergens (Grains, Dairy, Beans, Seeds, Peanuts, Sweeteners, Alcohols)
Along with the AEDs (Tegretol XR & Depakote ER), the anti-depressant (Prozac), and the anti-psychotic (Respirdal). {YIKES DRUGS!}

MY DIET
Eggs (hard boiled, scrambled, fried)
Fruit (raw)
Vegetables (raw & steemed)
Potatoes (mashed, boiled, baked, fried)
A Variety of Cooked Meats (Beef, Turkey, Chicken, Clams)
Juices (fresh squeezed)
Water (bottled or purified)
Prescribed Supplements & Medications

VITAMINS
B6 (Pyridoxal-5-Phospate)
Zinc
Evening Primrose Oil
Taurine w/p copper
Vitamin D3
Magnesium Gyconate
Vitamin C (ascorbic acid)
Folate
B12 (methylcobalamin)
Calcium Citrate
L-Tyrosine
L-Lysine
5-HTP
Potassium Iodide
Magnesium Citrate
Chromium Citrate
Molybdenum Citrate
Potassium Citrate
Boron Citrate
Vanadium Citrate
Digestive Enzymes
Multi-vitamin w/ lots of vegetables
As well as Chinese herbal & homeopathic remedies"(1.)

(1.) http://brain.hastypastry.net/forums/showthread.php?t=2727

L-Carnosine

One of the previous posts refers to L-Carnosine. This post will be updated with related info on L-Carnosine.

http://www.ethosplan.com/l-carnosine-information.asp

http://www.cherab.org/information/dietaryeffects/carnosine.html

http://cat.inist.fr/?aModele=afficheN&cpsidt=14508390

http://www.1stvitality.co.uk/az/carnosine/carnosine_an_antioxidant.htm

http://www.1stvitality.co.uk/az/carnosine/carnosine.htm

--gjh

AMPAKINE Structures

I'll reaserch what I can find on AMPAKINE Structures as they relate to seizures (not SZ)

--gjh

Patient Update December 11, 2006

Patient experienced "Keppra Anger" and psychosis side effects today. Patient was belligerent and almost violent. Made emergency call to Dr's office and spoke with neurologist. Result - Patient must stop Keppra today, evening dose was not taken. Side effects appeared about 4 days after starting medication (a couple pills were skipped due to poor memory and other emergencies attended by family. :( The dose was 250mg AM 250mg PM. Follow up call scheduled for Friday.

Patient had not had any seizures/dizziness since starting Keppra.

We think that we should see an endocrinologist and confirm we haven't missed something. Patient was said to have been hyperthyroid in the past.

--gjh

Saturday, December 9, 2006

Patient Update December 9, 2006

Patient had no dizzyness after lunch (rare), second day on drug Keppra. Noticed Patient speaking slower, perhaps both are indication that drug is already affecting GABA receptors.

No dizziness reported after evening meal.

--gjh

Aspartame Poisoning (Equal®, Nutrasweet® and Spoonful®) - seizures, memory loss, methanol poisoning

Whoops! YIKES! Did not know that! I suggest you read these links.

http://www.sweetpoison.com/aspartame-information.html

http://www.mercola.com/article/aspartame/hidden_dangers.htm

http://www.holisticmed.com/aspartame/adverse.txt

http://nccn.net/~wwithin/aspartame.htm

http://www.aspartamesafety.com/

http://aspartametruth.com/aspartamedotorg/

Friday, December 8, 2006

Questions to ask doctor

Should we have more tests taken to determine if patient has epilepsy?

What is Patient's measured CSF glutamate level presently? (1.)

What are Patient's compared DHEA to Cortisol Levels? (& melatonin)(2.)

What are Patient's food allergies, Dairy, Gluten, Sugar?

Is Patient Hypoglycemic? (3.)

(1.) http://www.worldwidehealthcenter.net/category.php?prod=659

(2.) http://www.blackwell-synergy.com/links/doi/10.1111/j.0013-9580.2005.59704.x/abs/

(3.) http://www.medhelp.org/forums/neuro/archive/14681.html

Patient Update December 8, 2006

Patient began Keppra in AM Experienced minor dizziness again after eating lunch.

Patient may be experiencing transient ischemic attack (TIA), or "mini-stroke" - dizzy spells have been how Patient described the experience. However, on at least two of these events the Patient fell to the ground and was seen shaking just before falling.

Patient's mother also had these at similar age. Patient also had seizures as a baby during high fever.

Thursday, December 7, 2006

Patient Update December 7, 2006

Neurologist prescribed Keppra for 2 weeks.

Researching L-Glutamine, GABA, Zinc, ALA as mentioned previously.

Patient needs tests for levels: zinc to copper (update later)

--gjh

Sleep-related Epilepsy

"In a review of 100 consecutive cases of nocturnal frontal lobe epilepsy [16], 28% occurred in sleep stages 3 or 4, and only 3% during REM. Clear epileptiform abnormalities on routine EEG occurred in less than half of patients. Forty-two patients showed a clear ictal discharge on polysomnography."(1.)

"O'Regan et al. [19] studied 25 children with an acquired disorder of communication and seizures, but not strictly meeting criteria for LKS. EEGs were uniformly epileptiform, usually (16 of 25 patients) worsening with sleep. Magnetic resonance imaging (MRI) was typically normal, but single photon emission computed tomography (SPECT) was abnormal (22 of 25 patients). Most were considered to have a receptive aphasia. Language deficits have been hypothesized to result from the persistent epileptic discharges, as evidenced by hypometabolism on SPECT [19]."(1.)

(1.)Sleep-related Epilepsy
Carl W. Bazil, MD, PhD
Current Neurology and Neuroscience Reports 2003, 3:167-172
Current Science, Inc. ISSN 1528-4042
Copyright © 2006 by Current Science, Inc.
http://www.current-reports.com/article.cfm?PubID=NR03-2-3-01&Type=Article&KeyWords=

Seizure Recovery Story - a natural approach

"Absorbing as much of the information as she could, she decided that she wanted a change for her son. She found the scientific information referenced in the article, “absolutely amazing”, and she was determined to try a natural approach. On her own she began giving her son supplements that were discussed in the article. She started him on 1000 mg of omega-3, 400 IUs of vitamin E, 500 mg L-Carnosine, 500 mg L-Glutamine, selenium, Vitamin C, zinc, and B-complex."(1.)

"She made changes in his diet, eliminating dairy and wheat and all processed food, which Jonathan frequently ate. “Now that I look back at it he had an awful diet.” She switched to all organic food and began using filtered water. She also started reducing the amount of Jonathan’s medication."(1.)

"Within two weeks Jonathan started showing some amazing changes. Denise noticed improved eye contact and increased “clarity”. He suddenly became more focused and articulate. He had more patience playing games and wasn’t as angry. Jonathan also began singing, something that he never really did before. Denise was happy and surprised, “He’s actually singing! Oh my God he’s singing!”(1.)

(1.) http://www.healthsentinel.com/org_news.php?id=111&title=Reversing%20autism%20and%20seizures%20?%20Jonathan?s%20story&event=org_news_print_list_item

--gjh

Glutamine and GABA

"The action of the heart is under considerable control of the nervous system, and the pathways involved in the neural control of cardiovascular function happen to rely on glutamate and GABA. If the brain has a faulty glutamine / glutamate / GABA metabolism, we can expect the development of cardiovascular dysfunction as well. In addition, glutamine serves as a substrate for the synthesis of a special type of beta-endorphin, glycyl-l-glutamine. This dipeptide appears to be important for the regulation of blood pressure and prevention of cardiorespiratory depression. Glycyl-l-glutamine is also important for the immune response, since it enhances the activity of the natural killer (NK) cells."(1.)

"The synthesis of glutamine protects the body, and the brain in particular, from ammonia toxicity. In fact, the synthesis of glutamine from glutamate is the key pathway for detoxifying ammonia. Excess ammonia is a crucial factor in the development of neurodegenerative diseases, since ammonia interferes with the oxidative metabolism of neurons and thus reduces the production of ATP, our "energy molecule." In addition, ammonia gives rise to very harmful nitrogen-based free radicals."(1.)

"In the brain, glutamine is a substrate for the production of both excitatory and inhibitory neurotransmitters (glutamate and gamma-aminobutyric acid, popularly known as GABA). Glutamine is also an important source of energy for the nervous system. If the brain is not receiving enough glucose, it compensates by increasing glutamine metabolism for energy-hence the popular perception of glutamine as "brain food" and its use as a pick-me-up. Glutamine users often report more energy, less fatigue and better mood."(1.)

"Glutamine also plays a part in maintaining proper blood glucose levels and the right pH range. The body has an exquisite mechanism for maintaining pH homeostasis. If the pH of the blood is too acidic, more glutamine is directed to the kidneys, where a certain type of glutamine results in the release of bicarbonate ions to correct acidosis. If the pH is too alkaline, more glutamine is sent to the liver, where a different kind of metabolism releases hydrogen ions to correct alkalosis."(1.)

"And there is still more. Due to its dependence on sodium transport, glutamine is one of the amino acids that control the volume of water in the cells, and the osmotic pressure (osmoregulation) in various tissues. Glutamine also plays a vital part in the control of blood sugar. It helps prevent hypoglycemia , since it is easily converted to glucose when blood sugar is low. In addition, glutamine regulates the expression of certain genes, including those that govern certain protective enzymes, and helps regulate the biosynthesis of DNA and RNA. Recently it has been discovered that glutamine is important for the cardiovascular system as well."(1.)

"The glutamine cycle in the brain is simple and elegant. Glutamine readily crosses the blood-brain barrier. Neurons take up glutamine and convert it to glutamate or GABA (through the additional step of decarboxylating the glutamate). Some glutamate is used for energy, some for synthesis of glutathione and niacin, some as neurotransmitter. After either glutamate or GABA are released into the synaptic junction, the supportive cells called glia, with their high supply of glutamine synthase, take up the glutamate or GABA and resynthesize glutamine, detoxifying ammonia in the process. The glutamate that is not converted to glutamine is used by the glia as a source of energy, and also to produce energy nutrients alanine and alpha-ketoglutarate, which are then released to the neurons."(1.)

"If excess glutamine accumulates through the action of the glia, the brain donates it to the body. Normally, however, very little glutamine is released by the brain, in contrast to muscle and adipose tissue, which donate a lot. In the brain, it's pretty much an internal affair. What we see is the glutamine glutamate GABA glutamine cycle."(1.)

"If the glia are dysfunctional due to reduced aerobic metabolism, or the release and/or activity of the glial glutamine synthase is inhibited in any way (free-radical damage, toxins, certain drugs), not only glutamate, but GABA as well might accumulate in excess, possibly causing lethargy and cognitive dysfunction. It has been suggested that this too is one of the phenomena we see in the aging brain. On the one hand, glutamate excitotoxicity damages or destroys some neurons, leading to deficiencies in memory and learning; on the other hand, excess of GABA can lead to lethargy. At the same time, excess ammonia, not detoxified through sufficient glutamine synthesis by the glia, leads to further neural damage."(1.)

"An interesting development related to glutamate is the increasing use of ampakines, a new class of drugs for Alzheimer's disease. Apparently an important factor in the pathogenesis of Alzheimer's disease is stroke or a series of undiagnosed mini-strokes. During stroke, the dying neurons release glutamate, which then unfortunately can cause more neuron death. Furthermore, ischemic episodes damage the glutamate receptors, so that later the glutamate can't work as a neurotransmitter. Without glutamate, there is no memory and no learning. Ampakines amplify the glutamate signal through a yet unknown mechanism, possibly by rebuilding glutamate receptors. In healthy people and in animals, ampakines have been shown to enhance cognitive performance, and can thus be classified as "smart drugs."(1.)

Glutamate

"One current hypothesis is that glutamate is also deficient in schizophrenia, though probably many neurotransmitters are out of balance in neurological disorders."(1.)

"At normal physiological levels, glutamate is beneficial and safe. It is an indispensable neurotransmitter that the brain produces according to need. When the central nervous system is aroused, surprisingly enough we do not see higher glucose consumption. Instead, some of the glucose is converted to glutamate. The other source of glutamate is, of course, glutamine. An abundant supply of glutamine makes it easier for the brain to maintain neurotransmitter balance, by increasing the production of glutamate when required for alertness, learning and memory, and the production of GABA when its inhibitory properties are needed. In fact, some people report feeling more centered and calm after they start taking glutamine. Others report a lifting of depression."(1.)

"Glutamate is our chief excitatory neurotransmitter. It is essential for learning and both short-term and long-term memory. Problems arise only if the normal process of glutamate removal and conversion to glutamine malfunctions and an excess of this excitatory neurotransmitter builds up in the synaptic junctions. Excess glutamate causes excessive influx of calcium ions into the neurons, causing excitotoxicity and ultimately even death of the neurons. It also destroys glutathione, a crucial brain-protective antioxidant. Low levels of brain glutathione are associated with neurodegenerative disorders. Glutathione depletion further leads to neuronal death."(1.)

"Under what conditions do we see excess levels of glutamate at the synapses? Not surprisingly, we see evidence of damage associated with excess glutamate in Alzheimer's disease patients, AIDS patients (the AIDS virus inhibits glutamate uptake by the glia), cancer patients (according to one hypothesis, cancer basically starts with brain dysfunction), and in those who have suffered a severe brain injury. Very high fever or artificially induced hyperthermia can also result in excess glutamate release, leading to seizures."(1.)

"GLUTAMINE--As well as cysteine it is recommended to take the other two aminos that make up glutathione as supplemental glycine and glutamine. Both glutamate and glutamine are forms of glutamic acid, the body easily converts the glutamine to glutamic acid. Glutamic acid readily passes the blood brain barrier and is considered a "brain fuel."(2.)

"In the brain, glutamine is a substrate for the production of both excitatory and inhibitory neurotransmitters (glutamate and GABA). Glutamine is also an important source of energy for the nervous system. Glutamic acid and cysteine are necessary for glucose regulation, and can decrease cravings for alcohol and sugar. If the brain is not receiving enough glucose, it compensates by increasing glutamine metabolism for energy. Glutamine users often report more energy, less fatigue and better mood.(sic.)"(2.)

"Glutamine is the most abundant single amino acid in the blood and in the muscle tissue comprising up to 60% of the amino acid pool in skeletal muscle; and is manufactured and released primarily by the skeletal muscle. Because it is important in the rapid growth of cells more is needed during stress or illness. Glutamine is utilized as a source of energy and for nucleotide synthesis by all rapidly dividing cells, such as the cells of the intestinal lining and certain immune cells thus without sufficient glutamine, the intestines atrophy and the immune function breaks down. Glutamine therapy was found to improve intestinal permeability in AIDS patients."(2.)

"Glutamine serves as a nitrogen donor and a carbon donor, and is thus an important muscle-building amino acid. Glutamine's unique structure, containing two nitrogen side chains makes it responsible for 35% of the nitrogen that gets into the muscle cell. It is anticatabolic, meaning it regulates protein synthesis in muscles, sparing muscle tissue and helps replenish muscle glycogen after exercise. It is also involved in glycogen synthesis in the liver and is a building block of many other amino acids. Glutamine can increase growth hormone levels by 43% thereby slowing aging. It also improves lymphocyte proliferation. Further more it reduces insulin resistance and high blood sugar which also counteracts aging."(2.)

"The amino acid glutamine strengthens the cell lining of both the small and large intestines, provides metabolic fuel for gut cells, brain cells, immune macrophages and lymphocytes. Glutamine has been reported to be helpful in reducing "leaky gut" and "brain fog". Glutamine is important as an energy source for our bodies, and is the primary fuel for the upper intestinal tract. It aids the immune system by increasing the integrity of the intestinal lining preventing toxins and pathogens from entering the bloodstream. Glutamine is also a component of folic acid. There is an association between folic acid deficiency and seizure. Disruptions of the intestinal lining may cause folate deficiency, and consequently lead to seizures."(2.)

"The small intestine uses 40% of the glutamine in the body, it being the primary amino acid for the cells that line the small intestine; it nourishes and repairs them. Insufficient glutamine increases the permeability of the gut leading to leaky gut syndrome. This lets in toxins, pathogens and partially digested molecules into the blood increasing the load on the liver. The large molecules entering the bloodstream stimulate antibody production, and then the liver subsequently has to cope with the waste products of antibodies. Which again increases the demands made on glutathione and other antioxidants."(2.)

"GABA--GABA is made from the amino acid Glutamic acid (Glutamine or Glucose). It reduces anxiety, elevates the pain threshold reduces the blood pressure and heart rate and reduces compulsive behavior. GABA promotes fat loss and stimulates the production of Human Growth Hormone (HGH). GABA can be taken as a supplement (L-Glutamine), produces a calming effect on people who struggle with temporal lobe symptoms like temper, irritability, and anxiety."(2.)

"GLYCINE--Glycine and glucose are the two most common amino acids in the body. Glycine is the simplest amino acid and is the only protein forming amino acid without a center of chirality, that is it is nonpolar. Because glycine has such a small side chain it can fit into many places where no other amino acid can. Hence it is the internal amino acid of a collagen helix, thus collagen is about one-third glycine. Most proteins however only contain a small quantity of glycine."(2.)

"Like GABA, Glycine activates Cl- ion conductance resulting in a hyperpolarization of the neuronal membrane and an antagonism of other depolarizing stimuli. This membrane hyperpolarization makes glycine the major inhibitory neurotransmitter in the brainstem and spinal cord, where it participates in a variety of motor and sensory functions. However in the forebrain it functions in an excitatory way by promoting the actions of the major excitatory neurotransmitter glutamate at the NMDA receptors. Other amino acids, including alanine and taurine, also activate glycine receptors, but with lower potency."(2.)

"Glycine may increase acetylcholine neurotransmission in the hippocampus, the memory center of the brain. This factor could be involved in having "ones life pass before ones eyes" during near death experiences. Increases blood sugar and Growth Hormone. Vitamin B6, magnesium and dimethylglycine are antiseizure and have increased speech in autistic children. Found in many foods, glycine is also synthesized in the human body where, among other functions it helps improve glycogen storage. It is utilized in the synthesis of hemoglobin, collagen and glutathione, and facilitates the amelioration of high blood fat and uric acid levels."(2.)

"It is essential for learning and both short-term and long-term memory. Glutamate, as a neurotransmitter, exists in the extracellular fluid only in very, very small concentrations--no more than 8 to 12 FM (micromoles/liter). When the concentration of this transmitter rises above this level, the neurons begin to fire abnormally. At higher concentrations, the cells undergo a specialized process of delayed cell death known as excitotoxicity; that is, they are excited to death. Some individuals may be especially sensitive and develop severe symptoms and even die suddenly from cardiac irritability, but in most instances the effects are subtle and develop over a long period of time. But, it is free glutamate that is the culprit. Bound glutamate, found naturally in foods, is less dangerous because it is slowly broken down and absorbed by the gut so that the tissues can utilize it, especially muscles, before toxic concentrations can build up. Infusions of MSG are used in mainstream clinical practice to reduce high ammonia levels in the blood (hyperammonemia) by stimulating the conversion of glutamate to glutamine. Both glutamate (as MSG) and glutamine are used by conventional medicine for treating several very serious conditions. Glutamine supplementation has shown better neural energy production and better neuro-transmitter balance are typical results, with improved mental performance and a sense of well-being. The glutamine cycle in the brain is simple and elegant. Glutamine readily crosses the blood-brain barrier. Neurons take up glutamine and convert it to glutamate or GABA (through the step of decarboxylating the glutamate). Some glutamate is used for energy, some for synthesis of glutathione and niacin, some as neurotransmitter."(3.)

"After either glutamate or GABA are released into the synaptic junction, the supportive cells called glia (more specifically, astroglia or astrocytes)--the most abundant type of cell in the central nervous system--with their high supply of glutamine synthase, take up the glutamate or GABA and resynthesize glutamine, detoxifying ammonia in the process. The glutamate that's not converted is used by the glia as a source of energy, and also to produce energy nutrients alanine and alpha-ketoglutarate, which are then released to the neurons. If excess glutamine accumulates through the action of the glia, the brain donates it to the body. Normally, however, the brain, releases very little glutamine, in contrast to muscle and adipose tissue, which donate a lot. During a stroke, ischemic episodes damage the glutamate receptors, so that later the glutamate can't work as a neurotransmitter. Without glutamate, there is no memory and no learning. Glutamate is also deficient in schizophrenia. It's an indispensable neurotransmitter produced in the brain according to need. When the central nervous system is aroused, we don't see higher glucose consumption. Instead, some of the glucose is converted to glutamate. An abundant supply of glutamine makes it easier for the brain to maintain neurotransmitter balance, by increasing the production of glutamate when required for alertness, learning and memory, and the production of GABA when its inhibitory properties are needed."(3.)

"What is the significance of the empty stomach?
Normally the blood-brain barrier protects the brain from excessive
amounts of any single amino acid. However that protection is reduced
dramatically when the amino acid is taken on an empty stomach in
isolation from other amino acids. In fact it is because of the natural
protection of the blood-brain barrier that it is considered necessary
to take glutamine on an empty stomach for purposes of stimulating the
release of growth hormone. If the glutamine is taken as part of
complete proteins, with a meal or on a full stomach, then it will be
forced to compete with other nutrients and amino acids for entrance to
the brain. But that competition between amino acids for entrance to
the brain is the normal state of nature; it ensures that no single
amino acid will flood the brain in isolation. Glutamine works for
stimulating GH release only if we intentionally defeat mother nature's
built-in protections, which in itself is an indication that some risks
are involved."(4.)

"Another concern is that the brain is more vulnerable to excitotoxicity
when the body is fasting. The brain derives most of its energy from
glucose (sugar), and it needs that energy to defend against any sudden
increase in glutamate. The worst time to take large amounts of
glutamine is in the morning before breakfast on an empty stomach, when
the body has been fasting overnight and blood sugar is low."(4.)

(1.) http://www.lef.org/magazine/mag99/sep99-report3.html

(2.) http://biologyofkundalini.com/article.php?story=SupplementList

(3.) Glutamine http://www.tuberose.com/Inflammation_Damage_&_Repair.html

(4.) http://groups.google.com/group/misc.fitness.weights/browse_thread/thread/c86779291cfa2781/a99488e2b334728c%23a99488e2b334728c

--gjh