LymeNet Home LymeNet Home Page LymeNet Flash Discussion LymeNet Support Group Database LymeNet Literature Library LymeNet Legal Resources LymeNet Medical & Scientific Abstract Database LymeNet Newsletter Home Page LymeNet Recommended Books LymeNet Tick Pictures Search The LymeNet Site LymeNet Links LymeNet Frequently Asked Questions About The Lyme Disease Network LymeNet Menu

LymeNet on Facebook

LymeNet on Twitter




The Lyme Disease Network receives a commission from Amazon.com for each purchase originating from this site.

When purchasing from Amazon.com, please
click here first.

Thank you.

LymeNet Flash Discussion
Dedicated to the Bachmann Family

LymeNet needs your help:
LymeNet 2020 fund drive


The Lyme Disease Network is a non-profit organization funded by individual donations.

LymeNet Flash Post New Topic  New Poll  Post A Reply
my profile | directory login | register | search | faq | forum home

  next oldest topic   next newest topic
» LymeNet Flash » Questions and Discussion » Medical Questions » Galactose - Amonia - Nitric Oxide, etc.

 - UBBFriend: Email this page to someone!    
Author Topic: Galactose - Amonia - Nitric Oxide, etc.
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
During chronic disease:

While the body tries to deal with the primary front, the energy metabolism, to keep us alive, dealing with the second front, which is the supply of material to keep up with the structural health of the cell and organs, is neglected. We can visualize it as follows:

During a cold winter you will need all the wood for heating in order not to freeze to death. But then, the wood needed for the repair of defective windows, doors, and roof is no longer available. If this condition lasts for any length of time and repeats itself every year, the house and living quarters become defective and possible irreparable. We may not freeze a lot and just a little, but the house is falling apart. A fatal event.

It is a similar happening with the glucose, which we might still have available to some degree for the basic energy to keep us upright, but it is no longer available for repair for upkeep and repair of our brain cells. That is when nature shows us a way out. But it is up to us to help the organism which cannot handle this on its own. It is up to us to take that course.

Nature offers us the sister-sugar to glucose, the galactose. The difference between the two is like two noses - one a stubby nose, the other a straight nose (we have or have not). But it is of importance for the metabolism and the cell structure.

The main function of galactose is the building and support of the cell unit (doors, windows, walls of the home), as opposed to glucose (fire and energy supply). It is possible to turn glucose into galactose, but only if the quantity is sufficient and not used up for the supply of energy (fire).

The door which nature holds open for us is easily entered. The needy patient is supplied with galactose and is then able to keep up the structure and building of his endangered or already damaged cells and repaired. The first advantage is that the cell needs little substance, i.e. little galactose, for the structural upkeep and repair, and it can be looked upon as a micro-nutrient. The second advantage is that any not needed galactose is turned back into glucose with great speed and without any loss this much larger ``leftover'' can be used to create more of the necessary energy.

Or, comparing it to the house and wood: I need little wood during the year, to keep windows, doors and ceiling or walls intact, but a lot to keep the home warm. For galactose that means: By supplying myself with little galactose I can keep endangered and damaged cells of the brain intact and even repaired. The left over galactose is quantitatively changed back to glucose for energy supply. Only the order is reversed. The second turns to be the first, thereby aiding the total organism.

Surprisingly, the changing of sequence has another advantage: part of the galactose changes into alpha-ketoglutarate and oxalacetat which in turn forms the connection to convert to amino acids (especially glutaminic acid/derivate and aspartate). For this ammonia is necessary which is part of the metabolism change, then turning into ``toxin'' for the cell if it is too highly concentrated, as it happens under metabolic stress. By giving galactose , a gentle way of detoxification is started when it changes into amino acids. These amino acids thus formed can serve the building of proteins. So not only is the giving of galactose aiding detoxification, but also has a protein-saving effect.


(I received this from the professor at a University involved for years in this research and medical doctors contributing some of their case histories. I have more wonderful case histories, in German, all of them involving some or more neuro symptoms, pain problems, problems many Lymies have, all of them benefiting from galactose permanently. I have several more multi-page papers written by these doctors/researchers discussing galactose use in general.. But I will not post until I find that you guys can see the forest for the trees!)

Here is one more, translated by one of the Europeans involved:

In a healthy state, a human being produces 2 to 10 g of a-D+galactose. It is a simple sugar structure, a basic element of life. Once advantage of galactose is its insuline-independent transport into the cells which leads to a protection of the pancreas in an insuline saving way. Galactorse also acts detoxifying by decomposing toxic ammonia, respectively of ammonium ions. It also acts purifying by synthesizing important amino acids for the organisms during the decomposition.

But the biggest accomplishment is its performance of recreation and its repair function within the cell metabolism. This means that galactose is important for the stability of the cell membransses and their contacting other cells and also the outer world, which becomes evident in concentration ability, alertness, long term and short term memory and social competence.


Why Galactose, what for?

Chronic stress finds its analogy in the life of cells. The fuel galactose is consumed excessively during stress, so that the nutrient most important for performance burns up. In this situation, sugar-protein combinations from the cell membrances are mobilized and burned up. That makes the cell membrane porous, weakens it and damages its stability. The receptors and contact spots to the outer world are degenerating more and more.

At that point essential and important messenger substances cannot get into the cells anymore. Glucose from the blood cannot get into the inner cell and the blood sugar level rises. By burning its own fuel and emergency fuel, not only the cell membranes are being damaged, but also toxins, such as ammonia, are created, which leads to further degeneration. Consequences of this stress metabolism can (depending on the load) lead to diseases like dementia, Alzheimers, Diabetes, Parkinsons, depressions and pain conditions.

Galactose serves as a natural building material for life, during disease as well as preventive during ongoing stress and before one of the above mentioned diseases can even set in.

Take care.

[ 06-02-2009, 04:13 AM: Message edited by: GiGi ]

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
lymie tony z
Frequent Contributor (1K+ posts)
Member # 5130

Icon 1 posted      Profile for lymie tony z     Send New Private Message       Edit/Delete Post   Reply With Quote 
Should'nt there be MORE study patients?

I know I read somewhere in your other posts that whoever thought this was not necessary.

However...Reading your other post also has IMHO an inadequate amount of case or individual studies on this stuff.

I think I'll wait and see.

zman

--------------------
I am not a doctor...opinions expressed are from personal experiences only and should never be viewed as coming from a healthcare provider. zman

Posts: 2527 | From safety harbor florida(origin Cleve., Ohio | Registered: Jan 2004  |  IP: Logged | Report this post to a Moderator
hardynaka
Frequent Contributor (1K+ posts)
Member # 8099

Icon 1 posted      Profile for hardynaka     Send New Private Message       Edit/Delete Post   Reply With Quote 
http://www.innvista.com/HEALTH/nutrition/essensug/galact.htm

Dietary Sources
(mg of Galactose per 100 grams of produce)

Dairy products
Fruit: Apples (800), Apricot (600), Banana (200), Blackberries (1,000), Cherries (400), Cranberries (1,200), Currants (800), Dates (800), Grapes (300), Kiwi Fruit (700), Mango (1,700), Orange (1,600), Nectarine (1,100), Peach (1,300), Pear (600), Pineapple (700), Plums (2,600), Prunes (1,600), Raspberries (900), Rhubarb (1,500), Strawberries (500), Passionfruit (300)
Herbs: Echinacea, Boswellia, Fenugreek, Chestnuts (2,700)
Vegetables: Broccoli (2,700), Brussels Sprouts (4,100), Avocado, Cabbage (4,400), Carrot (3,400), Cauliflower (3,200), Celery (2,700), Cucumber (1,600), Potato (1,800), Eggplant (3,500), Tomatoes (1,600), Leeks (6,600), Asparagus (2,800), Lettuce (2,000), Green Beans (4,100), Mushrooms (not buttons) (1,100), Beetroot (1,100), Onions (4,500), Parsnip (2,200), Green Peas (800), Pumpkin (2,400), Spinach (1,400)

Posts: 1086 | From Switzerland | Registered: Oct 2005  |  IP: Logged | Report this post to a Moderator
hardynaka
Frequent Contributor (1K+ posts)
Member # 8099

Icon 1 posted      Profile for hardynaka     Send New Private Message       Edit/Delete Post   Reply With Quote 
Functions
In animal studies, Galactose inhibits tumor growth and its spread (metastasis), especially to the liver. In addition, Galactose levels were found to be decreased in the intestinal mucins of colon cancer patients, suggesting that the addition of Galactose to the diet could help prevent or reverse the disease.

Galactose does not stimulate insulin secretion in humans. Therefore, serum Galactose levels are not affected in diabetics, which is good news.

Although Galactose can easily be converted into Glucose when needed for energy and can be formed from Glucose, dietary sources of Galactose are still important to maintain an epimerase enzyme-mediated equilibrium.

For instance, when Galactose was supplemented in the diet of patients with metabolic diseases being treated with low protein and low lactose diets, these patients showed a significant increase in Galactose concentrations in both the red and the white blood cells.

Galactose appears to help correct many disorders, including enhancing wound healing, decreasing inflammation, and stimulating calcium absorption. It also appears to help lower the risk of developing cataracts.

Galactose levels are usually lower in people with adult and juvenile arthritis and in those with Lupus, suggesting that this sugar is vital to preventing or correcting these conditions.

Galactose is widely distributed throughout the body, including the brain. Studies also indicate that the saccaride triggers long-term memory formation.

Galactose is another essential sugar concentrated in the testes, implying that these saccharides are vital in reproduction since it appears to help in the formation of sperm.

Found in both the proximal and distal tubules of the kidney, Galactose is obviously important for proper kidney function.

Galatose is also present in intestinal mucins which inhibit cholesterol absorption.

Since Galactose is found in immunoglobulins and macrophages, it appears to play a primary role in the immune system, especially that of rheumatoid arthritis.

In such patients, blood levels of the sugar were markedly reduced and proved that the less Galactose there was available, the more severe was the disease.

During remission, the reduction in the amount of Galactose was reversed. To make matters worse, a lack of Galactose seemed to set off a chain reaction involving other essential sugars.

A Galactose deficiency on the IgG of RA patients, also reduced the terminals for Glucosamine which, in turn, bind to Mannose proteins. This resulted in the activation of blood complement and the start of the inflammatory process.

Galactose levels are also altered in other diseases, especially in the severely ill. Levels of this saccharide are markedly reduced in upper airway epithelial cells.

This is important because such patients are more susceptible to opportunistic pathogens, especially those that target respiratory organs producing such diseases as pneumonia or bronchitis.

Dietary Galactose is also important in maintaining normal bacterial flora in the intestines. Prolonged use of Galactose has proven to increase the number of Bifidobacteria while providing the proper environment for other beneficial bacteria in the human gut.

Providing this type of environment not only strengthens digestive abilities, but also the immune system as well.

Scientists are now turning their attention to a link seen between Galactose deficiency and MS (multiple sclerosis). This disorder has already been linked to an inablility to absorb another essential sugar, Xylose, but there also appears to be abnormal Galactose molecules present as well.

In addition, the myelin sheath that covers nerves is attacked by overactive immune cells. The myelin sheath contains Galactose, as well as other essential sugars.

Therefore, supplementation of all eight essential sugars could help rebuild the system to where absorption is once again possible and could reverse the condition.

Safety
There does not appear to be any side effects from using a supplemental Galactose, unless one is Galactose-intolerant, but this is an extremely rare condition.

Based on research, some recommend as much as 50 grams in a healthy 150-pound adult as a safe dose. However, much less is more advisable, and since most of it is eliminated within 8 hours, dosing should occur at least twice a day to maintain optimal Galactose blood levels.

For the complete article:
http://www.innvista.com/HEALTH/nutrition/essensug/galact.htm

Posts: 1086 | From Switzerland | Registered: Oct 2005  |  IP: Logged | Report this post to a Moderator
hardynaka
Frequent Contributor (1K+ posts)
Member # 8099

Icon 1 posted      Profile for hardynaka     Send New Private Message       Edit/Delete Post   Reply With Quote 
Thanks Gigi!

Selma

Posts: 1086 | From Switzerland | Registered: Oct 2005  |  IP: Logged | Report this post to a Moderator
Marnie
Frequent Contributor (5K+ posts)
Member # 773

Icon 1 posted      Profile for Marnie     Send New Private Message       Edit/Delete Post   Reply With Quote 
I understand that our brain cells and our WBCs need glycogen.

I understand that Bb is PFK (phosphofructokinase) dependent. This enzyme, is "rate limiting" for glycoysis...using sugar, not oxygen, to make ATP. This enzyme is ACTIVATED by insulin. Several things can INactivate it.

But the following link gives me PAUSE...to evaluate whether or not galactose MIGHT BE potentially harmful:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10509875&dopt=Abstract

Posts: 9401 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
micul
LymeNet Contributor
Member # 6314

Icon 1 posted      Profile for micul     Send New Private Message       Edit/Delete Post   Reply With Quote 
Analytical Chemistry Laboratory, Institut National Agronomique, Paris, France.

"Lactose consumption has been associated with a high incidence of cataract in northern Indian and southern Italian populations. Galactose absorbed after hydrolysis of lactose from milk in individuals with normal lactase activity is considered responsible. However, lactase-deficient subjects who often avoid drinking milk are able to digest lactose and absorb free galactose in fermented milk and yogurt. This study was conducted to evaluate the relationships between milk and yogurt consumption, galactose metabolism and cataract risk. Milk ingestion was dose-related with cataract risk in lactose digesters (particularly in diabetics) but not in lactose maldigesters. Conversely, yogurt intake had a protective dose-effect on cataract formation for the whole population. Maximal galactose concentrations after an oral galactose test increased exponentially with age. Red blood cell galactokinase activity was significantly lower in elderly subjects than in young individuals , and galactose-1-phosphate uridyl-transferase activity was significantly lower in institutionalized subjects and in home-living elderly with cataract than in healthy elderly subjects . We conclude that the cataractogenic action of milk lactose is dependent on the disturbance of galactose metabolism in elderly subjects and that yogurt is not cataractogenic, although the mechanism of the protective effect of yogurt remains unknown."

PMID: 8336207 [PubMed - indexed for MEDLINE]

--------------------
You're only a failure when you stop trying.

Posts: 945 | From U.S | Registered: Oct 2004  |  IP: Logged | Report this post to a Moderator
SForsgren
Frequent Contributor (1K+ posts)
Member # 7686

Icon 1 posted      Profile for SForsgren         Edit/Delete Post   Reply With Quote 
zman,

Sure - wait and see....that's your option. The information is being provided for consideration. No one is pushing the product on anyone. The purpose of this board is to share information and GiGi in my opinion provides the most useful information I find here.

I am not sure what the value is in always being so negative. It certainly does not promote healing.

--------------------
Be well,
Scott

Posts: 4617 | From San Jose, CA | Registered: Jul 2005  |  IP: Logged | Report this post to a Moderator
lymie tony z
Frequent Contributor (1K+ posts)
Member # 5130

Icon 1 posted      Profile for lymie tony z     Send New Private Message       Edit/Delete Post   Reply With Quote 
SForsgren...

You are of course entitled to your opinion but I must say...
I don't have a negative bone in my body...

I just thought 4FOUR people as was stated in one study was a bit sparse to come to any conclusion good or bad...

And yes I agree GIGI has brought a whole host of information to this forum....

SOME useful and some not so useful...IMVHO>...

And you only bring opinions of opinions of opinions....
Not that there's anything wrong with that!

zman

--------------------
I am not a doctor...opinions expressed are from personal experiences only and should never be viewed as coming from a healthcare provider. zman

Posts: 2527 | From safety harbor florida(origin Cleve., Ohio | Registered: Jan 2004  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
If you do not read everything and all the details I have given you about Galactose, please quit your negative comments.

I have specifically pointed out that only 99.9% pure Galactose works. It is only available at one pharmacy in Germany. It is produced by one manufacturer in Italy.

This research is quite old, but this discovery is very recent. It has been put into practice in Germany about two years ago. I have a number of similar case histories, but they are all in German. And for people like you who do aboslutely nothing but try to pound everything I post into the ground, I am not making the effort trying to translate anything.

The info I have given you did not fly into my window on the wings of a bird. I worked my butt off communicating with the doctor/researchers involved (google w. reutter galactose parkinsonism alzheimers) and they were kind enough to take the time and respond to me. They have nothing to sell but goodwill and neither do I.

You will not find this info any place else, because it is new. Info about galactose, yes, but this info about the aboslutely pure form of it - no. It is new - so don't try to reinvent the old worndown wheel.

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
kelmo
Frequent Contributor (1K+ posts)
Member # 8797

Icon 1 posted      Profile for kelmo     Send New Private Message       Edit/Delete Post   Reply With Quote 
Just out of curiosity, could you explain the difference between galactose and the Mannatec Glyconutrients.

I only ask because someone gave me a wad of information and CD's to listen to years ago and I never did, thinking that it's just another miracle cure that an MLM was pitching.

Evidently, the guy who invented glyconutients won a Nobel prize.

But, according to what you wrote, we can get galactose from ordinary food. Gee, isn't THAT novel?

I need to reread everything you posted and read the articles. It's a lot to comprehend.

Thanks
Kelly

Posts: 2903 | From AZ | Registered: Feb 2006  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
The authors are talking a lot dementia, etc. But as you can tell from my previous posts, this approach (99.9% pure galactose) not a combination of anyother form of sugars, etc. Simply and plain -- 99.9% pure galactose --- prepared under high steam pressure (without metals as is usual for some methods o chemical hydrolization).
Range of Application used successfully: Parkinsons, Dementia, Alzheimers, Diabetes, Myoneulragia, Chronic Pain, Posttraumatic Stress disorder, General Stress Metabolism, State of Apoplexy, Depression. There are a few more that I won't repeat.

Do you think some of these positive case history outcomes had Lyme? The other day everybody chimed in on a thread confirming "Lyme causes Alzheimers". I don't agree with that because I firmly believe that preexisting conditions, yes, will eventually also make the brain the home for nasty microbes, such as Lyme. But it doesn't start all of a sudden with a spirochete descending on a healthy brain tissue or for that matter being able to find a foothold in a healthy body. Never.

Pasteur's Theory (which was also based on earlier German Work): said that when a certain microbe comes into you, the illness is specific to the microbe coming in. If the microbe is beta streptococcus A, you get tonisilitis. If it is Klebsiella pneumoniae, you get pneumonia.

On his deathbead, Pasteur said. "Le microbe est nil, le milieu est tout." (In English: the microbe is nothing. The milieu is all.) he realized he had been pushing the microbe theory because his name was attached to it. It was an ego thing. He was a charismatic speaker, and the world was under his spell, At the moment of death, he realized it was an ego trip, and that Bershan and the German researchers behind his work were right.

There are multiple reasons for this to be able to happen.


Cellular Stress and the Molecular Response

Werner Reutter, Kurt Mosetter
Institut fuer Biochemie und Molekularbiologie Campus Benjamin-Franklin
Charite-Universitaetsmedizin Berlin

Berlin-Dahlem

Cellular stress occurs at all ages and is a constant companion throughout life. Its origins, its actions on cells and responses of cells are many and various and they also depend on the age of the individual. Hunger is a continual source of cellular stress in infants. When the blood sugar concentration falls below a certain level, the central nervous system (CNS) intervenes, receptors are activated and finally the child cries. This is a natural and easily combated stress factor.

On the other hand, there are many unnatural stress factors. Thus, foreign substances or xenobiotics, heavy metals and in particular reactive oxygen radicals and UV-radiation can lead to premature aging, chronic inflammation and cancer.

Mitochondria play a crucial role in the occurrence of oxidative stress. Cell respiration, driven by oxygen and located in the mitychondria, provides the cell with energy in the form of ATP. Under conditions of oxidative stress, some of the oxygen can react with electrons produced during the activity of the respiratory chain proteins. The resulting oxygen radicals leave the mitochondria and can oxidize any cell proteins they encounter, leading to a reduction in, or loss of protein function. Depending on the proteins involved, the affected cells are damaged and the entire organ therefore suffers.

In Alzheimer's disease, oxidized forms of various macromolecules, e.g. lipids, nucleic acids and proteins, have been detected. A further biochemical expression of the cellular stress of this disease consists of the modification of proteins by the non-enzymatic attachment of sugars (in particular the monosaccharide, N-acetylglucosamine), observed in senile plaques and neural cell bodies.

Only a few years ago, a new form of stress was recognized, known as pstprandial oxidative stress. This occurs after ingestion of food rich in fat or carbohydrate. Macronutrients like that or starch can be oxidized following their uptake, or they may remain in a pro-oxidative form. Hyperlipidaemia and elevated blood sugar are accompanied by an increased oxidation of lipoproteins and a decrease of the antioxidative protection mechanism of the cell. LDL (low density lipoprotein) is the preferential target for oxidation. Consumption of lipid-rich food containing a high proportion of oxidized or easily oxidizable lipids leads to an increase in the concentration of lipid hydroperoxides, which can initiate the oxidation of LDL. Lipid hydroperoxides are significantly involved in the formation of artherogenic plaques and therefore in the occurrence of cardiovascular illnesses, as well as complications arising from diabetes.

If the body's own antioxidative stress mechanisms are no longer adequate, both of these last two forms of stress can be counteracted by the application of effective antioxidants like selenium, vitamin C and E, and flavonoids.

A further chronic source of stress for the cell lies in aging, which can also be considered as a physiological process. Fully operational energy metabolism and intact metabolism for the biosynthesis of cell material are basic prerequisites for the maintenance of cell structure and function. The substrate for both of these areas of metabolism is glucose.

Most of it is needed for energy metabolism, i.e. for the production of biological energy in the form of adenosine triphosphate (ATP). Often in old age and especially in Alzheimer's disease, the blood circulation of the brain is decreased, resulting in a decrese in the essential supply of glucose to the CNS.

A pathological insulin deficiency in certain brain areas also appears to contribute to the degeneration of nerve cells, thereby aiding the genesis of Alzheimer's disease. Insulin and its related proteins, growth factors IGF-1 and ll (Insulin-like Growth Factor l and ll), together with their receptors, are produced in various brain regions.

In addition, inadequate insulin production in the brain leads to a degernation of nerve cells characteristic of the early stage of Alzheimer's disese. Studies on brain tissue slices from deceased Alzheimer patients have shown that the production of insulin and IGF-l is significantly decreased in the hippocampus, which is responsible for memory storage. The same was found for the frontal cortex and the hypothalamus.

In these key brain regions, which are always affected in Alzheimer's disease, it was found that nerve cells had died as a result of insulin deficiency. It has long been known that diabetics carry an increased risk of Alzheimer's disease and these results represent the first evidence of a direct link between diabetes and this neurodegenerative illness.

In order tio differentiate clearly between Alzheimer's disease and diabetes mellitus, scientists refer to ``type 3 diabetes'', which affects only the CNS and has no consequences for the blood sugar level.

Poor blood circulation in the brain, together with insulin deficiency leading to a reduced uptake of glucose by brain cells provides a rather comprehensive clinical picture for the genesis of Alzheimer's disease. The brain cells receive an inadequate supply of their most important energy substrate, glucose. All the glucose is then channeled into energy metabolism, because, for obvious metabolic reasons, energy (i.e. ATP) production is the
most urgent priority of every cell.

Since glucose and its derivatives are also substrates for biosynthesis, the maintenance of cell structure is affected; in particular, biosynthesis of components of the plasma membrane is decreased. Membrane components affected in this way are receptors (e.g. for hormones or particular mediators of the CNS), ion channels, enzymes and other substances needed for structural maintenance. The decreased glucose uptake can be compensated by the application of galactose, because galactose, unlike glucose, enters cells independently of insulin. The galactose is converted quantitatively into glucose, thereby providing sufficient substrate for both biosynthesis (maintenance of cell structure) and for energy metabolism. Thus the harmful decrease in the supply of glucose to the CNS can be bypassed by the administration of galactose.

After administration of galactose, patients in an advanced stage of alzheimer's desease showed no improvement in memory, but they displayed a decided improvement in their subjective awareness and social behaviour. In cases of early Alzheimer's disease and mild cognitive impairment (MCI), even an improvement of memory was observed.

Take care.

[ 22. January 2007, 03:18 AM: Message edited by: GiGi ]

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
lymie tony z
Frequent Contributor (1K+ posts)
Member # 5130

Icon 1 posted      Profile for lymie tony z     Send New Private Message       Edit/Delete Post   Reply With Quote 
GIGI,
WHile I might admit to not reading all of your posts...it's mainly cuz you're not considerate enough to space them out enough for lyme brain

folks that have a hard time with big blocks of words.

Second...a lot of what you bring here is...you gotta admit...
somewhere from left of the north star...

Your terminology sounds a lot like it was made up to me by doctor who do the voo doo...
I read far enough usually....

There should be adequate translation of this recent stuff from germany...old or new...

Try researching that angle before bringing something to the table...

Get it in AMerican!

THanks ever so......zman

--------------------
I am not a doctor...opinions expressed are from personal experiences only and should never be viewed as coming from a healthcare provider. zman

Posts: 2527 | From safety harbor florida(origin Cleve., Ohio | Registered: Jan 2004  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
Mr. Z, you might consider doing your own research.

What I have posted on this subject is sent to me by the researchers and doctors who use it in practice. It is their text and their official publication. If you can't digest it as I post it, how about "copy and paste" and bringing the text into line with your capabilities. You don't seem to suffer from brain fog or other problems when it comes to dishing out ugly posts! I have enough work just trying to gather all the info and posting it. I spend hours on it taking it from pdf's to bringing it to Lymenet.

Whoever is truly interested, will find a way. Whatever I am not interested in, I do not bother to read either. This is the last post of yours that I will respond to specifically.

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
More on Galactose - received directly from the Reutter/Mosetter team of researchers who have given me all the other information I have posted.
I may have posted some of it earlier.

Evaluation of D(+)galactose as a dietary supplement:

D(+)Galactose

Only small quantities of galactose are found as the free monosaccharide in
animals and plants. It is a hexose, a group that includes glucose, as well
as mannose, glucosamine and galactosamine (the latter two occurring mostly
as their N-acetyl derivatives, and rarely in sulfated form). D-Galactose is
structurally related to the monosaccharide, L-fucose, a methyl pentose with
the same configuration as L-galactose.

Traces of free galactose are present in milk, sperm and urine, but levels of
galactose comparable to those of glucose are never found in any animal or
plant. In the absence of an exogenous supply, galactose is not normally
detectable in blood. It appears in blood and in significant quantities in
urine only during certain pathological processes. However, in animals and
plants, galactose occurs widely in glycosidic linkage with other
monosaccharides.

In particular, it is an essential component of glycolipids
(e.g. gangliosides) and glycoproteins, playing an important structural and
functional role in these complex structures.


The origin of galactose in animals


In infants, galactose is derived from lactose, which is split into equimolar
quantities of glucose and galactose by lactase, a disaccharidase secreted by
mucosal cells. In adults, the consumption of milk products is drastically
reduced, compared with that of infants, and galactose is then derived
principally from glucose. However, for this conversion of glucose into
galactose, the glucose must first be activated, i.e. converted into the
high-energy derivative, uridine diphosphate (=UDP)-glucose, which was
discovered by Leloir.

UDP-glucose is then converted into the activated form
of galactose, UDP-galactose (see below), which serves as a precursor for all
biosynthetic pathways leading to the incorporation of galactose residues, as
in glycoproteins and glycolipids. UDP-Glucuronic acid and UDP-xylose,
deriving from UDP-glucose, are precursors of glycosaminoglycans
(chondroitins, heparins) as well as UDP-hexosamines.


The interaction of glucose and galactose metabolism is represented in the
following scheme, which shows the macromolecular products derived from these
two activated hexoses. In addition to the homoglycan, glycogen, the scheme
shows the glycoconjugates known as heteroglycans, which are also derived
from UDP-galactose.


Interaction of glucose and galactose metabolism




Heteroglycans



From: Lffler, Petrides: Biochemie & Pathobiochemie, 7th edition (modified)


A critical step in this conversion is the epimerisation of UDP-glucose to
UDP-galactose. First, UDP-glucose is biosynthesized in three stages: (i)
phosphorylation of glucose to glucose 6-phosphate at the expense of ATP,
(ii) isomerization to glucose 1-phosphate, (iii) activation to UDP-glucose
with the aid of the coenzyme uridine triphosphate (=UTP).

In a process
involving the reduced form of the coenzyme nicotinamide-adenine-dinucleotide
(=NADH), UDP-glucose is then converted into UDP-galactose by epimerisation
at C-4. This energy-rich form of galactose is used in all synthetic
reactions. The described interconversion of glucose and galactose occurs in
all organs, most effectively in the liver.


Lactose


In the lactating mammary gland, lactose synthesis is mechanistically a
relatively simple process, but subject to fine hormonal regulation. Lactose
synthase is a heterodimeric protein, one subunit (A) being regulated by the
hormones estrogen, insulin and cortisol and the other (B) by progesterone.

Protein A is the galactosyl transferase, protein B the modifier protein
a-lactalbumin, which directs the synthesis towards lactose. Estrogen,
insulin and cortisol regulate the expression of galactosyl transferase.
Normally, UDP-galactose transfers galactose to N-acetylglucosamine, both in
the synthesis of free lactosamine and during the synthesis of
glycoconjugates.

Lactose synthesis is crucially regulated by progesterone,
which controls the activity of the modifier protein a-lactalbumin. After
parturition, progesterone decreases dramatically, so that galactose is
transferred to glucose, resulting in the synthesis of lactose rather than
lactosamine.


Glycoproteins


As indicated by their name, glycoproteins consist of a protein combined with
carbohydrate. These two constituents may be linked O-glycosidically via
serine, or N-glycosidically via asparagine in the consensus sequence
Asn-Xxx-Ser/Thr-. O-Glycans are encountered mostly in mucus, N-glycans in
membranes.

In membranes, glycoproteins are structurally important and some
membrane glycoproteins function as enzymes or specific receptors. Ordered
membrane structure is therefore not possible without glycoproteins. Together
with albumin, soluble glycoproteins represent the essential proteins of
serum. Without the mediation of glycoprotein receptors, important signals
from hormones or growth factors cannot enter target cells.

Without their
N-glycan moiety, some enzymes cannot fulfil their specific catalytic role.
Glycoproteins therefore play a crucial functional role in membranes, as well
as being fundamentally important for the formation and structural
maintenance of all plasma membranes of body cells.

Galactose occupies a key position in the structure and function of
glycoproteins. It occurs in the penultimate position of glycoprotein
glycans, having served as the docking site for N-acetylneuraminic acid (or
sialic acid) at the completion of glycoprotein synthesis. N-Acetylneuraminic
acid is an exceptional sugar acid. It consists of 9 C-atoms, carries a
negative charge in its free monosaccharide form, and possesses an N-acetyl
side group and a glycerol side chain. Each of these components is associated
with a defined biological function.

This unusual nona-sugar is always found
in the terminal position of glycoprotein glycans (it may then be linked to a
further residue of neuraminic acid, as in the polysialic acids). Sialic
acids determine the biological stability, structure, surface charge and
certain receptor functions of the cell. They can exist as components of the
cell surface only through the subterminal presence of galactose.


Glycolipids


Like glycoproteins, glycolipids are essential components of intracellular
membranes and the plasma membrane. Their concentration in membranes is
lower than that of the glycoproteins, and their biosynthesis is similarly
complex. Glycolipids are pathophysiologically important, since degradation
of their unusual structure depends on highly specific degradative enzymes,
which, when defective, lead to conditions known as glycolipid storage
diseases.

Glycoplipids also function as receptors, as well as controlling
the activity of proteins, e.g. enzymes.

Most of these membrane-localized glycolipids are gangliosides, formed by
attaching N-acetylneuraminic acid to the terminal galactose of a glycolipid.
In principle this is the same process as in glycoprotein synthesis, but the
relevant sialyl transferases have different specificity.

Again, a second
neuraminic acid residue may be attached to one that is already present.
However, neuraminic acid can never be attached to a glycolipid or nascent
glycoprotein, unless galactose is initially present as a docking site.
Galactose therefore plays a central, determining role in the structure and
function of both types of glycoconjugate.


Glycogen


Glycogen is a homopolymer of a1,4- and a1,6-linked glucose molecules. The
starting point for glycogen biosynthesis is an autoglucosylated glycoprotein
primer, to which individual activated glucose molecules (UDP-glucose) are
attached, in succession, by glycogen synthase. Through the activity of the
branching enzyme, the molecule attains a space-saving, spherical
configuration, with a molecular weight that can exceed 300 million, and
which is therefore visible under the electron microscope (g- and
d-clusters).

If a large pool of UDP-galactose is available, galactose can
also be incorporated into glycogen in the form of non-reducing end groups
(Nordein). More than 90% of glycogen degradation is due to the action of
hormonally controlled (glucagon, adrenaline) glycogen phosphorylase, which
removes terminal glucose molecules as glucose 1-phosphate in the presence of
the coenzyme pyridoxal phosphate (phosphorylation without ATP).

If high
concentrations of UDP-galactose are present, galactose is incorporated into
glycogen and some residues appear in a terminal position of the glycogen
molecule. This slows down glycogen degradation, with the result that the
glycogen molecule survives longer as an energy store. The mechanism of
galactose cleavage from glycogen is not yet known (unspecificity of
phosphorylase?)


Turnover


Glycoproteins and glycolipids undergo continuous synthesis and degradation.
It is characteristic of membrane glycoproteins that their glycan moieties
are degraded more rapidly than their protein backbone. Half-lives of
N-glycan moieties are between 10 and 24 h, while those of the protein are
between 60 and 80 h. This underlines the high requirement for
monosaccharides for the maintenance of the structure and function of
glycoproteins, in particular the high requirement for monosaccharides for
the renewal of the terminal monosaccharide residues (galactose for galactose
and N-acetylmannosamine for N-acetylneuraminic acid).

In certain metabolic
deficiencies (see below) glycan biosynthesis is affected sooner than that of
the protein. Such deficiency states (see below) profoundly affect the
structure and function of glycoproteins and glycolipids.


Disorders of galactose metabolism


Hereditary galactosemia


The most frequent inherited metabolic disorder affecting galactose
metabolism is hereditary galactosemia, with a frequency of 1:55,000. This
condition, which is manifested after galactose intake, is due to the absence
of uridyl transferase, the enzyme that synthesizes UDP-galactose from
galactose 1-phosphate. Since galactose is produced by cleavage of the
lactose of mothers milk, this defect gives rise to severe symptoms at an
early age (failure to thrive, reluctance to drink, vomiting, pronounced
neonatal icterus, hypoglycemia, hepatomegaly, splenomegaly, kidney damage in
the proximal tubules, formation of cataracts, mental retardation).

Galactose 1-phosphate accumulates, followed by galactose, both of which have
toxic effects. Particularly in the lens of the eye, galactose is converted
into galactitol (=dulcitol). Since this conversion requires NADPH as a
coenzyme, the concentration of NADPH-dependent reduced glutathione
decreases. The oxidized form of glutathione then forms mixed disulfides
with the crystallin of the eye, leading to the cataracts that are typical of
this disorder. The toxic effects of the accumulated galactose 1-phosphate
are even more serious. It inhibits various enzymes, including
phosphoglucomutase, glucose-6-phosphatase and glucose-6-phosphate
dehydrogenase. The toxicity is manifested especially in the liver,
frequently leading to fatal liver cirrhosis.


Hereditary galactokinase deficiency


This is a very rare illness, in which galactose cannot be phosphorylated.
There is no organ damage, since toxic metabolites are not produced and there
is no deficiency of UDP-galactose, which is synthesized via UDP-glucose.


Hereditary deficiency of UDP-glucose-4-epimerase


This genetic defect is also extremely rare and does not result in organ
damage. The necessary UDP-galactose is synthesized from free glucose, which
originates by digestion from the diet.


Compared with these primary or hereditary metabolic disorders of galactose
metabolism, secondary disorders occur much more frequently. They lead to a
deficiency of galactose, which is necessary for the biosynthesis of
important structural components. These galactose deficiency states, which
occur in adults, arise for different reasons and may have serious
consequences. In such cases the addition of galactose, e.g. as a dietary
supplement, is a health-promoting or restorative measure.

The most frequent cause of cellular galactose deficiency is


Metabolic stress.


This can have various origins, like physical or mental over-exertion,
consumptive illnesses, decreased blood circulation of organs (especially
brain) in old age, to mention only a few. As a result, energy metabolism
and metabolic turnover are affected.


The integrity of the organism is maintained by

1. energy metabolism and

2. metabolic turnover of the building materials of cells.


Energy metabolism is much more important for the life and survival of the
organism than metabolism concerned with synthesis of the building materials
of cells. Therefore, the provision of energy from nutrients is the urgent
goal of every body cell. The most important substrate for energy production
is glucose. Under normal conditions this applies especially to the brain
and erythrocytes, while in deficiency states (starvation, metabolic stress,
long-term intensive care) it applies to all cells.

Essential metabolic
processes of the cell are driven by the energy obtained by the oxidative
degradation of glucose. To mention only a few of these processes, ion
channels for the maintenance of the conduction of nerve impulses, or for
maintenance of the intracellular milieu are opened and closed, nutrients are
supplied to cells, impulses are conducted from cells to their neighbors.
Maintenance of these vitally necessary functions of the first front
(energy) is given priority over the functions of the second front (cell
and organ structure). Structural synthesis is therefore not only curtailed,
but a considerable quantity of cell material may also be used as a substrate
for energy production. This has dire consequences for the functional and
structural integrity of the cell, which slowly enters a situation of
metabolic stress then perishes. In order to obtain sufficient energy, the
cell formally burns its own housing.

This type of stress situation occurs in dementia, for example in Alzheimers
disease. In Alzheimer patients, the glucose requirement of the brain is
increased. Blood circulation in the brain is, however, decreased, owing to
the narrowing of blood vessels in old age (normally, 15% of the blood flows
through the brain). The imbalance of energy metabolism and structural
synthesis caused by the illness results in a sustained disordering of cell
structure, leading to cell death. A key reaction in this deleterious process
is the interconversion of UDP-galactose and UDP-glucose:


4-Epimerase

UDP-Galactose UDP-Glucose


At 1:3.5, the equilibrium of the reaction greatly favors glucose. This
means that UDP-galactose readily enters energy metabolism by conversion into
UDP-glucose and subsequently glucose. UDP-galactose is then no longer
available in sufficient quantity for the synthesis of glycoproteins and
glycolipids, and the integrity of the plasma membrane with its essential
components cannot be maintained.

At this point, Nature has provided an
escape route. It consists of the substitution of glucose with its sister
sugar, galactose. Galactose is readily taken up by cells, so that directly
after the provision of galactose, the intracellular concentration of
UDP-galactose is increased, and this can be used primarily for the
maintenance of structural synthesis. Any part of this UDP-galactose that is
not needed for structural synthesis flows quantitatively into energy
metabolism via UDP-glucose, catalyzed by the 4-epimerase. Compared with
glucose, galactose has the advantage that its uptake depends only on the
concentration gradient and is independent of insulin. It is therefore
important that galactose is administered as a bolus.

Administration of galactose has further advantages. It possesses
protein-sparing properties, since it is converted into amino acids,
primarily glutamate and its derivatives, and aspartate, as shown in rat
brain. Since amino acid synthesis consumes equivalents of ammonia, this
represents a detoxification process in hepatic encephalopathy.


Toxicology


As a micronutrient, galactose is not toxic, provided galactosemia is not
present. It has been reported that women suffering from galactosemia (very
rare in adults) show an increased incidence of ovarian carcinoma following
the administration of large amounts of galactose over several weeks,
compared with women without a dietary galactose supplement. These findings,
reported by only one research group, and which cannot be explained
biochemically, were recently disproved. It has also been reported that mice
display decreased learning ability after the lengthy administration of
galactose. Since galactose is crucially important in brain metabolism
(synthesis of gangliosides), this finding also cannot be explained
biochemically. It has so far only been reported for mice. Sophisticated
test methods are lacking for other species. A specific toxic effect cannot
be ascribed to galactose on the basis of this single finding. Furthermore,
it has been reported that rats on a diet consisting of 30% (!) galactose
(equivalent to 250-300 g/day for a human) display symptoms similar to those
of galactosemia. This is not surprising, since it leads to an intracellular
accumulation of galactose 1-phospate. A similar response is found in
pregnant rats, whose embryos die after such a metabolic ordeal. Also
chickens receiving these large quantities of galactose display neuronal
degeneration in the region of the basal ganglion, although this is not
observed in adult animals. These observations have no significance for the
use of galactose as a micronutrient, when it is administered to humans at
the rate of below 15 g per day.


Why not lactose instead of galactose?


Although half of the lactose molecule consists of galactose, it cannot
replace galactose as a dietary additive under any circumstances; it is even
dangerous. Severe galactose intolerance results in death at an early age, so
that the condition has never been described in an adult. In infants, the
frequency of the condition is 1:55,000. In contrast, lactose intolerance
(lactase deficiency) with the consequent intolerance of milk, occurs with
high frequency. In Germany it lies between 10 and 25%, worldwide 75%. For
galactose to be obtained from lactose, the lactose must first be cleaved by
lactase in the small intestine. Unlike the other disaccharidases, lactase
occurs in a relatively low concentration in the mucosal cells of the small
intestine. The provision of galactose by the cleavage of lactose is
therefore totally inadequate. Furthermore, many times the theoretical
quantity of lactose would be required for sufficient galactose to be
produced by the relatively low concentration of lactase. This in itself
would have severe pathological consequences, because large quantities of
uncleaved lactose would arrive in the large intestine, causing water
withdrawal and leading to serious side effects, like flatulence, spasms,
diarrhea and dehydration; the intestinal flora would also be altered.
Therefore, in cases of metabolic galactose deficiency, the administration of
only galactose is indicated, and under no circumstances lactose.

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
Mo
Frequent Contributor (5K+ posts)
Member # 2863

Icon 6 posted      Profile for Mo     Send New Private Message       Edit/Delete Post   Reply With Quote 
most of what's gotten me and my children to progress has been 'left of the north star'.

thank you to all who continue to clear the view. here's to collective gazing........

mo

Posts: 8337 | From the other shore | Registered: Jul 2002  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
This is my post from an old thread on Galactose. I bring it here to have it all together under one roof.

I received this today from medical doctors in Germany involved in the research and application in practice. Take care.

Range of Application:

Parkinson's Disease
Dementia
Alzheimer's Disease
Diabetic Metabolic Disorder
Myoneuralgia
Chronic Pain
Posttraumatic Stress Disorder
Meneral Stress Metabolism
State after Apoplexy
Depression


Application and Use of Galactose

1 .) D+ Galactose and brain tumors Two patients with glioblastoma and astocytoma III/IV, all therapeutic
possibilities of orthodox medicine exhausted (two regimes of
chemotherapy, one regime of radiation therapy, incomplete surgery
twice) were given palliatively 4 oral doses of 3 g of galactose to stabilize
their general condition.

Surprisingly, not only did their general condition improve with respect to
awareness, coordination of movement, self-awareness and general
capability, but also the primary tumor symptomatology like brain
pressure, occurrence of paroxysms, spasticity and visual ability.
Corresponding MRI controls not only showed a cessation of growth, but
also a slight regression of the primary tumor.

The favorable effect of galactose on tumor-derived pain conceivably
occurs on at least two levels. Otto Warburg, one of the most important
pioneers of modern biochemistry, showed that tumors have a high
glycolysis rate, obviously as a metabolic result of their state of stress.
This results in hyperacidity of the affected tissue. Assuming that
galactose obstructs glycolysis, the pain caused by hyperacidity would be
reduced. The dopamine and serotonin receptors are glycoproteins,
which require carbohydrates for their functional structure. Since they
contain galactose, a deficiency of this sugar may impede the proper
function of these receptors.

In the case of the dopamine receptor, this means loss of the obstructing dopamine effect. In the case of the serotonin receptor, galactose deficiency would lead to a reduction of vascular permeability, which is vital for the decrease of local hyperacidity, thus resulting in the presence of local pain stimuli. Toward the end of his scientific career Warburg found that cancer cells cease to grow when galactose is added to the culture medium in place of glucose.

2.) D+ Galactose and spasticity and tetraspasticity

Five youths with cerebral brain damage and tetraspasticity were given 3
times 3 g galactose per day to decrease the neuromuscular pain and
tension. Apart from a clear regulation of muscle tension, all youths showed much
improved attention as assessed by physical and cognitive
physiotherapeutic and neuropsychological learning processes.


3 .) D+ Galactose and coronary heart diseases and myocardial insufficiency

Two patients with therapy-resistant crisis after fourfold bypass with
coronary heart disease tachyarrhythmia, respiratory insufficiency,
sleeplessness and adynamia in the sense of a post-aggression-syndrome
were given 3 times 3 g galactose daily. They each regulated within less
than 24 hours towards sinus rhythm, respiratory regulation and
outstanding general condition.

4.) D+ Galactose and pain in joints, soft tissue and bones

24 patients with chronic (more than a year) neuromuscular pain, pain in
joints, soft tissue and spine and non-response to classical opiate
strategies, were treated within a period of four weeks with 3 times 3 g
galactose. Apart from the expected muscular release, 20 of the 24 patients reported an unexpected pain reduction of 6 units on the pain-analogue-scale (from 1 to 10)
.
5.) D+ Galactose and epileptic fits

Two patients with epileptic fits (one grand mal, one petit mal) were given
4 times 3 g galactose per day under the impression and the hypothesis of
a metabolic cerebral state of stress. The number of fits was impressively
reduced from two fits per day to one fit per week within 8 days of therapy.

6.) D+ Galactose and attention-deficit-hyperactivity-syndrome

Seven children diagnosed ADHS, all therapeutic possibilities of orthodox
medicine exhausted psychosocially and pharmacologically, with a
minimum of 25 sessions of behavior therapy and therapy with the
psychoactive drug Ritalin over 3 months, were given 3 times 1.5 g
galactose to regulate their attacks of hyperorexia, always immediately
before the attack.

Surprisingly, this not only regulated the attacks, but also the whole
spectrum of behavior with respect to concentration, the will and ability to
learn, motivation, social integration and intelligence performance.
The psychomotor abnormalities were regulated completely in 6 cases.

Background

Galactose is a naturally occurring hexose, which is commonly found in
the human diet. It is structurally very similar to glucose and can be
metabolised to this sugar in the body. D-galactose is a major nutrient in
the newborn and is a substrate for energy production and storage
(Kliegman and Sparks, 1985). However, there are inborn errors of
metabolism that result in D-galactosemia, which is accompanied by well
characterised signs and symptoms. There are also animal models
employing high levels of dietary D-galactose and these have been used
extensively to study such diseases.

This has provided a substantial body of background data on the toxicological effects of high doses of D-galactose. Certain factors may be considered as counterbalancing the need for a full formal toxicological assessment.
These include:

*D-galactose occurs naturally in the body and diet,
*the effects of D-galactosemia in humans are well defined,
*D-galactose has been used in humans for diagnostic purposes,
*there are existing pharmacokinetic data in human volunteers,
*D-galactose has already been used in a somewhat similar manner in
a clinical trial for prevention of hepatic metastases in patients with
colorectal cancer, and
*the product is proposed for use in patients with a poor prognosis.


Mechanisms for therapeutic effects of D-galactose

A preliminary study including five patients with HE grade IV has shown
that a D-galactose infusion in addition to standard therapy may be of
benefit for HE patients. Improvement of clinical symptoms (from grade IV
to grade II or I) was achieved within one to two days after the start of the
D-galactose infusion. On the first day of the additional D-galactose
treatment, patients were able to perform psychometric tests.

The underlying mechanisms for the therapeutic effect of D-galactose in
described diseases are thought to be the following:

*D-Galactose may contribute to a reduction of ammonia levels. It has
been shown that in the brain, D-galactose is converted into amino
acids, especially into glutamate and derivatives of aspartate. For this
conversion ammonia is required as donor of the amino group for
amino acid synthesis. This effect is also observed after administration
of glucose, but the D-galactose effect is of much longer duration.

*UPD-galactose, a derivative of D-galactose, is found in reduced
concentrations in patients with restricted liver function. UDPgalactose
serves as an essential precursor for the synthesis of
glycolipids and glycoproteins, which are both components of
biomembranes and of signal molecules like hormones or
neurotransmitters, as well as acting as receptors for hormones and
neurotransmitters. D-Galactose deficiency therefore results in a
disturbed metabolism of these substances, which can be prevented by
exogenous D-galactose administration.

*D-Galactose not only serves as precursor for
glycolipids/glycoproteins, but by conversion to glucose, which enters
glycolysis, it also serves as a substrate for energy metabolism.

*D-Galactose has been shown to bind endotoxins, which are found to
be increased in HE patients.
From this it is concluded that D-galactose may have a valuable impact on
the improvement of all described symptoms, when given in addition to
standard therapy.


Further Description of Galactose:

A healthy human produces 2 to 10 g of -D+galactose per day.
-D+Galactose is a structurally simple sugar and is, as it were, one of the
fundamental components of the living cell.

One advantage of galactose is its insulin-independent transport into cells,
which, by its sparing action on insulin, leads to a protection of the
pancreas. Galactose also acts as a detoxifying agent by removing toxic
ammonia and ammonium ions. In removing ammonia/ammonium ions, it
also serves for the synthesis of important amino acids required by the
organism.

Thus galactose both conserves and generates vital amino acids.
But the greatest contribution of galactose lies in its ability to support
resynthesis and repair in cell metabolism. Thus galactose is important for
the stability of cell membranes and their contacts with other cells and
their outer environment. This is reflected in improved concentration,
alertness, long term and short term memory and social competence.

Further Description of Galactose:

No data specifically on single dose lethality were found in the literature for
D-galactose (search of RTECS - Registry of Toxic Effects of Chemical
Substances, HSDB - Hazardous Substances Databank, Toxline). It
should be noted that in several reproductive studies in rats and mice
reported on RTECS, values for TDLo's (lowest dose producing toxicity)
were up to tens of gramsg/kg/day with oral dosing. It is reasonable to
assume that the acute lethality of oral D-galactose is greater than 5g/kg.

While not a single dose study per se, mice have been injected
intraperitoneally with 2g/kg at intervals of 8 hours for 4 days (Beuth et al,
1987; Isenberg et al, 1997). This allows the reasonable assumption that
the ip lethality of D-galactose is greater than 2g/kg. With 2g/kg of D-galactose
ip every 12 hours for 3 days in mice, no side effects were
reported (Beuth et al, 1988). Intraperitoneal administration is often
regarded as being close to an intravenous injection because absorption is
usually rapid and virtually complete.


Remarks/Comments Acute toxicity studies in mice, rats and dogs have been performed by the
company Schering with Echovist (a suspension containing D-galactose;
Registration No.: 28409.01.00; Registration date: 21.11.1994) and a 56%
(w/v) D-galactose solution and have been submitted to the BfArM. The
LD50-values as well as the LD50-ranges showed no clear-cut differences
between Echovist and the 56% (w/v) D-galactose solution.
Consequently further studies do not appear to be necessary.


Reference List

Alloussi S, Birlouez-Aragon I, Fevrier C and Papadopoulos H. Effects of 5% D-galactose
diet on D-galactose and dulcitol in plasma and lens of male and female pigs. Ann
Nutr Metab 33, 323 - 329, 1989.
Beuth J, Ko HL, Oette K, Pulverer G, Roszkowski K and Uhlenbruck G. Inhibition of liver
metastasis in mice by blocking hepatocyte lectins with arabinogalactan infusions
and D-Galactose. J Cancer Res Clin Oncol 113, 51 - 55, 1987.
Beuth J, Ko HL, Schirrmacher V, Uhlenbruck G and Pulverer G. Inhibition of liver tumor
cell colonization in two animal models by lectin blocking with D-Galactose or
arabinogalactan. Clin Exp Metastasis 6, 115 - 120, 1988.
Bird PH and Hartmann PE. The response in the blood of piglets to oral doses of D--
galactose and glucose and intravenous administration of D-galactose. Br J Nutr
71, 553 - 561, 1994.
Birlouez-Aragon I and Alloussi S. Effect of prolonged D-galactose consumption on D--
galactose tolerance in young healthy humans. Ann Nutr Metab 34, 1 - 7, 1990.
Chen YT, Mattison DR, Bercu BB and Schulman JD. Resistance of the male gonad to a
high D-galactose diet. Pediatr Res 18, 345 - 348, 1984.
Cramer DW, Muto MG, Reichardt JKV, Xu H, Welch WR, Valles B and Ng WG.
Characteristics of women with a family history of ovarian cancer: I. D-galactose
consumption and metabolism. Cancer 74, 1309 -1317, 1994.
Ferretti JL, Locatto ME, Savino D and Puche RC. The effect of D-galactose on bone
metabolism. Calc Tiss Res 14, 169 - 175, 1974:
Forcier NJ, Mizisin AP, Rimmer MA and Powell HC. Cellular pathology of the nerve
microenvironment in D-galactose intoxication. J Neuropathol Exp Neurol 50, 235 -
255, 1991.
Gibson JB. Gonadal function in D-galactosemics and in D-galactose-intoxicated
animals. Eur J Pediatr 154 (Suppl 2), S14 - S20, 1995.
Gona O. Cytoarchitectural changes in lens epithelium of D-galactose-fed rats. Exp Eye
Res 38, 647 - 652, 1984.
Greener Y and Youkilis E. Assessment of the cataractogenic potential of cyclohexanone
in guinea pigs and rabbits. Fund Appl Toxicol 4, 1055 - 1066, 1984.
Gurtler H and Hassane HM. Galaktosetoleranz nach intravenser
Galaktosestobelastung von Saugferkeln. Arch exper Vet Med 38, 778 - 780,
1984.
6
Isenberg J, Stoffel B, Stutzer H, Otte K and Beuth J. Liver lectin blocking with D--
Galactose to prevent hepatic metastases in colorectal carcinoma patients.
Anticancer Res 17, 3767 -3772,1997.
Juricek M, Gruz P, Veleminsky J, Stanek J, Kefurt K, Moravcova J and Jary J.
Mutagenic activity of 6-azido deoxyhexoses and azido alcohols in Salmonella
typhimurium and its inhibiton by a structure-similar carbon source in the medium.
Mutat Res 251, 13 - 20, 1991.
Keiding S and Mellemgaard L. Dose dependence of D-galactose cataract in the rat. Acta
Ophthalmologica 50, 174 -182, 1972.
Kliegman RM and Sparks JW. Perinatal D-galactose metabolism. J Pediatr 107, 831 -
841, 1985.
Leonardo JM, Dornfeld SS and Peak MJ. Evaluation of Escherichia coli K-12 343/113
and derived strains for microbial mutagenicity assays. Mutat Res 130, 87 - 95,
1984.
Mangeot M, Djabal A, Myara I, Cherruau B, Pourci ML and Lemonnier A. Metabolic
studies of a sustained D-galactose overload in rat. Ann Nutr Metab 31, 333 - 341,
1987.
Merkel C, Gatta A, Zoli M, Bolognesi M, Angeli P, Iervese T, Marchesini G and Ruol A.
Prognostic value of D-galactose elimination capacity, aminopyrine breath test,
and ICG clearance in patients with cirrhosis. Comparison with the Pugh score.
Dig Dis Sci 36, 1197 -1203,1991.
Meydani M, Martin A, Sastre J, Smith D, Dallal G, Taylor A and Blumberg J. Dose -
response characteristics of D-galactose-induced cataract in the rat. Ophthalmic
Res 26, 368 -374,1994.
Mizisin AP and Powell HC. Schwann cell changes induced as early as one week after
D-galactose intoxication. Acta Neuropatho193, 611 - 618, 1997.
Mizisin AP and Calcutt NA. Dose-dependent alterations in nerve polyols and (Na+,K+)--
ATPase activity in D-galactose intoxication. Metabolism 40, 1207 - 1212, 1991.
Mizisin AP, Myers RR, Heckman HM and Powell HC. Dose-dependence of endoneurial
fluid sodium and chloride accumulation in D-galactose intoxication. J Neurol Sci
86, 113 -124,1988.
Parkhurst GW and Mayes JS. D-galactose toxicity and activities of the D-galactose
metabolizing enzymes during development of the chick. Arch Biochem Biophys
150, 742 -745, 1972.
Segal S. The enigma of D-galactosemia. Int Pediatr 7, 75 - 82, 1992.
Segal S. In utero D-galactose intoxication in animals. Eur J Pediatr 154 (Suppl 2), S82 -
S86,1995.
Teshima R, Taura T and Okamura R. Effect of pregnancy on development of Dgalactose-
induced cataract in rat. Jpn J Ophthalmol 37, 56 - 61, 1993.
Watts RWE. Inborn errors of carbohydrate metabolism. In "Oxford Textbook of
Medicine", eds DJ Weatherall, JGG Ledingham, DA Warrell, Oxford University
Press, Oxford, pages 9.4 - 9.10, 1987.
Westhoff C. Ovarian cancer. Ann Rev Public Health 17, 85 - 96, 1996.
Winkler K, Henriksen JH and Tygstrup N. Hepatic, renal, and total body D-galactose
elimination in the pig. Am J Physiol 265, G9 - G14, 1993.

[ 14. December 2006, 11:41 PM: Message edited by: GiGi ]
--------------------------------------------------------------------------------
Posts: 4421 | From: Washington State | Registered: Oct 2000 | IP: Logged

GiGi
Frequent Contributor
Member # 259

posted 14 December, 2006 11:57 PM
--------------------------------------------------------------------------------
up, to be closer to my later post on Galactose

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
up for Marnie per my post entitled
"Nitric Oxide for blood flow, killing pathogens, etc."

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
Truthfinder
Frequent Contributor (1K+ posts)
Member # 8512

Icon 1 posted      Profile for Truthfinder     Send New Private Message       Edit/Delete Post   Reply With Quote 
So, if a person wanted to purchase some galactose, they would have to order it from Germany (or Italy?)

Or is it commercially avaliable at all?

And can we afford it even if we could get it?

Tracy

--------------------
Tracy
.... Prayers for the Lyme Community - every day at 6 p.m. Pacific Time and 9 p.m. Eastern Time just take a few moments to say a prayer wherever you are.

Posts: 2966 | From Colorado | Registered: Dec 2005  |  IP: Logged | Report this post to a Moderator
jblral
LymeNet Contributor
Member # 8836

Icon 1 posted      Profile for jblral     Send New Private Message       Edit/Delete Post   Reply With Quote 
up for that last question--is it available for us to buy?
Posts: 991 | From California | Registered: Feb 2006  |  IP: Logged | Report this post to a Moderator
kelmo
Frequent Contributor (1K+ posts)
Member # 8797

Icon 1 posted      Profile for kelmo     Send New Private Message       Edit/Delete Post   Reply With Quote 
My brain hasn't processed this information yet. But, I didn't get an answer to my question. Is this the same stuff that is sold by Mannatech?

They have glyconutrients. Someone gave information to me a couple of years ago when my daughter came down ill (it was unknown then). I tucked it away, not wanting to jump on the latest "miracle cure".

I need this information put into practical thought. It's not the information that's the problem, it's my brain.

Are glyconutrients, as sold by companies such as Mannatech, the same as galactase? Should we be considering this as a supplement? Or, can we glean this nutrient from regular food?

Thank you for the research!

Kelly

Posts: 2903 | From AZ | Registered: Feb 2006  |  IP: Logged | Report this post to a Moderator
Marnie
Frequent Contributor (5K+ posts)
Member # 773

Icon 1 posted      Profile for Marnie     Send New Private Message       Edit/Delete Post   Reply With Quote 
As far as "sugars" go...you might want to consider d ribose which is needed to make ATP and RNA.

Go here to learn:

http://www.holisticonline.com/Remedies/cfs/fib_new-hope-for-fibromyalgia.htm

Posts: 9401 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
SForsgren
Frequent Contributor (1K+ posts)
Member # 7686

Icon 1 posted      Profile for SForsgren         Edit/Delete Post   Reply With Quote 
Unfortunately, GiGi has left the board and will not be responding to any of these posts further. To many people giving her too much hassle for her incredibly helpful posts...

--------------------
Be well,
Scott

Posts: 4617 | From San Jose, CA | Registered: Jul 2005  |  IP: Logged | Report this post to a Moderator
breathwork
Frequent Contributor (1K+ posts)
Member # 567

Icon 1 posted      Profile for breathwork     Send New Private Message       Edit/Delete Post   Reply With Quote 
TO check out the research that Mannatech offers, go to...

www.glycoscience.com

They post papers about the glyconutrients in their products.

I do not sell the products...I just use them

Posts: 1062 | From CA USA | Registered: Jan 2001  |  IP: Logged | Report this post to a Moderator
kelmo
Frequent Contributor (1K+ posts)
Member # 8797

Icon 1 posted      Profile for kelmo     Send New Private Message       Edit/Delete Post   Reply With Quote 
Okay, that answers my question. It is the same thing.

Scott, can you incorporate some of her information on your website?

Kelly

Posts: 2903 | From AZ | Registered: Feb 2006  |  IP: Logged | Report this post to a Moderator
SForsgren
Frequent Contributor (1K+ posts)
Member # 7686

Icon 1 posted      Profile for SForsgren         Edit/Delete Post   Reply With Quote 
This is what I have learned from GiGi:

Only the absolutely "99.9% purified Galactose" works as posted. Nothing else. No other sugars etc. work in this direct manner. This straight from the scientists and medical doctors, not second or third hand. No use wasting money on stuff that doesn't work. There is only one source in Germany right now that carries it. There are several in Switzerland, but that is more expensive as all is in Swtizerland. The manufacturer that processes the galactose in this manner is in Italy.

For those interested further, I suspect GiGi will respond if you contact her directly via email even though she is no longer posting here on LN.

--------------------
Be well,
Scott

Posts: 4617 | From San Jose, CA | Registered: Jul 2005  |  IP: Logged | Report this post to a Moderator
kelmo
Frequent Contributor (1K+ posts)
Member # 8797

Icon 1 posted      Profile for kelmo     Send New Private Message       Edit/Delete Post   Reply With Quote 
Thank you, Scott. I won't waste money.

I would contact her directly, but I understand she disabled her private message.

I don't have any other way to contact her, and we have never spoken.

Posts: 2903 | From AZ | Registered: Feb 2006  |  IP: Logged | Report this post to a Moderator
susan2health
LymeNet Contributor
Member # 10446

Icon 2 posted      Profile for susan2health     Send New Private Message       Edit/Delete Post   Reply With Quote 
GiGi,

If you are still reading on this site: we may not let your last post die.

Up for GiGi!

Susan

Posts: 233 | From United States | Registered: Oct 2006  |  IP: Logged | Report this post to a Moderator
Marnie
Frequent Contributor (5K+ posts)
Member # 773

Icon 1 posted      Profile for Marnie     Send New Private Message       Edit/Delete Post   Reply With Quote 
Galactose metabolism - Borrelia burgdorferi

http://www.genome.jp/dbget-bin/get_pathway?org_name=bbu&mapno=00052

In this study the lipids of Borrelia burgdorferi, the causative agent of Lyme disease, were analyzed. Lipids comprise about 25-30% of the cell dry weight. The lipid fraction could be separated by HPTLC into 11 components.

Staining of these components revealed two glycolipids and two phospholipids. The glycolipids represented about 50% of the total lipids and comprised

only galactose as monosaccharide constituents.

PMID: 11522398

Posts: 9401 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
http://www.galactose.org/pharmacology.html
Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
pamoisondelune
Frequent Contributor (1K+ posts)
Member # 11846

Icon 1 posted      Profile for pamoisondelune     Send New Private Message       Edit/Delete Post   Reply With Quote 
I take alpha-galactosidase pills from Vitacost to prevent gas. Is this at all relevant or not relevant?

---Polly Polygonum (i'm taking this new name)

Posts: 1226 | From USA | Registered: May 2007  |  IP: Logged | Report this post to a Moderator
ping
Frequent Contributor (1K+ posts)
Member # 6974

Icon 14 posted      Profile for ping     Send New Private Message       Edit/Delete Post   Reply With Quote 
quote:
Originally posted by GiGi:
And for people like you who do aboslutely nothing but try to pound everything I post into the ground, I am not making the effort trying to translate anything.

The info I have given you did not fly into my window on the wings of a bird. I worked my butt off...

GiGi,

Please don't leave. I love to read your info and need it badly. There will always be people who disagree and I know you get a lot of that here, but please just "post & run" for the benefit of those of us who love you. [kiss]

ping
We are more than containers for Lyme"

--------------------
ping
"We are more than containers for Lyme"

Posts: 1302 | From Back in TX again | Registered: Mar 2005  |  IP: Logged | Report this post to a Moderator
ping
Frequent Contributor (1K+ posts)
Member # 6974

Icon 5 posted      Profile for ping     Send New Private Message       Edit/Delete Post   Reply With Quote 
Originally posted by kelmo:
My brain hasn't processed this information yet....

Wow, there's so much info. I noticed on the website something about contacting a physician if children haven't been tested for certain tolerance. I'm not a child but am very lactose intolerant and can't quite make out what role this plays re: galactose. Help!

ping
"We are more than containers for Lyme"

--------------------
ping
"We are more than containers for Lyme"

Posts: 1302 | From Back in TX again | Registered: Mar 2005  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
Ping, check out the Allergie Immun thread. All intolerances are addressed there and that is, in my opinion, the place to start. I did not start with AI because I was not aware of its existence. Read the English portion of the AI website. It explains a lot. You may want to use a translating engine (google and others) to translate more of the articles on their website. It really covers everything -- you only need to devote some time to it.

You can research the galactose later. Because nothing works well when your body has forgotten how to regulate properly at the energetic level (DNA), or, as often is the case, we are born with these errors. We inherit these like the blue eyes or the talent of the father or grandfather!

Thank you for your kind words.

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
ping
Frequent Contributor (1K+ posts)
Member # 6974

Icon 14 posted      Profile for ping     Send New Private Message       Edit/Delete Post   Reply With Quote 
Gigi - I will certainly take a look at the info. Great thanks for your reply and don't let anyone get you down. You are very much needed and wanted here. [group hug]

ping
"We are more than containers for Lyme"

--------------------
ping
"We are more than containers for Lyme"

Posts: 1302 | From Back in TX again | Registered: Mar 2005  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
Up for Runner and whoever else interested

D+ Galactose will be available in the US soon - so I heard at a recent lecture by K. Mosetter, Inventor of Myoreflex Therapy who has been involved in the research for many years and has been using D+ Galactose in his practices for a number of years successfully

Go to Page 11 of
http://www.neuraltherapy.com/FullAgendaHealingBrain.pdf

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
Up for Runner and whoever else interested

D+ Galactose will be available in the US soon - so I heard at a recent lecture by K. Mosetter, Inventor of Myoreflex Therapy who has been involved in the research for many years and has been using D+ Galactose in his practices for a number of years successfully

Go to Page 11 of
http://www.neuraltherapy.com/FullAgendaHealingBrain.pdf

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
GiGi
Frequent Contributor (5K+ posts)
Member # 259

Icon 1 posted      Profile for GiGi         Edit/Delete Post   Reply With Quote 
Up for Runner and whoever else interested

D+ Galactose will be available in the US soon - so I heard at a recent lecture by K. Mosetter, Inventor of Myoreflex Therapy who has been involved in the research for many years and has been using D+ Galactose in his practices for a number of years successfully

Go to Page 11 of
http://www.neuraltherapy.com/FullAgendaHealingBrain.pdf

Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
   

Quick Reply
Message:

HTML is not enabled.
UBB Code is enabled.

Instant Graemlins
   


Post New Topic  New Poll  Post A Reply Close Topic   Feature Topic   Move Topic   Delete Topic next oldest topic   next newest topic
 - Printer-friendly view of this topic
Hop To:


Contact Us | LymeNet home page | Privacy Statement

© 1993-2020 The Lyme Disease Network of New Jersey, Inc.
All Rights Reserved.
Use of the LymeNet Site is subject to the Terms and Conditions.

Powered by UBB.classic™ 6.7.3


The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:

The Lyme Disease Network of New Jersey
907 Pebble Creek Court, Pennington, NJ 08534 USA


| Flash Discussion | Support Groups | On-Line Library
Legal Resources | Medical Abstracts | Newsletter | Books
Pictures | Site Search | Links | Help/Questions
About LymeNet | Contact Us

© 1993-2020 The Lyme Disease Network of New Jersey, Inc.
All Rights Reserved.
Use of the LymeNet Site is subject to Terms and Conditions.