GiGi
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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 ]
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lymie tony z
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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
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hardynaka
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hardynaka
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posted
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.
hardynaka
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Thanks Gigi!
Selma
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Marnie
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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:
posted
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
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SForsgren
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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
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lymie tony z
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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
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GiGi
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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.
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kelmo
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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
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GiGi
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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 ]
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lymie tony z
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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
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GiGi
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posted
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.
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GiGi
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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.
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 mother�s 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 Alzheimer�s 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
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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 intraven�ser Galaktosesto�belastung 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
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GiGi
Frequent Contributor (5K+ posts)
Member # 259
posted
up for Marnie per my post entitled "Nitric Oxide for blood flow, killing pathogens, etc."
Posts: 9834 | From Washington State | Registered: Oct 2000
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Truthfinder
Frequent Contributor (1K+ posts)
Member # 8512
posted
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
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posted
up for that last question--is it available for us to buy?
Posts: 991 | From California | Registered: Feb 2006
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kelmo
Frequent Contributor (1K+ posts)
Member # 8797
posted
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?
SForsgren
Frequent Contributor (1K+ posts)
Member # 7686
posted
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
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breathwork
Frequent Contributor (1K+ posts)
Member # 567
posted
TO check out the research that Mannatech offers, go to...
SForsgren
Frequent Contributor (1K+ posts)
Member # 7686
posted
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
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kelmo
Frequent Contributor (1K+ posts)
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posted
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
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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: 9419 | From Sunshine State | Registered: Mar 2001
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GiGi
Frequent Contributor (5K+ posts)
Member # 259
pamoisondelune
Frequent Contributor (1K+ posts)
Member # 11846
posted
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
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ping
Frequent Contributor (1K+ posts)
Member # 6974
posted
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.
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
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ping
Frequent Contributor (1K+ posts)
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posted
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
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GiGi
Frequent Contributor (5K+ posts)
Member # 259
posted
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.
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ping
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posted
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.
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
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GiGi
Frequent Contributor (5K+ posts)
Member # 259
posted
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
GiGi
Frequent Contributor (5K+ posts)
Member # 259
posted
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
GiGi
Frequent Contributor (5K+ posts)
Member # 259
posted
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
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