“Beta cells surrounded by acids do not or cannot produce sufficient insulin. Acids destroy insulin receptor sites on the cellular membrane so body cells cannot properly use the hormone. If alkalinity is not soon restored, disease, including diabetes, takes hold. But without acidosis, there can be no sickness or disease – there can be no diabetes.”
Dr Robert O. Young,
Microbiologist and Scientist
Monosodium Glutamate (MSG) which can trigger the “Chinese Restaurant Syndrome” of headache and burning plus tightness in the chest, neck and face. Found in packet soups and instant drinks. (E 620 – E 635)
Allergic response – MSG is not a true allergen but may directly affect immune response by stimulating or damaging the nervous system. In studies done recently on animals, food allergies may be caused by a lack of Interleukin 12. This substance is made by cells in the body – oligodendrocytes, that are killed by excess glutamate. Also – Over 85% of individuals with Type 1 Diabetes have antibodies to the enzyme the body uses to turn Glutamate into GABA – glutamic acid decarboxylase (GAD). Their immune system attacks the means by which glutamate is metabolized, even though it does not attack glutamate itself. Because of their immune response to GAD, Type 1 diabetics are at risk of having an excess of glutamate in their systems already.
Hypoglycemia – MSG’s stimulation of pancreas decreases blood glucose, making hypoglycemia (low blood sugar) worse.
Pancreas – glutamate stimulates the pancreas and may cause Type II diabetes, obesity, and insulin resistance. In individuals with Type 1 diabetes, it may cause an excess of glutamate since 85% of those with Type 1 diabetes have antibodies which attack GAD – the enzyme responsible for converting glutamate into GABA.
Vision – There are glutamate receptors in the retina. Laboratory studies on animals have shown the retina to be damaged by MSG.
- Nervous system – MSG stimulates nerves in tongue and elsewhere directly (that’s why they use it). Glutamate in excess can overstimulate nerve cells until they die. Certain cells called oligodendrocytes which are found in the nervous system and make MYELIN are killed by excess glutamate. It is the inability to make myelin which defines the disease Multiple Sclerosis. In those patients, Interleukin 12 is low. IL 12 is also made by the oligodendrocytes – a clue that these cells are probably being killed by something. We firmly believe that something may be MSG and aspartame in the diet.
Hypothalamus – part of the brain most susceptible to attack because it is the “sensor” of the brain, out in the open so to speak, not protected by the blood brain barrier because it needs to monitor levels of hormones in the blood. This part of the brain directs the action of the pituitary gland which directs the action of the entire endocrine system. Many MSG sensitive persons become diagnosed with thyroid disfunction and are put on synthetic hormone due to hypothyroidism. This would suggest that the hypothalamus may be compromised and unable to effectively direct the pituitary gland and consequently the thyroid. The hypothalamus also regulates hunger, and body temperature. The hypothalamus is also responsible for rage and panic as well…
Brain – during periods of hypoglycemia where low blood glucose levels leave the brain with low defenses, or allergy response where the blood vessels become “leaky”, MSG may cross the blood brain barrier and damage brain cells by excitatory neurotoxicity. By affecting the pancreas and creating a situation of hypoglycemia, MSG may bring down the brain’s barriers, carrying it’s own key, in a sense, to get to the brain.
Proteins are globular and clumpy because the amino acid chains fold in on themselves. This is how the immune system recognizes proteins. They are large compared to single amino acids, and they are uniquely shaped. The immune system does not recognize tiny MSG as an allergen. However, trouble can begin because the body can attack the larger enzymes like GAD, responsible for turning excess MSG into GABA.
Glutamate – Protein Building Block and Excitatory Neurotransmitter….
Glutamate is just one of many amino acids used by the body and linked into the chains of protein in the body. However some amino acids are free to float around by themselves as well as being found linked into proteins because they serve vital functions – some are neurotransmitters which carry nerve cell impulses throughout the body. Amino acid neurotransmitters are like chemical messengers carrying news from nerve cell to nerve cell. Some amino acid neurotransmitters like glutamate trigger nerve cells to fire, others like taurine and gamma amino butyric acid tell those firing nerve cells to cease firing. It is a delicate balance. An important balance.
How does the body usually deal with excess amino acids?
Most amino acids if not used right away, are not stored as amino acids. The body has elaborate means of changing extra amino acids into other amino acids, and removing nitrogen and changing amino acids into fuel to be stored. There are processes such as “transamination” and “deamination” which occur mostly in the liver. In patients with compromised livers, however, they may have trouble transaminating cysteine, for example, into taurine, the amino acid that acts counter to glutamate. Also, an excess of the amino acid aspartate (found in Nutrasweet) may result in excess glutamate, since the body can convert aspartate directly to glutamate. Aspartate and glutamate affect some of the same receptors. In a different example, there is an enzyme that the body uses to convert excess glutamate into another neurotransmitter called GABA. In many patients with Type II Diabetes, their bodies view the enzyme responsible for turning MSG into GABA as an enemy and create antibodies to attack it so that it cannot do its job. This is a problem. The body is compromised in its job of getting rid of excess glutamate. It again is a question of balance, and what tips it.
Type 1 Diabetes
In the search to understand the mechanisms of diabetes because of its unprecedented rise in children, it was learned that roughly 85% of those studied with Type 1 diabetes had antibodies against glutamic acid debarboxylase (GAD) . GAD is an enzyme the body uses to turn glutamic acid, (glutamate) into gamma amino butyric acid (GABA).
Ingesting MSG may present the patient with an excess of glutamate, which the body has trouble converting because the immune system is attacking the very mechanism the body uses to metabolize excess glutamate. These people already have an excess of an amino acid the body can make – they do not need additional free glutamate in their diet.
Why should MSG matter to a diabetic?
MSG causes a very large insulin response after it is ingested since there are glutamate receptors in the pancreas. MSG manufacturers state that ingested MSG does not result in a corresponding increase in blood levels of free glutamic acid, but according to the following research done in Canada, ingested MSG DOES result in higher plasma concentrations of free glutamic acid AND higher insulin levels as well:
This study alone makes free glutamic acid’s role in diseases like Diabetes extremely relevant to the overuse of MSG and free glutamic acid in our food.
Type 2 Diabetes
It was also learned that 85% of children with Type 2 diabetes also suffer from obesity:
See page on MSG and Obesity
GAD65 is considered a key autoantigen in the diabetogenic process.
The serum antibodies are detected pancreatic island cells with antibodies specific cytoplasmic and membrane components (glutamic acid decarboxylase). This enzyme is found in the cytoplasm of pancreatic B cells. Cytosolic enzyme is found at the plasma membrane, which becomes the target of the immune system and induce synthesis of antibodies.
Is an enzyme that catalyzes Glutamatdecarboxilaza glutamate decarboxylation of gamma-amino butyric acid (GABA) and carbon dioxide (CO2).
GAD exists in two isoforms encoded by different genes: GAD 1 and GAD 2.
Initially it was found that the serum of young patients recently diagnosed with diabetes, precipitated a protein with a molecular weight of 64 kDa in human islets of Langerhans cells. Then protein was identified as glutamatdecarboxilaza, with the two forms. These isoforms are GAD 67 and GAD 65. GAD 1 and GAD 2 are expressed in the brain where the neurotransmitter GABA acts; GAD 2 is expressed in the pancreas.
GAD is an enzyme that because of some similarities with bacterial proteins can cause an autoimmune reaction against beta cells of the pancreas in type 1 diabetes.
In contrast to the ICAS and IaaS, GAD65 antibodies persist in serum of patients with type 1 diabetes years after diagnosis, despite the progressive decline in β cell function (J autoimmune 1994). A recent study found that 80% of subjects remained positive GAD65 antibody 12 years after their initial diagnosis. (Diabetes 2002).
GABA produced in β cells has been suggested to serve as a functional regulator of pancreatic hormone release as a paracrine signaling molecule communication between beta cells and other endocrine cells in islets of Langerhans. (Satin LS, Kinard TA 1998
GABA receptor inhibitors they could, by blocking the inhibitory effects of GABA on glucagon and somatotrophin secretion, increase their release.
An immediate effect of a rise in glucagon is insulin release with subsequent hypoglycaemia but chronic hyperglucagonaemia, much as hyper- secretion of growth hormone, is associated with the development of diabetes. This is a mechanism, therefore, that might be capable of leading to hyperglycaemia, or eventual diabetes, over time.
Reduced expression of GAD is produced by GABA inhibition and this in turn reduces autoimmune responses to GAD in rat islets and brain.
It has been suggested that such inhibition of GAD antigenicity might reduce the risk of the development of type 1 diabetes in those at risk.
(BJ BOUCHER & N. MANNAN – 2002)
about vitamin D deficiency and food allergens