Autoimmune Thyroid Disease

An Unfortunate and Lengthy Adventure in Misdiagnosis

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Glycine metabolism

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I haven’t been keeping this blog up to date. There’s so many things I need to blog about, but I just don’t have time! Hopefully this post will plug a few gaps for people.

Glycine is essential for the synthesis of nucleic acids, bile acids, proteins, peptides, purines, adenosine triphosphate (ATP), porphyrins, hemoglobin, glutathione, creatine, bile salts, one-carbon fragments, glucose, glycogen, and l-serine and other amino acids. Glucagon is a hormone that causes glycogen (stored in the liver) to convert to glucose which is needed by the body for energy. Glycine increases the release of glucose into the blood stream by stimulating the glucagon hormone. Glycine is an inhibitory neurotransmitter in the central nervous system, especially in the spinal cord. Glycine systems may be important in controlling epilepsy and other CNS disorders. Glycine also enhances the activity of neurotransmitters (chemical messengers) in the brain that are involved in memory and cognition. Glycine may be indicated to help alleviate the symptoms of spasticity. Glycine is an inhibitory amino acid with important functions centrally and peripherally. Molecular analogs and precursors can be used to augment these systems. The charged species have difficulty passing the blood-brain barrier and must be carried by transport pumps. Glycine helps convert many potentially harmful substances including toxic phenolic materials such as benzoic acid (sodium benzoate) into harmless forms. Vitamin Supplements

Glycine, along with Coenzyme A (derived from pantothenic acid) are required for salicylate detoxification through the amino acid conjugation pathway. This might be why I was dependent on pantothenic acid for a long time in order to feel normal, though it eventually threw my system so out of balance that it made me worse. However, glycine doesn’t seem to do much for me, which is why I’ve not bothered blogging about it. But trimethylglycine (betaine) does help a bit, especially with brain fog. As I am not protein deficient, I am producing enough glycine every day to meet my needs. For this reason I haven’t tried glycine on particularly bad reactions, or in really big doses, favouring TMG instead. I’ve only taken 500mg tablets of glycine in the past since I generally have a low tolerance of amino acid tablets. Glycine tablets tend to make me feel very depressed. It’s actually almost as though I’m having a glutamate reaction – probably because although glycine often antagonises glutamate in the brain, glycine also agonises glutamate on some receptors.

Vitamin B6 converts certain amino acids (glutamic acid, aspartic acid, glycine) to energy. This allows the body to process all dietary protein, even when the dietary protein is in excess of the body’s needs. Vitamin B6 also allows the body to synthesize certain amino acids. For example, if the diet is deficient or low in certain amino acids, such as glycine or serine, vitamin B6 enables the body to make them from sugar. Vitamin B6 is used also for the synthesis of certain hormones, such as adrenaline. enotes

B6 generally helps me a tiny bit when I am reacting, but it can make me feel worse if I take it every day.

Vitamin B-6 deficiency has been shown to increase urinary oxalate excretion. This represents the body’s inability to convert glyoxalate to glycine, which is necessary to synthesize glycine and serine. Springerboard

It’s interesting that a B6 deficiency causes a deficiency of glycine and an increase in oxalate production. I can see from this how prolonged, genuine B6 deficiency, OR a genotype/phenotype based low production of the enzymes involved, could cause hyperoxaluria in combination with a low tolerance for pharmaceutical doses of salicylate or benzoate.

The quantity of endogenous oxalate produced in these experiments must be related to the amount of oxalate precursors ingested and the degree of vitamin B6, deficiency produced. It appears from this study and that of Calhoun et al. in vitamin B6-deficient rats and the work of Archer et al. and Scowen et al. in cases of primary hyperoxaluria, that a considerable amount of urinary oxalate may be of endogenous origin and derived in great part from glycine. Oxalate has been shown to be formed from glycine via glyoxylic acid (10, 11) and inhibition of the system described by Cammarata and Cohen (12), i.e. glyoxylic acid plus glutamic acid, glycine plus a-ketoglutaric acid, could result in an accumulation of glyoxylic acid with increased oxalate formation. Endogenous Oxalate Synthesis and Glycine, Serine, Deoxypyridoxine Interrelationships in Vitamin B6-deficient Rats [pdf]

This is why glycine supplementation makes me very nervous, like everything else it can backfire and make things worse, and eventually it distorts something else. Unless you know exactly where the problem lies and what’s causing it, the odds are against you getting it right. This is why I don’t supplement regularly with anything anymore.

The body normally has plenty of glycine going spare – it is given to patients suffering from aspirin toxicity, but there is no evidence that someone who experiences side effects from the tiny quantities of salicylates in food (say, 1mg or so) would require supplementary doses of glycine. I think the human body would simply stop working if natural levels of glycine were so low they couldn’t soak up that little salicylate!

Written by alienrobotgirl

7 January, 2007 at 10:46 am

Posted in Don't Do This


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Something I have noticed is that lentils seem to give me energy and clear my head. Wheat germ seems to do the same thing, as long as I don’t eat it too often. I don’t think this is because they are low GI carbs because oysters and mussels have the very same effect – but scallops don’t. I could also blame it on the folic acid lentils and wheat germ contain, or the betaine wheat germ contains, but one common factor amongst all of these foods is they are particularly high in trace minerals. Oysters are high in zinc and copper, and mussels are high in manganese. Yet supplements do not have this effect on me, in fact, I have very negative experiences with zinc.

One thing they are all purportedly high in (there are no proper tables), is germanium. According to mainstream medicine, it’s a supposedly useless and potentially dangerous mineral. According to a standard safetly data sheet, absolutely harmless. According to the world of alternative medicine, something of a godsend. The claims are that germanium sesquioxide is somehow involved in processing oxygen in the body and releasing energy, that it’s extremely good for asthma, and that it fights cancer. On the packet it says “do not take at night.” I had to buy it from the US, of course, because the UK government forced a voluntary withdrawal of germanium sesquioxide from the UK market a few years ago (something this government seems to be very good at, forcing ‘voluntary’ withdrawals).

Being a total skeptic, I would rather make my own mind up as to what germanium does than listen to anyone else. So in typical fashion, I blew my lentil trial by taking some germanium yesterday morning. I didn’t go to bed until 1am because I wasn’t tired, and I woke up at 5am and couldn’t get back to sleep. I will probably collapse this afternoon!

[Edit: a number of further trials proved to me that germanium is quite a strong stimulant and should be avoided unless you really need a kick up the butt!]

Written by alienrobotgirl

26 November, 2006 at 10:48 am

Posted in Don't Do This

A few sulphur experiments

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First, determine whether you are sensitive to sulphites. This is a tricky experiment to perform, not because it is hard to get hold of sulphites, but because it is dangerous. If you have asthma or are prone to extreme reactions, you may want to determine whether you are sensitive to sulphites based on your history. If the reactions are controllable, you may want to determine with a test.

If you are sensitive to sulphites, you may be low on sulfite oxidase. Cofactors for this enzyme are heme and molybdenum. As far as I can find out, low sulfite oxidase can be caused by:

  • Depletion of molybdenum
  • Tungsten poisoning
  • Damage to pterin/folate metabolism
  • Porphyria-impaired Protoporphyrin IX production (part of the enzyme)
  • Severe anaemia (heme is part of the enzyme)
  • Genetic polymorphisms resulting in inefficient versions of SUOX

In my case, sulphites in wine give me asthma, sickness, and diarrhoea.

Try supplementing the cofactor molybdenum to see if it improves symptoms.

After establising this, find out if you are sensitive to MSM (methylsulfonomethane or methylsulfanylmethane). If you are sensitive to sulphites you probably will not tolerate MSM as it also requires sulfite oxidase in order to be converted to useable sulphate.

In my case, MSM gives me asthma.

Find out if you can tolerate magnesium sulphate (epsom salts). Inorganic sulphate is not well absorbed from the gut and can sometimes cause unpleasant reactions because it is broken down in the gut into sulphites. It is better taken in a bath or a footbath. Be sure not to attribute bad reactions to magnesium sulphate to the sulphate, it may be the magnesium that is the problem. Try ensuring a balance of calcium and magnesium.

In my case, I cannot tolerate epsom salts, even with calcium supplementation, even when taken only in baths and not orally. I get horrible heart-rhythm disturbance after using it.

Written by alienrobotgirl

15 August, 2006 at 2:30 pm

Posted in Don't Do This

The Sippy diet

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The Sippy diet was invented by a Chicago physician of the same name, Dr. Bertram Welton Sippy. He published a paper in 1915 describing his treatment for peptic ulcers, excess acid, and GERD (gastroesophagal reflux disease).

The diet consisted of measured amounts of milk and cream, farina cereal (a bland powdered cereal made from mixed roots and/or grains including wheat), and egg, taken at hourly intervals for a period of time. Patients were simultaneously treated with alkaline powders every half an hour. The powders were known as “Sippy powders” and consisted of sodium bicarbonate and calcium carbonate.

The diet fell out of favour in the 1960s after the publication of a medical article exposing doubled rate of heart attacks in patients who had been on the Sippy diet for a significant length of time. Most of the patients studied had been on the diet for over ten years. The paper in question blames butter fat in the first paragraph, without any supporting evidence.

This paper is often cited as one of the first to “prove” a connection between milk, butter fat, and heart disease. Many different vested interests have seized on this purported link between milk and heart disease, including the vegan society, in an effort to discredit dairy products as a valid food source. Search the internet for “sippy diet” and the vast majority of the articles you find will all be blaming milk and butter fat for heart disease.

In fact the truth is rather different.

Sippy’s diet actually caused a condition known as Milk-Alkali syndrome. This syndrome is caused by the ingestion of large quantities of calcium and absorbable alkali.

“[O]ral intake of more than 2 g/d of elemental calcium with absorbable alkali results in hypercalcemia and alkalosis […] not completely understood.” Says “Milk-alkali syndrome almost never results in death. […] A significant number of patients may be left with permanent renal impairment.”

“Calcium absorption is completed within 4 hours of intake. Avid absorption of large doses may lead to suppression of parathyroid hormone (PTH), which then produces enhanced bicarbonate retention by the kidney. Continuing ingestion of calcium carbonate and bicarbonate retention leads to alkalosis, which causes increased calcium resorption in the distal collecting system of the kidney. Also, hypercalcemia produces a renal concentrating defect that can be considered a form of nephrogenic diabetes insipidus. […] Chronic milk-alkali syndrome can result in metastatic calcification due to high serum calcium levels and relatively high phosphate levels (calcium times phosphate).”

In other words, large amounts of calcium in the form of antacids or supplements deposit in the arteries. Bicarbonate of soda increases the reabsorption of the calcium creating a cyclical effect that continues for as long as oral supplementation continues. This leads to the calcium deposition in the soft tissues including the arteries, which hardens them. Hardened arteries then lead to increased likelihood of heart attacks.

Calcium deposition in the soft tissues only occurs with inadequate amounts of vitamins A, D, and K, factors all heavily available in milk, cream, and yoghurt.

So it was not milk and butter fat at all that caused the observed heart disease, but Sippy powders! How come I am the first person on the internet to notice this stupendously obvious connection?

The moral of this story is to watch your supplementation of bicarb, calcium and other alkalines when you are treating food chemical reactions. Don’t make it a habit.

Written by alienrobotgirl

10 March, 2006 at 2:48 pm

Posted in Don't Do This