Category: Illness or disabilities
Introduction and description
Gout is a medical condition usually characterized by recurrent attacks of acute inflammatory red, tender, hot, swollen joints. Many pathogens and toxins can cause exactly the same sort of symptoms, but be classified medically by a different name. The disease called rheumatoid arthritis, for example, results in similar excruciatingly painful joints and swelling.
To be classified as gout, the ‘pathogens’ have to be uric acid crystals. The needle-like crystals of uric acid precipitate in joints, tendons, capillaries, skin, and other tissues. Kidney stones can also form through the process of formation and deposition of sodium urate microcrystals.
In some respects it is only the disease’s history that has caused a separation of it from other skeletal inflammatory diseases. The crystals, in this sense, are just another irritant getting into the joints. The main difference is that the crystals are produced by the body as a result of an agent [of which more in a moment], whereas many other arthritic diseases are caused directly by viruses, bacteria, toxins like smoke particles [from cigarette smoking or pollution ] or parasites.
Historically gout may even have been a disease caused directly by a toxin. In the days when wines and port was brewed in lead lined vats, the lead would often leech into the wine and cause lead poisoning. The symptoms of lead poisoning include aggression – and indeed gout sufferers of old were known for their aggression, as well as rheumatoid arthritis or arthritis. Some artists on this site had truly debilitating arthritis from the lead poisoning form their paints. Raoul Dufy and Renoir both suffered in this way.
Thus today’s gout may not be the same as the gout described in historical records, or it may still be, in part at least.
Gout was historically known as the disease of king’s and the rich man’s disease in the days when it was associated with wine, port and lead paints, but these days it is very common and even more important it is present in people who do not drink much wine, if any. So something is happening here that we need to take stock of. Havelock Ellis found in his A Study of British Genius (1904) that there was an unusually high rate of gout among eminent men in his study - the sort of people who drink their sherry and port from lead crystal decanters.
Gout affects about 1 to 2% of the Western population at some point in their lives.
America, Europe, Australia and South Africa are the countries where gout is most prevalent acording to this 2007-8 survey. One in every 40 'Brits' [British citizens] are affected by gout according to Gout Nation 2014.
The chart to the right is of added interest.
According to this chart, produced from a quick and therefore rough survey, [the numbers are in thousands], France has an unusually large number of gout sufferers.
And it may not be the wine consumption that is the culprit.
Gout is usually characterised by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. It is acutely excruciatingly painful.
After going to the emergency room they told me it was gout. The pain was unbearable. They sent me home with pain pills and that was it. A few weeks later it was now in my shoulder, ankle, and hip. Words can't describe my friends.
The joints in the toe are frequently the subject of the attack. However, it can attack other joints - toe joints, heels, knees, wrists, and fingers. It is noticeable that some people diagnosed with acute arthritis are actually suffering from gout but do not realise it.
There may be fever and fatigue from the pain. Gradually, over time, hard, deposits of uric acid crystals known as tophi build up and if they grow to any size they can deform the joints and lead to chronic arthritis due to bone erosion. The elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation.
Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance, and abnormal lipid levels, occurs in nearly 75% of cases. There can also sometimes be psoriasis – a symptom of lymph disease and a sure sign of pathogen or toxin invasion.
In theory, the pain from a gout attack is from the uric acid crystal shedding it's outer protein layer. White blood cells attack the raw crystal as a "foreign invader" because it appears new without its outer protein layer. You build up a new protein layer around the crystal and the pain subsides. There are however, extra facets to this explanation.
The gout James Gillray [from Wikipedia]
If you read the medical literature it says, and I quote:
“The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of gout.” [Wikipedia].
But this is not a cause, it is a symptom. This is better, but only a bit better:
“The clinical manifestations of gout occur as a result of immune responses to monosodium urate crystals.”
So the pain and inflammation is an immune response to the crystals, but this is just working back in the chain. Why did the crystals go there and why do they form?
Uric acid or ‘urate’ is not a toxin. It is present in the blood naturally. In humans, over half the antioxidant capacity of blood plasma comes from uric acid. Uric acid is a very powerful antioxidant and scavenger of singlet oxygen and radicals. Its presence provides the body with considerable protection from oxidative damage.
Raised uric acid is a symptom, not a cause, it is an indicator that the body has NEEDED to raise the scavenging and anti-oxidant activity in the blood, because there are pathogens in the blood. The technical term for raised uric acid levels is hyperuricemia. Hyperuricemia does not need to be treated, what needs to be treated and eradicated are the pathogens that have triggered its elevation. I repeat, it is a symptom and not a cause.
In effect we are asking the same question when we ask 'what causes the crystal to form' and then 'what has raised the uric acid levels' - because it is probably the same pathogen.
Gout can occur where serum uric acid levels are as low as 6 mg/dL (~357 µmol/L), but an individual can have serum values as high as 9.6 mg/dL (~565 µmol/L) and not have gout, so there is a question-mark here not only as to what causes the higher levels of uric acid, but also what makes the uric acid precipitate.
Toxins pathogens and crystal formation
When I was a child, my cousin Susan and I would grow crystal gardens on the window-sill of my uncle and aunty’s kitchen window. When crystals of a number of metallic salts are dropped into a solution of water glass, simple or branching stalagmites of coloured metal silicates are formed – just like those found in gout. Metal salts used included the sulfates and/or chlorides of copper, cobalt, iron, nickel and manganese.
Thus crystals form in the presence of a plasma like solution and in the presence of metals. They also form in the presence of a ‘seed’ crystal. A seed crystal is a small single crystal that you put in a saturated or supersaturated solution to grow a large crystal. The seed crystal does not have to be the same substance as the crystal you want to form, it just needs to be something similar and crystalline – which metals are.
In other words, gout crystals grow because there is a ‘seed crystal’ already in the joints – an agent or a toxin around which it can form. Heavy metals appear to be one sort of seed, and lead and mercury have both been already implicated as agents of gout. In thinking about this one should not forget the effect of faulty dental amalgam fillings.
But many smokers suffer from gout and rheumatoid arthritis, so the seed crystals here are the tiny smoke particles from the cigarette smoke that has entered their blood stream.
There may be other ‘seeds’. We are now being bombarded by any number of toxins in the form of pesticides, insecticides, and so on, all of which are chemical and all crystalline.
So we now need to ask, apart from all the multiple toxins in the environment, the vast majority of which could act as seed crystals, what other sorts of toxic substance could - by their ability to poison - have caused the raising of uric acid levels and by their ability to act as a seed crystal have provided the basic structure on which uric acid crystals could grow?
Pharmaceuticals may be acting as seed agents or may be creating the high levels of uric acid because they are toxic to the body. It may indeed be a good indicator of just how toxic a pharmaceutical is to measure uric acid levels.
The following links take you to eHealthme, and show the drugs that have actually been implicated in causing gout. The lists are based on Adverse Health Reports from doctors in the USA, so will continually change on a day to day basis, as new reports are added. The eHealthme site has a general category of gout and then some more specific categories. We have had trouble with the links to this site. The web site developers have moved pages and thus broken the links. We have provided a link to each symptom on eHealthme. If this ceases to work then the symptom chart on the site will need to be used instead. Scroll down the page for each symptom, until you get to the section 'Drugs that could cause'. Press this link and you will get a list of all pharmaceuticals implicated in causing that symptom :
- Gout - general - LINK - as of November 2016 about 1,150 pharms were implicated
- Gout - acute - LINK - as of November 2016 about 11 pharms were implicated
- Gout - chronic - LINK - as of November 2016 about 4 pharms were implicated
- Gouty arthritis - LINK - as of November 2016 about 350 pharms were implicated
- Gouty arthritis - acute - LINK - as of November 2016 about 11 pharms were implicated
- Gouty arthritis - chronic - LINK - as of November 2016 about 4 pharms were implicated
- Gouty tophus - LINK - as of November 2016 about 100 pharms were implicated
There is an interesting correlation here between the statistics shown in the introduction and these figures. The nations most affected are those who are big takers of pharmaceuticals. A druggy nation is a gouty poisoned nation! There are literally hundreds and hundreds of drugs in these lists, but if we take a look at some of the classes of drugs we can see some interesting patterns emerging:
- Pain killers and NSAIDs - Some of the more interesting drugs included on the list include aspirin, often prescribed to treat the pain of gout, but clearly in this case causing it. Other NSAIDs also appear in the list including COX-2 selective NSAIDs used to treat the symptoms of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and juvenile rheumatoid arthritis in patients two years or older. Vioxx alone has caused well over 600 ADRs. All these drugs could be acting as seed crystals for the uric acid.
- The immunosuppressants - The corticosteroids, specifically glucocorticoids, are also causative agents along with others like the TNF inhibitors. Since the disease is caused by pathogens, in general using immunosuppressants - drugs that suppress the immune system - are bound to have a negative effect. They also apparently upset the carbohydrate cycle meaning that fructose, which in moderate amounts helps in curing gout cannot do so.
- Gout treatments - Another drug which may be a surprise to some is Allopurinol, sold under the brand name Zyloprim/Lypurin and generics, and used "to treat excess uric acid in the blood and its complications, including chronic gout". It has resulted in literally thousands and thousands of ADRs and not a few deaths. Since uric acid is not the cause, but a cure, one assumes that by lowering uric acid one effectively removes all chance of the person ever getting better. It may also be acting as a seed crystal and causing gout.
- Beta blockers - also figure quite strongly as causative agents, which appears to indicate the body regards them as toxic
- Calcium channel blockers - which may result in calcium in the blood stream - another seed crystal, but also appears to indicate the body regards this class of drug as toxic
- Diuretics - particularly, but not exclusively, loop diuretics. Yet again indicating the body regards this class of drug as toxic
- Blood thinners - like Clopidogrel. Here the mechanism by which gout is produced are difficult to work out. It might be that simply altering the blood's composition results in lower uric acid concentrations and thus more chance for pathogens to act.
- Proton pump inhibitors - reduce stomach acid. Hydrochloric acid is required for the digestion of proteins and for the absorption of nutrients, particularly of vitamin B12 and of calcium, thus PPIs send undigested and unusable food through to the intestine. This may 'leak' into the blood stream, acting as a toxin. Furthermore a lack of stomach acid allows pathogens to proceed through to the intestines
- Anti-diabetic drugs - interfere with sugar levels and sugar levels seem to be key in determining uric acid levels. See fructose and sucrose digestion. Biguanides, for example, reduce hepatic glucose output and increase uptake of glucose by the periphery, including skeletal muscle. So in general they are interfering with the uric acid levels.
- Anti-biotics - whose action may serve to reduce the gut flora and thus allow pathogens and toxins to enter the system
- ACE inhibitors - these drugs act on the kidney and appear to have side-effects related directly to uric acid levels.
A low dose of MSU crystals, which did not induce inflammation in control animals, caused signs of acute gout attacks in ACEi-treated animals: PMID: 25344431
- Anti-histamines - also appear to figure strongly, which is to be expected. The histamine reaction by the body is to enable the immune system fight pathogens. If you suppress the immune system, the pathogens will of course multiply unchecked and gout, along with most arthritic conditions will become more severe.
- Statins - are present in large numbers as causative agents. Statins are used to lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, in the liver. Cholesterol is an essential structural component of animal cell membranes. It is required to establish proper membrane permeability and fluidity. It is thus a repair material. Statins take away the repair material, and furthermore, as cells are attacked by pathogens, ensure that there is nothing to do any more repairs with. They are a form of slow death. High cholesterol is a symptom not a cause - a symptom of attack by pathogens. Statins are treated as a toxin by the body.
- Osteoporosis treatments - also occur frequently in the list. This class of drugs results in numerous side effects, one of which is death, so it is not surprising to see it in this list. The example below covers just one of several drugs in this class
Source: eHealthme - On Dec, 04, 2016 81,353 people reported to have side effects when taking Fosamax. Among them, 464 people (0.57%) have Gout.
On Nov, 17, 2016: 81,344 people reported to have side effects when taking Fosamax.
Among them, 1,970 people (2.42%) have Death
One cause of gout appears to be vitamin supplements. If we take one example - niacin supplements [under the brand name niaspan] these are the figures from eHealthme
Source: eHealthme - On Dec, 04, 2016: 42,829 people reported to have side effects when taking Niaspan. Among them, 228 people (0.53%) have Gout
Taking another example, to show this is not an isolated example, the multivitamins have also had an effect
On Nov, 29, 2016, 13,820 people reported to have side effects when taking Vitamins.
Among them, 35 people (0.25%) have Gout
These figures may be a significant underestimate of the problem, as many people associate vitamins with 'health' and in the rather simple way people often think, more vitamins means more health - which it doesn't. Thus vitamin overdose as a cause may be being significantly under reported.
Vitamin tablets are mineral based and crystalline and in overdose are probably migrating via the blood stream to joints to act as seed crystals.
Mineral supplements appear to have a similar record.
A particle is defined as a small object that behaves as a whole unit with respect to its transport and properties.
The term Nanopowders then describes agglomerates of ultrafine particles or nanoparticles.
Nanometer-sized single crystals, or single-domain ultrafine particles, are often referred to as nanocrystals.
They are one of the most dangerous new inventions by science to have been released into the environment without adequate analysis and understanding of their damage. And they are being implicated as seed crystals in gout amongst many other diseases.
It is not generally recognised that bacteria can have a crystalline structure. Enteric bacteria [part of the gut flora] may have a crystalline structure; the diptheria bacteria has a crystalline structure. The gram positive group of bacteria are cystalline and of great importance is that they can cause painful crystalline deposition just like gout:
Gram-negative bacteria can cause infectious crystalline keratopathy but have no distinguishing features from infectious crystalline keratopathy caused by streptococci and other gram-positive bacteria. PMID: 9222227
Aerobic spore forming bacteria are crystalline. And so it can go on. Furthermore, research has already linked them with the formation of stones and crystals.
Several species of bacteria were found to form an intracellular crystalline material when grown in urine obtained from a subject with a history of infrequent renal calculi formation. The following species: Proteus mirabilis, Proteus rettgeri, Providencia stuartii, Enterobacter aerogenes, Enterobacter cloacae, Escherichia coli, and Candida albicans formed crystals of hydroxyapatite. Klebsiella pneumoniae, Pseudomonas aeruginosa, and Proteus vulgaris produced crystals of calcite -II. Several of these bacteria have been isolated from the kidneys of patients with renal caculi indicating that microorganisms may be involved in the nucleation process during calculogenesis. PMID: 844994
So bacteria can be seed crystals. And just as a little aside, syphilis is caused by bacteria:...
Review of data in very old charts sometimes brings new insights and perspectives, and suggests new hypothesis for illnesses of patients long deceased. Such applications can be made if enough information is available, e.g., autobiographical letters, skeletal remains, pictorial representations. ... When such an approach was applied to Erasmus (Rotterdam c 1466--Basle 1536), the differential diagnosis included gout, syphilitic arthritis and enteric rheumatism. PMID: 3550075
One factor believed important in triggering an acute episode of arthritis is cool temperatures. The increased precipitation of the uric acid at low temperatures partly explains why the joints in the feet are most commonly affected.
And what likes cold temperatures? Viruses.
Why is it categorised as 'seeding'? Because many viruses have a crystalline structure. A paper has been provided in the observations to show this - PMID: 26085142.
The possible presence of viruses [or other pathogens] is indicated by the fact that white blood cell counts are often elevated due to gout. A white blood cell count as high as 40.0×109/l (40,000/mm3) has been documented. But some of the links to viruses are particularly interesting.
Hippocrates noted that gout is rarely present in the sexually inactive – virgins, young boys and eunuchs. On the other hand it appears to be very prevalent in the very sexually active.
In 1683, Thomas Sydenham, an English physician noted:
Gouty patients are, generally, either old men, or men who have so worn themselves out in youth as to have brought on a premature old age—of such dissolute habits none being more common than the premature and excessive indulgence in venery, and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. The pain is like that of a dislocation, and yet parts feel as if cold water were poured over them. Then follows chills and shivers, and a little fever... The night is passed in torture, sleeplessness, turning the part affected, and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint, and being worse as the fit comes on.
Venery is “The practice or pursuit of sexual pleasure, or the indulgence of sexual desire”
And here we have Aulus Cornelius Celsus (30 AD):
[gout] seldom attacks eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery
This may help to explain why, according to Wikipedia “Rates of gout have approximately doubled between 1990 and 2010”.
Viral agents have been suspected as participants of immune-mediated disorders. In the case of rheumatic diseases, the synovial joint cavity represents a secluded area of inflammation which could harbor etiological agents. We analyzed by polymerase chain reaction the possible presence of DNA from various herpes viruses in blood and synovial fluid from patients with either rheumatoid arthritis (n = 18), axial spondyloarthritis (n = 11), or osteoarthritis (n = 8). Relevant findings were as follows: DNA from varicella zoster virus was found in synovial fluid but not in blood mononuclear cells from 33 % of patients with rheumatoid arthritis and in 45 % of patients with axial spondyloarthritis but not in patients with osteoarthritis. Also, DNA from herpes simplex viruses 1 and 2 was found both in the blood and in the synovial fluid from 33 % of patients with rheumatoid arthritis. PMID: 25980837
The name for a vaccine that has a live virus in it is an attenuated vaccine. Although most attenuated vaccines are viral, some are bacterial in nature. Examples include the viral diseases yellow fever, measles, rubella, and mumps, and the bacterial disease typhoid. As we can see from the description above, gout can be caused by viruses and bacteria. There appears to be a belief by those promoting vaccines that the immune system defeats the virus as it builds up an immunological record. But there is now enough research to show that this is not the case. A virulent strain of attenuated virus may replicate very fast before the immune system has had time to muster its defences - particularly if the virus is injected or administered by nasal spray. A virus is capable of then secreting itself in adipose tissue and the joints and 'laying low'. In those with shingles who are given anti-virals, there is a noticeable increase of rheumatoid arthritis and gout cases. Hypothetically this may mean that anti-virals not only do not work, but may cause the the viruses to escape to safer havens than they had previously enjoyed - the joints.
As such gout may be caused by viruses, obtained from vaccines, emerging at times of stress, or high emotion and thus low immunological function. It may also be caused by the excipient and/or adjuvant - particularly where these contains metals and heavy metals - aluminium and mercury - see this Wikipedia list.
Br J Gen Pract. 1992 Mar;42(356):131. Side effects of influenza immunization. Young G. PMID: 1303654
Fungi are known to be one of the agents responsible for rain drops and snow crystals, in other words they provide a seed crystal on which larger crystals can form. As fungal spores they can enter the body via numerous routes - lungs, vagina, nose etc and then if the immune system has been compromised by, for example, stress or antihistamines, they will get in the blood stream and migrate to any number of organs or joints. And cause gout.
Fungal spores can account for large proportions of air particulate matter, and they may potentially influence the hydrological cycle and climate as nuclei for water droplets and ice crystals in clouds, fog, and precipitation. Moreover, some fungi are major pathogens and allergens. The diversity of airborne fungi is, however, not well-known. By DNA analysis we found pronounced differences in the relative abundance and seasonal cycles of various groups of fungi in coarse and fine particulate matter, with more plant pathogens in the coarse fraction and more human pathogens and allergens in the respirable fine particle fraction (<3 microm). Moreover, the ratio of Basidiomycota to Ascomycota was found to be much higher than previously assumed, which might also apply to the biosphere. PMID: 19617562
Overdosing on Legumes
Raised uric acid levels are a symptom of the ultimate cause - pathogens.
Thus any drug or food that attacks the uric acid levels in a person will not only not cure them it may make them worse - by a considerable degree. High levels of uric acid may simply denote a very high level of attack by pathogens, heavy metals and other toxins.
The enzyme urate oxidase (UO), or uricase or factor-independent urate hydroxylase, catalyzes the oxidation of uric acid to 5-hydroxyisourate. It has the effect of lowering uric acid levels.
It is absent in human beings.
Urate oxidase, however, is found in nearly all other organisms, from bacteria to mammals. Thus by catching certain bacteria and eating certain parts of mammals - notably the liver - we are consuming urate oxidase anyway.
Furthermore, in certain plants, Urate oxidase is an essential enzyme in the ureide pathway, where nitrogen fixation occurs in the root nodules of legumes. The fixed nitrogen is converted to metabolites that are transported from the roots throughout the plant to provide the needed nitrogen for amino acid biosynthesis.
So let us suppose we have a pathogen ........... it is being kept in check by the uric acid levels the body has produced. We then overdose on, for example, legumes - lentils, peas, beans and so on. The uric acid plummets and the pathogens have a field day, reproducing, coming out of hiding and spreading like wildfire. We stop eating the legumes and suddenly the uric acid levels skyrocket in order to fight all these new pathogens. And as a consequence, because some of those pathogens may have reached the joints, we will get gout.
Overdosing on purines
Uric acid is the end product of catabolism of purines in humans. There are many naturally occurring purines:
- Theobromine – found in cocoa and chocolate, as well as tea
- Caffeine – coffee and tea
- Uric acid
Purines are found in high concentration in meat and meat products, especially internal organs such as liver and kidney.
In general, plant-based diets are low in purines.
Examples of high-purine sources include: sweetbreads, anchovies, sardines, liver, beef kidneys, brains, meat extracts (e.g., Oxo, Bovril), herring, mackerel, scallops, game meats, beer (from the yeast) and gravy.
A moderate amount of purine is also contained in beef, pork, poultry, other fish and seafood, asparagus, cauliflower, spinach, mushrooms, green peas, lentils, dried peas, beans, oatmeal, wheat bran, wheat germ, and hawthorn.
So let us suppose we are overdosing on purines but there are no pathogens - or at least relatively few - to fight. The uric acid levels skyrocket because we are overdosing and the body does not have the means to lower the levels because our diet is so unbalanced. Nothing may happen - uric acid levels may be incredibly high, but there are no pathogens in the joints. No gout.
But what if a small number of pathogens are secreted in the joints - and maybe nowhere else - perhaps only the big toe. The pathogen is found and treated as a seed crystal by the immune system and gout is the result.
Overdosing on fructose and sucrose
Fructose can raise uric acid levels. Sucrose is converted by the liver into fructose. A description of how fructose and sucrose are processed by the digestive system is provided in Fructose and sucrose digestion.
So let us suppose we are overdosing on fructose and sucrose but there are no pathogens - or at least relatively few - to fight. The uric acid levels skyrocket because we are overdosing and the body does not have the means to lower the levels because our diet is so unbalanced. Nothing may happen - uric acid levels may be incredibly high, but there are no pathogens in the joints. No gout.
But what if a small number of pathogens are secreted in the joints - and maybe nowhere else - perhaps only the big toe. The pathogen is found and treated as a seed crystal by the immune system and gout is the result.
Some people have an unfortunate gene mutation that means they are unable to process fructose:
Magnetic resonance spectroscopy studies of children with hereditary fructose intolerance revealed a readily detectable rise in phosphomonoesters with a marked fall in inorganic phosphate in their liver in vivo and a rise in serum urate in response to very low doses of oral fructose. Parents and some family members heterozygous for this enzyme deficiency showed a similar pattern when given a substantially larger dose of fructose. Three of the nine heterozygotes thus identified also had clinical gout, suggesting the possibility of this defect being a fairly common cause of gout. PMID: 2236043
In effect, in all cases like this where a food intolerance is found, the food acts as a poison and is treated like a pathogen. The body raises the uric acid to fight the pathogen - in this case fructose, though it could be any food to which a person is intolerant. The raised uric acid levels may then find other pathogens in the joints and gout result.
The more food intolerance or allergy the person has, the more the body becomes stressed if the food is eaten. In other words, uric acid levels may be extraordinarily high in these poor people, but may not always result in gout. It is important to read the section on food allergies, as they are becoming far more frequent and are linked to the excipient used in vaccines.
Prevention and treatment
Although reducing uric acid will certainly help with the symptoms of gout, in the longer term it may make things very much worse, so here we have a dilemma. Without the uric acid to help in your defences, the pathogens could spread all over the place. You will be gout free for months, maybe even years by cutting out all the foods that help in the production of uric acid. But long term, whatever pathogen has caused all this will be everywhere and you will find yourself with untold other illnesses. This thus has to be tackled on a step by step basis
Step one – managing the pain
In this you use a natural, plant based pain killer, we have included some observations on plants that can be used internally and as poultices. Meanwhile eat all the foods that maintain the uric acid levels as they are. The following all help with maintaining uric acid at the level needed by the body:
- Avoid legumes - for the reason explained above under legumes. A legume is a plant in the family Fabaceae (or Leguminosae), or the fruit or seed of such a plant. Well-known legumes include alfalfa, clover, peas, beans, lentils, [and pulses in general] lupins, mesquite, carob, soybeans, peanuts and tamarind.
- Avoid liver - for the reason explained above under legumes
- Eat more fructose containing foods - BUT DO NOT OVERDOSE. A description of fructose is given in the science section. There is also a description of how fructose is processed by the body.
One characteristic metabolic effect of fructose, present in sugar-sweetened beverages (SSB), is raised urate from hepatic processing of fructose. ….. PMID: 25928993
- Maintain purine containing foods - BUT DO NOT OVERDOSE. Uric acid is the end product of catabolism of purines in humans.
Step two – identify the pathogen [s]
This should be done in parallel with step one. This may take time. It may only be in that joint or it may be in other places. Test the lymph and the blood. It may help to test the crystals if this is at all possible.
For crystals to form there has to be a ‘seed’ so logic says you have a pathogen of some sort. One of the problems of the joints is that uric acid [and lymph] is about the only substance that the immune system can use to imprison the invader in a joint. In the rest of the body it tends to use cysts as a means of imprisonment, which on the whole do not hurt.
One of the more fascinating things about gout is that we have isolated it from all the other incidents of the body imprisoning pathogens, simply because it causes pian and is 'visible. We can get 'gout' in the head, but we don't necessarily feel it, for example
.... rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. PMID: 22224190
Step three – Identify the foods needed to fight the pathogen [s]
You then introduce foods into the diet that fight the pathogen – whatever it is, - for example liquorice as an anti-viral. Apples and some other malic acid based fruits like cherries as chelating agents. Since lead and other heavy metals appear to play a key role in starting gout, the chelating agents are key to removing the toxins responsible. Some pain killers also have pathogen related benefits, so this can be checked via their action. This site provides observations to help this process.
Step four – Fight the pathogen
In this you might use, foods, chelating agents as described above, heat, sleeping and so on. It depends on the pathogen
- Heat treatment - if the cause is a virus, heat treatment on the affected joints may be of benefit. ONLY SOME VIRUSES RESPOND TO HEAT TREATMENT. You have to be careful here as some classes of virus are activated by heat, although heat may subsequently kill even them. Saunas may be the best means of achieving this as they provide dry very hot conditions requiring only short exposure, but it may be that over a longer time period and with repeated action even very very warmth baths may have a positive effect. One of my friend cured her granny's shingles by roasting her overnight in a bed with the electric blanket turned up to full volume. I realise this is hardly scientific evidence, and entirely anecdotal, but some grannies are happy to be roasted - she slept like a top.
Terminal dry heat treatment effectively inactivated hepatitis A virus (HAV) and canine parvovirus .... After 24 h at 80 degrees C, HAV infectivity was reduced by > or = 4.3 log10 TCID50, as measured in a newly developed infectivity assay. ... PMID: 7701804
- Sleeping - which enables the body's defence mechanisms time to attack the pathogens
Step four – Dissolve the crystals
Once you know the pathogen has been eliminated – and for this more tests will be needed. You can dissolve the crystals by temporarily reducing the uric acid. Remember that in doing this you will release the pathogen from its crystal cage.
Before you release it you thus have to have a very good strategy for combatting that pathogen.[If it is still active]. Viruses and bacteria may well have been killed by the process, but toxins like lead and mercury will still be active when released.
Remember that the pathogen in the crystal may not be the same as that you have been fighting elsewhere, you may have multiple pathogens. To dissolve the uric acid you lower the uric acid levels by
- Eat more legumes - for the reason explained above under legumes. DO NOT OVERDOSE simply increase the amount you eat slightly. A legume is a plant in the family Fabaceae (or Leguminosae), or the fruit or seed of such a plant. Well-known legumes include alfalfa, clover, peas, beans, lentils, [and pulses in genral] lupins, mesquite, carob, soybeans, peanuts and tamarind.
- Eating liver and other foods containing the enzyme urate oxidase (UO),
- Avoiding all fructose and sucrose based foods - see Fructose and Sucrose to get a list of foods
- Avoid purine containing foods - or at least do not overdose on them [see above]
How it works
See the observations.
Some observations describe healing effects, the observations relating directly to gout have usually been caused either by the extreme pain or the medications.
References and further reading
- J Biol Chem. 2015 Jun 4. pii: jbc.M115.648352. [Epub ahead of print] - Crystal Structure of the Vaccinia Virus Uracil-DNA Glycosylase in Complex with DNA. Burmeister WP1, Tarbouriech N1, Fender P2, Contesto-Richefeu C3, Peyrefitte CN3, Iseni F4. PMID: 26045555
- Ann Rheum Dis. 2014 Dec;73(12):2101-6. doi: 10.1136/annrheumdis-2013-203600. Epub 2013 Sep 11. Sugar-sweetened beverage consumption: a risk factor for prevalent gout with SLC2A9 genotype-specific effects on serum urate and risk of gout. Batt C1, Phipps-Green AJ1, Black MA1, Cadzow M1, Merriman ME1, Topless R1, Gow P2, Harrison A3, Highton J4, Jones P5, Stamp L6, Dalbeth N5, Merriman TR1. PMID: 24026676
- Crystalline inclusions in aerobic spore-forming bacteria. HANNAY CL. Nature. 1953 Nov 28;172(4387):1004. PMID: 13111240
- Crystalline surface layers on bacteria. Sleytr UB, Messner P. Annu Rev Microbiol. 1983;37:311-39. Review. PMID: 6416145
- Crystalline inclusions in aerobic spore-forming bacteria. HANNAY CL. Nature. 1953 Nov 28;172(4387):1004. PMID: 13111240
- Conserved anchoring mechanisms between crystalline cell surface S-layer proteins and secondary cell wall polymers in Gram-positive bacteria Sára M. Trends Microbiol. 2001 Feb;9(2):47-9; discussion 49-50. Review. PMID: 11173224
- Crystalline bacteria arrays and specific long-range forces. GOLDACRE RJ. Nature. 1954 Oct 16;174(4433):732-4. PMID: 13213991
- [Electron microscopic study of a crystalline protein-toxin from diphtheria bacteria]. Kushnarev VM, Minenkova IB. Dokl Akad Nauk SSSR. 1973 Sep 1;212(1):240-2. Russian. PMID: 4584494
- [ELECTRON MICROSCOPE STUDY OF HAEMOPHILUS PERTUSSIS. II. ON THE ULTRASTRUCTURE OF HAEMOPHILUS PERTUSSIS WITH SPECIAL REFERENCE TO THE CRYSTALLINE-LIKE STRUCTURE OF THE BACTERIA]. HATASA K. Nihon Shonika Gakkai Zasshi. 1964 Oct;68:848-54. Japanese. PMID: 14215011
- [Crystalline proteins in certain bacteria of the enteric group]. HALKINA TO. Mikrobiol Zh. 1961;23:35-8. Ukrainian. PMID: 13710741
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