[nobody]

I can’t help you with the reflux other than to say that, like gout, it’s sometimes a misdiagnosis. Unless an examination has demonstrated that reflux is indeed the problem, it could be a stomach or gallbladder issue for instance.

Assuming you really are suffering from gout, it sounds like you’ve only had one uric acid test. If so, get it tested again!
You might well be able to win this battle with diet alone in the long run, especially if you count weight loss as part of diet. It would require patience however. Most of the information about gout and diet out there is also quite bad so make sure you aren’t wasting your time by trying to make the wrong changes to your diet.
Meds could be a great help while you are losing weight and ajusting your diet. The important thing, considering your liver issue and the 6.3 uric acid test (I assume you’re not misreading 0.63 mmol/l as 6.3 mg/dl which would completely change the picture), is to stick to very small doses of allopurinol (and if your doctor wants to give you febuxostat which is also known as Uloric, the dose you ought to try first should be no higher than 10mg which might well be a problem depending on where you live). You could also try completely different drugs or indeed foods known to lower uric acid but the nice thing about allopurinol and febuxostat is that they work well enough that a very small dose could well be sufficient. Even with common foods known to lower uric acid, you’d have to consume so much that it might be hard on your liver for all I know.
Possibly you might also get results by lowering your ferritin. See if that might have something to do with the fatigue you’re experiencing. But you should also find a way to lower your uric acid.

So far I have only been talking about drugs acting on uric acid but there are also drugs you could take to alleviate your symptoms. Unfortunately the drugs most people take for gout symptoms often cause liver function problems and you often need large doses for gout. If you can’t use regular anti-inflammatories because of your liver (if you haven’t tested what that does to your liver, I would strongly recommend against testing a regular anti-inflammatory at the same time as a drug which lowers uric acid), one thing you could do is to take a painkiller to help you sleep (keeping in mind you need to avoid anything containing paracetamol/acetaminophen).
If your doctor suggests colchicine instead of an anti-inflammatory, be aware that is also known to trigger liver function issues. They’d have to look into less common gout drugs if they want to suppress inflammation without endangering your liver.

[nobody]

Having joint symptoms where you never had any before (or only rarely) is expected when you are starting allopurionol.
But the big toe typically gets better quicker than this. Sometimes it lasts longer, especially with insufficient treatment.
2 weeks is not too soon to do a blood test but sometimes you’ve got to play along with your doctors when their ideas aren’t horribly wrong so waiting a little more for your blood test and allopurinol dose increase might make sense. But in the meantime perhaps you could see your doctor about a more effective treatment for your symptoms? Maybe you’re not taking enough colchicine. And if you didn’t get any side effects from Indocid, perhaps you could take it in addition to colchicine. The dose you took the first time wsa probably insufficient but, after being on colchicine for a while, you don’t need to take as much as would be necessary during the most acute phase of an attack and when there’s no colchicine in your system. Some doctors do not understand dosage (a gout attack isn’t a matter of life and death so they have more important things they need to know).
How long you’d need to take colchicine and/or Indocid (or similar) would depend on your symptoms. Unlike allopurinol, you can try to quit such drugs as often as you want. Worst case, you’ll get nasty symptoms.
And unlike allopurinol, these aren’t drugs you want to take every day for several months if you can avoid it (nevermind several years!).

As to the non-joint side effects you mentionned, all the investigation they might require is quitting colchicine. Colchicine has unusually strong side effects. They might even go away on their own while you are still taking colchicine.
But if they persist when you are taking allopurinol alone (or allopurinol together with a drug which has never given you such side effects), yes: I wouldn’t ignore them. Allopurinol is something you want to take for the long haul so you can’t accept the same side effects you’d accept for a drug you are only taking for a few weeks. It may be mere discomfort but it could also signal slow damage or simply a developing intolerance.

The main problem with diet is that most of the information you’ll find by looking around is worthless and that the useful information you can find isn’t comprehensive. When people aren’t told what reduces UA in the first place, naturally they will fail to achieve results.
Sticking to a diet tailored to lower UA isn’t very hard as long as you’re not an alcoholic. Giving up animal flesh is as easy as finding something else you like to eat. It might take some time (obviously you can’t simply yank something nutritious out of your diet without making other changes!) but it’s much easier than losing weight for instance (though losing weight is in some cases the main thing you’d need to do to lower UA!).
I wouldn’t overly concern myself with diet in your situation. You’ve already started allopurinol which works much better than diet. Some things still matter because they complement allopurinol but you’ll most likely be fine if you simply eat a healthy diet (with veggies and stuff) and avoid alcohol as well as other diuretics.

X-rays would only show something after years of pretty serious gout. MRIs are as I understand it not very specific (you wouldn’t ID crystals). Ultrasounds (is that the right word?) is another option which only shows the effects of crystals. Synovial fluid is very specific (it even discriminates between types of crystals) but hard to do correctly so can yield false negatives. I wouldn’t rely on any of these to guide treatment, only for diagnosis.
What works best apparently is DECT scans but that’s fairly new and not many gout sufferers can get them. That’s the one thing (besides blood tests) which could guide treatment effectively.

[nobody]

Hi Fire Titan,

You volunteered a lot of information but not your UA test results. It is NOT the case that simply taking allopurinol will eliminate crystals after a number of months. You must also take enough allopurinol… and how much is enough depends primarily on UA test results. 100mg a day is typically not enough. Maybe you understood this already but I wanted to make sure there was no misunderstanding.
Likewise, dosage also affects the effectiveness of anti-inflammatories.
Lots of people have had attacks on allopurinol. It seems you started very soon after you experienced your first clear gout symptoms so you are less at risk and a sufficient dose should cure you quicker than many others.

About side effects, it really depends on the individual.
You should AT LEAST get your your liver and kidney function markers tested. These are fine in most cases but not in every case! Allopurinol is a harmful drug to some people and a deadly drug to a few.
But this is not all about blood tests. The side effects you feel also matter and the ones you listed are somewhat worrying in my opinion.
I’d say the first thing to do is to determine which drug is causing this. AFTER getting a blood test, is it possible you could stop colchicine and take prednisone instead for a short while to see what that does to the side effects you’re experiencing? Ideally, you’d want to test allopurinol alone but that may not be practical depending on your ongoing inflammation.
There are alternatives to allopurinol nowadays if it turns out you are suffereing from persistent side effects. So don’t keep taking a drug which slowly grinds you down.
And if it turns out you aren’t getting serious side effects from either anti-inflammatories or colchicine, consider taking both to suppress gout symptoms (obviously you want to discuss drug combinations with your doctor before trying them). Some people have taken quite large amounts of both drugs which is obviously not ideal but as you’ve noticed gout can be debilitating so some people are motivated to do whatever it takes to suppress the symptoms.

The effectiveness of changes in diet and lifestyle also vary a lot between individuals. I was able to lower my UA by more than 1mg.
Fish and chicken are also meat, and no better than mammalian meat as far as UA is concerned. Avoiding mamallian meat might have an effect on your iron however but research this carefully before jumping to conclusions.

[nobody]

It was predictable that they’d bullshit you. There has been a little research on this and, equally predictably, the outcome was that you’d eat fewer of the problematic purines by going for soy instead of shrooms.
I’m sorry to say “moderate levels of purines”, “high in purines” and so forth are effectively bullshit as well.

Bottom line: eating the body of any organism tends to raise your uric acid. Best get most of your nutrition from stuff based on things like seeds and milk (that would include stuff like tubers, fruits and eggs for instance).
But the bodies of most land plants have very large cells so they don’t have many of the problematic purines. And relatively to these purines, they contain a lot of minerals, vitamins and the like so by eating the parts of land plants that are unlike seeds, you might get health benefits that outweigh the impact on uric acid (indeed, the beneficial effects could actually lower some people’s uric acid in spite of the purines).

Another problem with stuff like Quorn is that its nutritional value is poorly understood compared to stuff like soy. If you care to learn how to design a fact-baed vegan diet, you’ll have an easier time relying on a mix of well-known plant products than wannabe meat substitues.

[nobody]

Sure, you can afford to take your time.
Each additional mg has less effect so your estimate is too optimistic. On the other hand, SUA values often keep dropping a bit even if you don’t increase the dose during the first month or two. So yeah, 150mg might perhaps bring you down to around 5.5. But be aware there is some noise in test results so the next one could potentially be a disappointment. Averages are the most informative numbers.
As stated above, the main reason to aim at 5 (a pretty random target but you have to pick a number) would be the amount of time you left your gout to fester. This means you’ll probably be stuck with gout symptoms for quite a while and a lower SUA should theoretically both help keep these symptoms fairly mild and speed up the curing process a bit. The evidence for this is quite weak but that hasn’t stopped our host talking about taking the maximum dose without regard for SUA values. For what it’s worth my doctors don’t care much for targets either and figure that lower is better. At least there’s some support for using 5 as a target in the guidelines. In the end, you’ll have to observe the effect of the therapy on your symptoms over several months (keeping in mind the cognitive biases we are all subject to) and make an educated guess about what target might be right for you.

[nobody]

In my opinion, in your situation there’s no need to check again after an increasing your dose to a mere 150mg. It would be ideal to check very often but lots of doctors would have you go straight to 200mg anyway. So I think increasing first to 150mg and then to 200mg after only two weeks and without waiting for another blood test also makes sense.
And like I said above, I think it would be reasonable to target 5 rather than 6 in your case which is why I had already dismissed 150mg as a dose you would want to settle on. One always need to wait for several blood tests to confirm one’s guesses but 200mg looks like a more reasonable dose for you.
That said, as long as you seem to tolerate well the drugs targetting symptoms, there’s no urgency to increase your dose so you could justify being very careful. The one important thing was not to delay further the test you’ve just done. Since everything seems to be going smoothly, I don’t think there could be a strong argument against the details of any dose increase schedule you or doctor(s) might fancy at this point.

[nobody]

I would personally take colchicine or naproxen before pain gets to 5.
But these numbers are of course subjective. And everyone reacts differently to the drugs. It’s useful to read about what other people are doing because it gives you ideas you can try out. But you’ll have to come to your own conclusions.

This warning is probaly pointless but 60mg colchine may very well be a deadly dose. You’re not supposed to take much more than 1mg at once or more than a few mgs over the course of a day. The pills are usually 0.6mg, 1mg, or 0.5mg so I don’t think anyone would accidentally take 60mg but I’d rather clear this up just in case…

As to your original question, yes: trying smaller doses first generally makes a lot of sense when there is no emergency. There are exceptions like antibiotics but I’m not aware of a reason to avoid non-standard steroid doses. But steroids are something I know very little about. I don’t think there’s any forum regular who has much experience with this class of drugs unfortunately.

[nobody]

As you can see the forum isn’t very active and so the members of the forum pretty much all use words in their own way.
I’d say the duration, location and specificity of the symptoms matter as much as the pain. The main thing I take away from your description for instance is that you’d probably benefit from increasing your allopurinol dose sooner rather than later (assuming the blood test doesn’t come back with a red flag). And that’s got nothing to do with pain levels. Instead, I focused on things like “slightly puffy for months” because one of the points of increasing one’s dose slowly is to avoid triggering inflammation. But it looks like you might have constant inflammation to begin with! Inflammation in a single location which hasn’t resolved after a week also suggests you might have too much uric acid in your blood.
Either you take the time to describe your symptoms or you don’t. If you want to sum them up with a word or two, I don’t think the choice of word matters a great deal: absent a fairly detailed description, people will have trouble guessing what’s happening to you.
Gout symptoms vary quite a bit, which is part of why doctors have so much trouble diagnosing gout when you’re not in the middle of a textook acute MTP1 episode. Indeed I wouldn’t swear the ongoing symtpoms you’re experiencing on your second toe joint are due to gout. Don’t get me wrong: it’s probably gout. But if you didn’t have big toe attacks for several years previously, I would be more skeptical.

In all likelyhood, you had deposits there for years by the way (they haven’t migrated).
It’s your body’s irritation with the deposits which migrates, for instance because some dormant deposit becomes unstable or because fresh crystals develop next to it.

[nobody]

I don’t know that these words are defined anywhere in a standard manner. Some people might use these two words to mean the same thing.
Because of the different locations which might be affected, you could for instance have severe mobility issues or be unable to put your shoes on (not necessarily both at the same time) without much pain at rest. You might also not see much (if any) swelling or redness if the inflammation is deep under the skin.
So what we’ve got is mainly a standard description of the textbook MTP1 (big toe joint) attack: severe pain (at rest as well as to the touch), swelling (with unusually warm skin) and redness. But not having all the signs doesn’t mean it’s not gout, especially if a different location is affected. If you want to call it flare rather than attack when your big toe gets some but not all the symptoms or when the pain isn’t that bad, that makes sense but don’t expect everyone to use the word “flare” that way.

[nobody]

This is going to be a frustratingly slow process so there’s no point in trying to ask all the questions right now.
The only urgent questions relate to potentially serious side effects, especially if you noticed anything strange happening to your skin, lips and so forth. If the blood test comes back with strange values, that would of course also raise urgent questions.

Like I said, changing one’s dose is in the guidelines so it’s certainly not unheard of! In your case, the motivation for doing something a bit more complicated than usual would be the amount of time you allowed your gout to fester without treatment.
Most doctors are terrible at treating gout so imitating common practices isn’t a very good idea.

Initially, the effect of allopurinol often seems to increase over time but that’s probably not due to an increased effectiveness of the drug but to negative feedbacks. There are many confounding factors so you may not observe this increase.
There are also diminishing returns (or in other words a diminishing marginal effectiveness) with increasing doses but that’s a different issue.
Over longer periods, changes in your body’s ability to eliminate both uric acid and allopurinol metabolites will affect your SUA even if your lifestyle and diet didn’t change. It would be very difficult to tell whether there is a small change in the effectiveness of drug itself. I’m not aware of any conclusive results and the default assumption should I think be that the effictiveness doesn’t change over time.

[nobody]

I did find random pills purported to contain orotic acid online. Unlike the milk thistle pills which seemed serious enough, I can’t recommend them and so won’t link to them but there you go: there actually are pills containing compounds other than protein normally found in dairy and known to lower uric acid. 🙂 I should note that there is a concern about the carcinogenic effects of high doses. Best case scenario: you would only get a small fraction of the benefits of dairy so better consume regular dairy products if you can tolerate them both physiologically and ethically.

[nobody]

Sorry, I was mistaken. I looked it up and it turns out milk thistle is actually a plant! Maybe I should qualify my statements more carefully next time I’m working from old memories…
There have been studies using dairy extracts other than protein but I’m not remembering any other pill than the one which doesn’t actually contain dairy… which isn’t to say that there’s no such pill of course. And if you’ve got no particular reason to avoid dairy protein, you can use regular dairy extracts.

[nobody]

Yes, dairy provides protein but extracts containing (virtually) no protein also lower uric acid. It’s one of the best-established relationships in the field along with the effect of alcohol.
As to cherries, have you checked Jacob et al. (see the footnotes of the British guidelines)? Possibly it’s a junk paper but some expert thought it was worth referencing. I haven’t read it myself. It’s not the only one claiming an effect on uric acid anyway.

The fat metabolism does play a role in gouty inflammation… again, it’s not a cause of gout but modulates its expression. Keith has a page or two about this on Goutpal.
There is also as you mention the fat-related comordities of gout. Though it obviously isn’t relevant for every individual, certain fats are maligned for a reason regardless of the popularity of some truther barguments.
On top of that, there is weak evidence suggestive of fatty diets contributing to high uric acid. Carbs other than fructose (and of course sugar) seem to give better results in studies. Anectodally, many have come to this forum saying they developped gout after going on a low-carb diet. But this may of course be due to excessive protein intake or simply purines.

[nobody]

This stuff is quite complicated and there’s apparently not much motivation to research it. Basically, there are drugs that fix the problem so why bother?
I’m sorry to say that the studies actually looking at purines numerically (which isn’t the norm) rarely differentiate properly between purines. Outside of lab-type reasearch I’ve never seen a dietary study that actually does this. Which isn’t to say that there are no such studies. I didn’t look very hard and I’m not an expert.
I’ve seen fairly reasonable review articles, very focused clinical-type studies (here’s how these new food products or this specific diet we designed affects uric acid) as well as epidemiological-type studies reliant on self-reporting but nothing clinical about the broader dietary issues. Even the basic studies I found looking at fast human response to artifical intake of various compounds are quite old.

It does make sense to track purines but on the one hand most lists aren’t very useful and on the other there are lots of non-purine factors so it doesn’t make sense to focus too much on purines.
In the absence of adequate data, the basic rules I would propose for purines (even though they aren’t fully reliable) are:
-limit consumption of the bodies of organisms other than land plants, anything made from such as well as mystery foods (if you aren’t using an effective allopurinol dose or equivalent, make that drastically limit)
-try to look up the specific purine content (hypoxanthine and so forth) of the land plants you regularly eat in large amounts and look at alternatives in case it looks like they might be a problem
-if you’re eating foods other than land plants, also take a look at some of the very worst foods such as sardines and avoid them as much as possible

You are correct that chicken isn’t better than red meat in terms of purines. Indeed, if you discount organ meat, chicken is generally worse. But again, there are other concerns than purines such as cholesterol, hormones, allergenic compounds and heme iron.
Maybe this is good time to stress purines would normally not trigger gout attacks (unless perhaps you grossly induldge). They are a major factor in causing gout in the long run but triggers are something else. This distinction is poorly understood, including by doctors. Diurectics, certain fats and allergenics for instance might trigger attacks.
This is why some people might get attacks after eating fatty mammal meat but not chicken. From this they might incorrectly conclude that chicken doesn’t cause gout.
To be clear, after successful treatment triggers won’t do anything.

As to foods known to lower uric acid, dairy is the best known case. There are actually “natural” UA-lowering pills containing dairy extract for people who don’t want to consume actual dairy. For the same reasons chicken might be recommended over red meat, guidelines recommend consuming lots of low-fat dairy such as skimmed milk and yogurt made from such as opposed to cheese.
There are a few uric acid-lowering compounds occuring naturally in other foods (more so in herbs). This is why cherries are traditionally recommended to gout sufferers for instance. I think many berries have the same stuff. As you say, vitamin C also has an effect so I guess kiwi fruits could be said to be an UA-lowering food.
In some cases at least, alkalyzing urine also lowers uric acid. So one might argue many vegetables and even some fruits lower uric acid on that account.

[nobody]

It’s not clear what information you have about purines or where it comes from but it seems you’re using some kind of high/medium purine list. These are notoriously bad.
Beyond the obvious (even if the lists were based on good data, you’ve got to draw a line somewhere to make such lists while your body doesn’t care about the line between “high” and “medium”), purines too are merely a category and abstractions do not increase uric acid. Particular purines increase uric acid and different foods contain varying mixes of purines. So useful data about beer (or anything else) would tell you how much (a number, not “high” or some other word) hypoxanthine, xanthine and adenine there is in your beer.
This is why beer filtration matters. Dead yeast particles are a problem not so much because of the gross amount of purines but because of the specific purines they contain. Generally, non-plant cells are a problem.

Wine consumed with a low purine diet does increase UA. Whatever you eat, you’re producing uric acid. As you noted above, dietary purines are significant but are typically only a small part of the problem.
Traditionally, gout sufferers were warned against white wine in particular which (sometimes? again, I’ve never seen useful data about this) contains diuretic compounds other than alcohol. You’d be surprised where you can find diuretic compounds (some Turkish pastries for instance).

[nobody]

Yeah, I’m not aware of any real research on the issue. It doesn’t seem like a very productive research topic really since allopurinol can cure almost every gout patient who can tolerate it and its dosage has very little scientific basis to begin with.
Purines aren’t a big factor compared to the uncertainty regarding how low you should try to get your UA. Alcohol as such (not the purines in alcoholic drinks) is more of a problem in my opinion, as are nutritional deficiencies which can, together with allopurinol and excessive purine intake, contribute to kidney problems in the long run.

You can be much, much less strict with your diet after successful treatment. Again, the side effects of the drugs are the main concern, not gout attacks. In the initial phase of tratment, while you are still experiencing gout symptoms, I would recommend some caution but even at that stage, there’s little point in being very strict.
As long as you tolerate allopurinol well, you can eat meat without fearing gout. No question. Heart disease, kidney disease and so forth are much more serious concerns. Meat is only a serious problem for gout if you aren’t getting treatment or if you can’t moderate your consumption.

My turn to ask you a question since you care about your purine intake: where do you get informtion about the purines contained in your beer?
I’m not trying to justify consuming beer since I haven’t had a beer in decades but there’s bound to be great differences between beers and I strongly suspect beer is generally nowhere as bad as it’s made out to be. I have some idea of how dangerous beer yeast is but I don’t think I’ve ever seen useful data about actual beer.

[nobody]

Perceptions are all over the place. Really, I wouldn’t say most people are trying to be perceptive. Instead, they’re trying to justify the diet they want to have by any means necessary. And most people have very little dietary knowledge, including doctors. The scientific research is also scant and the published data inadequate. Diet is effectively a religious matter.
I’ve seen enough people killing themselves slowly with alcohol, meat and sugar that I’m kind of past caring. I remember a long-dead relative’s notebook about how he was poisoning himself better than his face because simply quitting the stuff was unconceivable.
So yeah, I’ve known people quite a few people who had (or are still having) a “normal” liefstyle on allopurinol. Certainly most people can control their UA while indulging. It simply takes a bit more allopurinol than would otherwise be necessary. The issue is, how does your liver like it? Side effects are more complicated than just the liver of course but be mindful that combining allopurinol and alcohol is going to have implications beyond UA over the years.

[Author]

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