Gout Diet Blog

Im 57 years old, and Ive suffered from gout in my right foot forabout fifteen years. The only medication the doctor has prescribedis colchicine which I only take when I feel the tinged of pain comingon.

Ive noticed that my gout episodes have increased over the last year.In the last four months I am averaging about two a month. I alsonote that the medicine seems to have no effect.

My question relates to diet. I am desperately trying to determine ifthere is something in my diet that is triggering the attacks. I quitdrinking alcohol last July (non-alcoholic beer only) and havedrastically reduced my red meat intake. A couple of months ago Icut out shrimp, but my attacks are increasing in their number. Iquestion whether any of the following could be the culprit:

Coffee (two pots a day)

Beans- Im eating vegetarian chili I make and it is made out ofkidney and pinto beans. I eat this twice a week (big bowl eachtime) and often put kidney or garbanzo beans on my salad that I eattwo or three times a week.

Cheese- grilled cheese sandwiches, string cheese, and grated cheeseon my salad.

You can tell from my question that Im not that knowledgeable butany advice would be appreciated. As an aside, Im wondering if Ishould be taking a different medication.

Concerning the possible effects of iron and molybdenumon gout:

I am NOT saying that these are necessarily proven oreven that there exists substantial evidence wherein itwould be sensible to rely on the supposed connectionactually existing.

However, females who menstruate and therefore loseiron, do not get gout. Females who cease menstruationare susceptible to gout. The crystals that precipitatein gout are sodium-urate-iron crystals. This makes therole of iron biologically plausible, but not proven.

Concerning Molybdenum:

It is extremely hard for a human to acquire too muchof this mineral as it is present in the normal diet inonly minute amounts. However, when sheep or cattleingest excessive amounts, they do develop a conditionthat bears similarities to gout. It has been suggestedthat Mo may inhibit certain enzymes at “high”concentrations and since people are so rarely testedfor Mo, no one would know that they have a high Molevel. Mo and S each bind to Cu in the kidneys andimpair kidney function leading to increased uric acidlevels. It seems ‘reasonable’ to consider Mo levels.I’m not saying it should be a primary consideration.

Concerning vitamin D:

It is possible that uric acid directly decreases serumlevels of Vitamin D by inhibiting 1 alpha-hydroxylaseaction. This is not proven, but again there areindications and it is biologically plausible. Since asupplement of Vitamin D would be cheap, have littlerisk and would not require an Rx, I thought it wouldbe a good issue to bring up

I think I have found a small glass-like crystal between a joint inthe article in New England Journal of Medicine.

Under the heading “Results” it states that

“Only 11 percent had undergone arthrocentisis, and of these, 65percent reported having urate crystals in their joint fluid.”

Well that’s not good enough

In Brian Emerson’s book <> it states on page 15

“Because the human body is so complex, nothing in medicineapplies invariably. However, one can work on the basis that crystalsare ALWAYS present in the joint fluid in an acute attack of gout andthat, provided an adequate sample can be obtained, urate crystalsshould be detectable in the joint fluid!

Well in my opinion club rules are club rules. I don’t care how muchpain you have, no crystals no gout - so hop it !

Professor Emerson also states (same page) that

“Ninety-five percent of people who suffer from acute gouthave high urate concentrations in the blood serum for many yearsprior to the first acute attack.”

I note that the New England JofM article found that of the new goutcases 72 percent reported hyperuricemia [high urate concentrations inthe serum].

My take on this is that crystals and hyperuricemia are not asabsolute as factors as they had appeared to be, although they areobviously still the most important ones.

Walter’s information about the build up of uric acid in the fattytissue for [presumably as long as] 10 to 15 years before an attack,makes lots of sense to me. For most of us getting the secretionlevel right in the kidneys and getting the uric acid out of thesystem, over time, must be the answer.

But all of this seems to me to point to (at least) two controlmechanisms at work, hyperuricemia and an unknown factor (or maybemore than one). The unknown factor can cause acute gout even inpatients with low hyperuricemia and even with no crystal formationbut it is rare. Without the unknown factor patients can havehyperuricemia and crystals and yet no gout.

This is a typical problem in engineering it’s the over temperatureswitch AND the lubrication but everyone hayes that, they alwayswant a nice simple solution.

That is probably all that is confusing us in the technology led lobbyin this debate.

But the fact that just because the influence of my theoreticalunknown factor is rare does NOT mean it should be ignored. Raremeans that it is there. And I wonder if it is not related toDIGESTION (and stress) rather than to DIET as such.

My Doc just increased my allo from 300 to 400 a week ago. I seem tobe tired a lot since then. Anyone ever have that happen ?

I just got through my first year without an attack. Alloprinol is the best. The only thing I really changed was no alcohol anymore….well, almost:) 100mga day and thats it. It’s nice to see everyone helping each other with thisgroup.

I’m taking 300mg of allopurinol, if I bruise my wrist. Will thebruise start a gout attack? Do I continue to take the allopurinol orlet the bruise heal, before resuming the medication?

Back from my trip and each day was an aggregation of little terror’s.I was on the end of a bad attack-about 6 weeks worth and had finishedthe last week of the attack with an agressive 1 week of cortizone,which bty the way, for me, does a great job of relieving theinflammation but nothing to make the cause, the crystal deposits,better.

When I am finishing a bout with the pain, my toe seems to be a verysensitive detector for what causes pain. That pain is alwaysassociated with meals. Particularly on a trip, where you are supposedto be having fun, you are under peressure. If not direct pressure,certainly a social kiknd of pressure, to eat some of the great foodthat you encounter on your trip.

Well, I have noticed that there are two kinds of pain stimuliassociated with food. The first will come within one hour of eatingand the second, often not related to the onset or the intensity ofthe second pain happens some 6 to 8 hours after the meal and usuallyhits in the middle of the night. that one, bacause I am now verycareful about what I eat, does not happen very often, but I do slipup and eat a steak or some other offender.

I believe I understand this pain after 1 hour phenomenon now.

Again it goes back to Chemistry but this time it is not really thatsimple. I will try to explain the principle and once you get it, youwill be able to remove some of the stimuli that get you into trouble.i.e. into the pain and swelling.

In the chemistry world there is a phenomenon that has been understoodand taught to chemistry majors for as long as our currentinstitutions have been standing. The Germans of old, I mean back inthe alchemy days had measured the solubility of compounds and thephenomenon dates well back into the 17th centruy. It has to do withsoluability of weakly soluable substances in water and there is, withevery substance, what is called a soluability constant. Ksp is theterm if you are going to ask your doctor but he is unlikely to knowwhat it really means.

Now don’t freak out because you see a formula..

NaU <=====> Na+ and U-This is an equillibrium situation and there is a soluability thatsodium urate will achieve when there is an excess of the solid formand this equillibrium will be establ;ished if the system is a testtube or if it is your foot. The constant K is the product of theamount of Sodium (Na+) times the amount of Urate (U-) that will bedissolved in an aqueous solution. If you increase the amount of, forexample, sodium that is in the solution, then the amount of urate (U-) that it takes to make the constant goes down.

In other words, if you put salt into your system, it will tend tomake the Sodium Urate that is dissolved in your blood want tocrystallize out. Increase your salt intake and you will inducecrystal formation.

I’ll finish this later but you have the overall conclusion.

I am proposing that we need to go onto a low salt diet during anattack. It is the salt in the ood we eat that makes that attack afteran hour of eating. the 6 to 8 hout one comes from breakdown of thefood into the uric acid and tha is different.

Low salt intake during an attack.

The link between lead and gout has been known for along time.I doubt that dental amalgams contribute to gout simplydue to the amount of material available.

Most tests such as serum and urine only indicaterecent exposure, not overall burden.

Often the damage is done and the heavy metals areexcreted.

i went to the doctors at the beginning of this week asi had ran out of drugs for it and was in the middle ofan attack. because of all the arguments on this listabout whether allopurinol should be taken during anattack, i asked him that specific question.

his exact words were “i wouldnt start takingallopurinol during an attack, but i would continuetaking it during an attack”. aaaah, more confusion!!

just my 0.02.

another point, has anyone had attacks in theirshoulder? if you have had this, did parts of your hand(at the end of the affected arm) go numb and remain sofor days? this has happened to me during this attack,although it may be from elevating the arm above myhead (only pain free place for it to go!)

BB guns will chase squirrels out of your yard, but don’t try it on abear.

Let’s talk about a minimalistic approach to gout for just a fewmoments. If your gout can be described as a sore toe once or twicea year, then lifestyle and dietary changes may do the trick foryou. My father only got gout after holiday binging on rich foodsand alcohol, and then he got it only in his big toe. SOMETIMES hewould take colchicine for it, but most of the time he just “rode itout” with lots of fresh water and no red meat for a few days. Hedid this his whole adult life. He is now 84 years old, and NEVERgets gout anymore (due primarily as I observe to the fact he is on arather restricted diet, can’t drink alcohol anymore, and lives astress-free life).

When I first started getting gout, I was able to stave off attacksthrough dietary and lifestyle modifications- BUT, in my case thegout was/ is highly progressive. In recent years, no matter WHAT Idid or did not drink or eat made no difference at all- the attackskept coming- monthly, weekly, daily until I hurt all the time anddeveloped knobby tophi all over the place. Who knows what kind ofpermanent damage gout has done to my joints over the past couplayears? I KNOW the damage it has done to my life. Going from beinga guy who could throw jumping spinning kicks over 7′ in the air allday long to a guy everybody now calls “gimp” is just one example.(I used to be a quite a dancer as well- now I am learning to justwalk again).

Anyway, my point is this- there ARE cases of gout that can betreated with changes in diet and lifestyle, BUT don’t be stubbornabout seeking aggressive medical treatment if the gout becomeschronic. If avoiding “triggers” and drinking lots of water does notprevent your attacks then seek treatment immediately and stay withit because every day with gout hurts your body irreparably.Unfortunately, we have only one true proven preventative treatmentfor gout right now and that is allopurinol. (Remember- NSAIDS,steroids, narcotics all only MASK pain and inflammation- they donothing to treat the underlying illness)