Traditional gout advice on protein rich foods has always been “Avoid them!”

High Protein Foods: How Do They Affect Gout?

But as awareness grows about nutrition in general, and proteins in particular, does this advice still hold true?

And if it doesn’t, what are the dangers of going too low on protein?

Protein Rich Foods: Contents

Protein Rich Foods: Introduction

I’ve experienced growing concern about the advice given to gout sufferers concerning protein. There appears to be confusion between purines and protein, and the advice on protein looks out-of-date in the light of gout research in the current millennium.

A quick look at the topic reveals little clear guidance from government or relevant professional bodies, so I started an in-depth study.

My research has led me down a few deep, dark, sometimes mythical alleyways.

To try to make sense of it all, I’ve decided to split this topic into at least 3 articles. This one looks at current American guidelines, or lack of them. I’ll look next at British guidelines, which in the absence of anything else are in danger of being adopted as a universal standard. Then, I will try and draw some conclusions.

Current Protein Guidelines For Gout Sufferers

High Protein Foods: Rheumatologist Advice

The first stop for gout guidelines should be the American College Of Rheumatologists (ACR). Their nearest thing to a guideline is a 2004 review of gout, diet and alcohol [1]. That document does mention the study into a 40:30:30 protein:carbohydrate:fats diet, but the recommendations are unclear:

Importantly, recent years have seen a surge in popularity of “low-carbohydrate, high protein diets” (e.g., Atkins, Zone, and South Beach diets). In a small, open study in overweight male gout subjects, a calorically restricted diet designed for IR management, with a 40/30/30 protein/carb/fat scheme and customized for high contents of seafood and mono-unsaturated fat as well as continued moderation in alcohol, achieved body weight lowering by ~17 pounds and also diminished hyperuricemia by 17 percent (3). But these results cannot be directly extrapolated to popular “low-carbohydrate” type diets, for which an adequately powered clinical trial in hyperuricemia and clinical gout has not yet been done.

The report is dismissive of evidence that milk protein may be beneficial to gout sufferers. This ignores Garrel’s 1991 investigation showing the acute effect of milk protein on uric acid levels. Also, it has not been updated to reflect Dalbeth’s similar 2009 investigation into milk and uric acid.
The report concludes with recommendations for gout patients, but these are not clearly defined. The protein advice is limited to:

concerns about the potential for ketosis and other effects of popular “low carb” diets heightened in animal protein and fat to exacerbate hyperuricemia and gout.
[and]
Consumption of vegetables with high purine content or a diet high in protein by themselves do not appear to raise the risk of developing gout.

There have been other studies since this recommendation, and I will review those investigations in a separate article. However, in the absence of clear guidelines, it is likely that nutritional and medical practitioners will seek guidance elsewhere.

High Protein Foods: Heart & General Advice

Guidance from the American Heart Association (AHA) is often quoted when health aspects of high protein foods are discussed. There are, in fact, two key protein-related guidelines from AHA, which refer, indirectly to nutrition advice from the Institute of Medicine.

The most authoritative reference, from a protein point of view is the second of their 2 guidelines, “Dietary Protein and Weight Reduction” [2] published in 2001. It is particularly likely to influence advisers to gouty arthritis sufferers, given the statement:

High-protein foods such as meat, poultry, seafood, eggs, seeds, and nuts are high in purines. Purines are broken down into uric acid, so excess consumption of these foods increases uric acid levels and may cause gout in susceptible individuals.

This is a very naive view of purine metabolism, and an unfortunate addition to the confusion that treats purines and proteins alike. Also, there is no reference to the, what was then, recent 2000 study on a 40% protein diet that appears to lower cholesterol as well as uric acid.

Anyway, they are strong recommendations in this AHA guidance to adopt a 15:55:30 protein:carbohydrate:fats ratio:

Total protein intake should not be excessive (average 50 to 100 g/d) and should be reasonably proportional ({approx}15% of kilocalories per day) to carbohydrate ({approx}55% of kilocalories per day) and fat ({approx}30% of kilocalories per day) intake.

It appears that in their haste to warn of the dangers of diets containing too high a proportion of animal protein and animal fat, they have adopted a low protein approach, primarily from the preceding year’s wider ranging “AHA Dietary Guidelines” [3].

I’ll confine myself to the protein part of these guidelines, and admit to some confusion, that might well arise from trying to analyze something from 10 years ago. The key point, echoed in my quote above from the later report, is the statement:

Although there are many conditions in which extra protein may be needed (growth, pregnancy, lactation, and some disease states), an average of 15% total energy or {approx}50 to 100 g/d should be adequate to meet most needs.

Note that the caution to recognize cases where extra protein is needed is lost between the two reports. Delving deeper, we can see how important this is. The AHA recommendations reference Advanced Nutrition and Human Metabolism (ANHM) by Goff, Gropper & Hunt (1995). Unfortunately, I only have access to the 2004 version, though the latest edition is 2008. This makes it difficult to understand if the dangers of low protein have been overlooked, or if they were not recognized when the 2000 Guidelines were published.

In a nutshell, the ANHM recognizes a 10% to 35% range for protein intake, noting that in some situations, especially where energy intake is restricted, 10% may be far too low, resulting in malnutrition. Where necessary, it might be more relevant to look at protein intake, which should be around 80g per day or 0.8g per kg body weight per day in normal circumstances.

The ANHM is a thorough explanation of nutrition issues and the main take-home is that cases need to be considered individually. Also, individual needs will change over time. Therefore fixed protein:carbohydrate:fats ratio’s might serve well as a starting point, but adjustments need to be made in the light of individual circumstances and test results.

Protein Rich Foods: Next Steps

I will continue this review of protein rich foods with an article on British Rheumatology Guidelines. Despite a focus on Great Britain, most of the issues affect every country, and the British guidelines are cited by many international gout studies.

To get a more complete view of current nutrition guidance for gout, especially with respect to protein, I have started the Protein Rich Foods Debate at GoutPal Interactive. If you have received specific nutrition advice from a professional advisor, please share it with us.

Protein Rich Foods: References

1. Author: Robert Terkeltaub. Titled: Health Professionals Follow-up Study on Gout: What Do We Now Tell Patients About Diet and Alcohol? Published: May 2004 Gout, Diet & Alcohol Guidelines
2. Author: St Jeor ST, Howard BV, Prewitt TE, Bovee V, Bazzarre T, Eckel RH; Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Titled: Dietary protein and weight reduction: a statement for healthcare professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Published: Circulation. 2001 Oct 9;104(15):1869-74. Dietary Protein & Weight Reduction
3. Author: Krauss RM, Eckel RH, Howard B, Appel LJ, Daniels SR, Deckelbaum RJ, Erdman JW Jr, Kris-Etherton P, Goldberg IJ, Kotchen TA, Lichtenstein AH, Mitch WE, Mullis R, Robinson K, Wylie-Rosett J, St Jeor S, Suttie J, Tribble DL, Bazzarre TL. Titled: AHA Dietary Guidelines: revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Published: Circulation. 2000 Oct 31;102(18):2284-99.

Milk Diet For Gout: Contents

Uric Acid Percent Change After Milk

Milk Diet For Gout: Introduction

The 1991 investigation claiming milk is beneficial for gout appears to be somewhat ignored by the medical profession. Now, almost 10 years later, a similar investigation reports similar findings. I have not done a full comparison of the two milk and uric acid studies. For one thing, I do not have full access to the latest study. However, you should find plenty of useful information in this summary taken from the American College of Rheumatology (ACR) press release.

Please note that I’ve paraphrased the original press release to make it more readable and relevant to us non-medical people. The full gout and milk report has subsequently been published in the British Medical Journal [1].

Milk Diet For Gout: Overview

The ACR’s press release, ‘Got Gout? Get Milk’, promotes the research presented at their Annual Scientific Meeting in Philadelphia, Pa.

It describes gout as a painful and potentially disabling form of arthritis with symptoms usually consisting of intense episodes of painful swelling in single joints, most often in the feet (especially the big toe).

They note that treatments are already available to prevent or control the arthritis associated with gout, but managing this disorder can be difficult, and treatment plans often have to be tailored for each person. I believe it is vital that treatment is planned individually, which is a key point in the Gout Freedom campaign.

They note that previous studies indicate that individuals who drink a lot of milk have a lower risk of developing gout. Though not specifically referenced, this is almost certainly Choi’s statistical analysis linking high dairy consumption with lower gout incidence.

Milk Diet For Gout: Research Report

The presentation is titled: “The Acute Effect of Skim Milk On Serum Urate Concentrations: A Randomized Controlled Cross-Over Trial” and it’s authors are listed as:

• Nicola Dalbeth, FRACP , Department of Medicine, University of Auckland, Auckland, New Zealand
• Sumwai Wong, Department of Medicine, University of Auckland, Auckland, New Zealand
• Greg Gamble, Department of Medicine, University of Auckland, Auckland, New Zealand
• Anne Horne, Department of Medicine, University of Auckland, Auckland, New Zealand
• Barbara Mason, Department of Medicine, University of Auckland, Auckland, New Zealand
• Lynette Fairbanks, Guy’s Hospital, London, United Kingdom
• Fiona M. McQueen, Department of Medicine, University of Auckland, Auckland, New Zealand
• Jillian Cornish, Department of Medicine, University of Auckland, Auckland, New Zealand
• Ian R. Reid, University of Auckland, Auckland, New Zealand
• Kate Palmano, Fonterra Research Centre, Palmerston North, New Zealand

Uric Acid Research Purpose

Recent observational studies have highlighted the beneficial role of skim milk in prevention of gout. The aims of this study were to determine the acute effects of intact skim milk on serum urate concentrations, and to examine the mechanisms of the urate-lowering effects of skim milk.

Uric Acid Research Method

This was a short-term randomized controlled cross-over trial of skim milk in 16 healthy male volunteers. The following products were tested (each 80g protein):

1. soy control
2. early season skim milk
3. late season skim milk (containing high concentrations of orotic acid, a naturally occurring uricosuric agent)
4. MPC 85 skim milk (an ultra-filtrated skim milk containing very low concentrations of orotic acid, purines and lactose)

Each participant received a single dose of each product (each containing 80 grams of protein) in random order. Researchers collected samples of blood and urine immediately before each participant drank one of the beverages and then hourly over a three-hour period. They completed this with each participant for each of the four beverages with a week in between each session.

Uric Acid Research Results

After drinking the soy milk, uric acid in the blood increased by about 10 percent. In contrast, all skim milks led to a decrease in serum uric acid by approximately 10 percent. All products (including the soy milk) rapidly increased the ability of the kidneys to remove uric acid from the body.

Additionally, researchers found that late season skim milk led to a greater increase in the removal of uric acid by the kidneys when compared to the other skim milks. Late season skim milk is primarily available from countries where milking is seasonal and cows are grass-fed, such as New Zealand and Australia, and is known to contain higher levels of orotic acid, a substance that promotes uric acid removal by the kidneys.

There were no significant differences over time or between groups in changes in serum oxypurines (xanthine and hypoxanthine) or purines (guanosine and inosine). However, all products led to an increased excretion of xanthine.

Uric Acid Research Conclusion

The press release concludes that the study showed that skim milk has a specific acute uric acid-lowering effect. The authors suggest long term studies for further proof that it might be a good dietary way to assist in the prevention and treatment of gout.

“This study has shown that skim milk can significantly reduce the serum uric acid concentration in the short term,” explains Nicola Dalbeth, MD, FRACP; senior lecturer, clinical medicine, University of Auckland, Auckland, New Zealand, and lead investigator in the study. “The results suggest that increasing the amount of skim milk in the diet may help with preventing the development of gout, and also assist with treatment for those with the disease. We are now continuing this work by studying the longer term effects of milk in people with gout.”

Milk Diet For Gout: Next Steps

Now is a good time to seriously consider improving your diet with skim milk. Do not forget that even the lowest fat skim milk still has some energy, so if you are counting the calories make sure you plan this diet change properly.

More importantly, you must realize that the uric acid lowering effects of skim milk, though significant, may not be enough to reduce you uric acid to a safe level. You must continue to check uric acid levels regularly to ensure that you remain safe.

If you are used to drinking full-fat whole milk, I found that by gradually reducing the fat content, I was soon happy with the taste of skim milk. In fact, I now find full fat milk far too creamy for my palate.

Milk Diet For Gout: References

1. Dalbeth N, Wong S, Gamble GD, et al. Acute effect of milk on serum urate concentrations: a randomised controlled crossover trial. Ann. Rheum. Dis. 2010;69(9):1677-1682.

I’m not one for scaremongering, but I do get frustrated by people who suffer years of gouty agony because they refuse to control uric acid. OK, so painkillers can mask the pain, but they cannot stop the inevitable invasive growth of uric acid deposits.

The big toe is the most common joint to get affected, but if left untreated, high uric acid levels will lead to urate deposits in every joint. This is more than a painful nuisance – these uric acid deposits known as tophi eat into bone, cartilage, and tendons causing permanent joint damage.

Most of us are lucky enough to live in a society where joint reconstruction surgery is a possibility, but why put yourself at that risk?

And I did mention every joint. Foot gout is a common problem because there are lots of joints in the foot. There are also lots of joints in the spine, and gout in the back, though fairly uncommon, is serious enough for you to be very afraid.

In gout management, there is too much emphasis on short term pain relief, and insufficient awareness of the consequences of allowing gout to reach the tophaceous stage. A single tophus (the name given to uric acid crystals when they form a lump in the body) often means severe joint movement restriction. This is quite common on the hands, where groups of tophi (the plural of tophus) tend to restrict finger movement. When this happens in the spine, back movement restriction becomes critical, and total incapacity from spine distortion is a real risk.

Samuels and colleagues reported a particularly bad case of spinal gout in the June issue of Bulletin of the NYU Hospital for Joint Diseases[1]. The image above shows how tophi in and around the spine have severely distorted the patient’s back. The report reveals that this impaired the ability to stand long enough to take a shower.

Fortunately, the patient responded well to allopurinol, even though he required a dose of:

750 mg daily to achieve a target serum uric acid level less than 6.0 mg/dL.

As I mentioned, uric acid back pain in the form of tophaceous spinal gout is uncommon, but the Samuels report does manage to cite 7 other cases, and there will be many more that go unreported.

It really is not worth letting gout go untreated this long. Are you showing any symptoms of tophaceous gout, or indeed gout symptoms of any kind, such as swollen joints? If so, you need to get your uric acid level checked by your doctor, and controlled today.

Uric Acid Back Pain References

1. Authors: Jonathan Samuels, M.D., Robert T. Keenan, M.D., M.P.H., Rena Yu, M.D., Michael H. Pillinger, M.D., and Tibor Bescke, M.D. Title: Erosive Spinal Tophus in a Patient with Gout and Back Pain. Published: June 2010.

To put it another way.

When most medics practicing today were in med school, the dietary control of gout was very simple: no high purine foods; limited medium purine foods; and unlimited low purine foods.

Then research in the 1970s and 80s began to question the simplicity of this view. In 1985, Zöllner[1] noted:

purine sources differ in their absorption rates, a fact not taken into account in our food tables.

[...] In summary it can be concluded that dietary purines are absorbed to a variable extent, depending on the degree of hydrolysis to nucleosides and/or nucleotides, and that they are oxidized to uric acid in the gut and excreted as uric acid, which is bad for gout but without influence on purine metabolism.

He concludes:

Supplements of dietary purines produce dose-proportional increases in plasma uric acid concentrations, uric acid pool size and renal uric acid excretion. The magnitude of these increases depends on the type of purine compound administered, which may limit the value of food tables for human dietetics. Purine content of food must be related not only to weight but also to energy and to protein, particularly if new foodstuffs or a vegetarian diet are ingested.

It is worth noting at this point, that foods never contain uric acid. Many do contain purines, which are a source of uric acid, but as Zöllner points out, there are different type of purine, and they metabolize to uric acid at different rates. He also points out that we do not really need to digest purines for uric acid, as we can make our own by reprocessing dead cells.

A turning point in our understanding of food high in uric acid came about in 2004. Choi and colleagues compiled statistics from a 12 year study of over 40,000 men. Though this statistical review adds nothing to our knowledge of how different purines affect gout in different ways, it certainly changed the way gout experts view diet.

Their conclusions set the foundation for today’s more effective gout diet plans:

Higher levels of meat and seafood consumption are associated with an increased risk of gout, whereas a higher level of consumption of dairy products is associated with a decreased risk. Moderate intake of purine-rich vegetables or protein is not associated with an increased risk of gout.

Though not the total story, as they do not factor in risks such as obesity and excess iron, those words should be tattooed on the hearts of all gout nutritionists. My simple view of purine control is to balance small portions (up to 4 oz) of meat or fish with low-fat dairy products. Fill the plate with whatever vegetable foods you enjoy. Simple and effective.

Finally, though we can see that some form of purine control may help gout, it is absolutely pointless to attempt this if you do not monitor your uric acid numbers. There is no correlation between gout pain and purines. You might still experience gout pain when uric acid is lowering because old urate crystals can cause a gout reaction before they dissolve completely. Make sure that you know and understand your uric acid level.

Food High In Uric Acid References

1. Author: Zöllner N . Title: Purine and pyrimidine metabolism. Published: Sep 1985.
2. Authors: Hyon K. Choi, M.D., Dr.P.H., Karen Atkinson, M.D., M.P.H., Elizabeth W. Karlson, M.D., Walter Willett, M.D., Dr.P.H., and Gary Curhan, M.D., Sc.D. Title:Purine-Rich Foods, Dairy and Protein Intake, and the Risk of Gout in Men . Published: March 2004.

See more articles related to food high in uric acid in the Gout Diet section.

The American Society for Clinical Investigation has recently reviewed the purpose of uric acid and it’s relationship with gout and other diseases.

“Uric acid transport and disease”[1] introduces its review with reference to the role of uric acid in evolution[2]. Humans have much higher levels of uric acid than many other animals because we no longer produce uricase naturally, which reduces uric acid to allantoin.

In other articles, I look at allantoin; how bacteria in our guts retain the ability to reduce uric acid; and how new drugs like rasburicase (sold under the Elitek brand) and peglioticase (sold under the Krystexxa brand) can reintroduce uricase to our bodies.

Here, I focus on what uric acid is. The report continues with some of the known benefits of uric acid.

Uric Acid: Vital Friend

The uric acid review highlights benefits of uric acid[3] including:

• Powerful antioxidant properties
• Fights heart disease
• Fights cancer
• Extends lifespan

Of course, these benefits are not always without consequences. We are aware that uric acid probably plays a part in raising blood pressure in order to walk upright, but this relies on several processes in our bodies to produce uric acid from dead body cells. These can be our own cells, or animal cells that we eat.

Our kidneys try to regulate the uric acid concentration in our blood. They filter out uric acid, then release back enough to maintain our vital functions. When systems go out-of-balance, complex factors can interact to cause problems in other areas. Often, we can see statistical associations with other diseases and conditions even though the causal links are not yet clear.

Uric Acid: Deadly Foe

The uric acid review continues to describe problems with high uric acid levels. This condition, known as hyperuricemia, is associated with several problems including:

• High blood pressure
• Heart disease
• Metabolic syndrome (a combination of diabetes or high blood pressure or obesity with heart disease or stroke or other blood circulation problems)

This of course is in addition to the problems directly associated with gout, discussed at length throughout this site, including:

• Kidney inflammation and stones.
• Bone, cartilage, and tendon destruction.

The report continues with a summary of emerging genetic investigation. I will review this area of gout research separately, as it addresses the “Why” rather than “What” of uric acid.

Next Steps To Answer “What Is Uric Acid?”

You’ve learned that uric acid is a component of our blood that is vital to human health, but destructive when we have too much. This is why you must control it to avoid serious longterm health problems, and not simply relieve gout pain.

You can learn more about the properties of uric acid and how it affects gouty arthritis in the “Understanding Uric Acid & Gout” section.

References For “What Is Uric Acid?”

1. Author: So A, Thorens B. Title: Uric acid transport and disease. Published: J Clin Invest. 2010 Jun 1;120(6):1791-9.
2. Author: Oda M, Satta Y, Takenaka O, Takahata N. Title: Loss of urate oxidase activity in hominoids and its evolutionary implications. Published: Mol Biol Evol. 2002 May;19(5):640-53.
3. Author: Ames BN, Cathcart R, Schwiers E, Hochstein P. Title: Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis. Published: Proc Natl Acad Sci U S A. 1981 Nov;78(11):6858-62.

Though this new report[1] adds nothing to the Austrian study[2] in terms of understanding why elevated uric acid leads to kidney impairment, it does confirm that the two are linked. It certainly adds weight to my position that asymptomatic hyperuricemia should be taken much more seriously.

High Uric Acid And Kidney Disease Investigation

The following information is extracted from the abstract of the uric acid investigation: “Association between serum uric acid and early kidney damage in middle-aged and elderly.”

Uric Acid Investigation Objectives

To investigate the association between uric acid in the blood and early kidney damage. Also investigate the prevalence of early kidney damage in the middle-aged and elders with normal serum creatinine.

Uric Acid Investigation Methods

The investigation surveyed 1023 subjects from the local population of Chengdu in China. The study group comprised of 539 men and 484 women aged between 57 and 69, selected randomly from the population with normal serum creatinine.

Subjects were divided into 4 groups determined by uric acid level in the blood:

1. Less than 4.74 mg/dL (0.282 mmol/L)
2. 4.74 mg/dL to 5.56 mg/dL (0.331 mmol/L)
3. 5.56 mg/dL to 6.37 mg/dL (0.379 mmol/L)
4. Greater than 6.37 mg/dL

Clearly not gout sufferers, but this is about uric acid, not necessarily gouty arthritis. The survey looked at cardiovascular risk factors, including serum UA and estimated glomerular filtration rate (eGFR) using the MDRD (modification of diet in renal disease) equation.

Uric Acid Investigation Results

Overall, 28.1% of subjects had early kidney damage, with men, at 35.8%, much more susceptible than women at 19.5%. The incidence of early kidney disease was analyzed to calculate the odds ratio across each of the 4 study groups. Taking the value of group A as 1, the other groups show the following risks:

1. 1.0
2. 1.740
3. 3.599
4. 5.488

Uric Acid Investigation Conclusion

The investigation concludes:

In the middle-aged and elders with normal serum creatinine, serum UA and eGFR are negatively correlated. And serum UA level is independently associated with early kidney damage.

GoutPal Conclusion

Given that the earlier study showed that uric acid levels above 9 mg/dL are associated with triple the incidence of kidney disease compared to below 7mg/dL, then any uric acid level above 5mg/dL suggests cause for concern.

Neither of these studies have shown whether high uric acid impairs kidney function or if kidney disease caused by something else causes uric acid levels to rise. Given that Siu and colleagues have shown allopurinol to be beneficial for kidney disease sufferers[3], I reckon there are good grounds to suggest that lowering the uric acid will lower the risk of kidney disease. As ever, this are cries out for more specific research. If you find some, please share it with the world on the gout forum.

High Uric Acid And Kidney Disease References

1. He S, Chen XP, Jiang LY, Peng Y, Gong L, Chen XN, Wu K, Cui KJ, Zhu Y, Huang DJ. [Association between serum uric acid and early kidney damage in middle-aged and elderly]. Zhonghua Yi Xue Za Zhi. 2010 Mar 16;90(10):658-61. [Article in Chinese]
2. Obermayr RP, Temml C, Gutjahr G, Knechtelsdorfer M, Oberbauer R, Klauser-Braun R. Elevated uric acid increases the risk for kidney disease. J Am Soc Nephrol. 2008 Dec;19(12):2407-13. Epub 2008 Sep 17.
3. Siu YP, Leung KT, Tong MK, Kwan TH. Use of allopurinol in slowing the progression of renal disease through its ability to lower serum uric acid level. Am J Kidney Dis. 2006 Jan;47(1):51-9.

Myth 1: Alkaline Foods Turn Red Litmus Blue

Alkaline Foods Image

Despite my best efforts to explain otherwise, people still believe that you can measure the power of alkaline foods by testing their pH. There are even lists of alkaline foods touted round the Internet that show the pH value for common foods. But these have nothing to do with the alkalizing effect, so why do they exist?

They stem from a US government table of pH values produced for the canning industry. Whilst they might help food packagers determine what balancing agents they need to avoid food reacting with it’s container, these values have absolutely nothing to do with the effect of food on our bodies.

The science of alkaline foods recognizes that elements and compounds in food cause different reactions in our body when digested. Some elements, e.g. proteins and phosphorous produce acidic salts. Other elements, e.g. potassium, magnesium and calcium, produce alkaline salts. These salts end up at our kidneys, where they alter the pH environment. This process has resulted in the Potential Renal Acid Load (PRAL) calculation, which is an approximate estimate of the effect of foods on the acidity/alkalinity of our bodies. Or more specifically, of urine, as this is the measurable result.

Still, people remain confused as to how an acidic food item, like lemons or vinegar, can have an alkalizing effect on urine and the kidneys. As I explained recently: Read the rest of Alkaline Foods: More Myths Exposed

Uric acid crystals must be dissolved to permanently get rid of gout pain, but how long does it take to get rid of them?

Like all gouty issues, the answer is never simple. However, we can see some factors that affect the time it takes for crystals to dissolve, and see that the time to start dissolving is now.

In an earlier article, I explained how tophi shrink quicker with lower uric acid concentrations. But this does not mean that once you lower uric acid to a safe level you will immediately stop all gout attacks. In fact, partially dissolved uric acid crystals can start a gout attack, as I explained in Allopurinol Medication: Why It Hurts To Get Rid Of Gout. Though that article looks specifically at allopurinol, the effects of dissolving uric acid crystals might occur with any urate lowering treatment, including diet, until all urate deposits dissolve. But how long does this cleansing period take?
Read the rest of this Uric Acid Crystals article…

Uric Acid Diagnosis Vs Uric Acid Management

There is a significant difference in interpreting uric acid blood test results between confirmed and suspected gout cases. For a confirmed gout patient, any number above 7mg/dL (0.4 mmol/L) is a clear risk of a gout attack. Blood tests for confirmed gouties should be used as an aid to managing gout. They indicate whether urate lowering therapy is set at the right dosage. This is a fairly simple process, though it does rely on the doctor understanding the need to set the right target uric acid level, and it relies on the patient taking the medication daily as directed.

The problems arise when a gout diagnosis is doubtful, and uric acid blood test results are being used to help form a definite diagnosis. There are two fundamental problems with this approach, which I explain below. Gout diagnosis from blood tests is possible, but needs a clear understanding of the gout process, preferably bolstered by more tests on a weekly basis.

We know that uric acid crystals can form in joints at normal temperatures with a uric acid concentration of slightly under 7mg/dL ^[1]. For confirmed gout patients, it is almost certain that uric acid will form crystals at that level. For unconfirmed gout patients, there is a strong probability that it will cause a gout attack, but this is not certain.

Uric Acid Blood Test Reporting Problem

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Acupuncture is commonly viewed as sticking needles into various parts of the body. Though needles are often involved, the aim is to stimulate energy flow in the body, and so other related techniques are often grouped under the acupuncture umbrella.

A detailed study of acupuncture is beyond the scope of this gout website, however I would like to draw your attention to 3 studies reported last year. (more…)