Note from Steve Phinney:  What this shows is that uric acid goes up promptly in the same time frame that ketones go up, but after 4-6 weeks, despite ketones staying up, uric acid starts to come back down. This graph, by the way, shows blood uric acid levels from the untrained subjects (VT) and bicycle racers (MIT) at various times over 4-6 weeks of sustained carbohydrate restriction (aka keto-adaptation). EDITOR’S NOTE:  Sometimes, the divide between experts who advise against a high-fat, low-carb diet and those who recommend it seems larger than the Grand Canyon. But occasionally, top thinkers from both sides break through to discover common ground, along with new paths for exploration.  With that in mind, here’s a discussion between two nationally recognized health researchers which refers to the uric data in this chart . STEVE:  Is the rise in uric acid due to protein breakdown that allows a cell to survive, such as proteins within a cell that are recycled or processed to make glycogen, or is it due to cell loss that’s caused by a cell dying, or if you will, being harvested for its protein, leading to the release of the nucleic acid in its DNA, and messenger RNA that are released when a cell actually dies. RICK:  You can synthesize uric acid from amino acids precursors, but a more common way is for cell turnover with nucleic acid release, and then the nucleic acids are broken down and the liver generates the uric acid from those breakdown products. So, it seems that you both agree that initially at least, when someone switches from a high carb to a low carb diet, their uric acid levels go up.  And that’s whether or not they’re eating purine rich foods.  But then, why do uric acid levels in the blood go up?   Are you both saying the same thing now, about why uric acid levels rise during the switch from carbohydrate burning to burning fats? RICK:  So the prediction is the uric acid would only be high during this phase and then would come down. SHELLEY:  Rick Johnson you’re interested in what happens to people’s blood pressure and what happens to them in ketosis and with their uric acid level variations.
RICK:  It sounds like you’re saying the blood pressure really didn’t change very much in these people. Steve Phinney:  This graph shows the blood ketones from my bike racer study, and illustrates the prompt rise in ketones by the first week of the diet. Steve Phinney:  This shows the treadmill times of my untrained subjects at baseline, then at one week and 6 weeks into the ketogenic diet. Steve Phinney:  This graph shows the performance and metabolic data from the bike racers, demonstrating no loss of peak aerobic power or endurance performance after 4 weeks on the very low carb diet. SHELLEY:  Are you both saying that uric acid in the blood can be protective from an antioxidant standpoint, but inside the cell, it may be causing problems, and the level in the blood may be a hint at what’s going on in the cell.
STEVE:  Is it due to lack of degradation of the glycogen, or is it increasing glycogen production because the metabolic trauma or stress of uric acid is driving gluconeogenic carbon from the periphery to the liver?  When you stress somebody, the peripheral musculature gives up what it’s got to help out the central viscera.
RICK:  Did you measure prostaglandins, or thromboxine derivatives to see if there was a change in patterns.
RICK:  The other thing is comparing a ketotic diet to one where there’s calorie restriction leading to ketosis, where you’re not getting fats fed to you and how that affects fat metabolism differences. RICK:  Sprague Dawley rat?  That’s a regular rat.  So what about the ketotic diet for rats again? STEVE:  The F3666 diet has been used for a decade to create rodent models to explain why a ketogenic diet helps kids with epilepsy. RICK:  You’re saying two different ketogenic diets have major differences on fatty liver.  What’s the difference?
STEVE:  The F3666 is very low in protein, so the animals don’t gain weight as fast, but  we think it’s inducing sarcopenia. STEVE:  Yes, and it’s preventing, we presume, lipoprotein production in the liver so you entrap fat in the liver because you can’t efficiently produce adequate surface proteins to get it out of the liver and into circulation. SHELLEY:  But in people eating a high fat diet, generally does that reduce fatty liver or increase it.
STEVE:  Perhaps you mentioned this interesting possibility, that it may be that the positive interaction with the circulating ketones is counteracting the initial transient problems with increased circulating uric acid.
Steve Phinney is emeritus professor of medicine at UC-Davis and a world-renowned expert on high fat diets, including how they affect uric acid levels.   Dr. Nor did I see any differences in blood uric acid levels when I was at University of Minnesota and we were making comparisons between ketogenic, meat-based diets and formula-based diets in cohorts of 40 people per group.  The metabolic profiles of the patients, in regards to uric acid and ketone levels, were pretty much the same, independent of the protein source, which leads me to think that the rise in uric acid was not determined by purines in the diet. It’s so low in protein that the animals are protein starved.  We think it’s making their liver very sick.
Bistrian and Blackburn together published 50 papers on that.  I got to be part of 5 or six of those during my fellowship.
Our work includes studies in cell culture, animal models, epidemiological studies and clinical trials. Recent studies include studies of fructose induced obesity, insulin resistance, leptin resistance, and fatty liver. We also are interested in the subcellular, and especially effects on the mitochondria in response to fructose and uric acid. Most recently our work has focused on how a reduction in ATP generation in response to fructose and uric acid may translate not only into obesity, but also into fatigue and decreased exercise.




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