Summary
In this episode of The Drive podcast, Dr. Rick Johnson, a professor of medicine at the University of Colorado, discusses his research on fructose and its metabolic effects. Dr. Johnson explains how his interest in fructose began while studying the relationship between high blood pressure and kidney disease. While conventional wisdom suggests that reducing sodium intake can lower blood pressure, Dr. Johnson explains that it is actually the concentration of salt in the blood that triggers a rise in blood pressure. He also discusses the role of serum osmolality in blood pressure and obesity.
The episode delves into the biochemistry of fructose and its effects on uric acid levels, as well as potential pharmacotherapy options for metabolic diseases. Fructose can lead to weight gain and metabolic effects by depleting intracellular phosphate levels, triggering the ampd pathway, and causing insulin resistance. The concentration and speed with which fructose arrives at the liver can affect the magnitude of these effects. Fructose generates uric acid, which can cause oxidative stress and inhibit fat burning, leading to fatty liver and insulin resistance. Fructose can also lower HDL cholesterol levels.
The context discusses the relationship between fructose and survival. Animals use fructose to survive in low oxygen states by switching to glycolysis and becoming insulin resistant. Fructose also helps store water and fat, which animals use to survive during hibernation or long flights without food. However, fructose is also the preferred fuel for many types of cancer cells, and blocking the fructose pathway can inhibit cancer growth.
The speaker discusses the benefits of lowering uric acid levels in the body, citing positive results in studies on insulin resistance, kidney disease, and blood pressure control. They mention that the risks associated with high uric acid levels increase when serum uric acid levels exceed 5.5, and that treatment with allopurinol is typically started when levels are 8 or higher. The speaker notes that xanthine oxidase inhibitors like allopurinol are the best at reducing intracellular uric acid levels.
The context discusses a study on the effects of glucose on animals and how it induces an enzyme to convert glucose to fructose, leading to fatty liver disease and insulin resistance. The study found that excess carbohydrates, even those not high in sugar, can lead to fatty liver disease. The context also touches on artificial sweeteners and their safety, with the conclusion being that they are the lesser of two evils compared to regular sugar.
Finally, the episode discusses the role of taste and its relation to weight gain. Sugar and salt are found to be the fastest drivers of weight gain, with umami being a receptor for uric acid type foods. High glycemic carbs, salty foods, and alcohol, especially beer, can also drive weight gain. The speaker recommends avoiding liquids with sugar or fructose, but natural fruit in moderation is okay. Berries, kiwi, lime, and lemon have low fructose content and are safe to eat in larger quantities, while grapes and pineapple have higher sugar content and should be consumed in moderation. For patients with non-alcoholic fatty liver disease, a restriction of 10 grams of fructose a day in the form of whole fruit is recommended.
