Uric Acid - A Pivotal Player in Metabolic Diseases - Dr. David Perlmutter
Having elevated uric acid indicates high blood pressure. New research demonstrates that lowering uric acid with allopurinol results in lower blood pressure.
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Alcohol Consumption and the Uric Acid Connection - YouTube
We want to do everything we can to keep our uric acid levels in the optimal range, typically below 5.5 mg/dl. And by far and away, the biggest contributor to the elevation of uric acid that we are seeing around the world seems to be the global increase in consumption of fructose sugar. That said, there are other contributors to the formation of uric acid, and one of them is alcohol.
As it turns out, when we look at the metabolism of alcohol and recognize that it directly contributes to the formation of uric acid, we shouldn't be surprised that alcoholic beverages do in fact increase uric acid. To a significant degree it depends on what type of alcohol is consumed, and indeed there are some gender-specific findings as well that are important.
This is important information that leverages the new and exciting research coming out from around the world on the threat posed by elevation of uric acid in terms of our health. In my new book, Drop Acid (https://www.drperlmutter.com/books/drop-acid/), I do a deep dive into the science of uric acid and provide a valuable game plan for getting uric acid levels under control.
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An Integrated Plan for Lowering Uric Acid - Dr. David Perlmutter MD
Let’s unpack a unique compilation of supplements and explore not just the value of each component and how they work synergistically to lower uric acid.
How Vegetables Affect Uric Acid The Acid Drop - YouTube
Unfortunately, there is still so much old-school information out there about Uric acid, mostly derived from the science surrounding gout. We know that purines, the breakdown products of DNA and RNA, do contribute to uric acid in the human body. That said, for many years, doctors were telling people to not consume vegetables that are high in purines for fear of raising their uric acid if that was a problem for them.
The great news is that we now know that these very helpful vegetables are actually associate with a lower uric acid level!
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What’s Making Us Fat The Uric Acid Connection - YouTube
So many people these days are having issues with weight gain and even obesity and with good reason. The diet that many people are consuming is remarkably different in comparison to what people ate even one hundred years ago. One of the biggest changes has been the amount of sugar, specifically fructose, that has entered the human diet.
Fructose consumption in humans enhances insulin resistance and the creation of body fat. Importantly, as well, fructose metabolism increases the production of uric acid, which further contributes to increasing body weight through several mechanisms. In fact, uric acid directly relates to overweight and obesity, even beyond its connection to fructose.
This video explores this relationship as well as what leads to elevation of uric acid, again in the context of overweight and obesity.
This study and so many more will be incorporated into my new book Drop Acid (https://www.dropacidbook.com), where you will learn the specifics of uric acid management including how to measure it and what to do to bring it under control.
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Marine Drugs Free Full-Text Fucoidan from Laminaria japonica Inhibits Expression of GLUT9 and URAT1 via PI3KAkt, JNK and NF-B Pathways in Uric Acid-Exposed HK-2 Cells
This work aimed to investigate the effect of fucoidan (FPS) on urate transporters induced by uric acid (UA). The results showed that UA stimulated the expression of glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1) in HK-2 cells, and FPS could reverse the effect. Moreover, UA could activate NF-κB, JNK and PI3K/Akt pathways, but both pathway inhibitors and FPS inhibited the UA-induced activation of these three pathways. These data suggested that FPS effectively inhibited the expression induction of reabsorption transporters URAT1 and GLUT9 by UA, through repressing the activation of NF-κB, JNK and PI3K/Akt signal pathways in HK-2 cells. The in vitro research findings support the in vivo results that FPS reduces serum uric acid content in hyperuricemia mice and rats through inhibiting the expression of URAT1 and GLUT9 in renal tubular epithelial cells. This study provides a theoretical basis for the application of FPS in the treatment of hyperuricemia.
Reduce Your Dementia Risk - The Role of Uric Acid The Acid Drop - YouTube
So many choices we make each and every day factor into our risk of developing dementia, basically an untreatable condition. We know that, for example, foods that raise blood sugar are associated with risk as is lack of exercise. Now we have learned that having a high uric acid also, dramatically, factors into our risk calculation. Understanding this is so empowering!
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Fucoidan from Laminaria japonica protects renal tubular epithelial cells from uric acid induced NLRP3-mediated pyroptosis through inhibition of NF-κB pathway - ScienceDirect
Hyperuricemia is a common metabolic disease with prominent morbidity, it can lead to many adverse effects and complications, such as chronic nephrosis…
Parkinsons Disease and the Uric Acid Sweet Spot - YouTube
The link between Parkinson’s and dairy may not just be explained by the pesticides and lactose.
Subscribe to NutritionFacts.org’s free newsletter to receive our B12 infographic that covers the latest research takeaways and Dr. Greger’s updated recommendations: https://nutritionfacts.org/subscribe/
Dairy and Parkinson’s? See Preventing Parkinson’s Disease With Diet (http://nutritionfacts.org/video/preventing-parkinsons-disease-with-diet)
Lactose and Parkinson’s? See Could Lactose Explain the Milk - Parkinson’s Disease Link? (http://nutritionfacts.org/video/could-lactose-explain-milk-parkinsons-disease-link)
Uric acid as an antioxidant? I’ve touched on that before in Miocene Meteorites and Uric Acid (http://nutritionfacts.org/video/miocene-meteorites-and-uric-acid/).
If levels are too high consider cutting down on Flesh and Fructose (http://nutritionfacts.org/video/flesh-and-fructose/) and eating cherries (see Gout Treatment with a Cherry on Top (http://nutritionfacts.org/video/gout-treatment-with-a-cherry-on-top/) and Treating Gout with Cherry Juice (http://nutritionfacts.org/video/treating-gout-with-cherry-juice/)). Check out Preventing Gout Attacks with Diet (http://nutritionfacts.org/video/preventing-gout-attacks-with-diet/).
Can a plant-based diet be used to treat Parkinson’s? See Treating Parkinson’s Disease With Diet (http://nutritionfacts.org/video/treating-parkinsons-disease-with-diet/). Any plant foods in particular that may help? Try nightshade veggies:
• Is Something in Tobacco Protective Against Parkinson’s Disease? (http://nutritionfacts.org/topics/Is-something-in-tobacco-protective-against-parkinsons-disease)
• Peppers and Parkinson’s: The Benefits of Smoking Without the Risks? (http://nutritionfacts.org/video/peppers-and-parkinsons-the-benefits-of-smoking-without-the-risks)
Have a question about this video? Leave it in the comment section at http://nutritionfacts.org/video/parkinsons-disease-and-the-uric-acid-sweet-spot and someone on the NutritionFacts.org team will try to answer it.
Want to get a list of links to all the scientific sources used in this video? Click on Sources Cited at http://nutritionfacts.org/video/parkinsons-disease-and-the-uric-acid-sweet-spot. You’ll also find a transcript of the video, my blog and speaking tour schedule, and an easy way to search (by translated language even) through our videos spanning more than 2,000 health topics.
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Thanks for watching. I hope you’ll join in the evidence-based nutrition revolution!
-Michael Greger, MD FACLM
Image Credit: Meditations via Pixabay. Image has been modified.
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Fructose Bad for The Brain - Dr. David Perlmutter Investigates - YouTube
There is an ever-increasing body of evidence that clearly shows the incredible threat posed by dietary fructose in multiple areas of human health. A diet higher in fructose is associated with increased risk for weight gain and type 2 diabetes, and just considering these two processes alone, the stage becomes set for all kinds of other downstream maladies.
We are now seeing robust data that relates fructose consumption to increased risk of brain degeneration and even compromised brain function. In this video, I explore one recent publication that was quite extensive and related fructose consumption in the form of beverages to a rapid increase in brain shrinkage as well as a significant decline in cognitive function. We then explore the mechanisms whereby this occurs including how fructose is metabolized into uric acid, compounding the threat to the brain.
In my new book, Drop Acid (https://amzn.to/309RuqN), we go much deeper into the science that reveals how elevated uric acid, a product of fructose metabolism, poses such a significant threat to the brain.
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Marine Drugs Free Full-Text Production Inhibition and Excretion Promotion of Urate by Fucoidan from Laminaria japonica in Adenine-Induced Hyperuricemic Mice
This work aims to explore the amelioration of fucoidan on adenine-induced hyperuricemia and hepatorental damage. Adenine-induced hyperuricemic mice were administered with fucoidan, allopurinol and vehicle control respectively to compare the effects of the drugs. Serum uric acid, urea nitrogen, hepatorenal functions, activities of hepatic adenosine deaminase (ADA), xanthine oxidase (XOD), renal urate transporter 1 (URAT1) and NF-κB p65 were assessed. As the serum uric acid, urea nitrogen, creatinine, glutamic oxalacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) data demonstrated, the adenine not only mediated hepatorenal function disorders, but also induced hyperuricemia in mice. Meanwhile, activities of hepatic ADA and XOD were markedly augmented by adenine, and the expression of URAT1 was promoted, which was conducive to the reabsorption of urate. However, exposure to fucoidan completely reversed those adenine-induced negative alternations in mice, and the activities of hepatic ADA and XOD were recovered to the normal level. It was obvious that hepatic and renal functions were protected by fucoidan treatment. The expression of URAT1 was returned to normal, resulting in an increase of renal urate excretion and consequent healing of adenine-induced hyperuricemia in mice. Expression and activation of NF-κB p65 was promoted in kidneys of adenine treated mice, but suppressed in kidneys of mice exposed to fucoidan from Laminaria japonica or allopurinol. In conclusion, the fucoidan is a potential therapeutic agent for the treatment of hyperuricemia through dual regulatory roles on inhibition of hepatic metabolism and promotion of renal excretion of urate.
Cherry consumption has been shown to successfully prevent gout arthritis attacks, but what about cherry juice concentrate?
Subscribe to NutritionFacts.org’s free newsletter to receive our B12 infographic that covers the latest research takeaways and Dr. Greger’s updated recommendations: https://nutritionfacts.org/subscribe/
Here are the other videos I’ve done on the power of cherries to control inflammation:
• Anti-inflammatory Life is a Bowl of Cherries (https://nutritionfacts.org/video/anti-inflammatory-life-is-a-bowl-of-cherries/)
• Gout Treatment with a Cherry on Top (https://nutritionfacts.org/video/gout-treatment-with-a-cherry-on-top/)
• Reducing Muscle Soreness With Berries (https://nutritionfacts.org/video/reducing-muscle-soreness-with-berries/)
Tart cherries (the kind people make pies out of, not the sweet kind) may also help with sleep (Tart Cherries for Insomnia: https://nutritionfacts.org/video/tart-cherries-for-insomnia).
What do you do with frozen cherries? I just eat them straight—suck on them like popsicles, but they’re also an integral part of my Healthy Chocolate Milkshakes (https://nutritionfacts.org/video/healthy-chocolate-milkshakes/).
Another way to help treat gout is to drink lots of water and keep one’s urine alkaline by eating lots of dark green leafy vegetables (see Testing Your Diet with Pee & Purple Cabbage: https://nutritionfacts.org/video/testing-your-diet-with-pee-purple-cabbage/).
Since this video came out, I have a newer one on gout: Preventing Gout Attacks with Diet (https://nutritionfacts.org/video/preventing-gout-attacks-with-diet/). And what role does uric acid play in Parkinson’s disease? See Parkinson’s Disease and the Uric Acid Sweet Spot (https://nutritionfacts.org/video/parkinsons-disease-and-the-uric-acid-sweet-spot/).
Have a question about this video? Leave it in the comment section at http://nutritionfacts.org/video/flashback-friday-treating-gout-with-cherry-juice and someone on the NutritionFacts.org team will try to answer it.
Want to get a list of links to all the scientific sources used in this video? Click on Sources Cited at http://nutritionfacts.org/video/flashback-friday-treating-gout-with-cherry-juice. You’ll also find a transcript and acknowledgments for the video, my blog and speaking tour schedule, and an easy way to search (by translated language even) through our videos spanning more than 2,000 health topics.
If you’d rather watch these videos on YouTube, subscribe to my YouTube Channel here: https://www.youtube.com/subscription_center?add_user=nutritionfactsorg
Thanks for watching. I hope you’ll join in the evidence-based nutrition revolution!
-Michael Greger, MD FACLM
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Marine Drugs Free Full-Text The Emerging Evidence for a Protective Role of Fucoidan from Laminaria japonica in Chronic Kidney Disease-Triggered Cognitive Dysfunction
This study aimed to explore the mechanism of fucoidan in chronic kidney disease (CKD)-triggered cognitive dysfunction. The adenine-induced ICR strain CKD mice model was applied, and RNA-Seq was performed for differential gene analysis between aged-CKD and normal mice. As a result, fucoidan (100 and 200 mg kg−1) significantly reversed adenine-induced high expression of urea, uric acid in urine, and creatinine in serum, as well as the novel object recognition memory and spatial memory deficits. RNA sequencing analysis indicated that oxidative and inflammatory signaling were involved in adenine-induced kidney injury and cognitive dysfunction; furthermore, fucoidan inhibited oxidative stress via GSK3β-Nrf2-HO-1 signaling and ameliorated inflammatory response through regulation of microglia/macrophage polarization in the kidney and hippocampus of CKD mice. Additionally, we clarified six hallmarks in the hippocampus and four in the kidney, which were correlated with CKD-triggered cognitive dysfunction. This study provides a theoretical basis for the application of fucoidan in the treatment of CKD-triggered memory deficits.
Glucosamine inhibits IL-1ß expression by preserving mitochondrial integrity and disrupting assembly of the NLRP3 inflammasome Scientific Reports
The NLRP3 inflammasome promotes the pathogenesis of metabolic, neurodegenerative and infectious diseases. Increasing evidences show that the NLRP3 inflammasome is a promising therapeutic target in inflammatory diseases. Glucosamine is widely used as a dietary supplement to promote the health of cartilage tissue and is expected to exert anti-inflammatory activity in joint inflammation, which is a nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome-associated complication. Here, we investigated whether GlcN inhibits the NLRP3 inflammasome and dissected the underlying molecular mechanisms. We found that GlcN suppressed the NLRP3 inflammasome in mouse and human macrophages. A mechanistic study revealed that GlcN inhibited the expression of NLRP3 and IL-1β precursor by reducing reactive oxygen species generation and NF-κB activation in lipopolysaccharide-activated macrophages. GlcN also suppressed mitochondrial reactive oxygen species generation and mitochondrial integrity loss in NLRP3-activated macrophages. Additionally, GlcN disrupted NLRP3 inflammasome assembly by inhibiting NLRP3 binding to PKR, NEK7 and ASC. Furthermore, oral administration of GlcN reduced peritoneal neutrophils influx and lavage fluids concentrations of IL-1β, IL-6 MCP-1 and TNF-α in uric acid crystal-injected mice. These results indicated that GlcN might be a novel dietary supplement for the amelioration of NLRP3 inflammasome-associated complications.
Anserine and glucosamine supplementation attenuates the levels of inflammatory markers in rats with rheumatoid arthritis SpringerLink
Rheumatoid arthritis (RA) is an autoimmune disorder that affects the joint synovium. Anserine is a functional dipeptide containing methylhistidine and β-alanine, and is present in the brain and skeletal muscle of birds and mammals. Glucosamine is an amino sugar used in the synthesis of glycosylated proteins and lipids. We evaluated the effects of anserine and glucosamine on RA. Rats were assigned into the control group, RA group, anserine group (1 mg/kg), glucosamine group (200 mg/kg), or anserine plus glucosamine group (anserine, 1 mg/kg + glucosamine, 200 mg/kg). Treatment was continued for 45 consecutive days and was administered orally. The serum levels of catalase, glutathione peroxidase (Gpx), superoxide dismutase (SOD), reduced glutathione (GSH), lipid peroxidation, uric acid, nitric oxide, ceruloplasmin, zinc, copper, prostaglandin E2 (PGE2), matrix metalloproteinase (MMP)-3, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 were assayed. The mRNA and protein levels of nuclear factor (NF)-κB and inducible nitric oxide synthase (iNOS) in synovial tissue were also determined. Anserine plus glucosamine significantly increased the catalase, SOD, Gpx, GSH, and zinc levels compared to the control, anserine, and glucosamine groups. Also, anserine plus glucosamine significantly reduced the PGE2, MMP-3, TNF-α, IL-1β, and IL-6 levels compared to the control, anserine, and glucosamine groups. Furthermore, anserine plus glucosamine significantly reduced the mRNA and protein levels of NF-κB and iNOS compared to the control, anserine, and glucosamine groups. Therefore, supplementation of anserine plus glucosamine shows therapeutic potential for RA.
Fucoidan Supplementation Relieved Kidney Injury and Modulated Intestinal Homeostasis in Hyperuricemia Mice | Journal of Agricultural and Food Chemistry
Hyperuricemia is a metabolic disease characterized by an excessively increased level of uric acid (UA) in the blood, with an increasing prevalence and often associated with kidney damage. Gut microbiota and endotoxins of gut origin are key mediators in the gut–kidney axis that can cause renal impairment. The study was to reveal the protective effects of fucoidan on renal injury caused by hyperuricemia. The hyperuricemia model was established in C57BL/6J mice. After 10 weeks of fucoidan supplementation, we found that the levels of serum UA and creatinine were reduced, and the levels of renal tumor necrosis factor α, interleukin-18 (IL-18), IL-6, and interleukin-1β (IL-1β) were also decreased. Fucoidan inhibited the expressions of phosphorylated NF-κB p65, NLRP3, and activated caspase-1 in the kidneys. Fucoidan also regulated the expressions of Bcl-2 family proteins and decreased the activation of caspase-3, thereby exerting antiapoptotic effect. In addition, fucoidan could reduce the expressions of glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1) proteins, thereby promoting the excretion of UA from the kidneys. Moreover, the protective effect of fucoidan on renal injury may be related to maintaining intestinal homeostasis. Fucoidan reduced serum lipopolysaccharide and improved the intestinal mucosal barrier function. Fucoidan decreased the abundances of Blautia, Muribaculaceae, and Dubosiella, and increased the abundances of Lactobacillus. High-dose fucoidan supplementation increased the content of butyric acid and enhanced the expression of ATP binding box transporter G2 (ABCG2) via the AMPK/AKT/CREB pathway in ileum. Conclusion: Fucoidan could protect against hyperuricemia-induced renal injury by inhibiting renal inflammation and apoptosis and modulating intestinal homeostasis in hyperuricemia mice.
Keto Diet & Parkinson's Disease with William Curtis - YouTube
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Key Timestamps:
01:55 Journalist Bill Curtis has had Parkinson's since 2000. As predicted, he was dramatically affected 10 years later with advanced Parkinson's. Now the only symptom he has is a slight tremor.
04:48 Within about 2 hours of eating carbs, Bill will begin to shake and feel rigid. He doesn't get the full on symptoms he had before.
07:38 Bill was in an exercise program. In an attempt to enhance the effects of the program, he fasted overnight and had nothing for breakfast before the workout. He found it alleviated his profound fatigue.
11:27 Fasting helped with the fatigue, but there were many more symptoms that were not reversed. Bill continued researching.
13:02 Bill exercised fasted every day for a year. He lost weight, but eventually, it stopped working. As you become fit, you make fewer ketones.
15:04 Dr. Veech suggested that Bill try Bulletproof Coffee after the night fast. Nearly all of his symptoms abated at the end of the first hour.
19:36 The military has been experimenting with Dr. Veech's ketone ester for radiation exposure.
22:26 A therapeutic ketogenic diet is one with 80 to 90% of your food as fat. Bill has devised 4 levels of ketosis.
30:33 Within the first 10 days of taking ketone ester, Bill no longer had urinary incontinence.
32:07 There is data that an elevation of uric acid it will delay the onset of Parkinson's. If you have Parkinson's, and your uric acid levels are higher, you decline more slowly.
36:14 BHB allows you to make more dopamine, serotonin, adrenaline, noradrenaline and nitric oxide.
38:00 In advanced Parkinson's neurotransmitters are negatively impacted. With ketosis, you are making serotonin, noradrenaline, adrenaline, dopamine and nitric oxide synthase.
38:52 Every antioxidant has to be recharged with an electron from NADPH, directly or indirectly.
39:50 Beta hydroxybutyrate raises NADPH levels using isocitrate dehydrogenase in the cytoplasm, outside of the mitochondria.
42:24 NADPH levels in the mitochondria does not correlate with NADPH levels in the cytosol. We should measure the cytosolic NADPH.
44:09 NADPH voltage is dependent upon the relative concentrations. More equals more resilience.
48:52 Dismutase does not get its electrons from the battery. It does this by taking 2 molecules of superoxide, oxidizing one and reducing the other.
52:59 You have the ability to use ketones to restore ischemia-reperfusion and turn off inflammation.
54:08 NADPH controls inflammation.
55:04 Dr. Veech found that treating Alzheimer's mouse models with beta hydroxybutyrate kept them from accumulating beta amyloid deposits.
58:03 Bill believes that TBI will respond very well to BHB, as evidenced by people close to him with head injuries.
01:02:41 Bill has created an online course to help people help each other. You need a cook, a coach, a nutritionist and a doctor.
01:04:36 Bill must still take his Parkinson's medications.