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The discussion revolves around the role of fructose in the human diet and the importance of fiber in mitigating its effects. It is argued that consuming whole fruits and juices containing fructose, along with fiber, can be health promoting and not harmful for humans.
Different individuals have varying levels of tolerance for carbohydrates, including starches and sugars. It is suggested that finding the right balance of carbohydrate sources based on individual activity levels and preferences can lead to optimal health.
Contrary to claims made in the podcast episode, it is highlighted that fructose is not inherently addictive or harmful. The activation of reward centers in the brain does not necessarily denote negative effects, and it is emphasized that glucose and fats can also activate these areas.
The connection between fructose and the inhibition of specific enzymes involved in mitochondrial function is discussed. However, it is clarified that this inhibition is primarily observed in cases of metabolic dysfunction and diabetes, rather than from the consumption of fructose in whole fruits or fruit juices.
The claim that fructose is a major fat-making molecule is misleading. While it is true that some fructose is converted to fat in the intestine, it is important to note that the conversion is minimal (less than 1% at the liver) and occurs when fructose is ingested in isolated and excessive amounts. Additionally, the metabolic effects of fructose should be considered in the context of whole fruits or fruit juice, which contain polyphenolic compounds that have been shown to minimize the negative effects of fructose. The mechanism behind fructose-induced increase in triglycerides is likely related to endotoxin production from bacterial metabolites in the intestine, rather than direct fructose metabolism. Studies on animals have shown that when the inflammatory response to endotoxin is blocked, the detrimental effects of fructose are also blocked. Thus, the focus should be on understanding the full context of fructose metabolism and considering dietary sources as well as other lifestyle factors when assessing its effects on health and insulin resistance.
Insulin resistance, a key factor in diabetes and metabolic dysfunction, is a complex issue with multiple contributing factors. One main factor is metabolic dysfunction at the mitochondrial level, which can result from various factors such as chronic stress hormone exposure, malabsorption of fructose leading to bacterial dysbiosis and endotoxemia, long-term consumption of polyunsaturated fats, and others. Correcting metabolic dysfunction at the cellular level, especially in the mitochondria, is crucial in addressing insulin resistance. Key lifestyle factors such as managing stress, getting enough sleep, exercise, and nutrient optimization can have a significant impact on improving cellular metabolism and insulin sensitivity. A comprehensive approach that considers all of these factors is essential in managing and potentially reversing insulin resistance.
Drawing parallels between fructose and alcohol can be misleading and oversimplified. While both can have negative effects on health, the mechanisms behind these effects are different. Ingested fructose, especially from whole fruits or fruit juice, does not exhibit the same negative impact as isolated fructose or excessive fructose in animal studies. The comparison might stem from the inflammatory response to endotoxin, which can be induced by both fructose and alcohol. However, it is important to note that endotoxin response is influenced by the involvement of the microbiome and that fructose from natural food sources has additional components that can mitigate any potential negative effects. Understanding the actual mechanisms involved and considering the full context of fructose metabolism is crucial in assessing its impact on health.
Insulin resistance is a complex issue that requires a multifaceted approach. Some key strategies include managing stress, optimizing nutrient intake, ensuring proper sleep, avoiding excessive polyunsaturated fat consumption, and maintaining a healthy body weight. The focus should be on improving metabolic function at the cellular level, particularly at the mitochondria, rather than demonizing specific nutrients or macronutrients. By addressing the underlying mechanisms of insulin resistance and adopting a comprehensive lifestyle approach, individuals can improve their insulin sensitivity and overall health outcomes.
This week, Paul talks to Mike Fave, critical care RN, about all things sugar & fructose. They share their thoughts on a recent podcast with Andrew Huberman and Alex Lustig, and why they disagree with certain points made about insulin, fruit juice, and fructose.
*Produced by Mountain Valley Media 00:00:00 Podcast begins 00:04:00 Mike’s background 00:05:15 Diving into fructose 00:13:00 Thoughts on honey and other carb sources 00:27:30 Robert Lustig rebuttal: is fructose addictive? 00:37:40 Fructose & fiber 00:47:00 How fructose affects the mitochondria 00:51:00 Clarifying hyperglycemia vs. a postprandial hyperglycemia 00:56:17 Is insulin the bad guy? 01:12:20 How insulin relates to diabetes, obesity, and insulin resistance 01:23:30 Balancing protein, fat and carbohydrates 01:30:00 Is fructose making us fat? 01:46:00 Final thoughts Connect with Mike: Mikefave.com https://m.youtube.com/@MikeFaveSimplified References: Review article: fructose malabsorption and the bigger picture: https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2006.03186.x A Relationship between Reduced Nucleus Accumbens Shell and Enhanced Lateral Hypothalamic Orexin Neuronal Activation in Long-Term Fructose Bingeing Behavior: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988143/ A High-Fat Meal, or Intraperitoneal Administration of a Fat Emulsion, Increases Extracellular Dopamine in the Nucleus Accumbens: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061790/ A Relationship between Reduced Nucleus Accumbens Shell and Enhanced Lateral Hypothalamic Orexin Neuronal Activation in Long-Term Fructose Bingeing Behavior: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988143/ The regulation of glucose metabolism: implications and considerations for the assessment of glucose homeostasis in rodents: https://journals.physiology.org/doi/full/10.1152/ajpendo.00165.2014?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org Consumption of Raw Orange, 100% Fresh Orange Juice, and Nectar- Sweetened Orange Juice—Effects on Blood Glucose and Insulin Levels on Healthy Subjects: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6770506/ The Effects of Soluble Dietary Fibers on Glycemic Response: An Overview and Futures Perspectives: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9736284/#B37-foods-11-03934 The Effects of Soluble Dietary Fibers on Glycemic Response: An Overview and Futures Perspectives: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9736284/#B37-foods-11-03934 Formation of Fructose-Mediated Advanced Glycation End Products and Their Roles in Metabolic and Inflammatory Diseases: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5227984/ Altered glycolytic and oxidative capacities of skeletal muscle contribute to insulin resistance in NIDDM: https://pubmed.ncbi.nlm.nih.gov/9216960/ Glucagon and type 2 diabetes: the return of the alpha cell: https://pubmed.ncbi.nlm.nih.gov/25344790/ Insulin, growth hormone and sport: https://pubmed.ncbi.nlm.nih.gov/11431133/ Effect of Mild Physiologic Hyperglycemia on Insulin Secretion, Insulin Clearance, and Insulin Sensitivity in Healthy Glucose-Tolerant Subjects: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7881846/ Fructose metabolism in humans – what isotopic tracer studies tell us: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533803/ Absorption capacity of fructose in healthy adults. Comparison with sucrose and its constituent monosaccharides: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433856/ Review article: fructose malabsorption and the bigger picture: https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2006.03186.x Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice: https://pubmed.ncbi.nlm.nih.gov/19637282/ Fructose Promotes Leaky Gut, Endotoxemia and Liver Fibrosis through CYP2E1-Mediated Oxidative and Nitrative Stress: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6783321/
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