Podcasts about physiology endocrinology

Iniziamo il primo di due episodi dedicati al dimagrimento localizzato. Analizziamo se è possibile perdere peso in aree specifiche del corpo e sfatiamo i miti comuni. Scopri come raggiungere i tuoi obiettivi di peso in modo sano e realistico. Segui Postura Da Paura su Instagram e Facebook per trovare altri consigli e informazioni per vivere una vita più equilibrata e serena. Per noi il movimento è una medicina naturale, visita il sito www.posturadapaura.com per trovare il programma di allenamento più adatto alle tue esigenze. Come promesso ecco le fonti citate durante la puntata: Hargreaves, M., & Spriet, L. L. (2020). Skeletal muscle energy metabolism during exercise. In Nature Metabolism (Vol. 2, Issue 9, pp. 817–828). Nature Research. https://doi.org/10.1038/s42255-020-0251-4 Heinonen, I., Bucci, M., Kemppainen, J., Knuuti, J., Nuutila, P., Boushel, R., & Kalliokoski, K. K. (2012). Regulation of subcutaneous adipose tissue blood flow during exercise in humans. J Appl Physiol, 112, 1059–1063. https://doi.org/10.1152/japplphysiol.00732.2011.-Regula Masullo, V., Fischetti, F., Esposito, G., & D'Elia, F. (2021). Pre-workout muscle vascularization and its effects on localized fat areas. Journal of Human Sport and Exercise, 16(Proc3), S1023–S1030. https://doi.org/10.14198/jhse.2021.16.Proc3.19 Paoli, A., Casolo, A., Saoncella, M., Bertaggia, C., Fantin, M., Bianco, A., Marcolin, G., & Moro, T. (2021). Effect of an endurance and strength mixed circuit training on regional fat thickness: The quest for the “spot reduction.” International Journal of Environmental Research and Public Health, 18(7). https://doi.org/10.3390/ijerph18073845 Pedersen, B. K., & Febbraio, M. A. (2008). Muscle as an Endocrine Organ: Focus on Muscle-Derived Interleukin-6. https://doi.org/10.1152/physrev.90100.2007.-Skeletal Polak, J., Bajzova, M., & Stich, V. (2008). Effect of exercise on lipolysis in adipose tissue. In Future Lipidology (Vol. 3, Issue 5, pp. 557–572). https://doi.org/10.2217/17460875.3.5.557 Purdom, T., Kravitz, L., Dokladny, K., & Mermier, C. (2018). Understanding the factors that effect maximal fat oxidation. In Journal of the International Society of Sports Nutrition (Vol. 15, Issue 1). BioMed Central Ltd. https://doi.org/10.1186/s12970-018-0207-1 Scotto di Palumbo, A., Guerra, E., Orlandi, C., Bazzucchi, I., & Sacchetti, M. (2017). Effect of combined resistance and endurance exercise training on regional fat loss. The Journal of Sports Medicine and Physical Fitness, 57(6), 794–801. https://doi.org/10.23736/S0022-4707.16.06358-1 Stallknecht, B., Dela, F., & Helge, J. W. (2007). Are blood flow and lipolysis in subcutaneous adipose tissue influenced by contractions in adjacent muscles in humans? American Journal of Physiology – Endocrinology and Metabolism, 292(2). https://doi.org/10.1152/ajpendo.00215.2006

Continuiamo e concludiamo con il secondo episodio dedicato al dimagrimento localizzato. Approfondiamo ulteriormente le strategie per perdere peso in modo sano e sfatiamo i miti sulla riduzione del grasso in aree specifiche. Impara le tecniche efficaci per un dimagrimento equilibrato e sostenibile. Segui Postura Da Paura su Instagram e Facebook per trovare altri consigli e informazioni per vivere una vita più equilibrata e serena. Per noi il movimento è una medicina naturale, visita il sito www.posturadapaura.com per trovare il programma di allenamento più adatto alle tue esigenze. Come promesso ecco le fonti citate durante la puntata: Hargreaves, M., & Spriet, L. L. (2020). Skeletal muscle energy metabolism during exercise. In Nature Metabolism (Vol. 2, Issue 9, pp. 817–828). Nature Research. https://doi.org/10.1038/s42255-020-0251-4 Heinonen, I., Bucci, M., Kemppainen, J., Knuuti, J., Nuutila, P., Boushel, R., & Kalliokoski, K. K. (2012). Regulation of subcutaneous adipose tissue blood flow during exercise in humans. J Appl Physiol, 112, 1059–1063. https://doi.org/10.1152/japplphysiol.00732.2011.-Regula Masullo, V., Fischetti, F., Esposito, G., & D'Elia, F. (2021). Pre-workout muscle vascularization and its effects on localized fat areas. Journal of Human Sport and Exercise, 16(Proc3), S1023–S1030. https://doi.org/10.14198/jhse.2021.16.Proc3.19 Paoli, A., Casolo, A., Saoncella, M., Bertaggia, C., Fantin, M., Bianco, A., Marcolin, G., & Moro, T. (2021). Effect of an endurance and strength mixed circuit training on regional fat thickness: The quest for the “spot reduction.” International Journal of Environmental Research and Public Health, 18(7). https://doi.org/10.3390/ijerph18073845 Pedersen, B. K., & Febbraio, M. A. (2008). Muscle as an Endocrine Organ: Focus on Muscle-Derived Interleukin-6. https://doi.org/10.1152/physrev.90100.2007.-Skeletal Polak, J., Bajzova, M., & Stich, V. (2008). Effect of exercise on lipolysis in adipose tissue. In Future Lipidology (Vol. 3, Issue 5, pp. 557–572). https://doi.org/10.2217/17460875.3.5.557 Purdom, T., Kravitz, L., Dokladny, K., & Mermier, C. (2018). Understanding the factors that effect maximal fat oxidation. In Journal of the International Society of Sports Nutrition (Vol. 15, Issue 1). BioMed Central Ltd. https://doi.org/10.1186/s12970-018-0207-1 Scotto di Palumbo, A., Guerra, E., Orlandi, C., Bazzucchi, I., & Sacchetti, M. (2017). Effect of combined resistance and endurance exercise training on regional fat loss. The Journal of Sports Medicine and Physical Fitness, 57(6), 794–801. https://doi.org/10.23736/S0022-4707.16.06358-1 Stallknecht, B., Dela, F., & Helge, J. W. (2007). Are blood flow and lipolysis in subcutaneous adipose tissue influenced by contractions in adjacent muscles in humans? American Journal of Physiology – Endocrinology and Metabolism, 292(2). https://doi.org/10.1152/ajpendo.00215.2006

In this episode, Charmaine, a seasoned dietitian, and Ghalia, an expert coach in the Reversing Diabetes Program, unravel the complexities of managing diabetes in the digital age. Navigating through the overwhelming and often conflicting information online, they shed light on scientifically backed blood glucose lowering hacks that actually work!Join the journey as they share two commonly overlooked factors that can help you progress further in your journey towards reversing diabetes!If you are looking to know more about what you can do starting from today to improve your insulin sensitivity and metabolic health so that you can reverse diabetes, then this podcast episode is a must-listen!ReferencesSpiegel, K., Leproult, R., & Van Cauter, E. (1999). Impact of sleep debt on metabolic and endocrine function. The Lancet, 354(9188), 1435-1439.Buxton, O. M., Pavlova, M., Reid, E. W., Wang, W., Simonson, D. C., & Adler, G. K. (2010). Sleep restriction for 1 week reduces insulin sensitivity in healthy men. Diabetes, 59(9), 2126-2133.Spiegel, K., Tasali, E., Penev, P., & Van Cauter, E. (2004). Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Annals of Internal Medicine, 141(11), 846-850.Chaput, J. P., Després, J. P., Bouchard, C., & Tremblay, A. (2007). Short sleep duration is associated with reduced leptin levels, elevated ghrelin levels, and increased body mass index. Sleep, 30(11), 1429-1437.Donga, E., Van Dijk, M., Van Dijk, J. G., Biermasz, N. R., Lammers, G. J., van Kralingen, K. W., ... & Romijn, J. A. (2010). A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. Journal of Clinical Endocrinology & Metabolism, 95(6), 2963-2968.Leproult, R., Copinschi, G., Buxton, O., & Van Cauter, E. (1997). Sleep loss results in an elevation of cortisol levels the next evening. Sleep, 20(10), 865-870.Rizza, R. A. (2010). Pathogenesis of fasting and postprandial hyperglycemia in type 2 diabetes: Implications for therapy. Diabetes, 59(11), 2697-2707.Rosmond, R., Dallman, M. F., & Björntorp, P. (1998). Stress-related cortisol secretion in men: Relationships with abdominal obesity and endocrine, metabolic and hemodynamic abnormalities. Journal of Clinical Endocrinology & Metabolism, 83(6), 1853-1859.Black, P. H. (2003). The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain, Behavior, and Immunity, 17(5), 350-364.Purnell, J. Q., Kahn, S. E., Samuels, M. H., Brandon, D., Loriaux, D. L., & Schwartz, R. S. (2009). Enhanced cortisol production rates, free cortisol, and 11β-HSD-1 expression correlate with visceral fat and insulin resistance in men: Effect of weight loss. American Journal of Physiology-Endocrinology and Metabolism, 296(2), E351-E357.Adam, T. C., & Epel, E. S. (2007). Stress, eating and the reward system. Physiology & Behavior, 91(4), 449-458.   12. Choi, J. H., Joseph, L., & Pilote, L. (2013). Obesity and C-reactive protein in various populations: A systematic review and meta-analysis. Obesity Reviews, 14(3), 232-244.⇰FREE WEBINAR TRAINING & OTHER LINKS: https://stan.store/reversingdiabetesrevolutionMy name is Charmaine and I'm the registered dietitian who helps people reverse Typ

This conversation is not your average discussion about testosterone; it's a journey into the physiological pathways, the intricacies of testosterone replacement therapy, and the crucial question of who should and shouldn't explore this avenue. Scott Howell, Ph.D., is the research director and primary investigator of Tier 1 Center for Clinical Research. He is an epidemiologist and exercise physiologist with research interests in the long-term safety of therapeutic androgen use, endocrine disrupting chemicals exposure, and preventative medicine. His work has been frequently published in notable peer-review journals including the American Journal of Physiology-Endocrinology and Metabolism and the Yale Journal of Biology and Medicine. Our discussion touches on making informed decisions about aromatase inhibitors and finasteride – the estrogen and DHT blockers, respectively. Dr. Howell also sheds light on the potential negative pathways of testosterone and offers valuable insights into navigating these aspects. Plus… we reveal some shocking facts about endocrine disruptors and their impact on the hormonal health of our species. – About Muscle Intelligence – We are raising the standard of men in their prime by helping aspirational men optimize their health so they can live longer, lead from the front and perform at their best everyday. Learn more: muscleintelligence.com/mipapply Support our Sponsors: Get a 10% discount on all BiOptimizers products at bioptimizers.com/muscle - use code MUSCLE10 Learn more from Dr. Scott Howell https://optimizeucenters.com/ https://www.researchgate.net/profile/Scott-Howell-2 Join the Mission: Private Email List: muscleintelligence.com/viplist Private Community: muscleintelligence.com/community Instagram: instagram.com/muscleintelligencecoaching YouTube: muscleintelligence.com/youtube

How do the experiences of our parents affect us? Do they affect only our learned behaviors? Or can they somehow affect our genes as well? Can the changes in someone's body due to a traumatic experience be passed on to their children and grandchildren? From famine in Ukraine to smells and diet in rats and mice, today we discuss how epigenetics plays a role in altering the biology of future generations. References: Bezo, B., & Maggi, S. (2015). Living in “survival mode:” Intergenerational transmission of trauma from the Holodomor genocide of 1932–1933 in Ukraine. Social Science & Medicine, 134, 87-94. Dias, B. G., & Ressler, K. J. (2014). Parental olfactory experience influences behavior and neural structure in subsequent generations. Nature neuroscience, 17(1), 89-96. Ingerslev, L. R., Donkin, I., Fabre, O., Versteyhe, S., Mechta, M., Pattamaprapanont, P., ... & Barrès, R. (2018). Endurance training remodels sperm-borne small RNA expression and methylation at neurological gene hotspots. Clinical epigenetics, 10(1), 1-11. McPherson, N. O., Owens, J. A., Fullston, T., & Lane, M. (2015). Preconception diet or exercise intervention in obese fathers normalizes sperm microRNA profile and metabolic syndrome in female offspring. American Journal of Physiology-Endocrinology and Metabolism, 308(9), E805-E821. https://en.wikipedia.org/wiki/Holodomor --- Support this podcast: https://anchor.fm/noggin-psychologypodcast/support

If you plan to eat a lot over the holidays, know that your body can compensate – for a little while. In a new study published in the American Journal of Physiology — Endocrinology and Metabolism, researchers analyzed eight young men to look at the effects that short-term overfeeding had on the body. The men […] The post 73. Our bodies can tolerate short periods of overeating appeared first on Dr. David Geier - Feel and Perform Better Than Ever.

@fabiodominski Fonte: Smith, J. A., Savikj, M., Sethi, P., Platt, S., Gabriel, B. M., Hawley, J. A., ... & Naslund, E. (2021). Three weeks of interrupting sitting lowers fasting glucose and glycemic variability, but not glucose tolerance, in free-living women and men with obesity. American Journal of Physiology-Endocrinology and Metabolism. --- Support this podcast: https://anchor.fm/fabio-dominski/support

Videos from Show  1. Scarborough 3 mins   2. COVID SHOTS EXPLAINED BY DR TENPENNY   3. Steve Deace on Twitter: "Pour one out for poor Bridgette from Washington, D.C     Anti-cancer and antidiabetic properties of maqui berry Nova Southeastern University (US), April 2, 2021 Researchers at NOVA Southeastern University in Florida reviewed the potential use of Aristotelia chilensis, also known as maqui berry, as a nutritional supplement to combat hyperinsulinemia and related diseases. Their report was published in the journal Food Science and Human Wellness. The scientific community has long considered nutritional supplementation to be a possible alternative medicine or adjunct treatment to conventional therapies for common ailments and diseases. Recent studies show that A. chilensis can reduce postprandial insulin levels by as much as 50 percent and is just as effective as metformin at increasing insulin sensitivity and stabilizing blood glucose levels. The berry’s mechanism of action involves inhibiting sodium-dependent glucose transporters in the small intestine and slowing glucose’s rate of entry in the bloodstream, which effectively reduces the likelihood of blood sugar spikes and the corresponding rise in insulin levels. At the same time, the A. chilensis contributes to cancer prevention since chronically high blood glucose levels are linked to the development of cancers. Studies have shown that diabetics and prediabetics have an elevated risk of developing cancerous growths. Based on the findings of previous studies, the researchers believe that consistent supplementation with A. chilensis could indirectly reduce the risk of cancer and other diseases that are promoted by hyperglycemia and hyperinsulinemia.   New research on vitamin D and respiratory infections important for risk groups   Karolinska Institutet (Sweden), April 1, 2021 Studies have shown that supplementary vitamin D seems to provide a certain degree of protection against respiratory infections. A new study involving researchers from Karolinska Institutet has now made the most comprehensive synthesis to date of this connection. The study, which is published in The Lancet Diabetes & Endocrinology, confirms that vitamin D protects against respiratory infections, a result that can have significance for the healthcare services. Whether vitamin D can reduce the risk of infection is a still an open issue. Four years ago, a synthesis of current research was published that showed that vitamin D supplementation can provide a certain degree of protection against respiratory infections. Now, the same researchers from, amongst other institutes, Karolinska Institutet, Harvard Medical School and Queen Mary University of London, have expanded the earlier material with an additional 18 studies and carried out new analyses. Their results are based on 43 randomized and placebo-controlled studies on the possible relationship between vitamin D and respiratory infections involving almost 49,000 participants. The material the researchers have drawn on comprised published as well as registered but as yet unpublished studies, and is the most comprehensive such compilation to date. The new study adds further information about vitamin D as a protection against respiratory infections, but does not cover the question of whether vitamin D can protect against COVID-19. Daily dose most effective While the total protective effect against respiratory infections was 8%, the researchers found, for example, that a daily dose of vitamin D is much more effective than one given every week or month. There is no reason, either, to exceed the recommended dose. "A particularly high dose doesn't seem necessary," says study co-author Peter Bergman, associate professor at the Department of Laboratory Medicine, Karolinska Institutet. "Those who received 400-1000 IU/day had the best response, as the group that received such a dose demonstrated a reduction in infection risk of 42%. I want to stress that there were no signals in the study that normal doses of vitamin D were dangerous or caused adverse reactions." Lower risk in vulnerable groups One conclusion that Dr. Bergman says can be drawn from the study is that the healthcare services should be more alert to groups that have a known risk of vitamin D deficiency, such as people with dark skin, overweight people and the elderly. "A daily dose of vitamin D can protect the bones and perhaps also reduce the risk of respiratory infections in vulnerable groups," he continues. "The wider population will probably not benefit as much from the supplement, though. Vitamin D doesn't make healthy people healthier." The researchers are now interrogating the mechanisms behind the protective effect of vitamin D against respiratory infections—for instance, what genetic factors determine why people respond differently to vitamin D supplements. One weakness of the compilation procedure is the possible influence of "publication bias," in that studies that do not demonstrate an effect are never published, which can create a false impression of how effective vitamin D is. To compensate for this, data from registered but as yet unpublished studies were also included. The study received no external funding. Some of the co-authors have declared the receipt of grants from pharmaceutical companies and/or vitamin supplement manufacturers, although outside of this study. See the scientific paper for a full list of potential conflicts of interest.   Role of inflammatory diet and vitamin D in link between periodontitis and cognitive function Instituto Universitario Egas Moniz (Portugal), March 25, 2021   According to news reporting originating from Almada, Portugal, research stated, “Patients suffering from periodontitis are at a higher risk of developing cognitive dysfunction. However, the mediation effect of an inflammatory diet and serum vitamin D levels in this link is unclear.” The news reporters obtained a quote from the research from Periodontology Department: “In total, 2062 participants aged 60 years or older with complete periodontal diagnosis and cognitive tests from the National Health and Nutrition Examination Survey (NHANES) 2011-2012 and 2013-2014 were enrolled. The Consortium to Establish a Registry for Alzheimer’s disease (CERAD) word learning subtest (WLT) and CERAD delayed recall test (DRT), the animal fluency test (AFT) and the digit symbol substitution test (DSST) was used. Dietary inflammatory index (DII) was computed via nutrition datasets. Mediation analysis tested the effects of DII and vitamin D levels in the association of mean probing depth (PD) and attachment loss (AL) in all four cognitive tests. Periodontitis patients obtained worse cognitive test scores than periodontally healthy individuals. DII was negatively associated with CERAD-WLT, CERAD-DRT, AFT and DSST, and was estimated to mediate between 9.2% and 36.4% of the total association between periodontitis with cognitive dysfunction (* * p* * < 0.05). Vitamin D showed a weak association between CERAD-DRT, AFT and DSST and was estimated to between 8.1% and 73.2% of the association between periodontitis and cognitive dysfunction (* * p* * < 0.05).” According to the news editors, the research concluded: “The association between periodontitis and impaired cognitive function seems to be mediated both by a proinflammatory dietary load and vitamin D deficiency. Future studies should further explore these mediators in the periodontitis-cognitive decline link.”     More protein doesn't mean more strength in resistance-trained middle-aged adults University of Illinois at Urbana, March 25, 2021 A 10-week muscle-building and dietary program involving 50 middle-aged adults found no evidence that eating a high-protein diet increased strength or muscle mass more than consuming a moderate amount of protein while training. The intervention involved a standard strength-training protocol with sessions three times per week. None of the participants had previous weightlifting experience. Published in the American Journal of Physiology: Endocrinology and Metabolism, the study is one of the most comprehensive investigations of the health effects of diet and resistance training in middle-aged adults, the researchers say. Participants were 40-64 years of age. The team assessed participants' strength, lean-body mass, blood pressure, glucose tolerance and several other health measures before and after the program. They randomized participants into moderate- and high-protein diet groups. To standardize protein intake, the researchers fed each person a freshly cooked, minced beef steak and carbohydrate beverage after every training session. They also sent participants home with an isolated-protein drink to be consumed every evening throughout the 10 weeks of the study. "The moderate-protein group consumed about 1.2 grams of protein per kilogram of body weight per day, and the high-protein group consumed roughly 1.6 grams per kilogram per day," said Colleen McKenna, a graduate student in the division of nutritional sciences and registered dietician at the University of Illinois Urbana-Champaign who led the study with U. of I. kinesiology and community health professor Nicholas Burd. The team kept calories equivalent in the meals provided to the two groups with additions of beef tallow and dextrose. The study subjects kept food diaries and McKenna counseled them every other week about their eating habits and protein intake. In an effort led by U. of I. food science and human nutrition professor Hannah Holscher, the team also analyzed gut microbes in fecal samples collected at the beginning of the intervention, after the first week - during which participants adjusted to the new diet but did not engage in physical training - and at the end of the 10 weeks. Previous studies have found that diet alone or endurance exercise alone can alter the composition of microbes in the digestive tract. "The public health messaging has been that Americans need more protein in their diet, and this extra protein is supposed to help our muscles grow bigger and stronger," Burd said. "Middle age is a bit unique in that as we get older, we lose muscle and, by default, we lose strength. We want to learn how to maximize strength so that as we get older, we're better protected and can ultimately remain active in family and community life." The American Food and Nutrition Board recommends that adults get 0.8 grams of protein per kilogram of body weight per day to avoid developing a protein deficiency. The team tried to limit protein consumption in the moderate-protein group to the Recommended Daily Allowance, but their food diaries revealed those participants were consuming, on average, 1.1 to 1.2 grams of protein per kilogram of body weight per day. Those in the high-protein group ate about 1.6 grams of protein per kilogram per day - twice the recommended amount. Burd and his colleagues hypothesized that getting one's protein from a high-quality source like beef and consuming significantly more protein than the RDA would aid in muscle growth and strength in middle-aged adults engaged in resistance training. But at the end of the 10 weeks, the team saw no significant differences between the groups. Their gains in strength, their body fat, lean body mass, glucose tolerance, kidney function, bone density and other "biomarkers" of health were roughly the same. The only potentially negative change researchers recorded between the groups involved alterations to the population of microbes that inhabit the gut. After one week on the diet, those in the high-protein group saw changes in the abundance of some gut microbes that previous studies have linked to negative health outcomes. Burd and his colleagues found that their strength-training intervention reversed some of these changes, increasing beneficial microbes and reducing the abundance of potentially harmful ones. "We found that high protein intake does not further increase gains in strength or affect body composition," Burd said. "It didn't increase lean mass more than eating a moderate amount of protein. We didn't see more fat loss, and body composition was the same between the groups. They got the gain in weight, but that weight gain was namely from lean-body-mass gain." Burd said the finding makes him question the push to increase protein intake beyond 0.8-1.1 grams per kilogram of body weight, at least in middle-aged weightlifters consuming high-quality animal-based protein on a regular basis. McKenna said the team's multidisciplinary approach and in-depth tracking of participants' dietary habits outside the laboratory makes it easier to understand the findings and apply them to daily life. "We have recommendations for healthy eating and we have recommendations for how you should exercise, but very little research looks at how the two together impact our health," she said. The study team included exercise physiologists, registered dietitians and experts on gut microbiology. "This allowed us to address every aspect of the intervention in the way it should be addressed," McKenna said. "We're honoring the complexity of human health with the complexity of our research."   Higher serum carotenoid levels linked with less visceral fat in women Hirosaki University & Kagome Ltd (Japan), March 24 2021.    Visceral fat resides within the abdomen, where it surrounds the internal organs. Visceral fat is not only challenging to lose but is associated with an increase in inflammation and disorders such as type 2 diabetes and cardiovascular disease. In fact, high visceral fat area is a greater predictor of cardiovascular disease than waist circumference and body mass index (BMI).  A study reported on March 11, 2021 in Nutrients revealed an association between higher levels of carotenoids and a reduction in visceral fat area. The investigation included 310 men and 495 women who received an annual health examination as part of the Iwaki Health Promotion Project in Japan. Blood samples were analyzed for the carotenoids alpha carotene, beta carotene, beta cryptoxanthin, lycopene, lutein and zeaxanthin. Visceral fat area was measured using an abdominal bioimpedance method and BMI was calculated from anthropometric data. Diet history questionnaire responses provided information concerning food intake. Total carotenoid levels were associated with the intake of leafy green vegetables, carrots and pumpkins, root vegetables and juice. Women’s carotenoid levels were significantly higher than those of men. Higher total carotenoid levels were associated with decreased visceral fat area and BMI in women, independent of fiber intake. Increased beta carotene, beta cryptoxanthin and lutein levels in women were also significantly associated with having a lower visceral fat area. The differences found between men and women in the study led the researchers to suggest that a threshold level of carotenoids might be necessary to influence visceral fat. “This is the first study to evaluate the association between serum carotenoids levels and visceral fat area in healthy individuals,” Mai Matsumoto and associates announced. “Ingestion of carotenoid-rich vegetables (particularly lutein and beta carotene) may be associated with lower visceral fat area, a good predictor of cardiovascular disease, especially in women.”       Research suggests optimal time of day to consume longevity-supporting supplements University of Waterloo (Ontario), March 24, 2021   Aging is a disease that can be fought with the appropriate combinations of supplements and behaviours, according to new research from the University of Waterloo. Using a comprehensive mathematical model, the researchers also found that the best time of day for someone to take these supplements depends on their age. Some anti-aging supplements should be taken by young people at night, while older people should take it midday for the greatest effectiveness. The two classes of drugs the researchers modelled are nicotinamide mononucleotide (NMN) and Resveratrol, which have been the subject of increased interest in recent years after reports emerged on their benefits on metabolism and increased lifespan of various organisms. A debate over whether to classify aging as a disease has been ongoing for decades, with the vast majority in the field of aging research now classifying it as such. As recently as 2015, a team of international scientists authored a paper calling it "time to classify biological aging as a disease"--and the World Health Organization has made moves that bring it closer to that definition. "It's really important to try and change this wrong paradigm that aging is not treatable," said Mehrshad Sadria, a PhD student in Waterloo'sDepartment of Applied Mathematics. "We shouldn't think like 30 years ago when we thought that once a person gets into their 70s or 80s, they must be lethargic and ailing.  The clear association of aging with various serious diseases is a stronger motivator for better understanding aging, Sadria said. Recognizing aging as a disease can encourage investment and promote research efforts in identifying therapies that can delay the aging process.  "We can take these drugs that can extend our lifespan and improve our health. This study is the first step in understanding when is the best time for young people and older folks to take these supplements." Sadria and Anita Layton, professor of Applied Mathematics, Computer Science, Pharmacy and Biology at Waterloo, developed a mathematical model that simulates the circadian clock and metabolism in the mouse liver. The model is age-specific and can simulate liver function in a young mouse or an aged mouse. They found that a young person, for example, should take NMN six hours after they wake up to achieve the highest efficiency. On the other hand, young individuals should take Resveratrol at night while older people should take it midday for the greatest effectiveness.  "The time you eat, what you eat, the time you sleep and the time you exercise are all factors that can affect your body, how you age and how you live," Layton said. "People should be mindful of when they eat and ensure that it coincides with other things in their environment that impact their sleep/wake cycle or body clock, such as exposure to light because if not, it could cause conflict within the body."  The study, Modeling the Effect of Ageing on the Circadian Clock and Metabolism: Implications on Timing of Medication, was recently published in the journal iScience.     Sugar not so nice for your child's brain development New research shows how high consumption affects learning, memory University of Georgia, April 1, 2021 Sugar practically screams from the shelves of your grocery store, especially those products marketed to kids. Children are the highest consumers of added sugar, even as high-sugar diets have been linked to health effects like obesity and heart disease and even impaired memory function.  However, less is known about how high sugar consumption during childhood affects the development of the brain, specifically a region known to be critically important for learning and memory called the hippocampus. New research led by a University of Georgia faculty member in collaboration with a University of Southern California research group has shown in a rodent model that daily consumption of sugar-sweetened beverages during adolescence impairs performance on a learning and memory task during adulthood. The group further showed that changes in the bacteria in the gut may be the key to the sugar-induced memory impairment. Supporting this possibility, they found that similar memory deficits were observed even when the bacteria, called Parabacteroides, were experimentally enriched in the guts of animals that had never consumed sugar. "Early life sugar increased Parabacteroides levels, and the higher the levels of Parabacteroides, the worse the animals did in the task," said Emily Noble, assistant professor in the UGA College of Family and Consumer Sciences who served as first author on the paper. "We found that the bacteria alone was sufficient to impair memory in the same way as sugar, but it also impaired other types of memory functions as well." Guidelines recommend limiting sugar The Dietary Guidelines for Americans, a joint publication of the U.S. Departments of Agriculture and of Health and Human Services, recommends limiting added sugars to less than 10 percent of calories per day. Data from the Centers for Disease Control and Prevention show Americans between the ages 9-18 exceed that recommendation, the bulk of the calories coming from sugar-sweetened beverages. Considering the role the hippocampus plays in a variety of cognitive functions and the fact the area is still developing into late adolescence, researchers sought to understand more about its vulnerability to a high-sugar diet via gut microbiota. Juvenile rats were given their normal chow and an 11% sugar solution, which is comparable to commercially available sugar-sweetened beverages.  Researchers then had the rats perform a hippocampus-dependent memory task designed to measure episodic contextual memory, or remembering the context where they had seen a familiar object before. "We found that rats that consumed sugar in early life had an impaired capacity to discriminate that an object was novel to a specific context, a task the rats that were not given sugar were able to do," Noble said. A second memory task measured basic recognition memory, a hippocampal-independent memory function that involves the animals' ability to recognize something they had seen previously. In this task, sugar had no effect on the animals' recognition memory. "Early life sugar consumption seems to selectively impair their hippocampal learning and memory," Noble said. Additional analyses determined that high sugar consumption led to elevated levels of Parabacteroides in the gut microbiome, the more than 100 trillion microorganisms in the gastrointestinal tract that play a role in human health and disease. To better identify the mechanism by which the bacteria impacted memory and learning, researchers experimentally increased levels of Parabacteroides in the microbiome of rats that had never consumed sugar. Those animals showed impairments in both hippocampal dependent and hippocampal-independent memory tasks. "(The bacteria) induced some cognitive deficits on its own," Noble said. Noble said future research is needed to better identify specific pathways by which this gut-brain signaling operates.  "The question now is how do these populations of bacteria in the gut alter the development of the brain?" Noble said. "Identifying how the bacteria in the gut are impacting brain development will tell us about what sort of internal environment the brain needs in order to grow in a healthy way."

In this episode, Dr. Grady and Dr. Garrett continue their conversation from last episode on the article "Modeling insulin resistance in rodents by alterations in diet: what have high-fat and high-calorie diets revealed?" This time we dive into how diets effect glucose metabolism, but how to also keep in mind your health goals when implementing a dietary lifestyle.   PLEASE SUBSCRIBE TO THE PODCAST For more Diabuddies content follow us on The Diabuddies Podcast Facebook page. Twitter: @TheDiabuddies Instagram: @thediabuddiespodcast You can email us at TheDiabuddiesPodcast@gmail.com   Time Stamps: 0:00 - Appreciating Nutritional Research Critically 4:40 - Range of Fat % in High Fat Diets (HFD) and Keto 11:30 - How Different Fatty Acids Create Different Metabolic Changes 14:50 - HFD + Omega 3 Supps Improve Insulin Sensitivity 19:30 - Saturated Fat Lengths and Fatty Sources 22:35 - Dr. Donohoe's MANY uses for coconut oil 27:35 - High Fat/High Sucrose (HSHS) diets AKA Standard American Diet (SAD) 29:55 - Epigenetics and HFHS 34:33 - Epigenetics and T1D Patterns 37:43 - Expansion on the SAD 43:00 - "Cafeteria" and "Choice" diets 46:48 - High Carb Diets (HCD): Picking a side is better then the combo 55:10 - HCD effect on Insulin Resistance (IR) 56:10 - Fructose's role on Hepatic IR 1:06:49 - Controls in HCD vs HFD 1:10:25 - Playing Devils Advocate Against One's Own Bias 1:14:10 - Altering Protein Content in Diets 1:18:23 - Dr. Panno's attempt at Amino Acid case study 1:20:50 - Protein Powder vs Food Sources 1:23:52 - Diabetic Win: Bone Broth Protein and night time blood sugars 1:27:00 - Diabetic Win: Mr. Incredible at Medtronic   Resources/Links Discussed in the episode: Small, Lewin, et al. “Modeling Insulin Resistance in Rodents by Alterations in Diet: What Have High-Fat and High-Calorie Diets Revealed?” American Journal of Physiology-Endocrinology and Metabolism, vol. 314, no. 3, 2018, doi:10.1152/ajpendo.00337.2017.

Conversion of Testosterone to Estradiol is a genetically regulated physiological function that is important to your wellbeing. Mess with is and all sorts of body organ symptoms are affected. Listen To This Podcast It May save your life. Scott Howell, Ph.D., is the research director and principal investigator of Tier 1 Center for Clinical Research https://tier1hw.com/  . He is a professor, epidemiologist, and exercise physiologist with research interests in the long-term safety of therapeutic androgen use, endocrine disrupting chemicals exposure, and preventative medicine. His primary expertise includes androgen metabolism, anabolic steroid abuse, pharmacogenetics, interpretation of clinical research, statistical analysis, and research methods.   Dr. Howell is an author with expertise spanning many fields. His authorships include a recent sport science text, Integrated Periodization in Sports Training and Athletic Development, coauthored with Dr. Tudor Bompa, University of Toronto, and Dr. James Hoffmann, East Tennessee State University. He has also served as a subject matter expert coauthoring the Encyclopedia of Sports Speed for The National Association of Speed and Explosion.   Dr. Howell has frequently published in notable peer-review journals including the American Journal of Physiology-Endocrinology and Metabolism, Karger Cardiology, Journal of Ethnopharmacology, Pharmacological Research, and the Yale Journal of Biology and Medicine.   Dr. Howell has received numerous acknowledgments for his contributions to academic scholarship and clinical research. He received the American Military University Academic Scholar Award in 2016 and has taken part in two major National Institutes of Health (NIH) and Department of Defense (DoD) funded studies at Wake Forest University: Strength Training for Arthritis Trial (START) and The Runners and Injury Longitudinal Study (TRAILS).      Dr. Howell holds a Ph.D. in Health Science-Epidemiology from Trident University, a Medical Degree from BMU School of Medicine, a Master of Science in Sport and Health Science from American Military University, a Bachelor of Science in Sport and Health Science from American Military University, and a Mechanical Engineering degree from Forsyth Technical College.   Dr. Howell is a former Ph.D. faculty member of the Trident University Health Sciences program where he taught the most rigorous courses of the Ph.D. program. He served as a Dissertation

In this episode, Dr. Grady and Dr. Garrett discuss the mechanisms of insulin resistance in various tissues in the body (muscle, liver, fat). This leads to several digressions about lifestyle habits that will that will affect these tissues directly to improve insulin resistance, such as exercise and muscle glucose metabolism. We also talk about what "Bursts Our Beta Cells" and a diabetic win that we recently had.   PLEASE SUBSCRIBE TO THE PODCAST For more Diabuddies content follow us on The Diabuddies Podcast Facebook page. Twitter: @TheDiabuddies Instagram: @thediabuddiespodcast You can email us at TheDiabuddiesPodcast@gmail.com   Time Stamps: 0:36 - Grady's "Burst My Beta Cells": Insurance and Pharmacies 9:53 - Garrett's "Bursts My Beta Cells": Margaritas, Celebration and T1D 15:03 - Diet Induced Obesity for Insulin Resistance (IR) Models and Studies 22:04 - Importance of Muscle Physiology 25:50 - Moving Your Body for Metabolism and Insulin Sensitivity 35:10 - 4 Major IR Models within Myocytes (Muscle Cells) 37:19 - Intracellular Lipids within Myocytes (Muscle Cells) 41:53 - Explanation on Glucose Sparing 45:07 - Athlete Paradox with Intracellular Lipids 50:06 - TAGs and Lipid Panels in Context of Muscle Physiology 55:10 - Mitochondria Dysfunction within Myocytes 1:02:38 - IR within Hepatocytes (Liver Cells) Definition 1:12:58 - IR in the Liver and NAFLD 1:15:43 - IR Liver Leads to Increased Lipogenesis and Transportation 1:19:33 - Brief Discussion on IR and Adipose Tissue 1:23:58 - Personal Diabetes Win   Resources/Links Discussed in the episode: Small, Lewin, et al. “Modeling Insulin Resistance in Rodents by Alterations in Diet: What Have High-Fat and High-Calorie Diets Revealed?” American Journal of Physiology-Endocrinology and Metabolism, vol. 314, no. 3, 2018, doi:10.1152/ajpendo.00337.2017.

A few weeks ago NBT Scientific Director Megan Hall and I met up to discuss the causes of postprandial fatigue, commonly known as “food coma”. We talked about two common causes, both associated with glucose dysregulation. Megan described some of the mechanisms causing hypoglycemia, including accelerated gastric emptying, periods of increased insulin sensitivity, and low hormonal states, while hyperglycemia is often associated with insulin resistance. This was such a big topic we only covered about half of it the first time around, so we’re continuing the conversation today. On this podcast, Megan and I discuss three additional causes of postprandial fatigue: endotoxin, inflammation, and mitochondrial dysfunction. Megan describes each of these scenarios in detail, discussing some of the upstream causes that can be targeted early on to avoid problems. She also provides practical steps you can take if you’re one of the millions dozing off after lunch every day. Be sure to follow along with Megan’s outline for this podcast.  Here’s the outline of this interview with Megan Hall: [00:01:42] Previous podcast: Postprandial Fatigue: Is It Normal To Need A Nap After Lunch?  [00:03:20] Hans Vink; Hyperglycemia reduces glycocalyx volume while NAC infusion prevents the reduction. Nieuwdorp, Max, et al. "Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo." Diabetes 55.2 (2006): 480-486. [00:03:51] Malcolm Kendrick on the glycocalyx; Podcasts: Why Cholesterol Levels Have No Effect on Cardiovascular Disease (And Things to Think about Instead) and A Statin Nation: Damaging Millions in a Brave New Post-health World. [00:04:51] NBT Strength and Conditioning Coach Zach Moore; Podcast: How to Strength Train Without a Gym. [00:06:21] Postprandial endotoxemia (PPE): definition, causes, downstream effects; Study: Kelly, Caleb J., Sean P. Colgan, and Daniel N. Frank. "Of microbes and meals: the health consequences of dietary endotoxemia." Nutrition in Clinical Practice 27.2 (2012): 215-225.  [00:11:04] What to do about PPE. [00:11:56] Probiotics; Podcasts: How to Optimise Your Gut Microbiome and Microbiome Myths and Misconceptions, with Lucy Mailing, PhD; How to Use Probiotics to Improve Your Health, with Jason Hawrelak, PhD. [00:12:10] Megasporebiotic; Study: McFarlin, Brian K., et al. "Oral spore-based probiotic supplementation was associated with reduced incidence of post-prandial dietary endotoxin, triglycerides, and disease risk biomarkers." World Journal of Gastrointestinal Pathophysiology 8.3 (2017): 117. [00:12:36] Chris' sister's story. [00:13:51] S. boulardii - may help with gut barrier function; Study: Terciolo, Chloe, Michel Dapoigny, and Frederic Andre. "Beneficial effects of Saccharomyces boulardii CNCM I-745 on clinical disorders associated with intestinal barrier disruption." Clinical and experimental gastroenterology 12 (2019): 67. [00:14:23] Additional supplements that may help with gut: Enteromend, Permaclear, GI Revive, SBI Protect. [00:17:09] Dietary interventions for PPE. [00:17:14] Plant polyphenols; Studies: 1. Wong, Ximena, et al. "Polyphenol extracts interfere with bacterial lipopolysaccharide in vitro and decrease postprandial endotoxemia in human volunteers." Journal of Functional Foods 26 (2016): 406-417; 2. González‐Sarrías, Antonio, et al. "The endotoxemia marker lipopolysaccharide‐binding protein is reduced in overweight‐obese subjects consuming pomegranate extract by modulating the gut microbiota: A randomized clinical trial." Molecular nutrition & food research 62.11 (2018): 1800160; 3. Kolehmainen, Marjukka, et al. "Bilberries reduce low‐grade inflammation in individuals with features of metabolic syndrome." Molecular nutrition & food research 56.10 (2012): 1501-1510.  [00:17:36] Sulforaphane; Studies: 1. Yanaka, Akinori, Junya Sato, and Shun Ohmori. "Sulforaphane protects small intestinal mucosa from aspirin/NSAID-induced injury by enhancing host defense systems against oxidative stress and by inhibiting mucosal invasion of anaerobic enterobacteria." Current pharmaceutical design 19.1 (2013): 157-162. 2. Yanaka, Akinori. "Role of sulforaphane in protection of gastrointestinal tract against H. pylori and NSAID-induced oxidative stress." Current pharmaceutical design 23.27 (2017): 4066-4075. [00:17:53] Hormetea. [00:20:20] Dietary oil composition plays a role in endotoxin transport; Study: Mani, Venkatesh, James H. Hollis, and Nicholas K. Gabler. "Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia." Nutrition & metabolism 10.1 (2013): 6. [00:21:55] Supporting detoxification; Studies: 1. Fox, Eben S., Peter Thomas, and Selwyn A. Broitman. "Hepatic mechanisms for clearance and detoxification of bacterial endotoxins." The journal of nutritional biochemistry 1.12 (1990): 620-628 (SciHub); 2. Munford, Robert S. "Invited review: detoxifying endotoxin: time, place and person." Journal of endotoxin research 11.2 (2005): 69-84. [00:22:20] Enterosgel. [00:24:04] Inflammation; Study: Mo, Zhenzhen, et al. "Endotoxin May Not Be the Major Cause of Postprandial Inflammation in Adults Who Consume a Single High-Fat or Moderately High-Fat Meal." The Journal of Nutrition 150.5 (2020): 1303-1312. [00:25:51] Lucy Mailing on gut barrier integrity: Article: Is a high-fat or ketogenic diet bad for your gut? Discussed on NBT Forum post. [00:26:26] Food sensitivities; Studies: 1. Ohtsuka, Yoshikazu. "Food intolerance and mucosal inflammation." Pediatrics International 57.1 (2015): 22-29; 2. Wilders-Truschnig, M., et al. "IgG antibodies against food antigens are correlated with inflammation and intima media thickness in obese juveniles." Experimental and clinical endocrinology & diabetes 116.4 (2008): 241. [00:27:58] IL-1 and postprandial fatigue; Study: Lehrskov, Louise L., et al. "The role of IL-1 in postprandial fatigue." Molecular metabolism 12 (2018): 107-112. [00:29:05] Mitochondrial dysfunction and glucose dysregulation; Study: Sergi, Domenico, et al. "Mitochondrial (dys) function and insulin resistance: From pathophysiological molecular mechanisms to the impact of diet." Frontiers in physiology 10 (2019): 532. [00:29:54] Normal vs pathological biochemistry. [00:32:53] TCA cycle and electron transport chain. [00:33:21] Insulin resistance is a cellular antioxidant defense mechanism; Study: Hoehn, Kyle L., et al. "Insulin resistance is a cellular antioxidant defense mechanism." Proceedings of the National Academy of Sciences 106.42 (2009): 17787-17792. [00:35:02] Blood sugar dysregulation and mito dysfunction; Studies: 1. Stefano, George B., Sean Challenger, and Richard M. Kream. "Hyperglycemia-associated alterations in cellular signaling and dysregulated mitochondrial bioenergetics in human metabolic disorders." European journal of nutrition 55.8 (2016): 2339-2345; 2. Rolo, Anabela P., and Carlos M. Palmeira. "Diabetes and mitochondrial function: role of hyperglycemia and oxidative stress." Toxicology and applied pharmacology 212.2 (2006): 167-178; 3. Kaikini, Aakruti Arun, et al. "Targeting mitochondrial dysfunction for the treatment of diabetic complications: pharmacological interventions through natural products." Pharmacognosy Reviews 11.22 (2017): 128. [00:36:26] How to support mitochondria. [00:36:46] Low-carb diet; Study: Miller, Vincent J., Frederick A. Villamena, and Jeff S. Volek. "Nutritional ketosis and mitohormesis: potential implications for mitochondrial function and human health." Journal of nutrition and metabolism 2018 (2018). [00:37:04] Exercise; Studies: 1. Oliveira, Ashley N., and David A. Hood. "Exercise is mitochondrial medicine for muscle." Sports Medicine and Health Science 1.1 (2019): 11-18; 2. Memme, Jonathan M., et al. "Exercise and mitochondrial health." The Journal of Physiology (2019); 3. Huertas, Jesus R., et al. "Stay fit, stay young: mitochondria in movement: the role of exercise in the new mitochondrial paradigm." Oxidative Medicine and Cellular Longevity 2019 (2019). [00:37:31] TRE or fasting, CR; Study: Lettieri-Barbato, Daniele, et al. "Time-controlled fasting prevents aging-like mitochondrial changes induced by persistent dietary fat overload in skeletal muscle." PloS one 13.5 (2018): e0195912. [00:38:03] Dietary polyphenols; Studies: 1. Sun, Chongde, et al. "Dietary polyphenols as antidiabetic agents: Advances and opportunities." Food Frontiers 1.1 (2020): 18-44; 2. Teixeira, José, et al. "Dietary polyphenols and mitochondrial function: role in health and disease." Current medicinal chemistry 26.19 (2019): 3376-3406. [00:38:47] Eat berries before a carb rich meal; 1. Törrönen, Riitta, et al. "Berries reduce postprandial insulin responses to wheat and rye breads in healthy women." The Journal of nutrition 143.4 (2013): 430-436; 2. Xiao, Di, et al. "Attenuation of postmeal metabolic indices with red raspberries in individuals at risk for diabetes: A randomized controlled trial." Obesity 27.4 (2019): 542-550. [00:39:34] Eat fatty fish; Studies: Lanza, Ian R., et al. "Influence of fish oil on skeletal muscle mitochondrial energetics and lipid metabolites during high-fat diet." American Journal of Physiology-Endocrinology and Metabolism 304.12 (2013): E1391-E1403; 2. de Oliveira, Marcos Roberto, et al. "Omega-3 polyunsaturated fatty acids and mitochondria, back to the future." Trends in food science & technology 67 (2017): 76-92. [00:39:53] Sleep; Studies: 1. Rodrigues, Nathane Rosa, et al. "Short-term sleep deprivation with exposure to nocturnal light alters mitochondrial bioenergetics in Drosophila." Free Radical Biology and Medicine 120 (2018): 395-406; 2. Schmitt, Karen, et al. "Circadian control of DRP1 activity regulates mitochondrial dynamics and bioenergetics." Cell metabolism 27.3 (2018): 657-666. [00:40:16] Supplements to support mitochondria; Study: Wesselink, E., et al. "Feeding mitochondria: potential role of nutritional components to improve critical illness convalescence." Clinical nutrition 38.3 (2019): 982-995. [00:42:22] Outline for this podcast.  [00:42:25] Dr. Josh Turkett’s 4-quadrant model. [00:44:47] 35% of pharmaceuticals cause mito dysfunction; Studies: 1. Meyer, Joel N., and Sherine SL Chan. "Sources, mechanisms, and consequences of chemical-induced mitochondrial toxicity." (2017): 2-4; and 2. Dykens, James A., and Yvonne Will. "The significance of mitochondrial toxicity testing in drug development." Drug discovery today 12.17-18 (2007): 777-785. [00:45:08] Environmental pollutants; Podcast: Environmental Pollutants and the Gut Microbiome, with Jodi Flaws, PhD. [00:45:22] Psychological stress; Podcast: Germline Exposures with Jill Escher. [00:46:35] Support NBT on Patreon. [00:46:51] Book a free 15-minute starter session with one of our coaches.

Reference: 1.Barone J, Roberts H. Caffeine consumption. Food and Chemical Toxicology. 1996;34(1):119-29. 2.Amin N, Byrne E, Johnson J, Chenevix-Trench G, Walter S, Nolte IM, et al. Genome-wide association analysis of coffee drinking suggests association with CYP1A1/CYP1A2 and NRCAM. Molecular Psychiatry. 2012;17(11):1116-29. 3.Svilaas A, Sakhi AK, Andersen LF, Svilaas T, Strom EC, Jacobs Jr DR, et al. Intakes of antioxidants in coffee, wine, and vegetables are correlated with plasma carotenoids in humans. The Journal of nutrition. 2004;134(3):562-7. 4.Pulido R, Hernandez-Garcia M, Saura-Calixto F. Contribution of beverages to the intake of lipophilic and hydrophilic antioxidants in the Spanish diet. European journal of clinical nutrition. 2003;57(10):1275-82. 5. SELFnutritionData know what you eat. Nutrient data for this listing was provided by USDA SR-21. Coffee, brewed from grounds, prepared with tap water [Internet]. 2018. (accessed on May 5, 2020) Available from: https://nutritiondata.self.com/facts/beverages/3898/2 6.Teketay D. History, botany and ecological requirements of coffee. Walia. 1999;20:28-50. 7.Fredholm BB. Adenosine, adenosine receptors and the actions of caffeine. Pharmacology & toxicology. 1995;76(2):93-101. 8.Nehlig A, Daval J-L, Debry G. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Research Reviews. 1992;17(2):139-70. 9.Dulloo A, Geissler C, Horton T, Collins A, Miller D. Normal caffeine consumption: influence on thermogenesis and daily energy expenditure in lean and postobese human volunteers. The American journal of clinical nutrition. 1989;49(1):44-50. 10.Bracco D, Ferrarra J-M, Arnaud MJ, Jequier E, Schutz Y. Effects of caffeine on energy metabolism, heart rate, and methylxanthine metabolism in lean and obese women. American Journal of Physiology-Endocrinology and Metabolism. 1995;269(4):E671-E8. 11.Huxley R, Lee CMY, Barzi F, Timmermeister L, Czernichow S, Perkovic V, et al. Coffee, decaffeinated coffee, and tea consumption in relation to incident type 2 diabetes mellitus: a systematic review with meta-analysis. Archives of internal medicine. 2009;169(22):2053-63. 12.Smith A. Effects of caffeine on human behavior. Food and chemical toxicology. 2002;40(9):1243-55. 13.Drake C, Roehrs T, Shambroom J, Roth T. Caffeine effects on sleep taken 0, 3, or 6 hours before going to bed. Journal of Clinical Sleep Medicine. 2013;9(11):1195-200. 14.J. Boekema MS, GP van Berge Henegouwen, AJPM Smout, P. Coffee and gastrointestinal function: facts and fiction: a review. Scandinavian Journal of Gastroenterology. 1999;34(230):35-9. 15.Mattioli AV, Pennella S, Farinetti A, Manenti A. Energy Drinks and atrial fibrillation in young adults. Clinical Nutrition. 2018;37(3):1073-4. 16.สำนักโภชนาการ กรมอนามัย กระทรวงสาธารณสุข. รายงานการศึกษาวิจัยปี 2552 เรื่อง สารอาหารในกาแฟเย็นแคลอรี ของกาแฟแต่ละชนิด. ออนไลน์. ค้นเมื่อ 5 พฤษภาคม 2563. เข้าถึงได้จาก : http://nutrition.anamai.moph.go.th/images/file/สารอาหารในกาแฟเย็น.pdf 17.Dalle Grave R, Sartirana M, El Ghoch M, Calugi S. Module 1: Monitoring Food Intake, Physical Activity and Body Weight. Treating Obesity with Personalized Cognitive Behavioral Therapy: Springer; 2018. p. 45-58. 18.Min JE, Green DB, Kim L. Calories and sugars in boba milk tea: implications for obesity risk in Asian Pacific Islanders. Food science & nutrition. 2017;5(1):38-45. 19.Jura YH, Townsend MK, Curhan GC, Resnick NM, Grodstein F. Caffeine intake, and the risk of stress, urgency and mixed urinary incontinence. J Urol. 2011;185(5):1775-80. 20.Lachenmeier DW, Schwarz S, Teipel J, Hegmanns M, Kuballa T, Walch SG, et al. Potential antagonistic effects of acrylamide mitigation during coffee roasting on furfuryl alcohol, furan and 5-hydroxymethylfurfural. Toxics. 2019;7(1):1.

Časovnica: [00:00:55] O projektu nadaljnjega izobraževanja o prehrani, vadbi in kritični presoji literature. Kultura pogovora preko socialnih omrežij ter epilog poizkusa svetovnega rekorda v mrtvem dvigu. [00:19:35] Inteligenca in kritično razmišljanje nista ista stvar. Zakaj pametni ljudje počnejo neumnosti. Zakaj je kritično razmišljanje ključ do dobrega življenja. [00:31:25] Kofein kot dopolnilo za izboljšanje zmogljivosti ter kako genotip vpliva na časovni vnos kofeina. [00:44:25] Vpliv mikrobiote in probiotikov na hujšanje. Visok vnos vlaknin in nižji vnos maščob za optimalno zdravje prebavil. [01:15:05] Zakaj vzdržljivostni športniki potrebujejo več beljakovin. [01:22:45] Zaključek.   Omenjeni članki: Zakaj pametni ljudje počnejo neumnosti: Why Do Smart People Do Foolish Things: https://www.scientificamerican.com/article/why-do-smart-people-do-foolish-things/ Vpliv genotipa na jemanje kofeina: Grgic et al. CYP1A2 genotype and acute effects of caffeine on resistance exercise, jumping, and sprinting performance. J Int Soc Sports Nutr 17, 21 (2020). https://doi.org/10.1186/s12970-020-00349-6 Mikrobiota in hujšanje: Fragiadakis. et al. (2020) ‘Long-term dietary intervention reveals resilience of the gut microbiota despite changes in diet and weight', The American Journal of Clinical Nutrition. Oxford University Press, pp. 1–10. https://doi.org/710.1093/ajcn/nqaa046  Hjorth et al. (2018) ‘Pre-treatment microbial Prevotella-to-Bacteroides ratio, determines body fat loss success during a 6-month randomized controlled diet intervention', International Journal of Obesity. Nature Publishing Group, 42(3), pp. 580–583. https://doi.org/10.1038/ijo.2017.220 Višji vnos vlaknin in nižji vnos maščob za optimalno zdravje prebavil: O'Keefe et al. (2015) ‘Fat, fibre and cancer risk in African Americans and rural Africans.', Nature communications, 6(May 2014), p. 6342. https://doi.org/10.1038/ncomms7342 Le Leu et al. (2015) ‘Butyrylated starch intake can prevent red meat-induced O6-methyl-2-deoxyguanosine adducts in human rectal tissue: A randomised clinical trial', British Journal of Nutrition, 114(2), pp. 220–230. https://doi.org/10.1017/S0007114515001750 Meta-analize o učinkovitosti probioikov pri hujšanju: Mazloom et al. (2019) ‘Probiotics: How Effective Are They in the Fight against Obesity?', Nutrients, 11(2), p. 258. https://doi.org/10.3390/nu11020258 Mohammadi et al. (2019) ‘Effects of pro-/synbiotic supplementation on anthropometric and metabolic indices in overweight or obese children and adolescents: A systematic review and meta-analysis', Complementary Therapies in Medicine. Elsevier Ltd, 44, pp. 269–276. https://doi.org/10.1016/j.ctim.2019.05.008 Cao. et al. (2020) ‘Effect of probiotic and synbiotic formulations on anthropometrics and adiponectin in overweight and obese participants: A systematic review and meta-analysis of randomized controlled trials', Journal of King Saud University - Science. The Author(s). https://doi.org/10.1016/j.jksus.2020.01.011 Potrebe vzdržljivostnih športnikov po beljakovinah: Kato et al. (2016). Protein Requirements Are Elevated in Endurance Athletes after Exercise as Determined by the Indicator Amino Acid Oxidation Method. PloS one, 11(6), e0157406. https://doi.org/10.1371/journal.pone.0157406 Bandegan et al. (2019). Indicator Amino Acid Oxidation Protein Requirement Estimate in Endurance-Trained Men 24h Post-Exercise Exceeds both the EAR and Current Athlete Guidelines. American Journal of Physiology-Endocrinology and Metabolism, 316(5):E741-E748. https://doi.org/10.1152/ajpendo.00174.2018   Sledite nam: Nenadov instagram: @nenad.feelgood Matjažev instagram: @matjaz.feelgood Feelgood Skupnost na Facebooku: https://bit.ly/feelgoodskupnost Spletna stran: https://www.feel-good.si   Poslušate nas lahko na: Podbean: https://bit.ly/podbean-zdp Stitcher: https://bit.ly/stitcher-zdp Pocket Casts: https://bit.ly/pocket-zdp Podcast Addict: https://bit.ly/addict-zdp Castbox: https://bit.ly/castbox-zdp iTunes: https://bit.ly/itunes-zdp  

Back on the podcast with me this week is sleep expert, Greg Potter, PhD. Through his articles, podcasts and live talks, Greg is helping an international audience understand the critical role sleep plays in health and wellbeing. Most recently, Greg has been studying the impact of circadian rhythm disruption, including sleep duration and meal timing, on the development of common cancers. In this interview, Greg and I discuss Alexey Guzey’s scathing critique of Matthew Walker’s book, Why We Sleep. We also talk about some of the biological processes affected by sleep restriction, including cognition, immune health, athletic performance, and appetite. Greg shares some of the ways poor sleep is associated with cancer formation, including the damaging effects of sleep restriction on DNA and metabolism. Here’s the outline of this interview with Greg Potter: [00:00:09] Greg's 4-part series of articles on sleep: 1. Having trouble sleeping? A primer on insomnia and how to sleep better; 2. Sleep-maintenance insomnia: how to sleep through the night; 3. Sleep-onset insomnia: how to get to sleep fast; 4. Sleep for athletes: are athletes a different breed? [00:00:28] Greg's previous podcasts: How to Entrain Your Circadian Rhythm for Perfect Sleep and Metabolic Health; Morning Larks and Night Owls: the Biology of Chronotypes; What to Do When You Can’t Sleep; Better Sleep for Athletes. [00:01:11] 2020 Metagenics International Congress on Natural Medicine. [00:03:36] Book: Why We Sleep, by Matthew Walker, PhD. [00:03:38] Article: Matthew Walker's "Why We Sleep" Is Riddled with Scientific and Factual Errors, by Alexey Guzey. [00:04:12] Book: Thinking, Fast and Slow by Daniel Kahneman. [00:10:23] Dimensions of sleep; Article: Buysse, Daniel J. "Sleep health: can we define it? Does it matter?." Sleep 37.1 (2014): 9-17. [00:12:34] The transtheoretical model of behavior change. [00:16:34] Stephan Guyenet’s Red Pen Reviews. [00:18:40] Chronotypes and the Sentinel Hypothesis. [00:19:39] Are people not sleeping enough? [00:21:56] Sleep duration in the US might be increasing; Study: Basner, Mathias, and David F. Dinges. "Sleep duration in the United States 2003–2016: first signs of success in the fight against sleep deficiency?." Sleep 41.4 (2018): zsy012. [00:26:12] People overestimate their sleep duration; Study: Lauderdale, Diane S., et al. "Self-reported and measured sleep duration: how similar are they?." Epidemiology (2008): 838-845. [00:28:29] Insulin sensitivity and testosterone higher after extended sleep; Killick, Roo, et al. "Metabolic and hormonal effects of ‘catch‐up’sleep in men with chronic, repetitive, lifestyle‐driven sleep restriction." Clinical endocrinology 83.4 (2015): 498-507. [00:29:00] Plasma IL-6 higher after sleep restriction; Study: Pejovic, Slobodanka, et al. "Effects of recovery sleep after one work week of mild sleep restriction on interleukin-6 and cortisol secretion and daytime sleepiness and performance." American Journal of Physiology-Endocrinology and Metabolism 305.7 (2013): E890-E896. [00:29:25] Better cognitive function with more sleep; Study: Kazem, Yusr MI, et al. "Sleep deficiency is a modifiable risk factor for obesity and cognitive impairment and associated with elevated visfatin." Open access Macedonian journal of medical sciences 3.2 (2015): 315. [00:29:37] Effects of sleep on appetite; Study: Al Khatib, H. K., et al. "The effects of partial sleep deprivation on energy balance: a systematic review and meta-analysis." European journal of clinical nutrition 71.5 (2017): 614-624. [00:30:02] Sleep extension and exercise performance; Study: Mah, Cheri D., et al. "The effects of sleep extension on the athletic performance of collegiate basketball players." Sleep 34.7 (2011): 943-950. [00:32:45] Assessing current sleep status. [00:33:11] Podcast with Ashley Mason: How to Use Cognitive Behavioral Therapy for Insomnia. [00:36:14] WHO (five) Well-Being Index; Short Form 12; Short Form 36. [00:38:55] NBT’s Health Assessment Questionnaire. [00:39:57] Sleep and all-cause mortality. [00:46:56] Sleep restriction leads to worse performance; Van Dongen, Hans, et al. "The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation." Sleep 26.2 (2003): 117-126. [00:47:31] Josh Turknett's 4-Quadrant Model; Podcast: How to Win at Angry Birds: The Ancestral Paradigm for a Therapeutic Revolution. [00:48:30] Sleep duration and cancer. [00:49:20] Short sleep duration associated with cancer among asians; long sleep duration associated with colorectal cancer; Study: Chen, Yuheng, et al. "Sleep duration and the risk of cancer: a systematic review and meta-analysis including dose–response relationship." BMC cancer 18.1 (2018): 1149. [00:51:02] Sleep deprivation and DNA damage: Study: Cheung, V., et al. "The effect of sleep deprivation and disruption on DNA damage and health of doctors." Anaesthesia 74.4 (2019): 434-440; and Carroll, Judith E., et al. "Partial sleep deprivation activates the DNA damage response (DDR) and the senescence-associated secretory phenotype (SASP) in aged adult humans." Brain, behavior, and immunity 51 (2016): 223-229. [00:51:16] Article: Seyfried, Thomas N., et al. "Cancer as a metabolic disease: implications for novel therapeutics." Carcinogenesis 35.3 (2014): 515-527. [00:56:22] Matthew Walker's website. [00:59:47] Greg’s website; Instagram, Twitter, LinkedIn. [01:02:55] Sleepio. (SHUTi no longer available).

Researcher Jon Ramsey, PhD is Professor in the Department of Molecular Biosciences within the School of Veterinary Medicine at UC Davis. His study of animals focuses on nutrition as it relates to obesity and aging. The goal of his research is to understand the biological mechanisms that contribute to the aging process and to develop dietary interventions that promote healthy aging and weight loss. In this podcast, NBT Scientific Director Megan Roberts interviews Dr. Ramsey about his research in the area of calorie restriction and its beneficial effects on longevity and healthspan. They examine the scientific literature on energy and macronutrient restriction, including some of the possible biological mechanisms driving the anti-aging effects of these interventions. They also discuss what this all means in practical terms for those seeking optimal health as they age. Here’s the outline of this interview with Jon Ramsey: [00:01:35] Calorie restriction for increasing lifespan. [00:02:01] Theories of aging. [00:04:40] Osborne and Mendel; Study: Osborne, Thomas B., Lafayette B. Mendel, and Edna L. Ferry. "The effect of retardation of growth upon the breeding period and duration of life of rats." Science 45.1160 (1917): 294-295. [00:04:58] Clive McCay; Studies: McCay, Clive Maine, and Mary F. Crowell. "Prolonging the life span." The Scientific Monthly 39.5 (1934): 405-414 and McCay, Carl M., Mary F. Crowell, and Lewis A. Maynard. "The effect of retarded growth upon the length of life span and upon the ultimate body size: one figure." The journal of Nutrition 10.1 (1935): 63-79. [00:06:25] Calorie restriction literature in animals. [00:07:39] Types of rodents studied. [00:08:09] Comparing effect of caloric restriction (CR) on different strains of mice; Study: Liao, Chen‐Yu, et al. "Genetic variation in the murine lifespan response to dietary restriction: from life extension to life shortening." Aging cell 9.1 (2010): 92-95. [00:09:08] Time restricted feeding in animal models. [00:11:51] Calorie restriction vs. malnutrition. [00:12:00] Different levels of calorie restriction. Study: Weindruch, Richard, et al. "The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake." The Journal of nutrition 116.4 (1986): 641-654. [00:13:36] Effects of 10% dietary restriction: Richardson, Arlan, et al. "Significant life extension by ten percent dietary restriction." Annals of the New York Academy of Sciences 1363.1 (2016): 11-17. [00:15:09] CALERIE study and resulting Publications. [00:17:56] Analyses of CALERIE data. Studies: Belsky, Daniel W., et al. "Change in the rate of biological aging in response to caloric restriction: CALERIE Biobank Analysis." The Journals of Gerontology: Series A 73.1 (2017): 4-10. and Redman, Leanne M., et al. "Metabolic slowing and reduced oxidative damage with sustained caloric restriction support the rate of living and oxidative damage theories of aging." Cell metabolism 27.4 (2018): 805-815. [00:19:21] Dietary restriction and oxidative stress; Study: Walsh, Michael E., Yun Shi, and Holly Van Remmen. "The effects of dietary restriction on oxidative stress in rodents." Free Radical Biology and Medicine 66 (2014): 88-99. [00:20:29] Podcast: How Oxidative Stress Impacts Performance and Healthspan, with Megan Roberts. [00:20:40] Effects of CR on reactive oxidative species production; Study: Ramsey, Jon J., Mary-Ellen Harper, and Richard Weindruch. "Restriction of energy intake, energy expenditure, and aging." Free Radical Biology and Medicine 29.10 (2000): 946-968. [00:20:59] Effects of fasting on the liver; Study: Salin, Karine, et al. "Decreased mitochondrial metabolic requirements in fasting animals carry an oxidative cost." Functional Ecology (2018). [00:21:56] Control of food intake: Do animal models accurately reflect human behavior? [00:25:06] Enriched environment; Study: McMurphy, Travis, et al. "Implementation of environmental enrichment after middle age promotes healthy aging." Aging (Albany NY) 10.7 (2018): 1698. [00:26:16] Monkey studies; Study: Ramsey, J. J., et al. "Dietary restriction and aging in rhesus monkeys: the University of Wisconsin study." Experimental gerontology 35.9-10 (2000): 1131-1149. [00:26:35] University of Wisconsin study: Colman, Ricki J., et al. "Caloric restriction delays disease onset and mortality in rhesus monkeys." Science 325.5937 (2009): 201-204. [00:26:35] National Institute on Aging study: Mattison, Julie A., et al. "Impact of caloric restriction on health and survival in rhesus monkeys from the NIA study." Nature 489.7415 (2012): 318. [00:31:34] Biological mechanisms behind the beneficial effects of CR. [00:33:09] Central metabolism sensors. [00:35:28] Mitochondrial proton leak. [00:37:41] Study: Bevilacqua, Lisa, et al. "Effects of short-and medium-term calorie restriction on muscle mitochondrial proton leak and reactive oxygen species production." American Journal of Physiology-Endocrinology and Metabolism 286.5 (2004): E852-E861. [00:40:59] The influence of dietary fat source; Study: Villalba, José Manuel, et al. "The influence of dietary fat source on liver and skeletal muscle mitochondrial modifications and lifespan changes in calorie-restricted mice." Biogerontology 16.5 (2015): 655-670. [00:42:16] Effects of protein restriction on longevity; Studies: 1. Davis, Teresa A., Connie W. Bales, and Roy E. Beauchene. "Differential effects of dietary caloric and protein restriction in the aging rat." Experimental gerontology 18.6 (1983): 427-435; 2. Pugh, Thomas D., Roger G. Klopp, and Richard Weindruch. "Controlling caloric consumption: protocols for rodents and rhesus monkeys☆." Neurobiology of aging 20.2 (1999): 157-165. [00:42:23] More recent studies on protein restriction: 1. Pamplona, Reinald, and Gustavo Barja. "Mitochondrial oxidative stress, aging and caloric restriction: the protein and methionine connection." Biochimica Et Biophysica Acta (BBA)-Bioenergetics 1757.5-6 (2006): 496-508; 2. Caro, Pilar, et al. "Effect of 40% restriction of dietary amino acids (except methionine) on mitochondrial oxidative stress and biogenesis, AIF and SIRT1 in rat liver." Biogerontology 10.5 (2009): 579-592. [00:43:42] Morris Ross study: Ross, Morris H. "Length of life and nutrition in the rat." The Journal of nutrition 75.2 (1961): 197-210. [00:44:03] Effects of dietary lipid composition on lifespan; Study: López-Domínguez, José A., et al. "The influence of dietary fat source on life span in calorie restricted mice." Journals of Gerontology Series A: Biomedical Sciences and Medical Sciences 70.10 (2014): 1181-1188. [00:45:07] Anthony J. Hulbert. [00:48:46] Omega-3 study: Aung, Theingi, et al. "Associations of omega-3 fatty acid supplement use with cardiovascular disease risks: meta-analysis of 10 trials involving 77 917 individuals." JAMA cardiology 3.3 (2018): 225-234. [00:50:02] Ketogenic Diets. [00:50:05] Study: Roberts, Megan N., et al. "A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice." Cell Metabolism 26.3 (2017): 539-546. Podcast: A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice, with Megan (Hall) Roberts. [00:53:47] Intermittent fasting study: Mitchell, Sarah J., et al. "Daily fasting improves health and survival in male mice independent of diet composition and calories." Cell metabolism(2018). [00:54:19] Valter Longo, PhD. [00:54:49] Weight cycling; Study: Smith Jr, Daniel L., et al. "Weight cycling increases longevity compared with sustained obesity in mice." Obesity 26.11 (2018): 1733-1739. [00:55:22] Exercise in the context of carb restriction and longevity. [00:56:08] Study: Holloszy, John O., et al. "Effect of voluntary exercise on longevity of rats." Journal of applied physiology 59.3 (1985): 826-831. [00:58:41] Take home points. [01:01:08] With unlimited resources, what would you study? [01:02:08] Jon Ramsey, PhD at UC Davis.

In letzter Zeit hat ein relativ neuer Trend seinen Weg in die Fitnessszene gefunden, das sogenannte Intermittent Fasting – oder auf Deutsch: Intermittierendes Fasten. Wir gehen auf die Vor- und Nachteile des Intermittent Fasting ein und erklären wie es funktioniert und für wen es Sinn machen kann Intermittent Fasting zu nutzen. Quellen: Adechian, S. et al., 2012. Protein feeding pattern, casein feeding, or milk-soluble protein feeding did not change the evolution of body composition during a short-term weight loss program. American Journal of Physiology - Endocrinology and Metabolism, 15 October, 303(8), pp. 973-982. Adlouni, A. et al., 1997. Fasting during Ramadan induces a marked increase in high-density lipoprotein cholesterol and decrease in low-density lipoprotein cholesterol.. Annals of Nutrition & Metabolism, 1 January, 41(4), pp. 242-249. Anson, M. R. et al., 2003. Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake. Proceedings of the National Academy of Sciences of the United States of America, 13 May, 100(10), pp. 6216-6220. Arnal, M.-A.et al., 2000. Protein Feeding Pattern Does Not Affect Protein Retention in Young Women1. The Journal of Nutrition, 1 July, 130(7), pp. 1700-1704. Atherton, P. J. et al., 2010. Muscle full effect after oral protein: time-dependent concordance and discordance between human muscle protein synthesis and mTORC1 signaling. American Journal of Clinical Nutrition, November, 92(5), pp. 1080-1088. Martin, B., Mattson, M. P. & Maudsley, S., 2006. Caloric restriction and intermittent fasting: Two potential diets for successful brain aging. Ageing Research Reviews, August, 5(3), pp. 332-353. Moro, T. et al., 2016. Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males. Journal of Translational Medicine, 13 October, 14(1), pp. 1-10. Schoenfeld, B. J., Aragon, A. A. & Krieger, J. W., 2013. The effect of protein timing on muscle strength and hypertrophy: a meta-analysis. Journal of the International Society of Sports Nutrition, 3 December, 10(1), p. 1. Wan, R., Camandola, S. & Mattson, M. P., 2003. Intermittent fasting and dietary supplementation with 2-deoxy-D-glucose improve functional and metabolic cardiovascular risk factors in rats. The FASEB Journal, June, 17(9), pp. 1133-1134. World Health Organization, 2017. Cardiovascular diseases (CVDs). [Online] Available at: http://www.who.int/mediacentre/factsheets/fs317/en/ [Zugriff am 26 September 2017].

Das sehr häufig verwendete Nahrungsergänzungsmittel BCAA hat nun wieder einen besonderen Hype in der Fitness und Bodybuildingszene erfahren, daher stellen wir uns die Frage ob dieser Hype gerechtfertigt ist oder ob BCAA-Produkte doch wieder nur unnötige Supplemente sind. Quellen: Churchward-Venne, T. A. et al., 2012. Supplementation of a suboptimal protein dose with leucine or essential amino acids: effects on myofibrillar protein synthesis at rest and following resistance exercise in men. Journal of Physiology, June, 590(11), pp. 2751-2765. Jackman, S. R. et al., 2017. Branched-Chain Amino Acid Ingestion Stimulates Muscle Myofibrillar Protein Synthesis following Resistance Exercise in Humans. Frontiers in Physiology, 7 June.8(390). Karlsson, H. K. R. et al., 2004. Branched-chain amino acids increase p70S6k phosphorylation in human skeletal muscle after resistance exercise. American Journal of Physiology - Endocrinology and Metabolism, 10 Junge, 287(1), pp. E1-E7. Moberg, M. et al., 2014. Absence of leucine in an essential amino acid supplement reduces activation of mTORC1 signalling following resistance exercise in young females. Journal of Applied Physiology: Nutrition and Metabolism, 39(2), pp. 183-194. Sharp, C. P. M. & Pearson, D. R., 2010. Amino Acid Supplements and Recovery from High-Intensity Resistance Training. Journal of Strength & Conditioning Research, April, 24(4), pp. 1125-1130. Witard, O. C. et al., 2014. Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise. American Journal of Clinical Nutrition, January, 99(1), pp. 86-95.

Coach and exercise physiologist Dr Mike T. Nelson pulled me to one side recently after seeing the results of my little experiment with a ketone ester supplement. In this interview, you’ll learn about why Dr. Mike thinks we should exercise caution before regularly simultaneously raising blood glucose and ketones. We also talk about why metabolic flexibility, not ketosis, should be the goal for most endurance athletes. Problems with impaired fat use: From  Nelson, Michael T., George R. Biltz, and Donald R. Dengel. "Repeatability of Respiratory Exchange Ratio Time Series Analysis." The Journal of Strength & Conditioning Research 29.9 (2015): 2550-2558. "Goedecke et al. (12) showed a very large interindividual variability in resting RER from 0.72 up to 0.93 that even persisted during exercise of increasing intensity. This corresponded to a relative rate of fat oxidation that ranged from 23 to 93%. This large interindividual variability in RER from 0.83 to 0.95 was also demonstrated by Helge et al. (16) during low-intensity steady-state exercise. This was quite similar to what we observed with a range of RER from 0.82 to 0.97.” (Nelson, MT, et al. 2015). Goedecke, Julia H., et al. "Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes." American Journal of Physiology-Endocrinology And Metabolism 279.6 (2000): E1325-E1334. Helge, Jørn W., et al. "Interrelationships between muscle fibre type, substrate oxidation and body fat." International journal of obesity 23.9 (1999): 986-991 Problems with impaired carb use: Research has shown that those are on a very low carb diet for prolonged periods of time demonstrate a reduced ability to fully use them during exercise (Burke, LM, et al.; Stellingwerf T. et al). Burke, Louise M., et al. "Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling." Journal of Applied Physiology 89.6 (2000): 2413-2421. Stellingwerff, Trent, et al. "Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration." American Journal of Physiology-Endocrinology and Metabolism 290.2 (2006): E380-E388. Finally, we discuss the potential interference effect of endurance exercise on strength training. Context matters! Only elite athletes probably need to worry about this, and at least one study has shown untrained women can use either order and get similar responses. Here’s the outline of this interview with Mike T. Nelson, PhD: [00:01:02] Keto Summit interview on Metabolic Flexibility. [00:03:25] Complete Blueprint To Faster Results...Without Pain and Plateaus. [00:06:14] Get the "Deadlift Re-alignment for Broken Meatheads." for free. [00:07:28] Online coaching. [00:08:58] http://www.miketnelson.com/podcast [00:09:15] HRV for Successful Online Coaching with Dr. Mike T. Nelson. [00:09:38] ithlete. [00:12:29] Zoom video conference software. [00:13:08] Instant Ketosis: 0.4 to 6.2mM in 30 Minutes. [00:13:47] Dominic D'Agostino: Researcher and Athlete on the Benefits of a Ketogenic Diet. [00:15:34] Cox, Pete J., et al. "Nutritional ketosis alters fuel preference and thereby endurance performance in athletes." Cell Metabolism 24.2 (2016): 256-268. [00:16:57] Ketone esters for endurance performance. [00:20:05] Ride time to exhaustion. [00:21:04] Professor Kieran Clarke at Oxford University. [00:22:27] Why You Should Skip Oxaloacetate Supplementation, Fueling for Your Activity and More! [00:25:19] Brooks, George A., and Jacques Mercier. "Balance of carbohydrate and lipid utilization during exercise: the" crossover" concept." Journal of applied physiology 76.6 (1994): 2253-2261. [00:26:10] Ketone salts and C8 (caprylic) oil to "push the process". [00:28:05] Fasting and carbohydrate adaptation. [00:28:18] Pyruvate dehydrogenase (PDH). [00:29:39] Ketone supplements and appetite suppression. [00:33:36] Jeff Rothschild. [00:34:20] FATMAX and the hard transition. [00:35:18] Peterson, Benjamin James. Repeated Sprint Ability: The Influence of Aerobic Capacity on Energy Pathway Response and Fatigue of Hockey Players. Diss. UNIVERSITY OF MINNESOTA, 2014. [00:37:42] Reintroducing carbs. [00:41:43] Sprints on wet tarmac (not recommended). [00:43:07] Terzis, Gerasimos, et al. "Early phase interference between low-intensity running and power training in moderately trained females." European journal of applied physiology 116.5 (2016): 1063-1073. Coffey, Vernon G., and John A. Hawley. "Concurrent exercise training: do opposites distract?." The Journal of physiology (2016). Also, 5-10x 2 minute intervals at 120-150% of LT (HIIT) and 15-30 minute continuous cycling at 80-100% of LT equally interfere with the adaptations to resistance training. So it’s not the intensity, more the total volume, that’s the problem. [00:46:22] Prioritising strength in the offseason. [00:48:40] Kiteboarding. [00:49:55] Fortaleza. [00:51:06] Mike's email.