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Click Here to Subscribe: http://Bit.ly/ThomasVid Get MY groceries at MY price with Thrive Market: http://ThriveMarket.com/Thomas My Website: http://ThomasDeLauer.com Burn Fat Faster | How to Enter 'Fat-Burning Mode' Quicker (Pre-Fasting Strategy) Study - American Journal of Physiology: Assessed the impact of the macronutrient content of a meal on the postprandial leptin response. 22 young healthy subjects (11 men and 11 women) were given, in a randomized order, an isoenergetic meal [carbohydrate (81%) or fat (79%)] or remained fasting. In both genders, leptin response was higher after the carbohydrate meal than after the fat meal and while fasting. In conclusion, a carbohydrate meal induces higher postprandial leptin levels than an isoenergetic fat meal. https://www.ncbi.nlm.nih.gov/pubmed/10567012 So we know that carbs will increase levels of leptin. However, the following study found that leptin levels need to be low in order for fat burning to take place. So trying to spike your leptin right before a fast could be counterproductive. Leptin & Fat Burning: To keep the human brain supplied with energy when food was scarce, mammals evolved the ability to switch from burning carbohydrates to burning fat in order to preserve skeletal muscle that would otherwise be metabolized and converted to glucose. Scientists long believed that the transition to fat metabolism was instigated solely by a drop in insulin. But a new study identified leptin as a key mediator - during starvation, plasma leptin levels fall, activating a pathway that promotes the breakdown of fat and mediates this critical shift from glucose to fat metabolism. While a drop in insulin also occurs, a decrease in leptin is also necessary for this process to happen. Study Summation: Researchers investigated the rate of carbohydrate and fat metabolism as rats went from a fed to a fasted state. The researchers observed that as the rats fasted, leptin levels decreased and activated a pathway that led to fat burning rather than carb burning. During fasting, the rats' use of stored glucose went down and sugar levels decreased as a result. In turn, levels of insulin and leptin decreased - the rats' bodies then broke down body fat to be turned into ketones for energy. Study – Cell: Researchers had rats fast for 48 hours - plasma non-esterified fatty acid (NEFA), glycerol, and bHB (β-OHB) concentrations increased progressively throughout the fast. Unsurprisingly, the reduction in plasma glucose concentrations that occurs as a fast progresses was accompanied by reductions in plasma insulin concentrations and increases in plasma glucagon concentrations. However, they also found that plasma leptin concentrations decreased by 80% between fed and 48-hr fasted rats. Next researchers specifically investigated the impact of reductions in net hepatic glycogenolysis on rates of endogenous glucose production, plasma leptin concentrations, and activation of the HPA axis. They treated post-absorptive rats fasted for 8, 16, and 48 hour with a small molecule inhibitor of glycogen phosphorylase, which resulted in reductions in plasma glucose and insulin concentrations. This was done as it’s consistent with the negligible contributions that hepatic glycogenolysis would be expected to have on plasma glucose concentrations in the glycogen-depleted state (during prolonged fasting.) Interestingly, the reductions in plasma glucose and insulin concentrations in fasted rats treated with the glycogen phosphorylase inhibitor were associated with reductions in plasma leptin concentrations and increases in HPA axis activity, as reflected by increases in plasma corticosterone and ACTH concentrations in these groups. The researchers next infused rats fasted for 48 hours with leptin and found: Increased leptin levels resulted in the suppression of plasma NEFA, glycerol, β-OHB, and lactate concentrations - suppressed HPA axis activity and plasma corticosterone levels as well. Leptin & Fat Burning: Leptin - corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone (cortisol in humans) concentrations. Corticotrophin-releasing hormone is secreted by the paraventricular nucleus of the hypothalamus - Corticotrophin-releasing hormone is given this name because it causes release of adrenocorticotropic hormone from the pituitary gland. Adrenocorticotropic hormone, in turn, travels in the bloodstream to the adrenal glands, where it causes the secretion of the stress hormones. Resources: 1) https://www.diabetes.co.uk/news/2018/jan/drop-in-both-insulin-and-leptin-needed-for-fat-burning-to-occur-90969878.html 2) https://www.cell.com/cell/fulltext/S0092-8674(17)31443-5 3) https://www.ncbi.nlm.nih.gov/pubmed/29307489 4) https://www.ncbi.nlm.nih.gov/pubmed/8717038/ 5) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430504/

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Click Here to Subscribe: http://Bit.ly/ThomasVid Find Good Culture in Whole Foods: https://www.goodculture.com My Website: http://ThomasDeLauer.com Belly Fat | Top 5 Causes of Belly Fat for MEN [2019] (Fat Loss 101) 1) Not enough Salt and Glucocorticoids (cortisol) out of balance Salt & Cortisol: Low sodium levels cause an increase in aldosterone, an adrenal hormone that seeks to preserve sodium in the body when it’s perceived to be scarce - aldosterone is responsible for telling the kidneys to retain the salt that your body needs. In other words, a lack of sodium can cause the brain to send signals to the adrenal glands to increase the release of aldosterone, which is responsible for water balance - cortisol is released alongside aldosterone. Cortisol & Belly Fat: Tissue cortisol concentrations are controlled by a specific enzyme (11-hydroxysteroid dehydrogenase) that converts inactive cortisone to active cortisol. This particular enzyme is located in adipose tissues - the gene for this enzyme is expressed more by obese conditions and has also been demonstrated in research that human visceral fat cells have more of these enzymes compared to subcutaneous fat cells. Thus, higher levels of these enzymes in these deep fat cells surrounding the abdomen may lead to obesity due to greater amounts of cortisol being produced at the tissue level. Additionally, deep abdominal fat has four times more cortisol receptors compared to subcutaneous fat. Cortisol can increase the activity of lipoprotein lipase (LPL), the major fat storing enzyme - there’s more cortisol receptors in visceral fat, hence more LPL activity there. Study – Oncotarget: The randomized, open-label pilot trial was conducted at a single institution. A total of 85 obese people were enrolled. All participants were served meals three times a day, and provided either a low salt diet or control diet with same calorie. Reductions in body weight (–6.3% vs. –5.0%) and BMI (–6.6% vs. –5.1%) were greater in the low salt group than in the control group. Extracellular water and total body water were significantly reduced in the low salt group compared to the control group. However, changes in body fat mass, visceral fat area, and skeletal muscle mass did not differ between the two groups. The observed decrease of body weight was caused by reduction of total body water, not by reduction of body fat mass or visceral fat mass. https://www.ncbi.nlm.nih.gov/pmc/arti... 2) Cardio in a Fed State (benefits of fasted training in general) Fat Loss (Intramyocellular Lipids) & Muscle Growth (P70S6K) Study - The Journal of Physiology: Findings- During F but not during CHO, the exercise bout decreased IMTG content in type I fibres from roughly 18% to 6% area lipid staining. Exercise-induced net glycogen breakdown was similar in F and CHO - however, compared with CHO, mean rate of postexercise muscle glycogen resynthesis was 3-fold greater in F. https://www.ncbi.nlm.nih.gov/pmc/arti... Study - European Journal of Applied Physiology A study from the European Journal of Applied Physiology had subjects split into two groups that were trained on two occasions separated by three weeks - one of the sessions was performed on an empty stomach after an overnight fast. Found: Increased p70s6k phosphorylation during intake of a protein–carb drink following resistance exercise in the fasted state - fasted training group saw a bigger increase in p70s6k. https://link.springer.com/article/10.... 3) Sleep Deprivation - Metabolic Health Study - Public Library of Science: Medicine: In this study, subjects (1,024 ) who consistently slept less than five hours a night had significant differences in the hormones leptin and ghrelin as compared with people who slept an average of eight hours a night. More specifically, subjects suffering a lack of sleep had 16% less leptin and nearly 15% more ghrelin than those who were well rested did. https://www.ncbi.nlm.nih.gov/pmc/arti... Molecular Level (endocannabinoids) Lack of sleep increases activity of endocannabinoid 2-arachidonoylglycerol (2-AG), which is mediated via the CB1 receptor. https://www.ncbi.nlm.nih.gov/pubmed/2... 4) Too Much Fructose: After the 100:0 glucose bolus, fractional lipogenesis rose to only 8%, which is quite low compared with the 23% observed previously (32). After consumption of the 50:50 and 25:75 solutions used here, the peak in lipogenesis was 17%. Lipogenesis increased 2-fold when as little as half the glucose was replaced with fructose. https://academic.oup.com/jn/article/1... 5) Estrogen & Alcohol Study – Toxicology: The study looked to investigate if ethanol alters aromatization of androgens and concentrations of hepatic estrogen and androgen receptors. In rats given ethanol, hepatic aromatization of androgen to estrogen was significantly increased by the ethanol administration. https://www.ncbi.nlm.nih.gov/pubmed/2...

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