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This is Sugar. On the left, we have Glucose, and on the right there is Fructose. The link between them gets broken down by the body and they both act independently of each other. Sugar is not 1 big molecule, it's 2 different ones. So why is all the hate going towards Sugar and not one of the smaller molecules?
Well that is because (((they))) don't want to bring attention to Fructose, the real culprit. All gym-goers already know about Glucose. Their best friend that helps refill the Glycogen storage in the Muscles and Liver to allow them to have the energy to lift in the gym.
What about Fructose? It surely couldn't be bad! Dr. Shekelstein told me it's good for me!
Let's see what the research says (there's surprisingly very high consensus on Fructose, probably because Dr. Shekelstein knows normies don't care for reading studies)
"During the fructolysis (Metabolism of Fructose), a high level of metabolic stress via ATP depletion is detected. ATP depletion causes oxidative stress and inflammatory response to disturb the function of tissues and organs, resulting in abnormal production of insulin, inflammatory cytokine, adiponectin, leptin and endotoxin. These indirect dangerous factors are secreted into systemic circulation, further aggravating metabolic burden in tissues and organs and even perturbing appetite and food intake."
"fasting or postprandial glucose concentrations are increased after high fructose consumption in clinical trials and animal experiments. The elevated glucose output may cause an increase of insulin demand and trigger insulin over-release."
"Impairment of β-cell mass and function inmales with high fructose diets result from dysregulation of leptin signaling and activation of protein kinase B (PKB/Akt)/Forkhead box protein (Fox) O1 in rat islets. ER stress occurs in pancreatic β-cells under high fructose diet, as it is closely associated with insulin resistance, inflammation and abnormal lipid metabolism, possibly leading to glucose intolerance and insulin resistance."
"High fructose increases postprandial lactate level, leading to hyperlactatemia. ... Lactate infusion induces insulin signaling impairment by inhibiting phosphatidylinositol 3-kinase (PI3K) and Akt activity in skeletal muscle of mice. On the other hand, lactate suppresses hexokinase (HK) and phosphofructokinase (PFK) in skeletal muscle, liver, heart and kidney, resulting in glucose consumption reduction. Meanwhile, glucose uptake is reduced by hyperlactatemia via suppressing GLUT4 to decrease glycolytic flux in skeletal muscle"
"High fructose consumption gives rise to hyperlipidemia" "Therefore, increased plasma FFAs, TG and VLDL-TG levels induce hyperlipidemia, as well as TG accumulation in extrahepatic tissues and organs. Fructose-induced lipotoxicity leads to NAFLD, lipid accumulation and autophagy in skeletal muscle, cardiac dysfunction, adipose inflammation, CKD, pancreatic islet dysfunction, brain oxidative stress and inflammation."
"ructose supplementation increases de novo ceramide biosynthesis and elevates ceramide concentrations in plasma [57], liver [58] and skeletal muscle [59], promoting local insulin resistance. Ceramide decreases the ability of insulin to activate Akt and GLUT4 translocation in 3T3-L1 adipocytes"
"Recently, fructose has been reported to be metabolized in several regions of brain, including cerebellum, hippocampus, cortex, and olfactory bulb, which express GLUTs and all of the enzymes in fructolysis, probably leading to central inflammation response. FFA elevation in plasma gives rise to hippocampal insulin signaling impairment and inflammation under high fructose consumption, since FFAs may cross the blood–brain barrier. Hypothalamus is the major site sensing energy status in the whole body. The possible mechanism relates to neuropeptides secretion via regulation of AMP-activated protein kinase (AMPK) signaling and malonyl-CoA concentration, compensating for the change in energy status. Rapid fructolysis results in ATP depletion to produce more AMP. Sensing increase of the AMP/ATP ratio, AMPK is activated under high fructose consumption. Moreover, peripheral indirect signals generated by fructose, including TNF-α can also activate AMPK in hypothalamus. Fructose triggers AMPK/malonyl-CoA signaling in hypothalamus, subsequently increasing food intake and the risk of obesity. Furthermore, fructose-induced hypothalamic AMPK activation increases hepatic gluconeogenesis by the elevation of circulating corticosterone level, further contributing to systemic insulin resistance."
I can copy and paste all day, you get it.
I am sure by this point you are shred to pieces. Dr. Shekelstein lied to you, me and everybody else.
It's over.
Well that is because (((they))) don't want to bring attention to Fructose, the real culprit. All gym-goers already know about Glucose. Their best friend that helps refill the Glycogen storage in the Muscles and Liver to allow them to have the energy to lift in the gym.
What about Fructose? It surely couldn't be bad! Dr. Shekelstein told me it's good for me!
Let's see what the research says (there's surprisingly very high consensus on Fructose, probably because Dr. Shekelstein knows normies don't care for reading studies)
"During the fructolysis (Metabolism of Fructose), a high level of metabolic stress via ATP depletion is detected. ATP depletion causes oxidative stress and inflammatory response to disturb the function of tissues and organs, resulting in abnormal production of insulin, inflammatory cytokine, adiponectin, leptin and endotoxin. These indirect dangerous factors are secreted into systemic circulation, further aggravating metabolic burden in tissues and organs and even perturbing appetite and food intake."
"fasting or postprandial glucose concentrations are increased after high fructose consumption in clinical trials and animal experiments. The elevated glucose output may cause an increase of insulin demand and trigger insulin over-release."
"Impairment of β-cell mass and function inmales with high fructose diets result from dysregulation of leptin signaling and activation of protein kinase B (PKB/Akt)/Forkhead box protein (Fox) O1 in rat islets. ER stress occurs in pancreatic β-cells under high fructose diet, as it is closely associated with insulin resistance, inflammation and abnormal lipid metabolism, possibly leading to glucose intolerance and insulin resistance."
"High fructose increases postprandial lactate level, leading to hyperlactatemia. ... Lactate infusion induces insulin signaling impairment by inhibiting phosphatidylinositol 3-kinase (PI3K) and Akt activity in skeletal muscle of mice. On the other hand, lactate suppresses hexokinase (HK) and phosphofructokinase (PFK) in skeletal muscle, liver, heart and kidney, resulting in glucose consumption reduction. Meanwhile, glucose uptake is reduced by hyperlactatemia via suppressing GLUT4 to decrease glycolytic flux in skeletal muscle"
"High fructose consumption gives rise to hyperlipidemia" "Therefore, increased plasma FFAs, TG and VLDL-TG levels induce hyperlipidemia, as well as TG accumulation in extrahepatic tissues and organs. Fructose-induced lipotoxicity leads to NAFLD, lipid accumulation and autophagy in skeletal muscle, cardiac dysfunction, adipose inflammation, CKD, pancreatic islet dysfunction, brain oxidative stress and inflammation."
"ructose supplementation increases de novo ceramide biosynthesis and elevates ceramide concentrations in plasma [57], liver [58] and skeletal muscle [59], promoting local insulin resistance. Ceramide decreases the ability of insulin to activate Akt and GLUT4 translocation in 3T3-L1 adipocytes"
"Recently, fructose has been reported to be metabolized in several regions of brain, including cerebellum, hippocampus, cortex, and olfactory bulb, which express GLUTs and all of the enzymes in fructolysis, probably leading to central inflammation response. FFA elevation in plasma gives rise to hippocampal insulin signaling impairment and inflammation under high fructose consumption, since FFAs may cross the blood–brain barrier. Hypothalamus is the major site sensing energy status in the whole body. The possible mechanism relates to neuropeptides secretion via regulation of AMP-activated protein kinase (AMPK) signaling and malonyl-CoA concentration, compensating for the change in energy status. Rapid fructolysis results in ATP depletion to produce more AMP. Sensing increase of the AMP/ATP ratio, AMPK is activated under high fructose consumption. Moreover, peripheral indirect signals generated by fructose, including TNF-α can also activate AMPK in hypothalamus. Fructose triggers AMPK/malonyl-CoA signaling in hypothalamus, subsequently increasing food intake and the risk of obesity. Furthermore, fructose-induced hypothalamic AMPK activation increases hepatic gluconeogenesis by the elevation of circulating corticosterone level, further contributing to systemic insulin resistance."
I can copy and paste all day, you get it.
I am sure by this point you are shred to pieces. Dr. Shekelstein lied to you, me and everybody else.
It's over.
