tek, thinks & la strada ☯ॐ☢ csmr@kapsi

On sugar - my enemy

TODO: This article is still pre-release, and is under editing process. All of my life, I've been force-fed sugar. And it goes on. Endless budgets go into selling products that contain mostly sugar - added sugar. But sugar will ruin health. And its damage in society is worse than alcohol.

Let me go through some studies

Fructose and metabolic health: governed by hepatic glycogen status?, Aaron Hengist et alFructose is a commonly ingested dietary sugar which has been implicated in playing a particularly harmful role in the development of metabolic disease. Fructose is primarily metabolised by the liver in humans, and increases rates of hepatic de novo lipogenesis Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children With Obesity, Schwarz et al 2017 Short-term (9 days) isocaloric fructose restriction decreased liver fat, VAT, and DNL, and improved insulin kinetics in children with obesity. These findings support efforts to reduce sugar consumption.

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans, Stanhope et al, 2009Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle–triglyceride and –cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose.

Insulin sensitivity index, acute insulin response, and glucose effectiveness in a population-based sample of 380 young healthy Caucasians. Analysis of the impact of gender, body fat, physical fitness, and life-style factors, Clausen et al 1996Obesity, abdominal fat distribution, and weight gain are important risk factors for the development of NIDDM (48–50). Also, obesity has been shown in prospective studies to be associated with increased risk of hypertension and mortality from cardiovascular disease (51–54). In the present study, obesity measured as BMI was the strongest determinant of the insulin sensitivity index explaining 29% of the variance of the insulin sensitivity index in men, which agrees with other studies (55).

Endocrine Influence on Cardiac Metabolism in Development and Regeneration, Niall Graham. 2021 Mammalian cardiomyocytes mostly utilize oxidation of fatty acids to generate ATP. The fetal heart, in stark contrast, mostly uses anaerobic glycolysis. During perinatal development, thyroid hormone drives extensive metabolic remodeling in the heart for adaptation to extrauterine life. These changes coincide with critical functional maturation and exit of the cell cycle, making the heart a post-mitotic organ. Here, we review the current understanding on the perinatal shift in metabolism, hormonal status, and proliferative potential in cardiomyocytes. Thyroid hormone and glucocorticoids have roles in adult cardiac metabolism, and both pathways have been implicated as regulators of myocardial regeneration. We discuss the evidence that suggests these processes could be interrelated and how this can help explain variation in cardiac regeneration across ontogeny and phylogeny, and we note what breakthroughs are still to be made. Insulin Downregulates Pyruvate Dehydrogenase Kinase (PDK) mRNA: Potential Mechanism Contributing to Increased Lipid Oxidation in Insulin-Resistant Subjects, Majer et al, 1998In contrast, our data indicate that insufficient downregulation of PDK mRNA in insulin-resistant individuals could be a cause of increased PDK expression leading to impaired glucose oxidation followed by increased FA oxidation.

Group 3 was given regular soybean oil including the oxidation prone ALA. This group developed pathological insulin resistance as determined by a high fasting blood glucose level in the context of massively higher circulating insulin.

Interactions between PPAR Gamma and the Canonical Wnt/Beta-Catenin Pathway in Type 2 Diabetes and Colon Cancer, Lecarpentier et al, 2017PPAR gamma is downregulated while the canonical Wnt/beta-catenin pathway is upregulated in both type 2 diabetes and colon cancer. Wnt activates some crucial metabolic key enzymes, such as PDKs in the two pathologies. In colon cancer, this leads to aerobic glycolysis or the Warburg effect.

Heterogeneity in Metabolic Responses to Dietary Fructose Ruixue Hou https://www.frontiersin.org/articles/10.3389/fgene.2019.00945/full

Advanced glycation end products and their receptors in serum of patients with type 2 diabetes, Diana Indyk, http://www.nature.com/articles/s41598-021-92630-0

Amadori Glycated Proteins: Role in Production of Autoantibodies in Diabetes Mellitus and Effect of Inhibitors on Non-Enzymatic Glycation Nadeem A. Ansari https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3570141/

Fructose alters hepatic fat metabolism by making it worse Samir Softic 2019 https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30504-2

Dr. Robert Lustig: "We need a low-insulin diet"

Copyright Casimir Pohjanraito 2021

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