If you are experiencing any of these situations, then your blood glucose levels are dramatically fluctuating up and down. It might be an early indication of hyperinsulinemia in your body.
When it comes to the body, many people often try to make sure that their body is healthy and strong by eating the right food, exercising regularly, and even getting a routine check-up from their primary healthcare providers. Even though people can achieve this, sometimes harmful pathogens like autoimmune diseases, metabolic syndrome, and chronic illnesses can affect the body. When harmful pathogens attack the body from the inside, it can cause the body to dysfunction, especially the body’s system. Many people have found ways to dampen the effects that harmful pathogens have caused in their bodies. However, there are some people who are autoimmune compromises or even have diabetes have taken the necessary precautions to make sure that they are in control of their bodies.
It is surprising that when people are controlling their insulin levels, they are accustomed to think that insulin is a blood sugar-regulating hormone. Research shows that when the blood glucose rises in the body, insulin is being secreted in the body to help bring the blood glucose down a bit. This is a partial stimulation known as insulin-sensitive glucose transporters, and this is one of the many roles that insulin provides that are unrelated to the body’s blood glucose. When the blood glucose levels are rising and falling dramatically in the body, it can cause anyone who has diabetes to go into DKA or diabetic ketoacidosis.
Studies have found that when diabetic individuals are keeping an eye on their blood glucose levels, they go on a ketogenic diet to keep their ketones under control. It is a surprise to many people that insulin is not required for cellular glucose uptake. The research study mentioned that when individuals are in a deficient carbohydrate diet, their bodies can regulate and control the production of the ketone bodies, causing a harmless physiological state known as dietary ketosis. The study even mentioned that when ketone bodies are flowing from the liver to the brain, it can be used as fuel. When this happens, spare glucose metabolism is very similar to the mechanism of spare glucose that is oxidizing fatty acids as an alternative fuel.
There is another study that shows that the use of exogenous insulin in individuals who have type 1 diabetes may need to suppress the free glucagon secretion that facilitates glucose transport into their cells. The hormone glucagon has a stimulatory effect on fuel production from the liver and can even modulate the hepatic glucose uptake and the hepatic glycogen synthesis in the body. The study even shows that the hormone glucagon has been longed dismissed as a minor contributor to metabolic diseases in the body. Not only that, but glucagon can even increase hepatic glucose from the liver to the brain and ketone production in the body.
What is interesting is that when insulin’s myopic focus is related to blood glucose. Research shows that many people have missed a host of health problems that can occur in the presence of average glucose in the body, but it is known as chronically elevated insulin. The research study showed that when there is a lack of insulin in the liver, it causes glycogenolysis and gluconeogenesis are being activated. When this happens, it can further enhance an overproduction of hormones like glucagon and cortisol, which can stimulate the process of insulin deficiency. A study has found that when a person has chronically elevated insulin or hyperinsulinemia, it can develop cardiometabolic diseases even if elevated glucose is absent. This is due to fasting glucose being part of a routine check-up and chronically elevated glucose.
Studies have shown that chronic hyperinsulinemia is the main factor in POS (polycystic ovarian syndrome) and that there is a high prevalence of undiagnosed insulin resistance with patients who have Parkinson’s disease. Chronic hyperinsulinemia can contribute to insulin resistance, as studies show that this factor can alter lipid metabolism in the body. The research study even shows that insulin sensitivity can be determined by hyper-insulinemic and can lead to weight gain, raised plasma triglycerides, and free fatty acids in the body.
Chronic hyperinsulinemia can be present long before there is a rise in blood glucose. Research shows that there are at least five stages in the progression of diabetes, and it can indicate any metabolic dysfunction that is happening in the body. In one study, it showed that there is an association between hyperinsulinemia in the fasting state and the development of diabetes. The study mentioned that basal hyperinsulinemia in adults who are normoglycemic could constitute an independent risk factor for metabolic deterioration to dysglycemia and can even help identify healthy subjects that may have an increased risk for diabetes.
All in all, if someone wants to make sure that their insulin levels are functioning correctly, they will have to be in a very low-carbohydrate ketogenic diet and keep an eye on their blood glucose levels. Individuals that are living with a condition due to chronic hyperinsulinemia, there are effective ways to manage this condition and even preventing it. Many people should start eating healthy, nutritional food, exercise regularly, and start developing healthy habits in order to achieve an overall sense of health and wellness. Some products are beneficial to regulate blood glucose by providing support to sugar metabolism with hypoallergenic nutrients, enzymatic cofactors, metabolic precursors, and phytonutrients.
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.
Dankner, R, et al. “Basal State Hyperinsulinemia in Healthy Normoglycemic Adults Heralds Dysglycemia After More Than Two Decades of Follow Up.” Diabetes/Metabolism Research and Reviews, U.S. National Library of Medicine, July 2012, pubmed.ncbi.nlm.nih.gov/22865584/.
Hogg, Elliot, et al. “High Prevalence of Undiagnosed Insulin Resistance in Non-Diabetic Subjects With Parkinson’s Disease.” Journal of Parkinson’s Disease, U.S. National Library of Medicine, Feb. 2018, pubmed.ncbi.nlm.nih.gov/29614702/.
Manninen, Anssi H. “Metabolic Effects of the Very-Low-Carbohydrate Diets: Misunderstood ‘Villains’ of Human Metabolism.” Journal of the International Society of Sports Nutrition, BioMed Central, 31 Dec. 2004, www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/.
Morita, Ippei, et al. “Chronic Hyperinsulinemia Contributes to Insulin Resistance under Dietary Restriction in Association with Altered Lipid Metabolism in Zucker Diabetic Fatty Rats.” American Journal of Physiology. Endocrinology and Metabolism, U.S. National Library of Medicine, 1 Apr. 2017, www.ncbi.nlm.nih.gov/pubmed/28143857.
Sonksen, P., and J. Sonksen. “Insulin: Understanding Its Action in Health and Disease.” British Journal of Anaesthesia, 1 July 2000, bjanaesthesia.org/article/S0007-0912(17)37337-3/fulltext.
Team, DFH. “Hyperinsulinemia: An Early Indicator of Metabolic Dysfunction.” Designs for Health, 12 Mar. 2020, blog.designsforhealth.com/node/1212.
Unger, Roger H, and Alan D Cherrington. “Glucagonocentric Restructuring of Diabetes: a Pathophysiologic and Therapeutic Makeover.” The Journal of Clinical Investigation, American Society for Clinical Investigation, Jan. 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3248306/.
Weir, Gordon C, and Susan Bonner-Weir. “Five Stages of Evolving Beta-Cell Dysfunction During Progression to Diabetes.” Diabetes, U.S. National Library of Medicine, Mar. 2004, pubmed.ncbi.nlm.nih.gov/15561905/.
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