Insulin Resistance
Episodes
In this clip, Dr. Peter Attia addresses the ideal targets for hemoglobin A1C levels, a key indicator of long-term blood glucose.
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
Dr. Michael Snyder discusses personalized medicine and the use of technologies that monitor metabolism and other health markers.
-
In this clip, Dr. Peter Attia addresses the ideal targets for hemoglobin A1C levels, a key indicator of long-term blood glucose.
-
Rhonda Vitamin D Gut Ketosis Insulin Resistance Fasting Sulforaphane Intestinal Permeability NRF2 Urolithin ADr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
-
Dr. Michael Snyder discusses personalized medicine and the use of technologies that monitor metabolism and other health markers.
-
In this clip, Tim Ferriss describes his efforts to mitigate the risk of Alzheimer's disease by managing his insulin levels using the ketogenic diet.
-
In this clip, Dr. Peter Attia explains his position on the relationship between insulin resistance and Alzheimer’s disease risk.
-
In this clip, Dr. Rhonda Patrick describes her personal experience with sleep deprivation and her subsequent altered metabolism.
-
Several studies have established causation showing that sleep duration is a major determinant of insulin sensitivity.
-
Dr. Dale Bredesen discusses treatments that may reverse symptoms of mild cognitive decline and Alzheimer’s disease.
-
Dr. Valter Longo on Resetting Autoimmunity and Rejuvenating Systems with Prolonged Fasting & the FMDFasting Cancer Obesity Aging Heart Disease Diabetes Insulin Resistance Inflammation Stem Cells Immune System Tissue Repair Autophagy Apoptosis Insulin AutoimmunityDr. Valter Longo discusses fasting as a means to treat or prevent age-related diseases such as cancer, Alzheimer’s disease, and others.
-
Sulforaphane Brain Cancer Aging Heart Disease Insulin Resistance Inflammation Depression Behavior Mental Health Autism Mortality NRF2This podcast is about one of the most important biological pathways you could possibly take the time to learn about: the NRF2 pathway.
-
Fasting Metabolism Breast Cancer Insulin Resistance Podcast Inflammation Video Insulin Time-Restricted EatingDr. Ruth Patterson discusses the role of fasting in the prevention and survivorship of breast cancer.
-
Ketosis Nutrition Brain Alzheimer's Diet Microbiome Performance Insulin Resistance Mitochondria Dementia Insulin SupplementsDr. Dominic D'Agostino discusses the health benefits associated with a modified Atkins diet, ketosis, and supplemental ketones.
-
Performance Brain Alzheimer's Cancer Gut Aging Ketosis Insulin Resistance Podcast Cholesterol Inflammation Immune System InsulinDr. Peter Attia discusses dietary strategies to promote longevity and optimal performance.
-
Obesity Nutrition Aging Heart Disease Insulin Resistance Cholesterol Inflammation Magnesium Vitamin K SeleniumDr. Bruce Ames discusses the CHORI Bar, a micronutrient- and fiber-dense nutrition bar developed in the Ames laboratory to manage obesity.
-
Biomarkers Vitamin D Nutrition Exercise Alzheimer's Gut Microbiome Performance Insulin Resistance Podcast CholesterolJim Kean is the CEO of National Pro Grid League (NPGL) and founder of WellnessFX.
-
Sauna Exercise Brain Aging Hormones Performance Insulin Resistance Depression Stress Heat Stress MuscleDr. Rhonda Patrick discusses how conditioning the body to heat stress through sauna use, called "hyperthermic conditioning" may cause adaptations that increase athletic endurance (by increasing plasma volume and blood flow to heart and muscles) and potentially even muscle mass.
Topic Pages
-
Cold exposure
Cold exposure triggers sympathetic norepinephrine activation of brown adipose tissue, augmenting GLUT4-mediated glucose uptake and mitigating insulin resistance.
-
Ultra-processed Foods (UPFs)
Ultra-processed foods exacerbate insulin resistance by delivering high-glycemic sugars, proinflammatory lipids, emulsifiers, and microbiome-altering additives.
News & Publications
-
Daily cinnamon supplementation averaging 2,100 milligrams – roughly a teaspoon – shows promise in managing type 2 diabetes. pubmed.ncbi.nlm.nih.gov
Cinnamon is one of the most consumed spices in the world, popular in both sweet and savory dishes in many cuisines. Evidence suggests cinnamon improves lipid profiles and protects against damage induced by oxidative stress. A recent systematic review and meta-analysis found that cinnamon helps maintain healthy blood glucose levels and reduces insulin resistance in people with type 2 diabetes.
Researchers analyzed the findings of 24 clinical trials investigating the effects of cinnamon supplementation on blood glucose levels. The various trials included more than 1,800 participants from 11 nations.
The analysis revealed that cinnamon supplementation reduced fasting blood glucose levels, hemoglobin A1c concentrations, and insulin resistance (without lowering insulin) in people with type 2 diabetes. The trials varied in duration from six to 16 weeks, and daily cinnamon doses ranged from 120 to 6,000 milligrams, averaging 2,100 milligrams – roughly a teaspoon.
These findings suggest that cinnamon improves symptoms of type 2 diabetes and may be a valuable adjunct to traditional therapies. Cinnamon is rich in polyphenols, a broad class of plant bioactive compounds. Learn more about polyphenols in our overview article.
-
Supplemental vitamin K2 improves diabetes markers and glycemic control. pubmed.ncbi.nlm.nih.gov
Vitamin K2 – a form of vitamin K produced in the gut – plays important roles in blood clotting, bone mass maintenance, and blood vessel contractility. But new research shows that supplemental vitamin K2 also improves diabetes markers. People with type 2 diabetes who took supplemental vitamin K2 had better markers of glycemic control than those who took a placebo.
Researchers performed a three-part study in humans and mice. First, they conducted a randomized controlled trial involving 60 adults who had type 2 diabetes. Half of the participants took vitamin K2 every day for six months, while the other half took a placebo. Then the researchers transplanted gut microbes from vitamin K2-supplemented mice into obese mice. Finally, they analyzed the gut microbial composition and their metabolites in both humans and mice.
They found that the participants who received supplemental vitamin K2 experienced marked reductions in levels of fasting blood glucose (13.4 percent), insulin (28.3 percent), and HbA1c (7.4 percent), indicating improved glycemic control. Similarly, the mice demonstrated improved glucose tolerance after receiving the gut microbe transplants. Lastly, the researchers found that certain metabolites that play roles in glucose metabolism, including bile acids and short-chain fatty acids, increased in the feces of both groups. Furthermore, they identified a specific type of bacteria that was responsible for producing these metabolites.
Vitamin K is a fat-soluble vitamin. The body has limited vitamin K storage capacity, so the body recycles it in a vitamin K redox cycle and reuses it multiple times. Naturally occurring forms of vitamin K include phylloquinone (vitamin K1) and a family of molecules called menaquinones (vitamin K2). Vitamin K1 is synthesized by plants and is the major form found in the diet. Vitamin K2 molecules are synthesized by the gut microbiota and found in fermented foods and some animal products (especially liver).
These findings suggest that vitamin K2 participates in maintaining glycemic control in people with type 2 diabetes. They also underscore the role of the gut microbiota in this process. Learn about other roles for the gut microbiota in this episode featuring Dr. Eran Elinav.
-
Even moderate light exposure during sleep harms heart health and increases insulin resistance www.sciencedaily.com
A single night of light exposure during sleep impairs glucose metabolism via activation of the “fight-or-flight” response.
Light is the primary signal that entrains the body’s master clock to set its 24-hour circadian cycle. Consequently, the body is synchronized to external light-dark cycles. In recent decades, exposure to light from artificial sources has increased, especially during the evening and nighttime hours, with negative effects on human health. Findings from a recent study suggest that a single night of light exposure impairs glucose metabolism via activation of the sympathetic nervous system.
The sympathetic nervous system is a division of the autonomic nervous system. It responds to both endogenous and exogenous stressors and is widely referred to as the coordinator of the body’s “fight-or-flight” response. The outcome of sympathetic nervous system activation is an increase in heart rate, cardiac output, and blood glucose levels, as well as other physiological responses that prepare the body for action. Evidence suggests that increased sympathetic nervous system activity alters sympathovagal balance (the balance between the sympathetic and parasympathetic nervous systems), driving poor heart rate variability.
The investigators recruited 20 healthy adults (average age, 26 years) who did not have sleep disorders. Participants spent two nights in a sleep laboratory, where they ate all their meals and went to bed at their habitual times. Half of the participants spent one night in dim light conditions (less than 3 lux, very dark) and one night in room light conditions (100 lux, from four 60-watt incandescent bulbs). The other half spent both nights in the dim light conditions. Participants provided blood samples and underwent oral glucose tolerance tests each morning.
The investigators found that participants who were exposed to room light conditions during sleep had increased nighttime heart rate, decreased heart rate variability, and increased morning insulin resistance, compared to when they slept in a dark room. They also spent less time in deep, slow-wave sleep.
These findings suggest that a single night of exposure to room light during sleep impairs glucose metabolism via activation of the sympathetic nervous system. Learn how light from devices impairs sleep in this clip featuring sleep expert Dr. Matthew Walker.
-
Fructose-containing beverages increase free fatty acid production in the liver, a marker of metabolic disease risk. www.sciencedaily.com
Metabolic diseases, such as type 2 diabetes, cardiovascular disease, and non-alcoholic fatty liver disease (NAFLD), represent a major public health burden. Dietary factors such as excess sugar intake are associated with greater metabolic disease risk; however, it is unclear how different types of sugars (e.g., glucose, fructose, or sucrose) differentially impact metabolic health. In this report, researchers investigated the effects of sugar-sweetened beverages on fatty acid synthesis, blood triglycerides, and hepatic insulin resistance in healthy males.
Following the consumption of glucose, the pancreas secretes insulin into the bloodstream so that insulin-sensitive organs such as the liver, skeletal muscle, and adipose tissue can transport glucose into their cells. Excess sugars are converted to fats in the liver via a process called de novo lipogenesis and then stored in adipose tissue; however, as fat levels in adipose tissue rise (i.e., overweight and obesity), fat accumulates in the liver leading to the development of NAFLD. Fructose, the main sweetener found in sugar-sweetened beverages, does not require insulin to be absorbed and is preferentially taken up by the liver, accelerating NAFLD development independent of weight gain.
The authors recruited 94 healthy lean males (average age, 23 years) and assigned them to consume beverages sweetened with moderate amounts of either glucose, fructose, or sucrose (a sugar that contains both glucose and fructose) in addition to their normal diet for seven weeks. The beverages contained an amount of sugar found in about two cans of non-diet soda. The researchers assigned a fourth group of participants to consume their normal diet with no added sugar-sweetened beverages. They assessed fatty acid and triglyceride synthesis by the liver and whole-body fat metabolism.
Daily consumption of beverages sweetened with fructose and sucrose, but not glucose, led to a twofold increase in the production of free fatty acids in the liver. Fructose intake did not increase triglyceride production in the liver or whole-body fat metabolism. Participants from all four groups consumed about the same amount of calories, and while body weight tended to increase for all groups, this relationship was only statistically significant for the group consuming glucose-sweetened beverages. Glucose and insulin tolerance did not change with sugar-sweetened beverage consumption.
The investigators concluded that consumption of beverages sweetened with fructose and sucrose increased free fatty acid production in the liver. While they did not observe changes in other metabolic markers such as insulin tolerance, they hypothesized that the alterations in fat production by the liver pave the way for metabolic disease development.