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Insulin Resistance

Episodes

insulin

Dr. Ben Bikman: How To Reverse Insulin Resistance Through Diet, Exercise, & Sleep

Posted on July 11th 2025 (4 days)

insulin resistance

How to Increase Insulin Sensitivity (and the optimal blood glucose for longevity) | Peter Attia

Posted on January 24th 2024 (over 1 year)

In this clip, Dr. Peter Attia addresses the ideal targets for hemoglobin A1C levels, a key indicator of long-term blood glucose.

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Q&A #37 with Dr. Rhonda Patrick (7/09/2022)

Posted on July 9th 2022 (about 3 years)

Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.

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

  • Long-term intervention with calorie restriction and high-intensity interval training doubles insulin sensitivity and greatly improves liver function in people with a form of fatty liver disease. pubmed.ncbi.nlm.nih.gov
    Exercise Obesity Metabolism Insulin Resistance Fatty Liver

    Metabolic dysfunction-associated steatohepatitis (MASH) is a form of fatty liver disease that promotes inflammation and damage over time. Closely connected to conditions like obesity and insulin resistance, MASH affects nearly one-third of people worldwide. A recent study found that a long-term intervention combining calorie restriction and high-intensity interval training (HIIT) in people with MASH improved liver function, doubling insulin sensitivity.

    Researchers assigned people with MASH to either a treatment group (16 participants) that received lifestyle counseling and exercise training or a control group (eight participants) that continued with standard medical care. The treatment group engaged in supervised HIIT three times a week while reducing caloric intake. The researchers assessed the participants' liver fat, measured blood biochemistries, and evaluated insulin sensitivity before and after the intervention.

    They found that the treatment group experienced notable reductions in body weight, fat mass, and liver injury. Their cardiorespiratory fitness improved considerably, and they exhibited a twofold increase in peripheral insulin sensitivity compared to the control group. Both groups saw reductions in total energy intake and liver fat.

    These findings suggest that combining caloric restriction with regular high-intensity exercise can yield marked improvements in liver health and insulin sensitivity, likely by redistributing excess nutrients to skeletal muscle. Learn more about calorie restriction in this clip featuring Dr. David Sinclair, and HIIT in this clip featuring Dr. Martin Gibala.

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  • Ketones may protect against cognitive decline by mitigating insulin resistance-induced neuronal damage. www.futurity.org
    Brain Aging Insulin Resistance Memory Insulin Ketogenic Diet

    Insulin regulates many processes involved in memory and cognitive function. However, age-related insulin resistance in the brain disrupts neuronal synaptic activity and contributes to cognitive decline. A recent study found that ketones may protect the brain from age-related insulin resistance in the brain.

    Researchers induced acute insulin resistance in mouse hippocampal tissue and determined its effects on neuronal function. Then, they administered beta-hydroxybutyrate, a type of ketone, to the tissues and evaluated the outcomes.

    They found that insulin resistance adversely affected aspects of neuronal communication, including synaptic activity, axonal conduction, network synchronization, synaptic plasticity, and action potential properties. However, ketones restored these functions.

    These findings suggest that ketones rescue the brain from the deleterious effects of acute insulin resistance. The high blood glucose levels associated with insulin resistance induce glucotoxicity, which causes structural damage and functional impairments of neuronal cells. Learn more about the effects of insulin resistance in the brain in this clip featuring Dr. Dale Bredesen.

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  • Daily cinnamon supplementation averaging 2,100 milligrams – roughly a teaspoon – shows promise in managing type 2 diabetes. pubmed.ncbi.nlm.nih.gov
    Diet Diabetes Insulin Resistance Insulin Polyphenol

    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.

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  • Supplemental vitamin K2 improves diabetes markers and glycemic control. pubmed.ncbi.nlm.nih.gov
    Metabolism Diabetes Insulin Resistance Vitamin K Insulin

    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.

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  • Omega-3s improve metabolic markers in women with gestational diabetes. www.sciencedirect.com
    Diabetes Insulin Resistance Omega-3 Inflammation Pregnancy Insulin

    Omega-3s improve metabolic markers in women with gestational diabetes.

    Gestational diabetes, a form of diabetes that occurs only during pregnancy, carries many health concerns for women, including an increased risk of developing type 2 diabetes in later life. A new study shows that omega-3 fatty acids may improve metabolic markers associated with gestational diabetes. Women who took omega-3s during their pregnancies had healthier blood glucose, triglyceride, and cholesterol levels than those who didn’t.

    Researchers analyzed the findings of six randomized controlled trials that investigated the effects of omega-3s in women with gestational diabetes. The studies included more than 330 pregnant women, and the duration of the various trials was six weeks. Omega-3 doses ranged from 1 to 2 grams per day.

    They found that across the six studies, markers of glucose metabolism (fasting glucose, fasting insulin, and insulin resistance), lipid metabolism (triglycerides and very low-density lipoprotein cholesterol), and inflammation (C-reactive protein) were lower among women who took omega-3s than those who took a placebo. Levels of high-density lipoprotein cholesterol – often referred to as “good” cholesterol – increased.

    This analysis suggests that omega-3 fatty acids, which are perhaps best known for their cardioprotective and neuroprotective properties, positively influence metabolism in pregnant women. It also aligns with the findings of a previous analysis, which found that compared to women who took a placebo, those who took supplemental omega-3s had considerably lower fasting blood sugar levels and insulin resistance. Learn about other health benefits associated with omega-3s in our comprehensive overview article.

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  • Polyphenols found in tea and coffee may reduce the risk of diabetes. pubmed.ncbi.nlm.nih.gov
    Diabetes Insulin Resistance Coffee Green Tea Polyphenol

    Drinking tea and coffee may reduce the risk of developing type 2 diabetes, a 2022 study found. Men that drank a beverage enriched in polyphenols present in tea and coffee had lower blood glucose levels and improved insulin sensitivity than those who drank a placebo.

    Eleven healthy men drank a beverage that contained either polyphenols from tea (catechins) and coffee (chlorogenic acids) or a placebo every day for three weeks. Both beverages provided 119 milligrams of caffeine – a little more than the amount present in one cup of coffee. At the end of the three weeks, they ate a high-fat, high-carbohydrate meal, and then researchers measured their blood glucose, insulin, and other metabolic markers.

    The researchers found that consuming the catechin- and chlorogenic-rich beverage reduced the men’s blood glucose levels when consumed with a high-fat or high-carbohydrate meal. Their insulin sensitivity and levels of hormones involved in glucose metabolism increased, as well.

    Catechins are polyphenolic compounds found in tea, cocoa, and berries. Evidence suggests that catechins ameliorate symptoms associated with diabetes. Chlorogenic acids are polyphenolic compounds found in coffee, apples, and berries. Evidence suggests that chlorogenic acids reduce inflammation, a key player in the pathophysiology of diabetes.

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  • Loss of estrogen receptor alpha led to aspects of metabolic syndrome, inflammation, and acceleration of atherosclerosis in mice. (2011) www.sciencedaily.com
    Hormones Insulin Resistance Inflammation Estrogen Blood Sugar Metabolic Syndrome Cardiovascular

    From the article:

    This early preclinical study in female mice demonstrated that removing estrogen regulator alpha alone was enough to reduce the immune system’s protective process and promote increased fat accumulation and accelerate atherosclerosis development. Without this protein, the mice developed additional aspects of metabolic syndrome such as glucose intolerance, insulin resistance and inflammation.

    This estrogen receptor is also expressed in many other non-reproductive tissues such as fat, muscle and liver and can also act independent of the hormone estrogen. However, little is known about the receptor’s actions in these tissues that are involved in blood-sugar regulation, which plays an integral role in metabolic syndrome.

    […]

    “Impairment of this receptor’s function could also play a role in the heightened incidence of metabolic syndrome being seen in younger women,”

    View full publication

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  • Sleep loss and lower sleep duration may be associated with lower morning, afternoon and 24-h testosterone levels. (2022) link.springer.com
    Sleep Hormones Insulin Resistance Cortisol Testosterone

    From the publication:

    When epidemiological and interventional studies are considered collectively, sleep loss and lower sleep duration are associated with lower morning, afternoon and 24-h testosterone; as well as higher afternoon, but not morning or 24-h cortisol. These reciprocal changes imbalances anabolic-catabolic signaling because testosterone and cortisol are respectively the main anabolic and catabolic signals in man. Fixing testosterone-cortisol balance by means of a novel dual-hormone clamp mitigates the induction of insulin resistance by sleep restriction and provided the first proof-of-concept that the metabolic harm from sleep loss can be ameliorated by approaches that do not require sleeping more. Obstructive sleep apnea is associated with lower testosterone, even after controlling for age and obesity whereas the conclusion that continuous positive airway pressure therapy has no effect on testosterone is premature because available studies are underpowered and better-quality studies suggest otherwise. High dose testosterone therapy induces OSA [obstructive sleep apnea], but more physiological dosing may not; and this effect may be transient or may dissipate with longer term therapy.

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  • Testosterone therapy increased tissue glucose uptake by 32% in response to insulin in men with type 2 diabetes and low testosterone (2015) www.sciencedaily.com
    Hormones Diabetes Insulin Resistance Testosterone Insulin

    From the article:

    The current study included 94 men with Type 2 diabetes. Prior to being treated, the 44 men in the study with low testosterone levels expressed significantly lower levels of insulin signaling genes and, thus, diminished insulin sensitivity. These men were randomized to receive a testosterone injection or a placebo every week for 24 weeks.

    The study found that while there was no change in body weight, testosterone treatment produced a reduction in total body fat of 3 kilograms (more than six pounds) while increasing muscle mass by the same amount.

    “Most importantly, we saw a dramatic increase in insulin sensitivity, demonstrated by a 32 percent increase in the uptake of glucose by tissues in response to insulin,” Dandona said. At the same time, there was a similar increase in the expression of the major genes that mediate insulin signaling.

    While patients' hemoglobin A1C (HbA1c) levels did not go down, a necessary indicator that testosterone can help control diabetes, Dandona noted that fasting glucose levels had diminished significantly, by 12 milligrams per deciliter. He said that a significant improvement in HbA1c may eventually be seen when longer term studies are carried out.

    View full publication

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  • Even moderate light exposure during sleep harms heart health and increases insulin resistance www.sciencedaily.com
    Sleep Insulin Resistance

    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.

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  • Strict 12-week keto without calorie counting: participants lost >5% percent body fat, 44% of their visceral fat, and 48% better insulin sensitivity www.sciencedaily.com
    Diet Obesity Ketosis Insulin Resistance Metabolic Syndrome Visceral Fat Ketogenic Diet

    This is a Jeff Volek study and used hard biomarkers, checking ketones daily.

    From the article:

    In the study, which appears in the journal Military Medicine, participants on the keto diet lost an average of almost 17 pounds and were able, with support of counselors, to maintain ketosis for 12 weeks. As a group, they lost more than 5 percent of their body fat, almost 44 percent of their belly, or visceral, fat and had a 48 percent improvement in insulin sensitivity – a marker that predicts risk of diabetes.

    […]

    The ketogenic diets in the study included no caloric restrictions, just guidance about what to eat and what to avoid. Carbs were restricted to about 30 to 50 grams daily, with an emphasis on nuts and non-starchy vegetables.

    […]

    Keto diet participants had near-daily check-ins during which they reported blood ketone measurements from a self-administered finger-prick test and received feedback, usually through text messages, from the research team. Ketosis was defined as a blood concentration of ketones, chemicals made in the liver, between 0.5 and 5.0 mM (millimolar).

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  • Visceral fat and total brain volume inversely linked independent of BMI and insulin resistance: a relationship between dementia and obesity www.sciencedaily.com
    Brain Obesity Insulin Resistance Metabolic Syndrome Visceral Fat

    From the article:

    Preliminary findings suggest a relationship between obesity and dementia that could lead to promising prevention strategies in the future.

    […]

    “Our results confirm the inverse association of increasing BMI with lower brain volumes in older adults and with younger, middle-aged adults and extends the findings to a much larger study sample,” […] “More importantly our data suggests a stronger connection between central obesity, particularly the visceral fat component of abdominal obesity, and risk of dementia and Alzheimer’s disease,” Dr. Seshadri added. The research showed the association between visceral adipose tissue and total brain volume was most robust and was also independent of BMI and insulin resistance."

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  • Visceral fat may be less circadian than (healthier) subcutaneous fat: only subcutaneous showed circadian rhythmicity in insulin sensitivity www.sciencedaily.com
    Obesity Insulin Resistance Circadian Rhythm Insulin Metabolic Syndrome Visceral Fat

    From the article:

    Using samples of adipose tissue from both visceral fat and subcutaneous fat from 18 people who underwent gastric bypass surgery, researchers found that subcutaneous fat has an intrinsic circadian rhythm in insulin sensitivity. Insulin sensitivity reached its maximum around noon, and was more than 50 percent higher than at midnight. Interestingly, the rhythm was not observed in visceral fat.

    […]

    “Our study demonstrates that subcutaneous human fat tissue has an internal clock that is able to regulate insulin sensitivity even when outside of the body. This tissue rhythm matches well with what has been observed in humans overall when examining how people cope with a meal or sugar load,”

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  • Fructose-containing beverages increase free fatty acid production in the liver, a marker of metabolic disease risk. www.sciencedaily.com
    Insulin Resistance Sugar Triglycerides Fatty Liver

    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.

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  • A single bout of aerobic exercise alters more than 9,000 molecules in the blood. www.nytimes.com
    Exercise Insulin Resistance Inflammation

    Exercise elicits a wide range of physiological changes in the body that improve multiple aspects of cardiovascular, neurological, and metabolic health. The molecular mechanisms that drive these improvements are not well understood. Findings from a new study suggest that an acute bout of aerobic exercise alters more than 9,000 distinct molecules in the human body to positively influence health.

    The study involved 36 adults between the ages of 40 and 75 years. The average body mass index among the participants was 28, which is considered overweight. Their steady-state blood glucose levels ranged from 86 to 220 milligrams per deciliter, suggesting a wide range of insulin resistance, from very low to very high.

    The authors of the study collected blood samples from all the participants before exercise and two, 15, 30, and 60 minutes afterward. They collected fasting blood samples from 15 of the participants the morning after the exercise protocol to assess inter-day variability. One group of participants engaged in an acute bout of aerobic exercise on a treadmill for eight to 12 minutes at their maximum capacity. A control group of 14 participants did not perform any exercise.

    Analysis of the participants' blood before and after exercise revealed that an acute bout of aerobic exercise induced extensive changes in 9,815 molecules, including proteins, lipids, genes, immune markers, and many others, that correlate with a person’s aerobic fitness.

    The authors of the study suggested that their findings could lay the groundwork for the development of a simple blood test that measures fitness in the future.

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  • Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes www.cell.com
    Insulin Resistance Fasting Insulin Time-Restricted Eating Blood Pressure Weight Loss

    A small randomized controlled clinical trial finds time-restricted eating within a 6-hour window (fasting for 18 hours) without reducing calories or losing weight improves insulin sensitivity, beta cell function, blood pressure, oxidative stress and reduces evening appetite.

    All eating was supervised and approached metabolic ward rigor. The improvements in metabolism were independent of weight loss and the reduction in blood pressure was so significant that it was comparable to the standard of care blood pressure medication (ACE inhibitors).

    The time-restricted eating they started early with the first meal at 8 am and dinner before 3 pm. The importance of time of day for this type of intermittent fasting is still an interesting open question, especially since there’s a lot of advocacy for late eating among 16:8 advocates, however, insulin sensitivity usually declines later in the day (and is exacerbated by the production of melatonin, which has an effect of shutting off insulin secretion). Interestingly, Dr. Satchin Panda has been gathering data via his mobile app (my circadian clock) that suggests an eating window later in the day may be comparable to an early eating window.

    To learn more about time-restricted eating and intermittent fasting check out the two separate podcasts I did with Dr. Satchin Panda. The episodes have summaries, timelines, and transcripts!

    Round 2 episode: https://www.foundmyfitness.com/episodes/satchin-round-2

    Round 1 episode: https://www.foundmyfitness.com/episodes/satchin-panda

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  • Genetically lowering plasma insulin levels by 25% extended median lifespan by 11% in female mice fed a low-calorie, high-carb low-fat diet. www.cell.com
    Diet Aging Insulin Resistance Insulin Protein Carbohydrates

    Genetically lowering plasma insulin levels by 25% extended median lifespan by 11% in female mice fed a low-calorie/high-carb/low-fat diet and by 3% in female mice fed a high-calorie/high-fat/low-carb diet.

    This study looked at the effects of genetically lowering insulin levels in older mice. Unfortunately, the male mice did not have lower plasma levels of insulin despite genetically lowering insulin-genes and so the effect on lifespan could not be determined in male mice.

    The female mice were fed two diets: (diet A: moderate-energy diet of 4.68 kcal/g, with 20% of calories from protein, 25% from fat, and 55% from carbohydrate; diet B: high-energy diet of 5.56 kcal/g, with 16% of calories from protein, 58% from fat, and 26% from carbohydrate).

    Interestingly, the lowering of circulating insulin through gene manipulation had a more profound effect on median lifespan in female mice fed the low-calorie/high-carb/low-fat diet (11% extension) versus the high-calorie/low-carb/high-fat diet (3% extension). It is important to note that diets A and B were not matched for the type of fat content, protein levels, or micronutrient composition, so there are numerous potential factors that could have impacted diet-dependent outcomes.

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  • Type 2 diabetics given broccoli sprout extract containing 150 μmol sulforaphane for 12 weeks lowered blood glucose levels by 10% compared to placebo. www.newscientist.com
    Diet Diabetes Insulin Resistance Sulforaphane Insulin NRF2 Metformin

    Broccoli sprout extract reduced HbA1c by 7.04% in obese patients with dysregulated type 2 diabetes. It has been demonstrated that a 1% decrease of HbA1c corresponds to 37% reduced risk of microvascular complications.

    Sulforaphane reduces glucose by suppressing liver enzymes that otherwise stimulate the production of glucose.

    In animals, sulforaphane also attenuated exaggerated glucose production and glucose intolerance by a magnitude similar to that of metformin.

    Further investigations showed that while both metformin and sulphoraphane cut blood glucose, they do it in different ways. Metformin makes cells more sensitive to insulin, so they sponge more surplus glucose out of the bloodstream. Sulphoraphane reduces glucose by suppressing liver enzymes that otherwise stimulate the production of glucose. For this reason, Rosengren thinks the broccoli extract is complementary to metformin, not competitive."

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  • VSL#3 improved HDL, insulin sensitivity, LDL, atherogenic factors, and inflammation www.ncbi.nlm.nih.gov
    Gut Obesity Microbiome Insulin Resistance Cholesterol Omega-3 Inflammation Microbes VSL#3 Insulin Triglycerides

    FTA

    … a clinical trial in 60 overweight (BMI > 25), healthy adults, aged 40-60 years. After initial screening, the subjects were randomized into four groups with 15 per group. The four groups received, respectively, placebo, omega-3 fatty acid, probiotic VSL#3, or both omega-3 and probiotic, for 6 weeks. […] The probiotic (VSL#3) supplemented group had a significant reduction in total cholesterol, triglyceride, LDL, and VLDL and had increased HDL (P < 0.05) value. VSL#3 improved insulin sensitivity (P < 0.01), decreased hsCRP and favorably affected the composition of gut microbiota. Omega-3 had a significant effect on insulin sensitivity and hsCRP but had no effect on gut microbiota. The addition of omega-3 fatty acid with VSL#3 had a more pronounced effect on HDL, insulin sensitivity and hsCRP. Table showing statistics of the study.

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  • Late-night eating increases weight gain, raised insulin, fasting glucose, cholesterol & triglycerides in small trial. www.sciencedaily.com
    Insulin Resistance Fasting Circadian Rhythm Fat Insulin Triglycerides Time-Restricted Eating

    A small clinical trial finds that eating later in the day (12 pm to 11 pm) increased weight gain, raised insulin, fasting glucose, cholesterol, and triglyceride levels compared to eating earlier in the day (8 am to 7 pm).

    In the small study, each of the nine healthy weight adults underwent each of the two conditions: daytime eating (three meals and two snacks between 8 a.m. and 7 p.m.) for eight weeks and delayed eating (the same three meals and two snacks eating from noon to 11 p.m.) for eight weeks after a 2-week washout period. This is a small trial and needs to be repeated but is in line with another study that showed when healthy adults eat meals that are identical for breakfast, lunch, or dinner, the postprandial glucose increase is lowest after breakfast and highest after dinner even though the meals were 100% identical.

    For more on meal timing and time-restricted eating…check out my podcasts with the experts, Dr. Satchin Panda and Dr. Ruth Patterson on youtube and iTunes.

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  • Unraveling Alzheimer’s: Making Sense of the Relationship between Diabetes and Alzheimer’s Disease1 www.drperlmutter.com
    Alzheimer's Diabetes Insulin Resistance Insulin

    Abstract. Numerous studies have documented a strong association between diabetes and Alzheimer’s disease (AD). The nature of the relationship, however, has remained a puzzle, in part because of seemingly incongruent findings. For example, some studies have concluded that insulin deficiency is primarily at fault, suggesting that intranasal insulin or inhibiting the insulin-degrading enzyme (IDE) could be beneficial. Other research has concluded that hyperinsulinemia is to blame, which implies that intranasal insulin or the inhibition of IDE would exacerbate the disease. Such antithetical conclusions pose a serious obstacle to making progress on treatments. However, careful integration of multiple strands of research, with attention to the methods used in different studies, makes it possible to disentangle the research on AD. This integration suggests that there is an important relationship between insulin, IDE, and AD that yields multiple pathways to AD depending on the where deficiency or excess in the cycle occurs. I review evidence for each of these pathways here. The results suggest that avoiding excess insulin, and supporting robust IDE levels, could be important ways of preventing and lessening the impact of AD. I also describe what further tests need to be conducted to verify the arguments made in the paper, and their implications for treating AD

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