What Causes Insulin Resistance? Lipid Overload
Over the past year I have interacted with hundreds of people with diabetes, and have come to learn one very important lesson that has changed my view of diabetes altogether. This realization came to me early on in my career as a nutrition and fitness coach for people with diabetes, and continues to hold true. While insulin resistance is a condition that is most commonly associated with type 2 diabetes, an increasing body of evidence is now shedding light on the fact that insulin resistance is a common thread that underlies many health conditions previously unassociated with blood sugar, including (but not limited to) heart disease, diabetes, atherosclerosis, the metabolic syndrome, obesity and cancer. What that means is simple: insulin resistance significantly increases your risk for the development of a collection of health conditions that can significantly reduce your quality of life and decrease your life expectancy. Watch this video for a synopsis of the causes of insulin resistance: What is insulin and why should you care? Insulin is a hormone which is released by the pancreas in response to rising blood glucose. When you consume carbohydrates, the glucose that enters the bloodstream knocks on the door of the beta cells in the pancreas as a signal to make insulin. Insulin serves as the key that unlocks the door to allow glucose to enter body tissues. Insulin tells your cells “Yoo hoo! Pick up this glucose. It’s all over the place.” Without insulin, cells in the liver, muscle, and fat have a difficult time vacuuming up glucose from the blood. These tissues are capable to vacuuming up only a small percentage (5-10%) of the glucose in circulation without the help of insulin. When insulin is present, the amount of glucose that can be transported into tissues sign Continue reading >>
Joslin Study Reveals That Dietary Fat Can Affect Glucose Levels And Insulin Requirements For People With Type 1 Diabetes
News Release Findings Have Major Implications for Insulin Dosing and Nutritional Recommendations BOSTON – March 27, 2013 – In a study of patients with type 1 diabetes, Joslin researchers found that dietary fat can affect glucose levels and insulin requirements. These findings, which appeared in the April edition of Diabetes Care, have major implications for the management of type 1 diabetes. Howard Wolpert, M.D., leads clinical trials that help to analyze the best ways to adopt technology for type 1 diabetes management. He is an Investigator in the Section on Clinical, Behavioral & Outcomes Research and Assistant Professor of Medicine at Harvard Medical School. Research has shown that dietary fat and free fatty acids (FFAs) impair insulin sensitivity and increase glucose production. Most studies have focused on the role of fat in the development of type 2 diabetes. However, studies of people with type 1 diabetes have shown that higher-fat pizza meals cause hyperglycemia hours after being consumed. In reviews of continuous glucose monitoring and food log data from adult patients with type 1 diabetes, Joslin clinicians observed that “several hours after eating high-fat meals, glucose levels went up,” says study lead author Howard Wolpert, MD, Senior Physician in the Joslin Clinic Section on Adult Diabetes and the Director of the Insulin Pump Program at Joslin. “We wanted to determine the underlying cause of these unexplained fluctuations.” Seven participants (adults with type 1 diabetes with an average age of 55) successfully completed the study. They spent two days at Beth Israel Deaconess Medical Center eating carefully controlled meals and having their glucose and insulin levels monitored. All breakfasts and lunches featured identical low-fat content. The t Continue reading >>
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Dear Mark: Does Eating A Low Carb Diet Cause Insulin Resistance?
157 Comments Despite all the success you might have had with the Primal way of life, doubts can still nag at you. Maybe it’s something you read, or something someone said to you, or a disapproving glance or offhand comment from a person you otherwise respect, but it’s pretty common when you’re doing something, like giving up grains, avoiding processed food, or eating animal fat, that challenges deeply-and-widely held beliefs about health and wellness. It doesn’t really even matter that you’re losing weight or seem to be thriving; you may still have questions. That’s healthy and smart, and it’s totally natural. A question I’ve been getting of late is the effect of reducing carb intake on insulin sensitivity. It’s often bandied about that going low carb is good for folks with insulin resistance, but it’s also said that low carb can worsen insulin resistance. Are both true and, if so, how do they all jibe together? That’s what the reader was wondering with this week’s question: Hi Mark, I’ve been Primal for a few months now and love it. Lowering my carbs and upping my animal fat helped me lose weight and gain tons of energy (not too shabby for a middle-aged guy!). However, I’m a little worried. I’ve heard that low carb diets can increase insulin resistance. Even though I’ve done well and feel great, should I be worried about insulin resistance? Do I need to increase my carb intake? I always thought low carb Primal was supposed to improve insulin function. Vince Going Primal usually does improve insulin sensitivity, both directly and in a roundabout way. It improves directly because you lose weight, you reduce your intake of inflammatory foods, you lower systemic inflammation (by getting some sun, smart exercise, omega-3s, and reducing or dea Continue reading >>
Saturated Fat And Insulin Sensitivity
Insulin sensitivity is a measure of the tissue response to insulin. Typically, it refers to insulin's ability to cause tissues to absorb glucose from the blood. A loss of insulin sensitivity, also called insulin resistance, is a core part of the metabolic disorder that affects many people in industrial nations. It is commonly asserted in journal articles and on the internet that saturated fat reduces insulin sensitivity. The idea is that saturated fat reduces the body's ability to handle glucose effectively, placing people on the road to diabetes, obesity and heart disease. Perhaps this particular claim deserves a closer look. The Evidence I found a review article from 2008 that addressed this question (1). I like this review because it only includes high-quality trials that used reliable methods of determining insulin sensitivity*. On to the meat of it. There were 5 studies in which non-diabetic people were fed diets rich in saturated fat, and compared with a group eating a diet rich in monounsaturated (like olive oil) or polyunsaturated (like corn oil) fat. They ranged in duration from one week to 3 months. Four of the five studies found that fat quality did not affect insulin sensitivity, including one of the 3-month studies. The fifth study, which is the one that's most commonly cited, requires some discussion. This was the KANWU study (2). Over the course of three months, investigators fed 163 volunteers a diet rich in either saturated fat or monounsaturated fat. The SAFA diet included butter and a table margarine containing a relatively high proportion of SAFAs. The MUFA diet included a spread and a margarine containing high proportions of oleic acid derived from high-oleic sunflower oil and negligible amounts of trans fatty acids and n-3 fatty acids and olive oil Continue reading >>
Study: Doubling Saturated Fat In The Diet Does Not Increase Saturated Fat In Blood
COLUMBUS, Ohio – Doubling or even nearly tripling saturated fat in the diet does not drive up total levels of saturated fat in the blood, according to a controlled diet study. However, increasing levels of carbohydrates in the diet during the study promoted a steady increase in the blood of a fatty acid linked to an elevated risk for diabetes and heart disease. The finding “challenges the conventional wisdom that has demonized saturated fat and extends our knowledge of why dietary saturated fat doesn’t correlate with disease,” said senior author Jeff Volek, a professor of human sciences at The Ohio State University. “It’s unusual for a marker to track so closely with carbohydrate intake, making this a unique and clinically significant finding. As you increase carbs, this marker predictably goes up,” Volek said.The researchers found that total saturated fat in the blood did not increase – and went down in most people – despite being increased in the diet when carbs were reduced. Palmitoleic acid, a fatty acid associated with unhealthy metabolism of carbohydrates that can promote disease, went down with low-carb intake and gradually increased as carbs were re-introduced to the study diet.In the study, participants were fed six three-week diets that progressively increased carbs while simultaneously reducing total fat and saturated fat, keeping calories and protein the same. When that marker increases, he said, it is a signal that an increasing proportion of carbs are being converted to fat instead of being burned as fuel. Reducing carbs and adding fat to the diet in a well-formulated way, on the other hand, ensures the body will promptly burn the saturated fat as fuel – so it won’t be stored. “When you consume a very low-carb diet your body prefere Continue reading >>
Eating Healthy Fats In Place Of Carbs Or Saturated Fats Improves Risk Factors For Diabetes
Follow all of ScienceDaily's latest research news and top science headlines ! Eating healthy fats in place of carbs or saturated fats improves risk factors for diabetes Eating more unsaturated fats in place of either dietary carbohydrate or saturated fat reduces blood sugar, insulin levels, and other metrics related to type 2 diabetes, according to a new meta-analysis of data from 102 randomized feeding trials in adults. A large-scale meta-analysis finds consumption of unsaturated fats in place of either saturated fats or carbohydrates could aid in the prevention and management of type 2 diabetes Eating more unsaturated fats, especially polyunsaturated fats, in place of either dietary carbohydrate or saturated fats lowers blood sugar levels and improves insulin resistance and secretion, according to a new meta-analysis of data from 102 randomised controlled feeding trials in adults. The study, led by Dariush Mozaffarian M.D., Dr.P.H., dean of the Friedman School of Nutrition Science and Policy at Tufts University, and Fumiaki Imamura, Ph.D., at the Medical Research Council (MRC) Epidemiology Unit, University of Cambridge, provides novel quantitative evidence for the effects of dietary fats and carbohydrate on the regulation of glucose and insulin levels and several other metrics linked to type 2 diabetes. The results were published in PLOS Medicine on July 19. Rates of insulin resistance and type 2 diabetes are rising sharply worldwide, highlighting the need for new, evidence-based preventive strategies. While a healthy diet is clearly a cornerstone of such efforts, the effects of different dietary fats and carbohydrate on metabolic health have been controversial, leading to confusion about specific dietary guidelines and priorities. "The world faces an epidemic of ins Continue reading >>
Diet And Diabetes: Why Saturated Fats Are The Real Enemy
This is the seventh article in our “Controversies” series and the third piece focusing on the subject of fats. Today, we are going to explore the very important relationship between saturated fat intake and the onset of diabetes. As we mentioned in The Ultimate Guide to Saturated Fats, “Once we control for weight, alcohol, smoking, exercise and family history, the incidence of diabetes is significantly associated with the proportion of saturated fat in our blood.” Today we will take a deep dive to fully understand why there is such a strong link between diabetes and saturated fat consumption. We will also discuss how a plant-based diet may protect you from (or even reverse!) the disease. What Is Insulin Resistance? Insulin resistance is a hallmark of both prediabetes and type 2 diabetes. So what is insulin resistance exactly (and why is it important)? Let me explain. Insulin is what permits glucose (sugar) in the blood to enter our (muscle) cells. In essence, insulin ‘unlocks’ the door, allowing the glucose to come in. If there is no insulin at all (the case of type 1 diabetes), the blood sugar ‘hangs out’ in the bloodstream because it cannot get inside. That causes the blood sugar levels to rise. But what happens if the insulin is there but is simply not working properly? In that case, the lock to the cell door is ‘blocked.’ This is what is called insulin resistance. So what causes insulin resistance in the first place? Insulin resistance is caused by fat. Fat build-up inside (muscle) cells creates toxic fatty breakdown products and free radicals that ‘block’ the insulin-signaling process, close the ‘glucose gate,’ and make blood sugar levels rise. And this cycle can happen really fast. In fact, insulin resistance can occur in 180 short minu Continue reading >>
Influence Of Dietary Fat Composition On Development Of Insulin Resistance In Rats: Relationship To Muscle Triglyceride And Ω-3 Fatty Acids In Muscle Phospholipid
High levels of some but not all dietary fats lead to insulin resistance in rats. The aim of this study was to investigate the important determinants underlying this observation. Insulin action was assessed with the euglycemic clamp. Diets high in saturated, monounsaturated (ω-9), or polyunsaturated (ω-6) fatty acids led to severe insulin resistance; glucose infusion rates [GIR] to maintain euglycemia at ∼1000 pM insulin were 6.2 ± 0.9, 8.9 ± 0.9, and 9.7 ± 0.4 mg · kg−1 · min−1, respectively, versus 16.1 ± 1.0 mg · kg−1 · min−1 in chow-fed controls. Substituting 11% of fatty acids in the polyunsaturated fat diet with long-chain ω-3 fatty acids from fish oils normalized insulin action (GIR 15.0 ± 1.3 mg · kg−1 · min−1). Similar replacement with short-chain ω-3 (α-linolenic acid, 18:3ω3) was ineffective in the polyunsaturated diet (GIR 9.9 ± 0.5 mg · kg−1 · min−1) but completely prevented the insulin resistance induced by a saturated-fat diet (GIR 16.0 ± 1.5 mg · kg−1 · min−1) and did so in both the liver and peripheral tissues. Insulin sensitivity in skeletal muscle was inversely correlated with mean muscle triglyceride accumulation (r = 0.95 and 0.86 for soleus and red quadriceps, respectively; both P = 0.01). Furthermore, percentage of long-chain ω-3 fatty acid in phospholipid measured in red quadriceps correlated highly with insulin action in that muscle (r = 0.97). We conclude that 1) the particular fatty acids and the lipid environment in which they are presented in high-fat diets determine insulin sensitivity in rats; 2) impaired insulin action in skeletal muscle relates to triglyceride accumulation, suggesting intracellular glucose–fatty acid cycle involvement; and 3) long-chain ω-3 fatty acids in phospholipid of sk Continue reading >>
Association Between Dietary Fat Intake And Insulin Resistance In Chinese Child Twins
Abstract Dietary fat intake is correlated with increased insulin resistance (IR). However, it is unknown whether gene–diet interaction modulates the association. This study estimated heritability of IR measures and the related genetic correlations with fat intake, and tested whether dietary fat intake modifies the genetic influence on type 2 diabetes (T2D)-related traits in Chinese child twins. We included 622 twins aged 7–15 years (n 311 pairs, 162 monozygotic (MZ), 149 dizygotic (DZ)) from south-eastern China. Dietary factors were measured using FFQ. Structural equation models were fit using Mx statistical package. The intra-class correlation coefficients for all traits related to T2D were higher for MZ twins than for DZ twins. Dietary fat and fasting serum insulin (additive genetic correlation (r A) 0·20; 95 % CI 0·08, 0·43), glucose (r A 0·12; 95 % CI 0·01, 0·40), homoeostasis model of assessment-insulin resistance (Homa-IR) (r A 0·22; 95 % CI 0·10, 0·50) and the quantitative insulin sensitivity check index (Quicki) (r A −0·22; 95 % CI −0·40, 0·04) showed strong genetic correlations. Heritabilities of dietary fat intake, fasting glucose and insulin were estimated to be 52, 70 and 70 %, respectively. More than 70 % of the phenotypic correlations between dietary fat and insulin, glucose, Homa-IR and the Quicki index appeared to be mediated by shared genetic influence. Dietary fat significantly modified additive genetic effects on these quantitative traits associated with T2D. Analysis of Chinese twins yielded high estimates of heritability of dietary fat intake and IR. Genetic factors appear to contribute to a high proportion of the variance for both insulin sensitivity and IR. Dietary fat intake modifies the genetic influence on blood levels of in Continue reading >>
Dietary Fat Content Alters Insulin-mediated Glucose Metabolism In Healthy Men1,2,3
Abstract Background: A high dietary fat intake is involved in the pathogenesis of insulin resistance. Objective: The aim was to compare the effect of different amounts of dietary fat on hepatic and peripheral insulin sensitivity. Design: Six healthy men were studied on 3 occasions after consuming for 11 d diets with identical energy and protein contents but different percentages of energy as fat and carbohydrate as follows: 0% and 85% [low-fat, high-carbohydrate (LFHC) diet], 41% and 44% [intermediate-fat, intermediate-carbohydrate (IFIC) diet], and 83% and 2% [high-fat, low-carbohydrate (HFLC) diet]. Insulin sensitivity was quantified by using a hyperinsulinemic euglycemic clamp (plasma insulin concentration: ≈190 pmol/L). Results: During hyperinsulinemia, endogenous glucose production was higher after the HFLC diet (2.5 ± 0.3 μmol•kg−1•min−1; P < 0.05) than after the IFIC and LFHC diets (1.7 ± 0.3 and 1.2 ± 0.4 μmol•kg−1•min−1, respectively). The ratio of dietary fat to carbohydrate had no unequivocal effects on insulin-stimulated glucose uptake. In contrast, insulin-stimulated, nonoxidative glucose disposal tended to increase in relation to an increase in the ratio of fat to carbohydrate, from 14.8 ± 5.1 to 20.6 ± 1.9 to 26.2 ± 2.9 μmol•kg−1•min−1 (P < 0.074 between the 3 diets). Insulin-stimulated glucose oxidation was significantly lower after the HFLC diet than after the IFIC and LFHC diets: 1.7 ± 0.8 compared with 13.4 ± 2.1 and 19.0 ± 2.1 μmol•kg−1•min−1, respectively (P < 0.05). During the clamp study, plasma fatty acid concentrations were higher after the HFLC diet than after the IFIC and LFHC diets: 0.22 ± 0.02 compared with 0.07 ± 0.01 and 0.05 ± 0.01 mmol/L, respectively (P < 0.05). Conclusion: A high-fat, l Continue reading >>
- This Incredible Detox Drink Helps You Burn Fat, Boost Metabolism, Fight Diabetes And Lower Blood Pressure.
- This Incredible Detox Drink Helps You Burn Fat, Boost Metabolism, Fight Diabetes And Lower Blood Pressure
- This Incredible Detox Drink Helps You Burn Fat, Lower Blood Pressur,Fight Diabetes And Boost Metabolism
Dietary Fat, Insulin Sensitivity And The Metabolic Syndrome.
Abstract Insulin resistance is the pathogenetic link underlying the different metabolic abnormalities clustering in the metabolic syndrome. It can be induced by different environmental factors, including dietary habits. Consumption of energy-dense/high fat diets is strongly and positively associated with overweight that, in turn, deteriorates insulin sensitivity, particularly when the excess of body fat is located in abdominal region. Nevertheless the link between fat intake and overweight is not limited to the high-energy content of fatty foods; the ability to oxidize dietary fat is impaired in some individuals genetically predisposed to obesity. Insulin sensitivity is also affected by the quality of dietary fat, independently of its effects on body weight. Epidemiological evidence and intervention studies clearly show that in humans saturated fat significantly worsen insulin-resistance, while monounsaturated and polyunsaturated fatty acids improve it through modifications in the composition of cell membranes which reflect at least in part dietary fat composition. A recent multicenter study (KANWU) has shown that shifting from a diet rich in saturated fatty acids to one rich in monounsaturated fat improves insulin sensitivity in healthy people while a moderate alpha-3 fatty acids supplementation does not affect insulin sensitivity. There are also other features of the metabolic syndrome that are influenced by different types of fat, particularly blood pressure and plasma lipid levels. Most studies show that alpha-3 fatty acids reduce blood pressure in hypertensive but not in normotensive subjects while shifting from saturated to monounsaturated fat intake reduces diastolic blood pressure. In relation to lipid abnormalities alpha-3 fatty acids reduce plasma triglyceride Continue reading >>
- Ultraviolet Radiation Suppresses Obesity and Symptoms of Metabolic Syndrome Independently of Vitamin D in Mice Fed a High-Fat Diet
- Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2 Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA)*
- Effects of resveratrol on glucose control and insulin sensitivity in subjects with type 2 diabetes: systematic review and meta-analysis
The Influence Of Dietary Fat On Insulin Resistance
Abstract Dietary fat has been implicated in the development of insulin resistance in both animals and humans. Most, although not all, studies suggest that higher levels of total fat in the diet result in greater whole-body insulin resistance. Although, in practice, obesity may complicate the relationship between fat intake and insulin resistance, clinical trials demonstrate that high levels of dietary fat can impair insulin sensitivity independent of body weight changes. In addition, it appears that different types of fat have different effects on insulin action. Saturated and certain monounsaturated fats have been implicated in causing insulin resistance, whereas polyunsaturated and omega-3 fatty acids largely do not appear to have adverse effects on insulin action. Given the importance of insulin resistance in the development of diabetes and heart disease, establishing appropriate levels of fat in the diet is an important clinical goal. Preview Unable to display preview. Download preview PDF. Continue reading >>
Does Fat Cause Insulin Resistance?
For decades now, we have been told that fatness (or “obesity”) is a major cause of diabetes. Health “experts” have warned about this, but they could never say how being overweight could cause insulin resistance (IR). Without IR, you can’t have Type 2 diabetes, so the whole “blame fat” theory has been suspect. Well, now they have a plausible explanation. Obesity may cause inflammation, causing IR, leading to diabetes. But is this theory true? Does adipose (fat) tissue really create inflammation? Or do both obesity and inflammation come from some other cause? Get ready for some science as I try to explore these questions. In a new report in the Journal of Leukocyte Biology, two Japanese scientists report that “obesity is associated with a state of chronic, low-grade inflammation.” They explain that as fat cells get larger, they seem to attract immune cells called macrophages. These cells produce inflammatory chemicals called cytokines that help cause insulin resistance. Chief among these chemicals are interleukin-6 and tumor necrosis factor-alpha. In animal models, insulin resistance doesn’t occur until after macrophages invade the fat cells. So the question remains, which comes first, the inflammation or the fatness? What draws the immune cells into adipose tissue? Remember that most overweight people never develop diabetes. And some overweight people have much more inflammation than others. (The same is true of thin people, of course.) Why do some develop this fat-related inflammation and some don’t? Some think that weight itself provokes inflammation. According to French scientists writing in the journal European Cytokine Network, weight loss is associated with reduced “macrophage infiltration” and reduced inflammation. Also, another chemical, Continue reading >>
What Causes Insulin Resistance?
Michael: You wrote: ” Part of the question in my mind are the relative benefits of higher HDL vs lower LDL; a topic I would love to see taken up on a NF video.” I have suggested that this be a topic of future videos. In the meantime, below is some information I’ve gathered about HDL which may be helpful to you. . **************** I am not an expert on the topic of HDL, but some of my favorite NutritionFacts forum members and some experts have had a thing or two to say on the matter. BOTTOM LINE: I synthesize the information below to mean we do not need to worry about HDL levels or HDL falling in the context of a whole plant food based diet, when LDL goes down or is already at a healthy level. . In other words, if you have high/unsafe cholesterol levels (total and LDL) overall, then also having high HDL can be protective (especially if you got that high HDL through exercise or some other healthy behavior rather than diet). But in the face of healthy LDL levels, the HDL level doesn’t seem to matter. I may be wrong about this, but see what you think. ************************************ . First, check out the following article from heart health expert Dean Ornish. He does a great job of explaining the role of HDL and when we need to worry about it’s levels vs when we do not. “A low HDL in the context of a healthy low-fat diet has a very different prognostic significance than a low HDL in someone eating a high-fat, high-cholesterol diet.” . Two of our more knowledgable forum particpants, Gatherer and Darryl, have put together for us some of the strongest evidence–a list of good studies. Gatherer wrote (from comment ) : . “”Don’t put too much stock in HDL levels. Here is a news release “Raising ‘good’ cholesterol doesn’t protect against heart di Continue reading >>
Insulin resistance (IR) is a pathological condition in which cells fail to respond normally to the hormone insulin. The body produces insulin when glucose starts to be released into the bloodstream from the digestion of carbohydrates in the diet. Normally this insulin response triggers glucose being taken into body cells, to be used for energy, and inhibits the body from using fat for energy. The concentration of glucose in the blood decreases as a result, staying within the normal range even when a large amount of carbohydrates is consumed. When the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. This often remains undetected and can contribute to the development of type 2 diabetes or latent autoimmune diabetes of adults. Although this type of chronic insulin resistance is harmful, during acute illness it is actually a well-evolved protective mechanism. Recent investigations have revealed that insulin resistance helps to conserve the brain's glucose supply by preventing muscles from taking up excessive glucose. In theory, insulin resistance should even be strengthened under harsh metabolic conditions such as pregnancy, during which the expanding fetal brain demands more glucose. People who develop type 2 diabetes usually pass through earlier stages of insulin resistance and prediabetes, although those often go undiagnosed. Insulin resistance is a syndrome (a set of signs and symptoms) resulting from reduced insulin activity; it is also part of a larger constellation of symptoms called the metabolic syndrome. Insuli Continue reading >>