- Insulin Resistance and Type 2 Diabetes
- What Is Insulin Resistance? Everything You Ever Wanted to Know
- Defining Insulin: How the Hormone Helps Regulate Blood Sugar
- Understanding Insulin Resistance and Its Effect on Blood Sugar Control
- The Potential Causes of Insulin Resistance
- What Are the Main Symptoms of Insulin Resistance?
- How Is Insulin Resistance Diagnosed?
- Should You Be Tested for Insulin Resistance?
- Can Insulin Resistance Be Prevented or Reversed?
- How to Change Your Lifestyle and Diet to Prevent, Manage, or Help Reverse Insulin Resistance
- How do I know if I am Insulin Resistant?
- Insulin Resistance Syndrome in the Elderly
- Insulin Resistance: Dealing With the Diagnosis
- What is insulin resistance?
- Symptoms of insulin resistance
- Causes of insulin resistance
- Can insulin resistance be reduced or reversed?
- What Is Insulin Resistance?
- How Are Insulin Resistance and PCOS Connected?
- How Do I Know If I Have Insulin Resistance?
- 1. You Have Severe Hangry Attacks
- 2. You Store Weight Around Your Belly
- 3. No Matter How Many Spin Classes, Miles Run, and Salads Ate, You Can’t Lose Weight
- 4. You’ve Developed Dark Velvety Patches in the Folds of Your Skin
- 5. You’ve Got Skin Tags
- Summary of Insulin Resistance and PCOS
- What does insulin do in the body?
- What does it mean to be insulin resistant?
- What causes insulin resistance?
- What are the symptoms of insulin resistance?
- What are the complications of insulin resistance?
- Is there an insulin resistance test?
- Can you reverse insulin resistance?
Insulin Resistance and Type 2 Diabetes
For well over half a century, the link between insulin resistance and type 2 diabetes has been recognized. Insulin resistance is important. Not only is it the most powerful predictor of future development of type 2 diabetes, it is also a therapeutic target once hyperglycemia is present. In this issue of Diabetes, Morino et al. (1) report a series of studies that provide evidence of a genetic mechanism linking expression of lipoprotein lipase (LPL) to peroxisome proliferator–activated receptor (PPAR)-δ expression and mitochondrial function. This is likely to contribute to the muscle insulin resistance that predisposes to type 2 diabetes.
Observation of abnormal mitochondrial function in vitro in type 2 diabetes (2) was soon followed by in vivo demonstration of this abnormality in insulin-resistant, first-degree relatives of people with type 2 diabetes (3). Further reports of a modest defect in muscle mitochondrial function in type 2 diabetes were published shortly thereafter (4,5). These studies raised the question of whether type 2 diabetes could be a primary disorder of the mitochondria. However, the study of first-degree relatives tended to be misinterpreted as having shown a major defect in mitochondrial function in type 2 diabetes, although it had studied nondiabetic groups from the opposite ends of the insulin resistance–sensitivity spectrum. Indeed, other studies showed no defect in mitochondrial function in type 2 diabetes (6,7), which led to further confusion. Mitochondrial function was then shown to be acutely modifiable by changing fatty acid availability (8) and that it was affected by ambient blood glucose concentration (9). When ambient blood glucose levels were near normal in diabetes, no defect in mitochondrial function was apparent.
But if mitochondrial function in well-controlled type 2 diabetes is not abnormal, is a defect in insulin-resistant, first-degree relatives clinically relevant? The answer is provided in Fig. 1, which shows population distributions of insulin sensitivity for normoglycemia, impaired glucose tolerance, and type 2 diabetes. The wide range of insulin sensitivity in the normoglycemic population fully encompasses the range observed in type 2 diabetes. Even though mean insulin sensitivity in diabetes is lower than that of matched control subjects, values are drawn from the same distribution and, with matching for body weight and physical activity, differences will be relatively small. Differences in insulin sensitivity will be particularly evident when making comparisons between groups selected from the extreme ends of the population distribution (Fig. 1). When parameters directly linked to muscle insulin resistance are compared between groups selected in this way, any linked difference will be maximized, making this strategy entirely appropriate to investigate the pathophysiology of muscle insulin resistance.
Distribution curves of insulin sensitivity as measured by the euglycemic-hyperinsulinemic clamp showing that people with type 2 diabetes sit within the range of the nondiabetic distribution, but toward the lower range. Identification of factors underlying muscle insulin resistance itself can be investigated by comparing groups drawn from the extremes of the total population distribution. Such factors may not be clearly discernible when type 2 diabetic individuals are compared with normoglycemic control subjects matched for weight and physical activity. The data are from previously published population studies of normal glucose tolerance (n = 256), impaired glucose tolerance (n = 119), and type 2 diabetes (n = 194) (20,21).
Muscle insulin resistance as determined by the euglycemic-hyperinsulinemic clamp is clearly a risk factor for development of type 2 diabetes (10). However, the pathophysiology of hyperglycemia in established diabetes relates to hepatic not muscle insulin resistance. This distinction has been elegantly demonstrated in studies of moderate calorie restriction in type 2 diabetes, which resulted in a fall in liver fat, normalization of hepatic insulin sensitivity, and fasting plasma glucose, but no change in muscle insulin resistance (11). More recent work employing severe calorie restriction confirmed previous findings and also demonstrated a longer-term return of normal insulin secretion as intrapancreatic fat content fell (12). The fact that fasting and postprandial normoglycemia can be restored in type 2 diabetes without change in muscle insulin resistance should not be surprising. Mice totally lacking in skeletal muscle insulin receptors do not develop diabetes (13). People with inactive muscle glycogen synthase are not necessarily hyperglycemic (14), and many normoglycemic individuals maintain normal blood glucose with a degree of muscle insulin resistance identical to that among people who develop type 2 diabetes (Fig. 1). The relevance of muscle insulin resistance for development of type 2 diabetes is more subtle. Over many years and only in the presence of chronic calorie excess, hyperinsulinemia steadily brings about hepatic fat accumulation and hepatic insulin resistance. Onset of hyperglycemia is ultimately determined by failure of nutrient-stimulated insulin secretion (15). This new understanding is described by the twin cycle hypothesis (16). So what actually determines this critical primary insulin resistance in muscle?
Morino et al. (1) report analyses of mRNA in muscle biopsies to compare expression of genes involved in mitochondrial fatty acid oxidation. Their experiments compare data for subjects at opposite extremes of the insulin resistance spectrum. Findings were confirmed in independent groups selected in the same way and two genes were found to be consistently lower in expression. Using knock down of expression by appropriate inhibitory RNA, Western blotting showed that LPL was the important gene product. In both human rhabdomyosarcoma cells and L6 myocytes, such knock down of LPL induced a decrease in mitochondrial density. The function of LPL is to release fatty acids from triglyceride for direct cellular uptake. The biological relevance of the link between decreased mitochondrial numbers and RNA interference (RNAi) inhibition of LPL was confirmed by observing that the effect was only seen if fat was present in the extracellular media. To test the hypothesis that fatty acid flux into cells regulates mitochondrial biogenesis by a PPAR-dependent process, knock down of PPAR-δ was also shown to decrease mitochondrial density. Furthermore, limitation of fatty acid uptake by directly inhibiting the transmembrane fatty transporter CD36 was shown to achieve the same effect. Overall, these studies suggest that insulin resistance is related to decreased mitochondrial content in muscle due, at least in part, to reductions in LPL expression and consequent decreased PPAR-δ activation.
This important article establishes a biological mechanism whereby insulin resistance in muscle is causally linked to genetic influences that are measurable in the general population. It focuses on insulin resistance by comparing extremes of the distribution of this characteristic in the normal population. But does insulin resistance cause mitochondrial dysfunction, or vice versa? The former appears more likely on the basis of current evidence. Exercise can reduce insulin resistance and ameliorate mitochondrial dysfunction (17), whereas established mitochondrial dysfunction does not necessarily produce insulin resistance in animal models or in humans (18,19). Understanding the nature of common insulin resistance in muscle and its relationship to type 2 diabetes is long overdue. Future work should determine whether specific therapeutic manipulation can offset the effect of identifiable genetic influences and interrupt the long run-in to type 2 diabetes.
No potential conflicts of interest relevant to this article were reported.
The author is grateful to Leif Groop of Lund University for permission to use combined data from the Botnia Study and the Malmö Prospective Study in Fig. 1 and to Jasmina Kravic of Lund University for replotting the data.
See accompanying original article, p. 877.
- © 2012 by the American Diabetes Association.
Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
- Morino K,
- Petersen KF,
- Sono S,
- et al
. Regulation of mitochondrial biogenesis by lipoprotein lipase in muscle of insulin-resistant offspring of parents with type 2 diabetes. Diabetes 2012;61:877–887
- Kelley DE,
- He J,
- Menshikova EV,
- Ritov VB
. Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes. Diabetes 2002;51:2944–2950pmid:12351431
- Petersen KF,
- Dufour S,
- Befroy D,
- Garcia R,
- Shulman GI
. Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes. N Engl J Med 2004;350:664–671pmid:14960743
- Szendroedi J,
- Schmid AI,
- Chmelik M,
- et al
. Muscle mitochondrial ATP synthesis and glucose transport/phosphorylation in type 2 diabetes. PLoS Med 2007;4:e154pmid:17472434
- Phielix E,
- Schrauwen-Hinderling VB,
- Mensink M,
- et al
. Lower intrinsic ADP-stimulated mitochondrial respiration underlies in vivo mitochondrial dysfunction in muscle of male type 2 diabetic patients. Diabetes 2008;57:2943–2949pmid:18678616
- De Feyter HM,
- van den Broek NM,
- Praet SF,
- Nicolay K,
- van Loon LJ,
- Prompers JJ
. Early or advanced stage type 2 diabetes is not accompanied by in vivo skeletal muscle mitochondrial dysfunction. Eur J Endocrinol 2008;158:643–653pmid:18426822
- Lim EL,
- Hollingsworth KG,
- Smith FE,
- Thelwall PE,
- Taylor R
. Effects of raising muscle glycogen synthesis rate on skeletal muscle ATP turnover rate in type 2 diabetes. Am J Physiol Endocrinol Metab 2011;301:E1155–E1162pmid:21917633
- Lim EL,
- Hollingsworth KG,
- Smith FE,
- Thelwall PE,
- Taylor R
. Inhibition of lipolysis in Type 2 diabetes normalizes glucose disposal without change in muscle glycogen synthesis rates. Clin Sci (Lond) 2011;121:169–177pmid:21388348
- Schrauwen-Hinderling VB,
- Kooi ME,
- Hesselink MK,
- et al
. Impaired in vivo mitochondrial function but similar intramyocellular lipid content in patients with type 2 diabetes mellitus and BMI-matched control subjects. Diabetologia 2007;50:113–120pmid:17093944
- Lillioja S,
- Mott DM,
- Spraul M,
- et al
. Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus. Prospective studies of Pima Indians. N Engl J Med 1993;329:1988–1992pmid:8247074
- Petersen KF,
- Dufour S,
- Befroy D,
- Lehrke M,
- Hendler RE,
- Shulman GI
. Reversal of nonalcoholic hepatic steatosis, hepatic insulin resistance, and hyperglycemia by moderate weight reduction in patients with type 2 diabetes. Diabetes 2005;54:603–608pmid:15734833
- Lim EL,
- Hollingsworth KG,
- Aribisala BS,
- Chen MJ,
- Mathers JC,
- Taylor R
. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia 2011;54:2506–2514pmid:21656330
- Brüning JC,
- Michael MD,
- Winnay JN,
- et al
. A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance. Mol Cell 1998;2:559–569pmid:9844629
- Savage DB,
- Zhai L,
- Ravikumar B,
- et al
. A prevalent variant in PPP1R3A impairs glycogen synthesis and reduces muscle glycogen content in humans and mice. PLoS Med 2008;5:e27pmid:18232732
- Ferrannini E,
- Nannipieri M,
- Williams K,
- Gonzales C,
- Haffner SM,
- Stern MP
. Mode of onset of type 2 diabetes from normal or impaired glucose tolerance. Diabetes 2004;53:160–165pmid:14693710
- Taylor R
. Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetologia 2008;51:1781–1789pmid:18726585
- Ritov VB,
- Menshikova EV,
- Azuma K,
- et al
. Deficiency of electron transport chain in human skeletal muscle mitochondria in type 2 diabetes mellitus and obesity. Am J Physiol Endocrinol Metab 2010;298:E49–E58pmid:19887598
- Zechner C,
- Lai L,
- Zechner JF,
- et al
. Total skeletal muscle PGC-1 deficiency uncouples mitochondrial derangements from fiber type determination and insulin sensitivity. Cell Metab 2010;12:633–642pmid:21109195
- Maassen JA,
- ‘t Hart LM,
- van Essen E,
- et al
. Mitochondrial diabetes: molecular mechanisms and clinical presentation. Diabetes 2004;53(Suppl. 1):S103–S109pmid:16703328
- Groop L,
- Forsblom C,
- Lehtovirta M,
- et al
. Metabolic consequences of a family history of NIDDM (the Botnia study): evidence for sex-specific parental effects. Diabetes 1996;45:1585–1593pmid:8866565
- Tripathy D,
- Eriksson KF,
- Orho-Melander M,
- Fredriksson J,
- Ahlqvist G,
- Groop L
. Parallel manifestation of insulin resistance and beta cell decompensation is compatible with a common defect in Type 2 diabetes. Diabetologia 2004;47:782–793pmid:15114470
What Is Insulin Resistance? Everything You Ever Wanted to Know
Having insulin resistance may increase the risk of prediabetes, type 2 diabetes, and metabolic syndrome. But changing your diet and lifestyle can help reverse this health state.
The hormone insulin helps keep blood sugar levels steady, but when insulin resistance occurs, glucose accumulates in the blood, either leading to or exacerbating prediabetes and type 2 diabetes. Thinkstock
Carbohydrates — sugars and starches found in many foods — are a main source of fuel for your body. Your digestive system breaks down carbs into glucose, or sugar, which is then released into your bloodstream. And with the help of insulin, glucose can absorb into the cells of your body to be used for energy or storage. (1) But if you have insulin resistance, your cells will have trouble absorbing this glucose, and your body will require more insulin to function properly. (2)
It is possible to overcome insulin resistance. But before you can deal with this problem, you must understand what insulin is, and how insulin affects control of blood glucose. (2)
Defining Insulin: How the Hormone Helps Regulate Blood Sugar
Insulin is a hormone produced by your pancreas, and it plays an important role in metabolism. Your pancreas secretes insulin into your bloodstream after you eat a meal. Insulin allows sugar in your bloodstream to enter into muscles, cells, and fat. (2)
This hormone is also important because it stops sugar from accumulating in your bloodstream. The more you eat, the more insulin your body releases to regulate your blood sugar and keep it within a healthy range. (3)
RELATED: Everything You Need to Know About Insulin if You Have Type 2 Diabetes
Understanding Insulin Resistance and Its Effect on Blood Sugar Control
Although the production and release of insulin is a natural metabolic response after eating, some people don’t use insulin properly.
To receive energy, your cells, fat, and muscles must be able to absorb the glucose in your bloodstream. If your body doesn’t respond well to insulin, glucose can build up in your blood and raise your blood sugar level. To help you maintain a normal blood sugar level, your pancreas compensates for this resistance by releasing more insulin. (3)
The effects of insulin resistance on the body vary from person to person. Sometimes, the increased production of insulin by the pancreas is enough to overcome insulin resistance and normalize blood sugar levels. But other times, the pancreas is unable to produce sufficient amounts of insulin to overcome the resistance. This triggers high blood sugar (hyperglycemia) and other health problems. (3)
RELATED: How to Stabilize Your Blood Sugar
Although insulin resistance can exist on its own without another diagnosis, it relates to certain health conditions, too. Here are a few:
If your pancreas struggles to produce enough insulin to handle the glucose in your body, your blood sugar level can become mildly elevated and you may develop prediabetes. This means your blood sugar is higher than normal but not high enough to be diagnosed with diabetes.
This condition — which affects about 84.1 million people — is a precursor to type 2 diabetes. Having prediabetes also is associated with an increased risk for heart disease, stroke, eye problems, neuropathy (nerve damage), and kidney disease.
Type 2 Diabetes
In the case of prediabetes, your pancreas works overtime to secrete enough insulin to regulate your blood sugar. But if your pancreas can’t keep up with the demand, insulin resistance can progress from prediabetes to type 2 diabetes. Most people diagnosed with prediabetes end up with type 2 diabetes within 10 years. (3)
Metabolic syndrome is also closely related to insulin resistance. Interestingly, metabolic syndrome isn’t a condition in itself but rather a collection of metabolic risk factors that can set the stage for type 2 diabetes and heart disease. Insulin resistance is included among these risk factors, along with high blood pressure, abnormal cholesterol levels, high triglycerides (a form of fat storage often related to lifestyle factors), and a large waist circumference.
RELATED: 10 Things Your Doctor Won’t Tell You About Metabolic Syndrome
The Potential Causes of Insulin Resistance
Although the exact cause of insulin resistance is unknown, certain factors have been linked with this condition. These include: (4)
- Obesity (defined as having a certain body mass index, or BMI)
- Eating a high-calorie, high-sugar diet
- Lack of physical activity
- Taking high doses of a steroid
- Chronic stress
- Having polycystic ovary syndrome (PCOS) or Cushing’s disease
Some people are also at higher risk for developing insulin resistance. These include people: (3)
- With a family history of type 2 diabetes
- With a personal history of gestational diabetes
- Over the age of 45
- Who are Hispanic, African-American, Native American, or Asian-American
- With a waist circumference larger than 40 inches (men) or larger than 35 inches (women)
- With a history of high blood pressure (hypertension) or high triglycerides
The risk factors for insulin resistance are similar to the risk factors for prediabetes and type 2 diabetes. But lifestyle changes can help your body use insulin properly, which can reduce your risk of diabetes.
RELATED: 10 Bad Habits That Raise Your Diabetes Risk
What Are the Main Symptoms of Insulin Resistance?
Insulin resistance may not cause any noticeable symptoms, so you can have insulin resistance and not know it. Symptoms don’t usually occur until you develop prediabetes or type 2 diabetes.
If your blood sugar level becomes elevated and you have prediabetes, symptoms may include increased thirst and hunger, tiredness, and blurry vision. Insulin resistance can also cause the formation of dark patches on the neck, groin, and armpits called acanthosis nigricans. (5)
When insulin resistance progresses to type 2 diabetes, you may also have tingling sensations in your hands or feet. (6)
How Is Insulin Resistance Diagnosed?
Although insulin resistance doesn’t usually have symptoms, your doctor may recommend testing your blood sugar if you have risk factors for this condition, such as obesity, a sedentary lifestyle, or high blood pressure.
This involves a series of tests, which are the same for diagnosing prediabetes and type 2 diabetes. (7)
Hemoglobin A1C Test This blood test measures your average blood glucose level over a period of two to three months. This test can determine your blood sugar level, and help your doctor assess how well you’re managing the diabetes. A normal A1C test result is under 5.7 percent; results between 5.7 percent and 6.4 percent is prediabetes; and results equal to or above 6.5 percent is type 2 diabetes. (7) You’ll repeat testing at different intervals over three months to confirm an initial diagnosis.
RELATED: 5 Ways to Lower Your A1C
Fasting Plasma Glucose (FPG) You will not consume food or liquids for at least eight hours, and then your doctor will draw blood to measure your blood sugar level after fasting. If you have an elevated blood sugar, you’ll return a few days later to repeat the test. A repeatedly high level can indicate either prediabetes or diabetes. A number under 100 milligrams per decliliter (mg/dL) is normal; a number between 100 to 125 mg/dL signals prediabetes; and a number greater than 125 mg/dL signals type 2 diabetes. (7)
Glucose Tolerance Testing (OGTT) Your doctor measures your blood glucose level, gives you a sugary liquid to drink, and then repeats the test two hours after you drink the liquid. If after two hours your blood sugar level is less than 140 mg/dL, your blood glucose level is considered normal. A number between 140 mg/dL and 199 mg/dL is considered prediabetes, and a number 200 mg/dL or higher signals type 2 diabetes. (7)
Should You Be Tested for Insulin Resistance?
You should be tested for insulin resistance if you’re showing signs of having a high blood sugar level. (3) Again, there’s no specific test to confirm insulin resistance. But if you’re experiencing fatigue, brain fog, or increased hunger, see your doctor. Getting tested may reveal an elevated blood sugar or prediabetes. With an early diagnosis, you can take steps to help reverse the condition and avoid full-blown type 2 diabetes.
RELATED: 7 Blood Sugar Testing Mistakes to Avoid
If you see your doctor for symptoms, your doctor can perform a random blood sugar test.
This may happen if you’re having obvious symptoms of diabetes, and you have risk factors for insulin resistance and diabetes, like obesity, high cholesterol, or high blood pressure. A random blood sugar test can be completed anytime of the day. Results over 200 mg/dL may confirm diabetes. (7)
Can Insulin Resistance Be Prevented or Reversed?
This metabolic condition doesn’t have to progress to prediabetes or type 2 diabetes. Making lifestyle changes can help reverse insulin resistance so that your body can respond properly to insulin. (4)
Lose weight. One study found that losing weight combined with getting regular exercise could improve insulin sensitivity in obese older individuals. (8) Reduce your fat and calorie intake and get physically active. Do a moderate-intensity exercise, like biking or speed-walking, five days a week at minimum. (9)
RELATED: Reversing Diabetes Is Possible Through Weight Loss, Study Finds
Choose activities that you find enjoyable, such as walking, biking, swimming, or playing sports. Losing as little as 10 to 15 pounds may help reverse and prevent insulin resistance. (7)
Eat a low-carb diet. Reducing your intake of carbohydrates may also improve glucose metabolism and reduce insulin resistance. Other research found that eating three low-carb meals in a 24-hour period could reduce post-meal insulin resistance by more than 30 percent. Study participants limited their carbohydrate intake to no more than 30 percent per meal. (10) Although more research is needed to confirm these results, eating a balanced diet that consists of moderate portions of carbohydrates and sugars may improve how your body uses insulin and reverse insulin resistance.
RELATED: 10 Foods That Can Help With Blood Sugar Control
Change your medication with doctor supervision. You may have insulin resistance if you take steroid medication to treat pain and inflammation. (11) These drugs prompt the liver to release extra glucose, increasing the risk for steroid-induced diabetes. Lowering your dosage or slowly weaning yourself off steroids may improve insulin sensitivity. Speak with your doctor before modifying your medication.
Quit smoking. Giving up cigarettes may also reverse insulin resistance. Nicotine can cause your body to produce extra glucose, which makes it harder to control your blood sugar level. (12)
Get plenty of sleep. Aim for seven to nine hours of sleep a night for optimal health. (13) Not getting enough sleep may increase your risk for diabetes or make it harder to control. (14) Speak with your doctor if you’re having trouble sleeping. This may indicate a sleep disorder.
Manage stress well. When you’re under stress, your body produces higher amounts of cortisol, which is a stress hormone. (15) This hormone can make your muscles and cells resistant to insulin, resulting in higher blood sugar. As a result, chronic stress may increase your risk for prediabetes and type 2 diabetes. (16)
How to Change Your Lifestyle and Diet to Prevent, Manage, or Help Reverse Insulin Resistance
Having insulin resistance doesn’t mean that you’ll develop prediabetes or type 2 diabetes, but this can happen if you don’t make changes to your diet and lifestyle habits.
RELATED: What Makes for a Good Type 2 Diabetes Diet?
Consuming carbohydrates in moderation, prioritizing fitness, and giving up bad habits like smoking not only may help you avoid diabetes but also all the health complications related to the disease, including heart disease, stroke, nerve damage, and vision problems. (17)
How do I know if I am Insulin Resistant?
And should I care? Well yes you should care. A lot. You are likely pre-diabetic…
You’d care because being insulin resistance combined with a moderate to high carbohydrate diet makes you “hyperinsulinemic” – you have high insulin all the time. This means you are now metabolically dysregulated meaning your body:
- turns fat burning off
- promotes fat storage
- dials down your physical activity (feel lethargic and lazy)
- disrupts the hunger control mechanisms in the brain
- has all the physiological factors in play (reactive oxygen species, inflammation, IGF-1 etc) which eventually result in the range of metabolic diseases which will kill most of us with a reduced quality of life for a decade before we die – diabetes, cancer, heart disease and dementia.
Understanding how your own body reacts to different types of food, stress, and other environmental factors is absolutely key to long term health, especially weight control.
That’s why we care about insulin resistance and maybe you should too…..read on
Insulin is a protein produced by the pancreas. It helps in the regulation of nutrients and energy around the body. It is best known for helping move glucose (carbs) into cells so it can be used for energy. That’s a pretty crucial function; without insulin you will die. Type 1 diabetes is a failure of the pancreas to produce insulin, so Type 1 diabetics can inject synthetic insulin.
But insulin is way more interesting than just that. It is part of a complex hormonal and neural system that affects all parts of our body. That system controls energy storage and energy use. That system controls:
- Fat burning – elevated insulin turns off fat burning
- Fat storage – elevated insulin promotes nutrients (both carbs and fat) to be stored away in fat cells
- Physical activity – elevated insulin dials down (your brain suppresses your body) energy output
- Hunger – a more complex interaction with insulin, leptin and ghrelin (other hunger hormones), the hypothalamus (hunger centre in the brain), inflammation and other anabolic (growth) promoting agents switch hunger off and on. We are still learning exactly how this might work, but insulin in short spikes might switch off hunger, but when chronically high (longer term) keeps the “I’m still hungry” switch on.
People are said to be insulin resistant when they have trouble getting glucose into their cells. One way to think about it is that the cells become “resistant” to insulin trying to open them up and get glucose in. This can be temporary – for example when we starve ourselves our body wants to divert any glucose away from most cells in the body and have it used by some cells which require more glucose (eg, brain cells, red blood cells). In the meantime the rest of the body runs off fat. The same is true when we eat excessive amounts of carbohydrates. We can become temporarily insulin resistant, helping us pack away that extra energy into fat for a famine in the future.
When the body is properly regulated, the whole metabolic machine works perfectly. We produce insulin when we need to, become insulin resistant to help us when we are starving, and store extra energy when we are in times of plenty. In an evolutionary sense, this is a system designed to work across feast and famine.
Unfortunately the whole system can become “uncoupled” by modern life. Stress, lack of famine and constant feast, too little exercise, poor quality foods and much more all make you insulin resistant. Modern human life promotes insulin resistance. In fact, my colleagues at Otago University have shown that in older New Zealanders, pre-diabetes may affect as much as 50% of the populaiton.
I’d say that this condition called “pre-diabetes” really indicates the start of “end stage” failure of the body. This is because pre-diabetes is the point where people start to be unable to get glucose into their cells, regardless of how much insulin they produce OR their pancreas has started to fail because of having to produce so much insulin for so long (it’s burnt out), then we can be almost certain that the majority of the older and other higher risk groups (Maori and Pacific people in New Zealand) are insulin resistant.
We need to identify insulin resistance way before you start to fail the tests your doctor currently uses. We’ll look at that now.
How can you tell if you are insulin resistant?
The main reason I wrote this post was because I am often asked how you tell if you are insulin resistant. That’s a great question and hard to answer, but very very important to your health. Read on.
The health system has some serious diagnostics which will show you if you are insulin resistant. I’ve listed everything below. You’ll know some of these already .
- High fasting blood sugar
- 110 to 125 mg/dL (6.1 mM to 6.9 mM) – WHO criteria
- 100 to 125 mg/dL (5.6 mM to 6.9 mM) – ADA criteria
- High HbA1C (glycated Haemoglobin) between 5.7 and 6.4 percent.
- Oral glucose tolerance testing: High and prolonged levels of glucose to carbohydrates ingested (usually administered as 75g of pure glucose drink). Diagnosed with a blood sugar level of 140 to 199 mg/dL (7.8 to 11.0 mM) after two hours.
So these are the techniques your doctor will use to screen you to understand whether you have Type 2 diabetes or pre-diabetes. All of these by definition indicate moderate to severe insulin resistance, which has probably been persistent for decades.
But it’s not the end of the story. The problem is that you can pass any one of these tests fine but still have insulin resistance and all the problems described above.
Why? Because current medical testing looks at our inability to get glucose into cells, rather than how much insulin we are producing. Many people can move glucose into their cells at an acceptable rate but need to do so with massive amounts of insulin.
Therein lies the biggest unnoticed problem in modern medicine. We have a large part of the population told they are metabolically healthy when they are not. We send them away, tell them all is good, and it is only when they show “end stage” symptoms that we act.
Do you see a problem?
Bottom line 1: High and prolonged levels of insulin because of carbohydrates ingested, even with normal blood glucose responses, is dangerous to your health.
There is a better way – that is measuring both insulin and glucose response in the oral glucose tolerance test. That way we can see if you have this condition called “hyperinsulinemia” even with good glucose disposal. The trouble is that would cost you nearly $1000 in New Zealand, if you could find someone willing to do it and interpret the results. It’s costly, time consuming (a few hours in a lab) and messy and painful (lots of blood samples).
You could measure fasting insulin – but I’m not convinced that most insulin resistant people show problems here.
But can you observe symptoms yourself without a clinical diagnosis? I think if you have a few of the symptoms below then it is likely you have insulin resistance.
- I’ve had trouble controlling my weight my whole life
- I have a high waist circumference (I’ve got a fat gut) – more than 100 cm men, 85 cm women
- I always feel hungry
- I feel like something sweet after dinner to stop my hunger
- Fatigue, exhaustion, depression
- High blood pressure
- Frequent hypoglycemia (low blood sugars)
- You are over 50 years old
BTW – if you have failed one of the glucose tests then don’t bother with the checklist, you are already insulin resistant.
Bottom line 2: If you have some of these symptoms, the easy “try it yourself” work around is to severely restrict the amount of carbohydrate you eat for a couple of weeks and see how you feel. I’d say if you are insulin resistant, then the carb restriction is the method which can best help you reset your metabolism.
Insulin Resistance Syndrome in the Elderly
IRS is increasingly recognized as a harbinger of classical disease states, including diabetes and metabolic syndrome X. It has been postulated that insulin resistance, diabetes, and metabolic syndrome X are all associated with a proinflammatory state, but it has been difficult to determine whether the proinflammatory state is a cause or effect of these conditions. Furthermore, it is unclear what proinflammatory cytokines are most likely to be elevated early in the course of these conditions, especially in insulin resistance. All these conditions also become increasingly common with aging. Here, we examined functional, chemical, metabolic, and inflammatory status in a relatively healthy and uniform population of elderly women. We excluded any person taking diabetes medications and used strict criteria for euglycemia (i.e., fasting glucose <110 mg/dl).
These residents had significant impairments in their abilities to care for themselves, requiring nursing home placement. They were, however, the healthiest members of the nursing home population, having on average mild to moderate cognitive and functional impairments. Mean insulin levels were 280 pmol/l in the IR group and 58.4 pmol/l in the NIR group. It is significant that the majority of recruited residents did not have IRS, fasting hyperglycemia, or frank diabetes, as it is generally assumed that residents this debilitated would have near-universal insulin resistance (13).
Those with IR did not differ from the NIR group in age, height, weight, smoking history, drinking history, or nutritional risk, as measured by the mini–nutritional assessment tool. Importantly, the two groups did not differ in BMI, although the IR group had a BMI that was ∼6% greater (P = 0.09). The groups did not differ on measures of severe illness as measured by the comorbidity scale of Charlson, a medical record–based inventory of 19 conditions associated with in-patient mortality. Functional status did not differ between the two groups, as measured by four different measures: the functional index measure, the activities of daily living, the 6-m walk, and the 6-min walk. This lack of difference suggests that the muscle wasting, sarcopenia, and frailty associated with insulin resistance (13) is confounded by aging and other associated factors and is more likely a later association with IRS. Levels of depression, as measured by the geriatric depression scale, or dementia, as measured by the mini–mental status examination, were similar between the groups. Balance and risk of falls as measured by the timed get-up-and-go test was also similar. This lack of difference shows that any deleterious effects of insulin resistance had not yet manifested themselves in common indexes of health status.
These groups did not differ in the indicators of general inflammation, including C-reactive protein, prealbumin, albumin, transferrin, or immune cell levels, or in hemoglobin or hematocrit. They also did not differ in cholesterol levels. Hyperlipidemia is a hallmark of metabolic syndrome X, whereas low cholesterol (<160 mg/dl) is used in geriatrics as an index of malnutrition. Overall, therefore, insulin resistance had little impact on immediate general health, giving us the opportunity to examine an early stage of IRS.
Although the study included only those with a fasting blood glucose of <110 mg/dl, glucose was higher (P < 0.05) in the IR (94.2 mg/dl) versus the NIR group (87.9 mg/dl). The IR group fasting glucose was well within normal limits and only 7% higher than in the NIR group. Nevertheless, it is a clear indication that even this early stage of IRS is associated with impairments in glucose handling.
In contrast to the lack of differences in routine laboratories, several hormone levels were elevated in the IR group. As expected, insulin C-peptide was elevated but only by ∼15%. Interestingly, the insulin/C-peptide level was about fivefold higher in the IR group, suggesting that insulin or C-peptide clearance or degradation was affected more than secretion. Any difference in insulin clearance cannot be ascribed to renal failure, as serum creatinine did not differ between the IR and NIR groups. Amylin, cosecreted with insulin in a 1:1 molar ratio from the pancreas, was also elevated over fourfold in the IR population. The ratio of insulin and amylin did not differ between the two groups, suggesting that the two peptides were cleared and secreted in a similar fashion.
Serum insulin levels were highly correlated with serum leptin levels, consistent with insulin resistance being associated with obesity. As expected from numerous other studies, leptin also correlated positively with BMI and inversely with adiponectin. Leptin was increased ∼70% in the IR population (P < 0.01). This was unexpected, given that the average BMI for the IR group was only marginally (6%), and not significantly, higher than in the NIR group. However, BMI is a cruder measure of adiposity than serum leptin, as BMI does not distinguish between lean and adipose tissue. The leptin-to-BMI ratio was also ∼70% higher in the IR group in comparison with the NIR group (P < 0.005). This suggests that either those in the IR group were hypersecreting leptin per unit of fat mass or that a greater percent of their body weight was adipose tissue. The latter seems more likely, considering the recent description of the sarcopenic obese. These residents, despite having a normal or high BMI, have decreased muscle mass, and so a greater proportion of their BMI is adipose tissue. Such residents are at an increased risk for mortality and morbidity. The current findings suggest that insulin resistance could be an early component of sacropenic obesity.
The strong associations of leptin and leptin/BMI with serum insulin and their segregation between the NIR and IR groups suggest a strong association between obesity and insulin resistance. However, BMI only showed a trend toward association with insulin (P = 0.06), whereas the leptin-to-BMI ratio correlated better with serum insulin than did leptin alone. This again suggests that serum levels of leptin are much more sensitive at inventorying the metabolic parameters associated with insulin resistance than is BMI. This is further suggested by the finding that the leptin-to-insulin ratio did not differ between the IR and NIR groups, even though each of these components alone were very different. Thus, leptin and insulin overlap to some degree in their abilities to distinguish the IR and NIR groups but likely retain independent predictive abilities.
In contrast, serum adiponectin levels correlated even more strongly with leptin than did insulin. Adiponectin is secreted from fat and can reverse insulin resistance and hyperglycemia, possibly through its ability to regulate proinflammatory cytokines (14–17). However, adiponectin did not distinguish insulin resistance from non–insulin resistance, being decreased in the IR group by ∼25% (P = 0.08).
Evidence for a proinflammatory state was most clearly revealed by a significant (P < 0.01) elevation in TNF. TNF levels were 50% higher in IR compared with NIR residents. Arithmetic increases that did not reach statistical significance were evident in every other proinflammatory and anti-inflammatory cytokine measured with the exceptions of MIP-1α and RANTES. The lack of statistical significance in the elevations of some of the cytokines may have been caused in part by the large variance within groups. To further assess a global trend of cytokine elevation and to negate variance, we computed two proinflammatory indexes, both of which included TNF that assessed elevations on nonparametric scoring. However, neither of these summations was different between the two populations. This suggests that even with the power of including a statistically significant component (TNF), there is no evidence for a statistically meaningful global cytokine increase. This supports TNF as being the primary cytokine whose elevation is relevant in early insulin resistance.
The role of serum TNF is further supported by a strong correlation with serum insulin levels. This correlation between TNF and insulin was even stronger than that between leptin and insulin. One source of serum TNF could be from adipose tissue. However, serum TNF levels did not correlate with serum leptin levels. In some studies, TNF and leptin levels correlate, presumably because both can be secreted from fat. However, TNF has sources in addition to adipose tissue, whereas adipose tissue is essentially the sole source of serum leptin. Therefore, the lack of correlation between leptin and TNF suggests that the source of elevated TNF was not adipose tissue. Further supporting this were the findings that the TNF-to-BMI ratio did not distinguish between IR and NIR groups the way leptin-to-BMI ratio did, and the TNF-to-insulin ratio, unlike the leptin-to-insulin ratio, still distinguished the IR and NIR groups. Therefore, TNF and leptin behaved very differently, making it unlikely that adipose tissue was the source of the elevation in TNF. TNF did show a statistical trend with C-reactive protein (P = 0.07), suggesting that it might have arisen from a generalized proinflammatory condition.
In conclusion, we examined early insulin resistance in a population of elderly women living in a long-term care facility before debility ascribable to insulin resistance had arisen. Although no functional impairments were found between the IR and NIR groups, we found that other parameters were already changing. Despite exclusion of any person with a serum fasting glucose ≥110, a slight, statistically significant increase in serum glucose of 7% demonstrated an early glucose intolerance in the IR group. Differences in C-peptide and the insulin–to–C-peptide ratio suggested an increased insulin secretion and a decreased insulin clearance in the IR group. Increased leptin and leptin-to-BMI ratios in the absence of differences in BMI suggest that the IR group had a higher percent of body fat mass and that IR could be related to sarcopenia of obesity. TNF was the one proinflammatory cytokine statistically elevated in the IR group. The lack of correlation of TNF with BMI or leptin suggests that the TNF did not originate from fat. Thus, early insulin resistance is associated with elevations of leptin, even after correction of BMI and a proinflammatory state, as evidenced by elevated levels of serum TNF.
If you have insulin resistance, following a healthy lifestyle can reduce your chances of developing Type II diabetes. Studies have shown that combining:
- Healthy eating
- Weight loss
- Regular physical activity
can all help reduce your risk of Type II diabetes in the years to come. These lifestyle changes were shown to be at least as effective as a common medication used to treat insulin resistance.
Smart eating tips for improving insulin resistance
- If you are overweight, losing some weight will improve insulin resistance. Eating smaller portion sizes, being more physically active and eating less energy dense foods (‘extra’ foods) can assist with weight reduction.
- Physical activity is not only beneficial for weight management but can also independently assist with improving insulin resistance. Include 30 minutes of physical activity on most days of the week.
- Resistance training (e.g. hand weights) can also help with insulin resistance. Also try to increase your incidental activity. Examples of incidental activity include gardening, housework and walking around the shops.
Healthy eating tips
- Eat at least five serves of vegetables and two pieces of fruit each day.
- Eat wholegrain foods everyday such as high fibre breakfast cereals, multigrain bread, oats, barley and cracked wheat.
- Enjoy legumes (dried peas, beans and lentils) on a regular basis.
- Include low glycaemic index (GI) foods. Low GI foods can help by slowing the rate of absorption of glucose into the blood stream, so not as much insulin is required.
- Reduce the amount of saturated fat in your diet. Limit commercial cakes and biscuits, fried take-away foods, butter, lard, cream and trim the visible fat off meat.
An Accredited Practising Dietitian (APD) can help you plan and implement these lifestyle changes.
Insulin Resistance: Dealing With the Diagnosis
When my daughter was a pre-teen, her routine blood glucose test came back a little high. Her pediatrician had her undergo a special test called a fasting blood glucose test, which was followed by a series of other tests. The results prompted her doctor to come back with a chilling diagnosis: insulin resistance.
As a pediatric nurse, I was familiar with the topic of diabetes and insulin resistance, but this was a frightening diagnosis. My daughter was very upset, thinking she now had a terrible disease. And both my husband and daughter turned to me for ways to deal with this new diagnosis.
What is insulin resistance?
It’s a condition in which the hormone, insulin, becomes less effective at managing sugar levels in the blood glucose after eating or drinking anything that contains a simple sugar.
Insulin is produced by the pancreas and acts to open the doors of the cells, taking glucose out of the bloodstream and putting it into the cells for energy. When cells don’t respond enough to insulin, blood glucose levels rise as a result.
How serious is insulin resistance?
The presence of insulin resistance typically precedes the diagnosis of type 2 diabetes, previously known as adult onset diabetes. When an individual has diabetes, his or her pancreas does not make enough insulin to keep blood sugars level. This is a chronic disease which can result in a number of side effects and disabilities.
How do I know if my child has insulin resistance?
The signs and symptoms can vary with each person, but some are very noticeable. In my nursing career, I have taken care of children who seem to have a dark ring around their necks that looks like oily dirt. This is not dirt and can’t be washed away. It also can occur under the arms or in the groin area. This ring is called acanthosis nigricans and is a sign of insulin resistance.
Other signs of insulin resistance include:
- Brain fogginess or inability to focus,
- High blood sugar,
- Higher blood pressure,
- Increased hunger,
- Intestinal bloating,
- Sleepiness, especially after meals.
If your child is exhibiting these symptoms, make an appointment with their pediatrician and be sure to let his or her doctor know exactly what signs your child has been displaying.
At Children’s Hospital Los Angeles, the Division of Endocrinology and Metabolism provides clinical care and research focused on childhood diabetes, growth, weight management, endocrinology and bone metabolism. For more information, visit their webpage.
Diet and Exercise to Avoid Diabetes
As we researched more on the subject of insulin resistance, what became clear to my family was that this condition was something we could treat and correct, and if we did so early enough, it didn’t have to mean “diabetes” for my child. There are some medications available, but what else could we do? The answer was, two things:
- Healthy eating
Everything we read indicated that insulin resistance and diabetes have a relation to nutrition. I knew that from nursing school and also had some tools to work with because I have a long on-and-off relationship with Weight Watchers!
The Family Plan
So, as a family, we came up with a plan to make meaningful changes in our lifestyle, but none so drastic or difficult to maintain that we couldn’t stick to them.
- My daughter remembers some of the basics:
- No more fast food,
- No excessively sugary drinks (including juice),
- Lots of fruits and vegetables,
- Reading food labels,
- My Food Pyramid Website (Website is interactive for adults and children)
And, sadly, we also had to stop Dad from making his wonderful buttery and cheesy sauces, except as a rare treat!
- Fresh, colorful vegetables and fruits,
- Whole grains,
- Healthy fats, not trans fats,
- Avoid heavily processed foods, high fructose corn syrup and excessively-sugared beverages.
Many weight-loss programs are low in carbohydrates (carbs), but some are needed in the diet so as not to starve the cells of energy, which can otherwise upset the body’s blood sugar balance. The carbs that do this well come from whole grains, fruits and vegetables. It’s best to avoid refined sugars (or carbohydrates) and grains.
My daughter’s doctor prescribed Vitamin D for her, as this is often deficient in those with insulin resistance. However, your child’s doctor may or may not prescribe something different, depending on your child’s needs.
What Works at Our House
To be a better role model for my daughter, I went back to Weight Watchers and my daughter came with me for a few months. We joined a gym and made a promise to the dog to walk her more often. We stopped going to fast food places, except as a rare treat. And we gave up sodas.
Thankfully, I had given my daughter broccoli as a baby, so she already had one vegetable she liked. From there, we explored and tasted to integrate more vegetables and fruits into our diet. We steamed them or ate them raw to avoid adding any additional oil when possible. I tried out “lighter” recipes from books and magazines to introduce variety and make these changes into a lifestyle and not a diet.
My daughter discovered that she loved to eat couscous, a whole grain, with vegetables. There are healthier choices for snacks in every grocery store these days, but we read the labels to find the best ones.
Insulin Resistance Success Story
My daughter’s blood sugar levels are now normal and she no longer has insulin resistance. Knowing that once you are insulin resistant, you continue to be at risk for insulin resistance and hyperglycemia, however, it can be controlled with diet and exercise. Because she made some simple life changes and stuck with them, she was able to successfully lower her risk of developing diabetes later in life.
Insulin resistance is the name given to when cells of the body don’t respond properly to the hormone insulin.
Insulin resistance is the driving factor that leads to type 2 diabetes, gestational diabetes and prediabetes
Insulin resistance is closely associated with obesity; however, it is possible to be insulin resistant without being overweight or obese.
Modern research has shown that insulin resistance can be combatted by treatment methods that reduce how much insulin the body is producing or taking via insulin injections or insulin pumps.
Reducing insulin resistance can be achieved by following low-carbohydrate and ketogenic diets.
What is insulin resistance?
The role of insulin is to allow cells of the body to take in glucose to be used as fuel or stored as body fat.
It also means that glucose is more likely to build up in the blood and this can lead to too high blood sugar levels
When the body becomes resistant to insulin, it tries to cope by producing more insulin. People with insulin resistance are often producing too more insulin than healthy people.
Producing too much insulin is known as hyperinsulinemia
Symptoms of insulin resistance
Initially, insulin resistance presents no symptoms. The symptoms only start to appear once it leads to secondary effects such as higher blood sugar levels. When this happens, the symptoms may include:
- Lethargy (tiredness)
- Difficulty concentrating (brain fog)
Other signs that often appear in people with insulin resistance include:
- Weight gain around the middle (belly fat)
- High blood pressure
- High cholesterol levels
If insulin resistance develops into prediabetes or type 2 diabetes, the symptoms will include increased blood glucose levels and more of the classic symptoms of type 2 diabetes
Causes of insulin resistance
Whilst the exact cause of insulin resistance is still not fully understood, it is well-known which factors can lead to insulin resistance developing.
Insulin resistance can commonly develop if one or more of the following factors apply:
- If you are overweight or obese
- Having a high-calorie diet, high-carbohydrate or high-sugar diet
- Sedentary lifestyle – taking little physical activity
- Taking high doses of steroids over an extended period of time
- Having chronic stress
- Having Cushing’s disease or polycystic ovary disease
In terms of what is happening inside the body that causes insulin resistance, researchers have observed that insulin resistance occurs in people that have:
- High levels of insulin circulating in their blood
- Excessive fat stored in the liver and pancreas
- High levels of inflammation
Insulin resistance is a state where the body does not respond to insulin as well as it should. It’s almost like a lack of communication between insulin and the cells of the body. Insulin resistance is a key feature of type 2 diabetes.
Insulin resistance is a problem because it affects the body in a number of ways.
Resistance to insulin causes the body to produce more insulin which leads to increased hunger higher blood pressure and weight gain.
It is still not fully understood what causes insulin resistance. There does seems to be a strong link between weight gain and insulin resistance.
Studies have shown that significantly reducing calorific intake can improve the body’s sensitivity to insulin.
Download a FREE blood glucose chart for your phone, desktop or as a printout.
Can insulin resistance be reduced or reversed?
It is certainly possible to reduce the effects of insulin resistance and there are a number of effective ways to do this.
Effective methods include:
- Low-carbohydrate and ketogenic diets
- Very-low-calorie diets
- Weight loss surgery
- Taking a lot of exercise in combination with a healthy diet
These methods share a similar way of working in that they all help to reduce the body’s need for insulin and help people to lose weight.
Read more on reversing the effects of diabetes
What Is Insulin Resistance?
Insulin resistance and PCOS. You may have been diagnosed with the latter, but are not sure whether you also have the former. An insulin resistance test should be one of the first that your doctor does after diagnosing PCOS. Unfortunately, that’s not always the case…
In this article I’ll outline some classic signs and symptoms to help inform you of whether you should be pushing for further testing. Of course, you’re smart women, you know this is not a diagnosis. I’m not a doctor, I’m a degree-qualified nutritionist. Even if I was a doctor, I could not diagnose you via a blog. You need to get a blood test done to know for sure. So, book one as soon as you can.
Insulin is our storage hormone. When we eat, our body detects a rise in blood sugar (glucose). Our body doesn’t like blood sugar to be high. This is because cells can be damaged if it’s high for prolonged periods of time. These cells include those in the brain, liver, pancreas, heart, and eyes. Therefore, in response to high blood sugar, the body stores excess glucose in muscle and liver cells for later use.
Insulin is the hormone that allows this to happen. It tells the cells to open up and let the glucose in. Insulin is excreted by the pancreas. It binds to a receptor on the cell and tells it to open up. This process is similar to the way a key opens a door. Insulin resistance occurs when insulin no longer works effectively due to chronic low grade inflammation. The key has been used too much, the lock gets worn and the key no longer fits.
As a result, the blood glucose level stays high. The brain believes that more insulin is required. It sends a message to the pancreas to get it to make even more. However, the ‘lock’ is still worn so the extra insulin doesn’t help. If this process continues over a long period of time, the pancreas becomes so fatigued that it’s unable to produce enough insulin. This is called Type 2 diabetes.
How Are Insulin Resistance and PCOS Connected?
70% of women with PCOS have insulin resistance. Studies have shown that improving insulin resistance can reduce:
– Testosterone levels
– Body weight
Metformin is a drug that you may already know about. It’s often prescribed to help with fertility – you may have even been prescribed it yourself! Metformin is a drug that improves insulin sensitivity. However, it’s not thing that improves insulin sensitivity. In fact, it’s not even effective for many women.
Studies have shown that a very low carbohydrate (ketogenic) diet can be very successful alternative. It can improve insulin resistance, help weight control, and reduce testosterone levels. Reducing testosterone levels is especially important if ovulation is to happen.
How Do I Know If I Have Insulin Resistance?
The stats say that insulin resistance and PCOS often go hand in hand. A blood test can tell you whether you have insulin resistance. This should measure fasting blood glucose, fasting insulin, and HbA1c (long-term blood glucose performance).
It’s important that you don’t just accept them telling you that your levels are normal. Make sure that you ask for the actual results. The ‘normal’ range for fasting blood glucose is 3.61-5.50 mmol/L. Your level could be deemed ‘normal’ even when it’s 5.49mmol/L. Get the actual figure and then make an informed decision about how normal it actually is.
Here are some more indicators that you should get your levels checked:
1. You Have Severe Hangry Attacks
I know you know what I’m talking about! One minute you’re not even hungry, and the next you must eat everything in sight. No food? No problem! The closest boyfriend’s, friend’s, or colleague’s head will suffice. If no food’s available, then you might even start to feel shaky, jittery, and faint. You’re experiencing severe blood sugar crashes. These show that your blood glucose isn’t stable and is not doing what it should be.
2. You Store Weight Around Your Belly
This is true even if you’re not overweight, or ‘Lean PCOS.’ If you put on weight, where does it go? If the answer is your stomach, then that’s a really good sign that you’ve got some insulin resistance going on. Studies that have looked at both overweight and normal weight women have shown that weight gain around the stomach is a significant sign you have insulin resistance.
3. No Matter How Many Spin Classes, Miles Run, and Salads Ate, You Can’t Lose Weight
Feel like you’re doing everything ‘right’ and still not losing weight? Insulin resistance might be playing a factor in this.
Studies have shown that insulin resistance impacts the ability to burn fat. In fact, one study showed that the muscles of people with insulin resistance are geared towards fat storage, not fat burning. No wonder it’s hard to lose weight!
4. You’ve Developed Dark Velvety Patches in the Folds of Your Skin
These could be under your arms or on the back of your neck. The proper name for them is acanthosis nigricans. It’s caused when insulin-like growth factor (increased by insulin resistance) stimulates the cells in the skin to produce more keratin and dermal fibroblasts.
Studies have shown that insulin resistance is not the only reason that these patches develop. However, they are still a potential indicator of it.
5. You’ve Got Skin Tags
Skin tags are little bits of skin that hang off. I know what you’re thinking, “Oh is that what they’re called?” Yes, I admit, until recently I didn’t know either. Studies have shown that multiple skin tags are a really good indicator of insulin resistance, so if you have them then go and get them checked out.
Summary of Insulin Resistance and PCOS
Insulin resistance and PCOS often go hand in hand.
Insulin resistance causes excess androgens, which causes a lot of the horrible PCOS symptoms.
Longer term, insulin resistance can develop into Type 2 diabetes and put us at risk for all manner of nasty metabolic diseases. But it is reversible, so you need to address it now.
It needs to be diagnosed by blood tests from your doctor, but some signs that you may be insulin resistant include:
– Blood sugar crashes (aka hangry attacks)
– Putting on weight around your belly
– Struggling to lose weight
– Dark velvety patches on your skin
– Skin tags
by Dr. Will Cole
A staggering 50 percent of us are now either prediabetic or have full-blown type 2 diabetes. No, that is not a typo; one out of two of us have some serious blood sugar problems, making a condition that was once a rarity completely commonplace.
Much of the blood sugar problems we see today are due to one thing: insulin resistance. Insulin is a hormone that directs blood sugar into cells to create energy in the form of ATP, but when you become resistant to its effects, your cell receptor sites are blunted and you’re left with a backup of insulin and blood sugar, which is no bueno. If this condition goes on for too long without intervention, you could get diabetes, which is one of the leading causes of heart attacks and strokes!
Know the signs of blood sugar imbalance
If more than one of these is true for you, I suggest getting your blood sugar levels checked stat.
- You crave sweets or breads and pastries….a lot!
- Eating sweets doesn’t relieve your sugar cravings and even increases them.
- You become irritable and “hangry” if you miss a meal.
- You find yourself needing caffeine to get through the day.
- You become lightheaded if you miss a meal.
- Eating makes you exhausted and in need of a nap.
- It’s difficult for you to lose weight.
- You feel weak, shaky, or jittery pretty frequently.
- You have to pee a lot.
- You get agitated, easily upset, or nervous, out of proportion to the reason for these feelings.
- Your memory is not what it used to be.
- Your vision is blurry.
- Your waist measurement is equal to or larger than your hip measurements.
- You have an atypically low sex drive.
- You’re always thirsty.
Natural ways to improve blood sugar balance
You don’t have to settle for a future of diabetes. Intervene now with these tips for restoring a healthy blood sugar/insulin balance.
1. Find your baseline.
The labs I run on my patients to assess their blood sugar balance and check for insulin resistance are:
2. Sip on matcha.
EGCG is a compound in green tea, EGCG has demonstrated a stabilizing effect on blood sugar levels. Drinking the whole green tea leaf in the form of matcha powder is a great way to up your ECGC intake.
3. Try alpha-lipoic acid.
In several studies, alpha-lipoic acid supplements helped balance blood sugar levels and improved insulin resistance. This antioxidant also strengthens immunity, improves energy production in cells, protects brain cells against excitotoxicity, and helps the body remove excess toxic metals. For blood sugar control, take 200 milligrams three times a day.
4. Take magnesium.
According to research published in the medical journal Circulation, in a group of nearly 5,000 people, those who took higher levels of magnesium over a period of 15 years had a decreased risk of metabolic syndrome, a condition that is often a precursor to diabetes. A similar study, published in the American Journal of Epidemiology, followed more than 1,000 healthy adults for five years and found that greater magnesium intake improved insulin sensitivity. Other studies have shown that magnesium improves triglycerides and high blood pressure – two other hallmarks of metabolic syndrome and diabetes.
5. Add chromium.
When chromium levels are low, good cholesterol tends to drop and the risk of insulin resistance, as well as triglyceride levels, go up. Chromium supplementation has been shown to improve blood sugar receptor function. The best food sources of chromium include onions, tomatoes, potatoes, and sea vegetables.
6. Increase Nrf-2.
The protein Nrf-2 plays a role in regulating antioxidant gene induction by turning on genes that are responsible for antioxidant and detox pathways. When Nrf-2 is activated, inflammation tends to subside. There are many antioxidant rich foods that tend to activate Nrf-2, including:
- EGCG from green tea
- Quercetin from apples
- Curcumin from turmeric
- Resveratrol from grapes
- Rosmarinic acid from rosemary
- L-sulforaphane from broccoli
- Thiosulfonateallicin from garlic
7. Bring in vitamin E.
This fat-soluble tocopherol has been shown to support insulin sensitivity. Standard doses range between 600 and 900 milligrams.
8. Sprinkle cinnamon.
Proanthocyanidin, a bioflavonoid found in cinnamon, may alter the insulin-signaling activity in fat cells, making it a potential diabetes buster. The spice has also been shown to significantly reduce blood sugar levels and triglycerides in people with type 2 diabetes.
9. Seal and heal the gut.
Your gut health and blood sugar balance are inextricably connected – one study found that transplanting the microbiome of diabetic mice into healthy mice made the recipients diabetic! Among the culprits are advanced glycation end products (AGE) – harmful compounds that have the potential to cause leaky gut. A high sugar diet can also tip your microbiome in the wrong direction, causing candida overgrowth, which is also linked to blood sugar problems. What’s good for your gut is good for your blood sugar, and vice versa.
10. Get more sun.
Most people have low vitamin D levels, which can cause a host of problems, but in one study, supplementing with vitamin D for 12 weeks decreased body fat by 7 percent, and lower weight correlates with better blood sugar control. Low D levels have also been linked to metabolic syndrome. Aim for 60 to 80 ng/mL per day.
11. Eat more healthy fats.
One study found that higher blood sugar in non-diabetics decreased function in areas of the brain affected by Alzheimer’s disease (AD). This is one reason why Alzheimer’s is often referred to in the medical literature as “type 3 diabetes.” On the other hand, a ketogenic diet – where fat, not sugar, is your primary source of energy – has been shown to do some remarkable things for your brain health.
Healthy fats provide a slow, sustainable form of energy, subverting the more drastic ups and downs that can happen with sugar burning. Humans were meant to rely more on fat and less on sugar – for example, babies primarily use the fat in breast milk for brain development and energy. From a biological and evolutionary perspective, the most sustainable form of energy for optimal brain health as well as blood sugar control is healthy natural fat.
12. Take B-vitamins for the win.
Methylation is a complex process that supports many crucial function in the body, including healthy blood sugar balance. Activated B vitamins – like B9 L-Methylfolate (L-5-MTHF) and B6 Pyridoxyl-5-Phosphate (P5P) – are a great way to support methylation pathways. Food medicines to focus on are spinach, okra, and turnip greens, and meats like chicken liver or grass-fed beef liver, which have the highest levels of bioavailable B vitamins.
13. Activate your PPARs.
Studies suggest that PPARs, or peroxisome proliferator-activated receptors, may help improve inflammatory conditions such as atherosclerosis, asthma, colitis, MS, and other autoimmune conditions. Some PPAR activators for you to bring into your life: wild-caught fish, green tea, astragalus, ginger, and sea buckthorn.
14. Get your omega-3s on.
You’ve probably heard that omega-3 fatty acids can lower the risk of stroke and heart attacks, but these healthy fats most prevalent in fish oil also convert the potentially harmful very low-density lipoproteins (VLDL), which are linked to diabetes, into less dangerous low-density lipoproteins (LDL).
15. Never forget adaptogens!
Adaptogens are awesome at balancing out hormones and inflammation. A study found the adaptogen American ginseng berry juice could significantly improve glucose tolerance and normal bloods sugar levels after just 10 days.
If you want to learn more about your own health case please check out our free health evaluation. We offer in person as well as phone and webcam consultations for people across the country and around the world.
The information on this website has not been evaluated by the Food & Drug Administration or any other medical body. We do not aim to diagnose, treat, cure or prevent any illness or disease. Information is shared for educational purposes only. You must consult your doctor before acting on any content on this website, especially if you are pregnant, nursing, taking medication, or have a medical condition.
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Your body naturally produces the hormone, insulin, to help keep your blood sugar at healthy levels, but sometimes your body doesn’t respond to insulin the way it should. When this happens, it’s called insulin resistance. Here, we’ll discuss what insulin resistance is, how it can cause complications like type 2 diabetes, and what you can do to prevent it.
What does insulin do in the body?
Insulin is a hormone that helps regulate your blood sugar and is made by an organ known as the pancreas that sits behind your stomach. Your pancreas sends insulin into your bloodstream after you eat or if it detects that your blood sugar levels are high.
Once insulin enters your blood, it has 2 major jobs:
1) Insulin takes sugar out of your blood and sends it into your cells to be used for energy.
When you eat a meal with carbohydrates (also called carbs or sugars), you often get a burst of energy. Well, your cells get energy from sugar too, but how does the sugar get into the cells? That’s where insulin comes in.
Most of the cells in your body contain insulin receptors. Think of an insulin receptor like a lock and the insulin hormone like a key. When the key opens the lock—or when insulin binds to the insulin receptor—the cell opens to let sugar in. By attaching to insulin receptors, insulin helps take sugar out of the blood and sends it into cells to be put to good use. As a result, your blood sugar levels should return to normal.
2) Insulin takes sugar out of your blood and stores it in muscles, fat cells, and the liver for later use.
Even though it’s helpful for your cells to take in blood sugar for energy, they don’t need immediate access to that sugar all the time. In fact, insulin will take any extra blood sugar that your cells can’t use right away and send it to your muscle cells, fat cells, and liver to be stored for later use. When it’s stored, the original form of sugar, glucose, becomes another form of sugar known as glycogen.
What does it mean to be insulin resistant?
Both of insulin’s primary jobs require your cells—specifically, the insulin receptors on your cells—to respond to insulin. But for several reasons, your cells may stop responding to insulin as well as they should. In other words, instead of being sensitive to the effects of insulin, they become resistant to the effects of insulin—hence, the name insulin resistance. When cells become insulin resistant, sugar stays in your bloodstream, which can lead to high blood sugar.
What causes insulin resistance?
There are numerous potential causes of insulin resistance. Some of the most common causes include:
- Polycystic ovary syndrome (PCOS). PCOS is a condition that affects a woman’s reproductive health but also causes high levels of insulin, which can lead to insulin resistance over time.
- High doses of steroids taken for longer than a few weeks. When taken for extended periods of time, steroids can cause continuously high blood sugar, which can lead to insulin resistance.
- Chronic stress. Persistent stress can have the same effects as high doses of steroids, since stress causes your body to release its own stress steroids like cortisol.
- Being overweight or obese. Although scientists don’t know exactly how, being overweight or obese contributes to poor insulin sensitivity.
- Sedentary lifestyle. Living an inactive lifestyle can lead to insulin sensitivity, but the opposite—living an active lifestyle—can actually improve insulin sensitivity.
- Poor diet (high-carbohydrate or high-sugar diet). Any diet that is high in carbs or sugars will increase blood sugar levels, which can lead to insulin resistance over time.
There are also some unchangeable factors that can increase your risk of developing insulin resistance—for example, having a family history of insulin resistance or diabetes or belonging to Black, Asian, and/or Hispanic ethnic groups.
What are the symptoms of insulin resistance?
At first, your pancreas tries to fight the effects of insulin resistance by releasing more insulin. Even though your cells are not responding to insulin as well as they should, the fact that there is more insulin in your bloodstream helps keep your blood sugar levels normal. Therefore, you may not have any noticeable symptoms of insulin resistance initially.
Over time, as insulin resistance gets worse, even more insulin won’t be able to make up for your cells’ weak response to insulin. At this point, high blood sugar levels often become the first key sign of insulin resistance. As high blood sugar persists, you may begin to notice symptoms like excessive thirst, frequent urination, and headaches.
What are the complications of insulin resistance?
High blood sugar levels can contribute to several complications associated with insulin resistance. One of the most severe complications is a condition called metabolic syndrome, also known as insulin resistance syndrome. This chronic condition involves a combination of:
- high cholesterol
- high blood pressure
- high blood sugar (which can lead to prediabetes and type 2 diabetes)
- excess body fat around the waist
Insulin resistance can also lead to each of the symptoms of metabolic syndrome individually.
Metabolic syndrome, prediabetes, and type 2 diabetes are the most common complications of insulin resistance. Prediabetes and type 2 diabetes result from high blood sugar levels that may have to be controlled with medications if changing your diet and exercising aren’t enough. These complications are especially serious because they increase your risk of heart disease, heart attacks, and strokes.
Is there an insulin resistance test?
Unfortunately, there is no insulin resistance test that is commonly used in medicine. Your doctor can use a blood glucose test or hemoglobin A1C test to evaluate your blood sugar levels. But remember that in the early stages of insulin resistance, your blood sugar levels may still appear normal, so a blood glucose or A1C test is not always a reliable test of insulin resistance.
Can you reverse insulin resistance?
On the bright side, there are ways you can help improve insulin sensitivity and reverse insulin resistance:
- Engage in at least 30 minutes of physical activity most days of the week. Exercise is one of the fastest and most effective ways to reverse insulin resistance.
- Lose weight, especially around the middle. Losing weight around the abdomen not only improves insulin sensitivity but also lowers your risk of heart disease.
- Adopt a high-protein, low-sugar diet. Protein helps keep your body’s blood sugar levels stable, whereas high-sugar diets can cause spikes in blood sugar that only make insulin resistance worse. Even though being insulin resistant doesn’t necessarily mean you have diabetes, following a meal plan recommended by the American Diabetes Association can help improve insulin sensitivity.
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