Insulin Resistance: Prevention, Nutrition And Treatment

Marko Balašević Author: Marko Balašević Time for reading: ~19 minutes Last Updated: August 09, 2022
Insulin Resistance: Prevention, Nutrition And Treatment

Insulin is a protein hormone secreted by the beta cells of the pancreas. This is a kind of policeman who strictly monitors the level of glucose in the blood and, when it rises, includes various mechanisms and ways to return to the starting point.

In the article we will tell:

  1. What is insulin and insulin resistance
  2. Causes of insulin resistance
  3. Symptoms of Insulin Resistance
  4. Types of insulin resistance
  5. Diagnosis of insulin resistance
  6. Complications and consequences of insulin resistance
  7. Nutrition for insulin resistance
  8. Treatment of insulin resistance
  9. Intermittent fasting for insulin resistance
  10. Prevention of insulin resistance

What is insulin and insulin resistance

Insulin is a protein hormone secreted by the beta cells of the pancreas. This is a kind of policeman who strictly monitors the level of glucose in the blood and, when it rises, includes various mechanisms and ways to return to the starting point - that is, to physiological values ​​that are optimal for the functioning of organs.

Insulin, contrary to popular misunderstanding, does not transport glucose on itself - it, in principle, does not tolerate anything or anyone. Its mechanism of action is somewhat different: for example, in adipose tissue and muscles, it promotes the movement of a specific GLUT 4 transporter from the cytoplasm (that is, the internal environment, cell suspension in which organelles and the nucleus “float”) into the membrane.

So, the task of this hormone is to drive naughty glucose into the cell. However, it is not limited to this only, given how freely and easily this monosaccharide can return back to the blood - that is why it uses various ways of its utilization (in particular, glycogen synthesis).

However, the cells themselves can form a substrate so beloved and relatively easily metabolized by them - due to gluconeogenesis. This is a biochemical process that consists in the synthesis of glucose from various non-carbohydrate components, which can be keto acids and even amino acids. This somewhat increases the range of functions of insulin - after all, now, having reduced the concentration of glucose in the blood, it is necessary to prevent its re-increase - not because of food intake, but because of its intracellular production.

Thus, this hormone inhibits lipolysis (the process of breaking down fat) and catabolism (breakdown) of proteins, stimulating, on the contrary, the uptake of amino acids by cells, as well as the formation of proteins and lipids.

At the heart of all actions of insulin, as, indeed, of most biologically active substances, is the interaction between it and cell receptors, which mediates a number of signal reactions. You cannot come to someone else's house without an invitation - and he cannot arbitrarily send glucose into the cell.

In general, the processes proceed measuredly and evenly - at least as long as the receptors respond to insulin. However, the more often and longer it circulates in the blood, the less susceptible they become - our cells are capricious, they simply get bored with this hormone with its same type of interaction pattern, memorized by memory. There is such a pathological condition as INSULIN RESISTANCE - when the pancreas performs its work on the production of hormones responsibly and carefully, but the receptors simply become resistant. Now glucose cannot enter the cell.

Causes of insulin resistance:

  1. Frequent, fractional meals - for each intake of food (or rather, for proteins and carbohydrates), insulin is secreted by the cells of the pancreas. And it does not matter whether it will be a candy, an apple or a full breakfast - the answer will be the same: in the form of the secretion of this hormone.

  2. Insufficient physical activity - moderate exercise increases the sensitivity of insulin receptors (and even, according to some reports, promotes the synthesis of new ones!).

  3. Excess consumption of fast carbohydrates - yes, and simple sugars such as glucose with fructose, and polysaccharides (glycogen, starch, etc.) cause insulin secretion. The only difference is that complex carbohydrates increase blood sugar levels slowly - and its subsequent decline will be just as smooth.

  4. Polymorphisms in genes. Of course, genetics does not always take a leading place in the list of causes of diseases, but its role, nevertheless, cannot be disputed. To date, several genes are known, violations in which ("breakdowns" in other words) can lead to obesity and diabetes - of course, under favorable conditions for this (such as the lack of a rational, properly selected diet, triggers in the form of stress and chronic diseases, sedentary Lifestyle).

    • The FTO (fat mass and obesity associated) gene affects metabolic processes in general by expressing a specific protein compound in the brain structures responsible for energy exchange.

      Research: Study of metabolic features in individuals with the RS9939609 polymorphism of the FTO gene

      In numerous studies, the polymorphism of this gene has been associated with overweight, an increase in the circumference of the hips and waist, as well as the total amount of fat mass.

    • The KCNQ1 gene encodes an organic compound that is also expressed in the cells of the islets of Langerhans of the pancreas and thus participates in the control of insulin secretion. Its polymorphism is associated with an increased risk of developing type 2 diabetes mellitus.

    • TCF7L2 gene - indirectly regulates the expression of glucagon-like peptide 1 (with insulin-like action) in intestinal cells; it is also noted in the cells of the heart, the nervous tissue of the brain, the heart and in the pancreas.

      Research: Study of associations of new genetic markers of type 2 diabetes mellitus in the West Siberian Caucasian population

    • IRS-1 and IRS-2 genes - mutations in them lead to the development of insulin resistance and hypofunction of pancreatic beta cells.

  5. Lack of sleep and lack of normal sleep hygiene. Hunger and satiety hormones (leptin and ghrelin), growth hormone (growth hormone, known for its fat-burning effect), TSH (thyroid-stimulating hormone), cortisol and melatonin are largely associated with sleep-wake cycles.

    Various sources cite, on average, such disappointing statistics: 35% or more of the adult population of the world sleeps less than 7 hours a day, and over the past decades, the total duration of sleep has decreased, in general, by 1.5-2 hours.

    Interestingly, limiting sleep to 5.5 hours for 2 weeks was associated with a decrease in TSH and free thyroxine levels - and thyroid hormones are known to play a central role in metabolism.

    Disturbances in the sleep-wake cycle are also accompanied by a decrease in the production of leptin by adipose tissue, which affects the saturation centers in the hypothalamus (one of the leading structures of the brain) and thereby suppresses appetite - all because at night its level increases by 30%. There are statistics that indicate that people who work in shifts are more at risk of obesity, cardiovascular disease and type 2 diabetes.

    Study: Obesity and sleep

  6. Chronic stress - the hormones of the cortex and the adrenal medulla, released under the action of adverse, dangerous factors, stimulate an increase in blood glucose levels: after all, you need strength, energy to run away or fight. So, for example, cortisol is responsible for the formation of key enzymes of gluconeogenesis, already mentioned earlier; it also reduces the sensitivity of insulin receptors.

 

Insulin resistance can also be caused by:

  • abnormal structure of insulin;

  • violation of the number or decrease in the sensitivity of receptors;

  • violation of intracellular signal transmission;

  • failure in the mechanisms of glucose transport.

Symptoms of Insulin Resistance

  1. The constant feeling of hunger and the desire to have a snack - on the one hand, this is mediated by the loss of sensitivity to glucose receptors - it simply CANNOT enter the cells and remains in the blood. On the other hand, insulin resistance, as a rule, accompanies LEPTIN RESISTANCE - in essence, their mechanisms are similar to each other.

    Leptin is a protein hormone encoded by the ob gene that regulates eating behavior. Violation of its functions is associated with polymorphisms of this gene, as well as failures in its transport to the nervous tissue of the brain (that is, crossing the control border - the blood-brain barrier), loss of sensitivity of leptin receptors or malfunctions in conducting intracellular signals from them.

    However, it must be answered that mutations in the ob gene are extremely rare, as are changes in the structures of genes encoding leptin receptors.

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    A much more significant factor is the violation of the transport of this hormone through the blood-brain barrier (the barrier between the blood circulating through the vessels and the nervous tissue of the brain, giving the latter a certain selectivity in terms of nutrient permeability) - and this occurs with an increased content (more than 25-30 ng / ml) leptin in blood serum - at such high concentrations, the level of leptin in the cerebrospinal fluid, as well as directly in the brain tissue, ceases to increase.

    In addition, it is noted that the constant circulation of leptin leads to a decrease in the number of receptors for it - in particular, in the hypothalamus. This is called “leptin-induced leptin resistance”.

    Study: Leptin resistance, unresolved diagnostic issues

  2. Acantosis nigricans or darkening of the skin in places of friction and folds (in the area of ​​\u200b\u200bthe armpits and groin, on the bends of the elbow joints; “dirty neck effect”).

     

  3. Acne, oily skin, male-pattern hair growth, anovulation, and infertility are all a characteristic bouquet of hyperandrogenism found in polycystic ovary syndrome (PCOS).

    In the pathogenesis of PCOS, the insulin theory still occupies a central place. In particular, it has been shown that insulin reduces the production of sex hormone-binding globulin (SHBG) in the liver, thereby increasing the fraction of free, ACTIVE androgens in the blood, stimulating, say, the production of sebum (which leads to the development of acne).

    In addition, adipose tissue, the excess of which, as a rule, accompanies any violation of carbohydrate metabolism, stimulates an increase in the activity of 17-beta-steroid dehydrogenase, an enzyme that catalyzes the formation of testosterone.

  4. Puffiness - occurs due to the excretion of potassium and retention in the body of sodium, which pulls water molecules with its tail.

  5. Decreased flow of bile due to increased levels of lipids and cholesterol - increases the risk of developing gallstone disease.

  6. An increase in blood pressure is partly mediated by sodium retention, which leads, respectively, to water retention and, as a result, an increase in circulating blood volume; partly - the loss of magnesium.

  7. “Red dots” or vascular angiomas are another striking manifestation of impaired cell sensitivity to insulin.

     

  8. The appearance of papillomas due to excessive division of epithelial cells. This is not surprising, given the nature and biological role of insulin, the hormone of synthesis (anabolism). Everything grows on it like yeast: from cancer cells to muscles.

  9. Bacterial overgrowth syndrome (SIBO) - pathogenic microflora loves glucose, and its increased concentration in the blood is ideal conditions for active reproduction and an increase in the number of their colonies.

    Signs of SIBO are rather nonspecific and are usually manifested by the following symptoms:

    • bloating;

    • diarrhea;

    • weakness, fatigue, lack of strength;

    • nausea;

    • rumbling in the stomach.

  10. Fungi grow no less actively - candidiasis is observed, the manifestations of which largely depend on the localization of the pathological process (for example, candidiasis of the oral cavity, intestines, and genital organs occurs, accompanied by characteristic cheesy discharge and severe itching).

  11. Androgenetic alopecia or hair loss in typical male areas (occiput and temples) is usually one of the symptoms of PCOS. It arises due to insulin stimulation of the activity of 5-alpha-reductase, an enzyme that catalyzes the transformation of testosterone into a much more metabolically active DIHYDROTESTOSTERONE.

  12. Outbursts of aggression - due to a sharp drop in blood glucose concentrations.

Types of insulin resistance

  1. Physiological - occurs during puberty, pregnancy, menopause, as well as in conditions of hypoxia, iron deficiency and a sedentary lifestyle.

  2. Pathological - caused by lifestyle and nutrition.

    In addition, insulin resistance can accompany many endocrine diseases: thyrotoxicosis, hypothyroidism, Cushing's syndrome (in which there is excessive production of ACTH by the pituitary gland - adrenocorticotropic hormone), pheochromocytoma (a tumor of the adrenal glands that autonomously secretes adrenaline and norepinephrine). It also accompanies an increase in the concentration of uric acid (hyperuricemia), which can subsequently lead to gout, rheumatoid arthritis, heart failure, and cirrhosis of the liver.

    Research: Insulin resistance and its significance in the pathogenesis of carbohydrate metabolism disorders and type 2 diabetes mellitus

Diagnosis of insulin resistance

  • Waist circumference over 80 cm for women and over 90 cm for men.

  • Body mass index >25.

     

  • Fasting insulin concentration > 6 mmol/l.

  • Fasting glucose >5 mmol/L.

  • Glycated hemoglobin >6%.

  • Triglycerides >1.7 mmol/L.

  • High density lipoproteins (HDL) < 1 mmol/L.

  • Low density lipoproteins (LDL) >3 mmol/L.

  • HOMA index >1.4.

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Additionally, we recommend checking the following indicators for the presence of concomitant pathologies:

  1. Uric acid (increased fructose intake is often associated with an increase in uric acid and the development of gout).

  2. Homocysteine ​​(in PCOS, there is usually a deficiency of B vitamins, which leads to an increase in serum homocysteine ​​levels).

  3. Cortisol in daily urine.

  4. Thyroid panel: TSH, T4 St., T3 St., antibodies to thyroperoxidase and thyroglobulin.

  5. ALT, AST, alkaline phosphatase, bilirubin fractions.

  6. Ultrasound of the abdominal organs, mammary glands, and adrenal glands.

  7. Prolactin.

Complications and consequences of insulin resistance

Insulin resistance is the last, key step in the development of type 2 diabetes. It is also important to understand that the pancreas begins to compensatory produce more and more insulin - so that its avalanche-like flow somehow makes glucose squeeze inside the cells, pass through their closed doors. But its resources and capabilities are far from endless - over time, its depletion also occurs. And then patients have to resort to an insulin needle.

In diabetes mellitus, both types 1 and 2, there is a decrease in cognitive functions, and the risk of dementia increases by as much as 50%!

Patients, as a rule, suffer from microcirculatory disorders, obesity, dyslipidemia and hypertension.

 

Insulin resistance and polycystic ovary syndrome (PCOS) are inseparable companions in life, complementary to each other in the context of the development of metabolic disorders. Statistics show that in patients with type 2 diabetes, PCOS occurs 1.5-2 times more often than in women who do not have such a pathology.

It is interesting that the hepatitis C virus is able to directly influence the signaling cascade triggered by insulin - it is noteworthy that insulin resistance was detected in 32.4% of persons suffering from the chronic course of this disease.

Nutrition for insulin resistance

  1. It is necessary to switch to a 3-time diet. The exceptions are patients with adrenal insufficiency, gastrointestinal diseases in the acute stage and professional athletes - they are just shown snacks with fractional meals.

  2. A high-fat, moderate-protein and low-carbohydrate diet, and the basis of the diet should be foods with a low glycemic index.

     

    GLYCEMIC INDEX - an indicator that reflects how much the concentration of glucose in the blood will change after eating a particular product.

    The following foods should be excluded:

    • refined sugar in its pure form or as part of sweets, waffles, cakes;

    • honey;

    • dried fruits;

    • sweet fruits;

    • oatmeal, pearl barley, corn and semolina porridge;

    • bakery products;

    • starch;

    • sauces (mayonnaise, ketchup) and store-bought dressings;

    • soft drinks (lemonade, packaged juices, mojitos, soda);

    • beer and wine;

    • chips, crackers, french fries and hamburgers;

    • ready-made culinary dishes;

    • dairy.

  3. It is recommended that you consider a paleo diet or other low-carbohydrate protocols. In particular, the diet should contain:

    • meat - preferably chicken or turkey (red is recommended to be limited);

    • fatty sea fish (you can also use river fish, but remember to carefully examine the muscle fibers and take a long time to cook due to the high degree of parasitic worm infestation);

    • non-starchy vegetables;

    • nuts - with the exception of peanuts (highly allergenic and usually infected with mold) and cashews (contains a lot of carbohydrates in the composition);

    • gluten-free cereals: quinoa, green buckwheat, brown rice;

    • vegetable oils;

    • olives;

    • eggs;

    • cod liver and other sources of fats;

    • seasonal berries;

    • as sweeteners, erythritol is acceptable in moderation.

       

  4. Observe “hungry” intervals of at least 4-5 hours - remember that for any food intake, the pancreas will secrete insulin, the sensitivity to which is already impaired.

Treatment of insulin resistance

  1. Medication - the drug "Metformin" (it is prescribed strictly by a doctor!). As a rule, indicators for its use will be type 2 diabetes mellitus and / or a body mass index of more than 35.

  2. Biologically active supplements (non-drug) can be conditionally divided into two categories: aimed at replenishing deficiencies and at correcting carbohydrate metabolism.

 

In general, we recommend considering the reception:

  • Berberine (500 mg 2-3 times a day before meals, course - 3-6 months) - has a choleretic effect, lowers cholesterol and normalizes the lipid profile.

    In addition, studies have shown its protective function in relation to the cardiovascular system - in particular, in diabetic rats, it protected myocardial cells from apoptosis (self-programmed death).

    One of the important functions of insulin - the production of nitric oxide, which leads to the expansion of the lumen of blood vessels, increased blood flow and, as a result, increased glucose utilization in target tissues - is impaired in the conditions of the development of insulin resistance and type 2 diabetes mellitus. However, in animals, berberine treatment enhanced this insulin-induced vasorelaxant effect.

    Study: Berberine improves mesenteric artery insulin sensitivity through up-regulating insulin receptor-mediated signaling in diabetic rats

  • Magnesium (400-800 mg) - prevents an increase in blood pressure and the appearance of edema, has an analgesic effect.

  • Chromium (200 mcg / 3 times) - improves the sensitivity of cellular receptors to insulin, and also reduces cravings for sweets.

    However, it should be borne in mind that inorganic forms of this metal are quite toxic and have a low absorption rate. That is why its organic compounds are commonly used as biological additives: chromium picolinate, chromium nicotinate and chromium malate.

    Study: Type 2 Diabetic Rats on Diet Supplemented With Chromium Malate Show Improved Glycometabolism, Glycometabolism-Related Enzyme Levels and Lipid Metabolism

  • Myoinositol is recommended in the treatment of PCOS. Improves the quality of germ cells, normalizes tissue sensitivity to insulin, prevents the development of intrauterine malformations in the fetus. (Drink courses, 3-4 g / day).

     

  • Taurine (1000 mg 2 times a day on an empty stomach) - reduces the level of insulin in the serum, prevents an increase in blood pressure. Indicated for problems with bile flow.

  • Omega-3 polyunsaturated fatty acids (PUFAs) - eicosapentaenoic and docosahexaenoic acids (EPA and DHA) - have shown anti-inflammatory, antithrombotic properties, as well as positive effects on kidney function - especially in the context of diabetes-related pathologies on their part (including nephropathy, polycystic kidney disease and other). In particular, high intakes of EPA and DHA have been associated with lower risks of proteinuria (the presence of protein in the urine).

    Study: The effects of omega-3 fatty acids on diabetic nephropathy: A meta-analysis of randomized controlled trials

    The scientists also note that combination therapy with omega-3 PUFAs and vitamin D3 was well tolerated and had significant beneficial effects on the function of insulin-producing beta cells in patients with type 1 diabetes. In addition, omega-3 supplementation was associated with an increase in circulating calciferol levels.

    Study: The effects of vitamin D and omega-3 fatty acids co-supplementation on biomarkers of inflammation, oxidative stress and pregnancy outcomes in patients with gestational diabetes

  • Zinc (15-20 mg) - a mineral necessary for the normal functional activity of many antioxidant enzymes: superoxide dismutase and catalase. Its deficiency leads to the oxidation of pancreatic beta cells and the development of oxidative stress, to which they are already prone, given the large amounts of reactive oxygen species they form.

    A study of 82,000 American women published impressive results: low zinc intake was associated with a 17% increased risk of developing diabetes.

    Study: Role of Zinc Homeostasis in the Pathogenesis of Diabetes and Obesity

Reduce cravings for sweets:

  1. Licorice.

  2. Nutmeg.

  3. Ginseng root.

  4. Ashwagandha.

  5. Tulsi.

Intermittent fasting for insulin resistance

Intermittent fasting is a diet that consists in observing certain “hungry” intervals, the number of which directly depends on the chosen system. So, 16/8 is the most popular - that is, a complete refusal of food for 16 hours (including sleep) and a window of 8 hours during which you can eat (as a rule, these are two, less often - three meals).

 

Intermittent fasting is now being talked about more and more - but usually in the context of autophagy (that is, the degradation of old / unnecessary / diseased cells and / or their components). However, it plays a significant role in the correction of metabolic disorders.

In lab rats on a daytime fast and time-restricted feeding, the following beneficial effects were observed:

  • decreased levels of leptin and insulin;

  • reduction of body fat (especially visceral);

  • increased levels of ketones (and their use as an energy source);

  • decrease in heart rate and, as a result, blood pressure at rest;

  • increased tone of the parasympathetic nervous system;

  • maintaining muscle mass.

Intermittent fasting in animal models slowed down the development of neurodegenerative disorders - in particular, Alzheimer's, Parkinson's, and Huntington's diseases.

In addition, such a nutrition system increases the resistance of the whole organism to stress factors and common diseases that occur in the realities of the modern world with its sedentary lifestyle.

However, we do not recommend intermittent fasting without the advice of a nutritionist in patients with chronic adrenal fatigue, acute gastrointestinal diseases, impaired bile flow, hypoglycemia, and heavy physical exertion.

Prevention of insulin resistance

  1. Sufficient physical activity. Insulin resistance, like type 2 diabetes, is a lifestyle disease that can be corrected - most importantly, an integrated approach.

    You can sit on Metformin all your life, but without changing your eating habits and without adding moderate physical activity, you will not see improvements in laboratory and functional analyzes.

    No time for 10,000 steps a day? Start small - Rome was not built in a day either. Get off a few stops early for a leisurely walk to work; climb the stairs - forget about the existence of the word "elevator"; go for evening walks with children, friends and parents - you will also fall asleep faster as a bonus.

  2. Stick to intermittent fasting - the easiest system that does not require much effort will be 12/12. So, let's say if you have dinner at 7 pm, then at 7 am you can have breakfast. In addition, this mode will allow you to easily give up snacking and switch to a 3-time diet.

  3. Do not abuse carbohydrates. Especially the simple ones. Especially without fiber. A glass of freshly squeezed juice will only contribute to a sharp jump in blood glucose - the rest of the effects of this nuclear weapon against the pancreas are very doubtful.

    Love smoothies? Replace sweet fruits with berries, add a generous bunch of greens and a handful of seeds - and enjoy a green cocktail of youth and beauty.

  4. Limit foods with a high insulin index (such as red meat and cottage cheese) - they cause increased insulin secretion, although they often do not affect the immediate rise in blood sugar levels.

  5. Work with stress tolerance. Can't completely limit adverse factors? Then change your focus and your attitude towards them!

  6. Do yoga, breathing practices and Pilates - increasing the tone of the Parasympathetic system is a key point in working with the digestive system and its diseases.

The material is based on research:
  • The study of metabolic features in individuals with the RS9939609 polymorphism of the FTO gene

  • Study of Associations of New Genetic Markers of Type 2 Diabetes Mellitus in the West Siberian Caucasoid Population

  • obesity and sleep

  • Leptin resistance, unresolved diagnostic issues

  • Insulin resistance and its significance in the pathogenesis of carbohydrate metabolism disorders and type 2 diabetes mellitus

  • Berberine improves mesenteric artery insulin sensitivity through up-regulating insulin receptor-mediated signaling in diabetic rats

  • Type 2 Diabetic Rats on Diet Supplemented With Chromium Malate Show Improved Glycometabolism, Glycometabolism-Related Enzyme Levels and Lipid Metabolism

  • The effects of omega-3 fatty acids on diabetic nephropathy: A meta-analysis of randomized controlled trials

  • The effects of vitamin D and omega-3 fatty acids co-supplementation on biomarkers of inflammation, oxidative stress and pregnancy outcomes in patients with gestational diabetes

  • Role of Zinc Homeostasis in the Pathogenesis of Diabetes and Obesity

 

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