Insulin Resistance: Background, Pathophysiology, Etiology. Ahr. Islet adaptation to insulin resistance: mechanisms and implications for intervention. Diabetes Obes Metab. Mari A, Ahr. Assessment of insulin secretion in relation to insulin resistance. Curr Opin Clin Nutr Metab Care. Pathophysiology of insulin resistance in human disease. Physiol Rev. 7. 5(3): 4. Leptin, a hormone that plays a key role in regulating energy intake and energy expenditure, may be one of the most important hormones in your body.Obesity is caused by a variety of factors, and leptin resistance may be one of them. A Paleo Diet may help reverse the effects of leptin resistance. Nutrition experts for years have recommended the healthy Mediterranean diet. It’s linked to longer life span and reduced rates of heart attack, stroke, cancer. Kim JA, Wei Y, Sowers JR. Role of mitochondrial dysfunction in insulin resistance. Feb 2. 9. 1. 02(4): 4. Insulin resistance and inflammation may have an additional role in the link between cystatin C and cardiovascular disease in type 2 diabetes mellitus patients. Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Reaven G, Abbasi F, Mc. Laughlin T. Obesity, insulin resistance, and cardiovascular disease. Recent Prog Horm Res. Inflammation and insulin resistance. Inflammatory mechanisms in the regulation of insulin resistance. Mar- Apr. 1. 4(3- 4): 2. Inflammatory, atherothrombotic aspects of type 2 diabetes.
Curr Med Res Opin. Suppl 1: S5- 1. 2. Florez H, Castillo- Florez S, Mendez A, Casanova- Romero P, Larreal- Urdaneta C, Lee D, et al. C- reactive protein is elevated in obese patients with the metabolic syndrome. Diabetes Res Clin Pract. Laaksonen DE, Niskanen L, Nyyss. C- reactive protein in the prediction of cardiovascular and overall mortality in middle- aged men: a population- based cohort study. Eur Heart J. 2. 6(1. High- sensitivity C- reactive protein: a useful marker for cardiovascular disease risk prediction and the metabolic syndrome. Semple RK, Cochran EK, Soos MA, Burling KA, Savage DB, Gorden P, et al. Plasma adiponectin as a marker of insulin receptor dysfunction: clinical utility in severe insulin resistance. Diabetes Care. 3. Brabant G, M. Hepatic leptin signaling in obesity. Fuke Y, Fujita T, Satomura A, Wada Y, Matsumoto K. Alterations of insulin resistance and the serum adiponectin level in patients with type 2 diabetes mellitus under the usual antihypertensive dosage of telmisartan treatment. Diabetes Technol Ther. Meilleur KG, Doumatey A, Huang H, Charles B, Chen G, Zhou J, et al. Circulating adiponectin is associated with obesity and serum lipids in West Africans. J Clin Endocrinol Metab. Omentin plasma levels and gene expression are decreased in obesity. Tan BK, Adya R, Farhatullah S, Lewandowski KC, O'Hare P, Lehnert H, et al. Omentin- 1, a novel adipokine, is decreased in overweight insulin- resistant women with polycystic ovary syndrome: ex vivo and in vivo regulation of omentin- 1 by insulin and glucose. Moreno- Navarrete JM, Catal. Circulating omentin concentration increases after weight loss. Nutr Metab (Lond). The role of the adipocyte hormone adiponectin in cardiovascular disease. Curr Opin Pharmacol. Diamant M, Tushuizen ME. The metabolic syndrome and endothelial dysfunction: common highway to type 2 diabetes and CVD. Curr Diab Rep. 6(4): 2. Dushay J, Abrahamson MJ. Insulin resistance and type 2 diabetes: a comprehensive review. Medscape Today . Insulin resistance is associated with microangiopathy in type 1 diabetic patients treated with intensive insulin therapy from the onset of disease. Exp Clin Endocrinol Diabetes. Lutsey PL, Steffen LM, Stevens J. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation. 2. 00. Feb 1. 2. 1. 17(6): 7. Low- dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial. Diabetologia. 5. 4(8): 2. Baudrand R, Campino C, Carvajal CA, Olivieri O, Guidi G, Faccini G, et al. High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome. Clin Endocrinol (Oxf). De Wit S, Sabin CA, Weber R, Worm SW, Reiss P, Cazanave C, et al. Incidence and risk factors for new- onset diabetes in HIV- infected patients: the Data Collection on Adverse Events of Anti- HIV Drugs (D: A: D) study. Diabetes Care. 3. HIV lipodystrophy and its metabolic consequences: implications for clinical practice. Curr Med Res Opin. Yu IC, Lin HY, Sparks JD, Yeh S, Chang C. Androgen receptor roles in insulin resistance and obesity in males: the linkage of androgen- deprivation therapy to metabolic syndrome. The prevalence of impaired fasting glucose and type 2 diabetes in a population- based sample of overweight/obese children in the Middle East. Pediatr Diabetes. Sarti C, Gallagher J. The metabolic syndrome: prevalence, CHD risk, and treatment. J Diabetes Complications. Mar- Apr. 2. 0(2): 1. Levy- Marchal C, Arslanian S, Cutfield W, Sinaiko A, Druet C, Marcovecchio ML, et al. Insulin resistance in children: consensus, perspective, and future directions. J Clin Endocrinol Metab. Beck- Nielsen H. General characteristics of the insulin resistance syndrome: prevalence and heritability. European Group for the study of Insulin Resistance (EGIR). Suppl 1: 7- 1. 0; discussion 7. Hirschler V, Ruiz A, Romero T, Dalamon R, Molinari C. Comparison of different anthropometric indices for identifying insulin resistance in schoolchildren. Diabetes Technol Ther. Savino A, Pelliccia P, Chiarelli F, Mohn A. Obesity- related renal injury in childhood. Horm Res Paediatr. Einhorn D, Reaven GM, Cobin RH, Ford E, Ganda OP, Handelsman Y, et al. American College of Endocrinology position statement on the insulin resistance syndrome. Endocr Pract. 2. 00. May- Jun. 9(3): 2. American Association of Clinical Endocrinologists Position Statement on Metabolic and Cardiovascular Consequences of Polycystic Ovary Syndrome. Endocr Pract. 2. 00. Mar- Apr. 1. 1(2): 1. Essah PA, Nestler JE. The metabolic syndrome in polycystic ovary syndrome. J Endocrinol Invest. Pasquali R, Patton L, Pagotto U, Gambineri A. Metabolic alterations and cardiovascular risk factors in the polycystic ovary syndrome. Minerva Ginecol. 5. Cheng AY, Leiter LA. Metabolic syndrome under fire: weighing in on the truth. Can J Cardiol. 2. Definitions of metabolic syndrome: Where are we now? Curr Vasc Pharmacol. The metabolic syndrome: is this diagnosis necessary? Am J Clin Nutr. 8. Kahn R, Buse J, Ferrannini E, Stern M. The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care. 2. De Taeye B, Smith LH, Vaughan DE. Plasminogen activator inhibitor- 1: a common denominator in obesity, diabetes and cardiovascular disease. Curr Opin Pharmacol. Endothelial inflammation in insulin resistance. Feb 1. 2- 1. 8. 3. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta- cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 2. 8(7): 4. Katz A, Nambi SS, Mather K, et al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab. Muniyappa R, Lee S, Chen H, Quon MJ. Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. Am J Physiol Endocrinol Metab. E1. 5- 2. 6. Antuna- Puente B, Faraj M, Karelis AD, et al. HOMA or QUICKI: is it useful to test the reproducibility of formulas? Diabetes Metab. 3. Vaccaro O, Masulli M, Cuomo V, et al. Comparative evaluation of simple indices of insulin resistance. Rossner SM, Neovius M, Mattsson A, Marcus C, Norgren S. HOMA- IR and QUICKI: decide on a general standard instead of making further comparisons. Acta Paediatr. 9. Sobngwi E, Kengne AP, Echouffo- Tcheugui JB, Choukem S, Sobngwi- Tambekou J, Balti EV, et al. Fasting insulin sensitivity indices are not better than routine clinical variables at predicting insulin sensitivity among Black Africans: a clamp study in sub- Saharan Africans. BMC Endocr Disord. Impact of metformin and rosiglitazone treatment on glucose transporter 4 m. RNA expression in women with polycystic ovary syndrome. Eur J Endocrinol. Salpeter SR, Buckley NS, Kahn JA, Salpeter EE. Meta- analysis: metformin treatment in persons at risk for diabetes mellitus. Quinn CE, Hamilton PK, Lockhart CJ, Mc. Veigh GE. Thiazolidinediones: effects on insulin resistance and the cardiovascular system. Br J Pharmacol. 1. Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. N Engl J Med. 2. 00. Jun 1. 4. 3. 56(2. Rasouli N, Raue U, Miles LM, Lu T, Di Gregorio GB, Elbein SC, et al. Pioglitazone improves insulin sensitivity through reduction in muscle lipid and redistribution of lipid into adipose tissue. Am J Physiol Endocrinol Metab. E9. 30- 4. Lee WJ, Lee YC, Ser KH, Chen JC, Chen SC. Improvement of insulin resistance after obesity surgery: a comparison of gastric banding and bypass procedures. Herman WH, Hoerger TJ, Brandle M, Hicks K, Sorensen S, Zhang P, et al. The cost- effectiveness of lifestyle modification or metformin in preventing type 2 diabetes in adults with impaired glucose tolerance. Ann Intern Med. 1. Treatment of the metabolic syndrome: the impact of lifestyle modification. Curr Atheroscler Rep. Exercise as a therapeutic intervention for the prevention and treatment of insulin resistance. Diabetes Metab Res Rev. Sep- Oct. 2. 0(5): 3. Hawley JA, Lessard SJ. Exercise training- induced improvements in insulin action. Acta Physiol (Oxf). Shih KC, Janckila AJ, Kwok CF, Ho LT, Chou YC, Chao TY. Effects of exercise on insulin sensitivity, inflammatory cytokines, and serum tartrate- resistant acid phosphatase 5a in obese Chinese male adolescents. Ioannides- Demos LL, Proietto J, Mc. Neil JJ. Pharmacotherapy for obesity. Jayagopal V, Kilpatrick ES, Holding S, Jennings PE, Atkin SL. Orlistat is as beneficial as metformin in the treatment of polycystic ovarian syndrome. J Clin Endocrinol Metab. Kiortsis DN, Filippatos TD, Elisaf MS. The effects of orlistat on metabolic parameters and other cardiovascular risk factors. Diabetes Metab. 3. Analysis of the XENDOS study (Xenical in the Prevention of Diabetes in Obese Subjects). Endocr Pract. 2. 00. Leptin, Thyroid, and Weight Loss By. Byron J. Richards, Board Certified Clinical Nutritionist. It is very common for overweight individuals to have a majority of the symptoms associated with a hypothyroid- like condition. This is especially true for those who have a history of yo- yo dieting or have difficulty losing weight by cutting back on calories and trying to exercise more. A great deal of confusion exists among patients and the medical community itself regarding the precise role that thyroid hormone plays in obesity. This is partly because thyroid lab tests often don’t correlate with the patient’s hypothyroid symptoms (patient is complaining, yet the lab tests are normal or not too far off). And it is partly because many people who are normal weight or underweight also have hypothyroid- like symptoms or hypothyroidism by lab test. I’ll explain these paradoxical situations in this article. Numerous discoveries in the past 1. Discoveries in the past year have elucidated how problems with nerves in the subconscious brain induce thyroid malfunction. These discoveries open a whole new world of possibilities for those struggling with long- standing hypothyroid- like problems and difficult body- weight issues. To understand how simple and basic problems—left unresolved—can lead to more complex problems that are much more difficult to solve (though solvable), let’s begin by understanding simple- case thyroid and leptin problems. Simple- Case Thyroid Problems. A shortage of active thyroid hormone, known as T3 (triiodothyronine), is a primary and simple reason why so many individuals struggle with the symptoms of hypothyroid. Another common problem is that your thyroid lacks nutrients to make basic thyroid hormone, known as T4 (thyroxin). Your thyroid can be inflamed or “stressed,” which gets in the way of making T4 at an optimal rate. Your liver can be inflamed or stressed, which gets in the way of converting T4 to T3 at an optimal rate. Cells around your body require basic nutrition to carry out the metabolic instructions that T3 gives them; otherwise it is no different than not having enough T3. Any or all of these simple- case thyroid problems happen long before true hypothyroidism, even though they cause a person to have some or many of the symptoms of hypothyroidism (this is one reason lab tests often don’t show a frank thyroid hormone problem – there really isn’t one). Even when a person has true hypothyroidism by lab test, there may be a co- existing simple- case thyroid problem, often of long duration. Thus, people with thyroid symptoms, even those on thyroid medication, can seek to improve their healthy metabolic function by providing basic nutrients that enhance the formation of thyroid hormone in the thyroid gland, enhance the activation of T4 to the biologically active T3, and enhance the nutritional ability of cells to utilize thyroid hormone. Supplements for Thyroid Health. I designed different dietary supplements to fill these specific needs. Thyroid Helper. Along with selenium, manganese provides a boost of specific antioxidant enzymes inside your thyroid gland and in your liver, so that both organs can function in a less stressed and inflamed manner. Tyrosine is added to boost dopamine and nerve related thyroid formation, as well as provide the core molecule of thyroid hormone (T4 is one molecule of tyrosine surrounded by four molecules of iodine). Several herbs that are synergistic with these functions round out the very popular Thyroid Helper formula.*I recommend a water- soluble and extremely biologically active form of iodine called Iosol Iodine. It is one of the best supplements to help individuals warm up. Iodine is needed for thyroid hormone formation. Unlike potassium iodide, which can clog the thyroid gland due to its poor solubility, Iosol readily washes away if it is not needed. It is hands down the best iodine on the market today.*Daily Energy Multiple Vitamin contains biologically active co- enzyme B vitamins along with Krebs cycle cofactor nutrients that help turn on cellular engines so they can respond to T3 instructions. The superior biological uptake of these nutrients is key to helping your metabolism get in gear. Thus, our basic Thyroid Energy Package to support simple- case thyroid problems is Thyroid Helper. This may be all the support you need to feel better or it may be part of the support. Regardless, it is the basic place to get started – and this is true whether you are overweight, normal weight, or underweight. Simple- Case Leptin Problems. Leptin is known as the fat hormone; it is made in your white adipose tissue or stored fat. Following a meal, leptin is released from your fat, enters your blood, and travels up to your brain where it delivers a message that you are full and also lets your subconscious brain know how much fuel you have on hand (like the gas gauge in your car). One of the simple- case leptin problems encountered by people who are overweight is that their leptin “gas gauge” is sticky, or in more advanced cases, broken. This is called leptin resistance because leptin is either not getting into your brain correctly or not registering properly in your hypothalamus gland once it does enter your brain. For a more complete description, read the article What is Leptin? If you are overweight you must eat in harmony with leptin or you cause considerable confusion in your subconscious brain. This results in fatigue and increased inflammation, along with great difficulty losing weight. Following the Five Rules of The Leptin Diet helps optimize leptin function in your body and unlock easier weight loss. Rule 1: Never eat after dinner. Rule 5: Reduce the amount of carbohydrates eaten. You can solve many simple- case leptin problems by following these guidelines. Learn more about The Leptin Diet. Leptin problems create inflammation in your brain and around your body. In addition to eating quality food and following The Leptin Diet, various dietary supplements can enhance the way leptin works. I designed Leptinal. Leptinal is a unique combination of DHA, GLA, tocotrienols, pomegranate, and citrus- derived polymethoxylated flavones. Because the essential fatty acids of DHA and GLA are woefully lacking in the typical American diet, they are key basics that should be supplemented to promote optimal leptin function that assists easier weight loss.*Another simple- case leptin issue involves problems relating to how insulin functions in your body, resulting in food cravings – especially for sweets, and easy weight gain from eating carbohydrates. It is a potent combination of metabolically- activating first milk colostrum, insulin- supportive chromium and vanadium, and the sweet- tooth- busting herbs gymnema sylvestre and inula racemosa.*Covering your basic nutrient bases with Leptinal. Simple- Case Thyroid- Leptin Problems. How well leptin registers in your brain has a major bearing on how thyroid hormone is produced in your body. This is because one function of leptin is to set the long term energy spending policy of your body based on available food supply. Your subconscious brain interprets leptin resistance to mean a famine is going on, even though you are often eating too much on a regular basis. This is a faulty perception of starvation. Your hypothalamus then has a major influence over how much TSH (thyroid stimulating hormone) your pituitary will produce, meaning that your subconscious brain intentionally turns down the volume on your metabolism so that you can survive a famine, which may not even exist. This is a different issue from every other simple- case thyroid problem that I mention above, and if you have any of those problems as well, it just makes this thyroid- leptin problem even worse. This is also the reason for yo- yo dieting, as after a diet that evokes the leptin- driven starvation response, leptin commands that calories are stored as fat when more food is eaten. And the more times you have yo- yo dieted in the past the more likely you are to have thyroid- leptin problems when you try to diet in the future. Researchers now believe that even small elevations in TSH (thyroid stimulating hormone), rather than indicating a looming thyroid problem, in some cases actually predict an emerging leptin and insulin problem associated with weight gain. It was found that when weight was lost, TSH scores returned to normal. Another study shows very clearly that leptin driven weight gain actually inflames the thyroid gland and induces thyroid autoantibodies to form, as if the leptin driven obesity problems are punching the thyroid gland in the nose. Once again, thyroid autoantibodies returned to normal when weight was lost. Another study shows one key symptom that flags a leptin and thyroid problem is a decrease in coordination. Are you bumping into things too often? This is because leptin- driven TRH signals that produce thyroid hormone also signal your cerebellum, which is involved with coordinating your physical movements. Once your thyroid- leptin system starts to stress out you may also not get a normal amount of coordination- related nerve conduction. These studies, combined with a basic understanding of how and why leptin needs to have a main say in how much thyroid hormone is produced, indicate that leptin problems are a driving force behind thyroid problems. While some may think their sluggish thyroid problems led to obesity, it is mostly the other way around. Thus, improving simple- case leptin problems and losing weight will improve thyroid function. This issue is always made worse if your internal plumbing systems aren’t up to the challenge (constipation, irritable bowel, liver issues, lymph stagnation, chemical sensitivity, fibromyalgia, etc.)Some chemicals like perchlorate, chlorine, and fluoride can directly bind to your thyroid gland and reduce iodine uptake.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. Archives
October 2017
Categories |