In this post I link to and excerpt from Insulin Resistance from StatPearls, Jan. 2020.
Spoiler alert: This article had no useful tips on the diagnosis and management of insulin resistance for weight loss.
Insulin resistance is said to make weight loss very difficult and for some (many) people impossible.
Obesity fuels insulin resistance and insulin resistance fuels obesity.
However, I’ve been unable to find clear practical guidelines on the diagnosis and mitigation of insulin resistance. The article from Stat Pearls was not helpful.
I next reviewed Insulin Resistance
Updated: Aug 07, 2019
Author: Samuel T Olatunbosun, MD, FACP, FACE from emedicine.medscape.com.
I didn’t find the above article particularly helpful either. I’ll just have to keep looking.
Here are excerpts from Insulin Resistance from StatPearls, Jan. 2020 [Although I didn’t find the article helpful after I had reviewed it, I left it in the blog so I don’t later re-review it by mistake]:
Introduction
Insulin resistance is identified as an impaired biologic response to insulin stimulation of target tissues, primarily the liver, muscle, and adipose tissue. Insulin resistance impairs glucose disposal, resulting in a compensatory increase in beta-cell insulin production and hyperinsulinemia. [1][2][3]The metabolic consequences of insulin resistance can result in hyperglycemia, hypertension, dyslipidemia, visceral adiposity, hyperuricemia, elevated inflammatory markers, endothelial dysfunction, and a prothrombic state. Progression of insulin resistance can lead to metabolic syndrome, nonalcoholic fatty liver disease (NAFLD), and type 2 diabetes mellitus.
Insulin resistance is primarily an acquired condition related to excess body fat, though genetic causes are identified as well. The clinical definition of insulin resistance remains elusive as there is not a generally accepted test for insulin resistance. [4][5]Clinically, insulin resistance is recognized via the metabolic consequences associated with insulin resistance as described in metabolic syndrome and insulin resistance syndrome.
The gold standard for measurement of insulin resistance is the hyperinsulinemic-euglycemic glucose clamp technique. This is a research technique with limited clinical applicability; however, there are a number of clinically useful surrogate measures of insulin resistance, including HOMA-IR, HOMA2, QUICKI, serum triglyceride, and triglyceride/HDL ratio. In addition, several measures assess insulin resistance based on serum glucose and/or insulin response to a glucose challenge.
The predominate consequence of insulin resistance is type 2 diabetes (T2DM). Insulin resistance is thought to precede the development of T2DM by 10 to 15 years.
In addition to T2DM, the spectrum of disease associated with insulin resistance includes obesity, cardiovascular disease, nonalcoholic fatty liver disease, metabolic syndrome, and polycystic ovary syndrome(PCOS). These are all of great consequence in the United States with a tremendous burden being placed on the healthcare system to treat the direct and indirect conditions associated with insulin resistance.
Lifestyle modification should be the primary focus for the treatment of insulin resistance. Nutritional intervention with calorie reduction and avoidance of carbohydrates that stimulate excessive insulin demand are a cornerstone to treatment. Physical activity helps to increase energy expenditure and improve muscle insulin sensitivity. Medications also can improve insulin response and reduce insulin demand.
Etiology
Insulin resistance etiology can be divided into acquired, hereditary, and mixed. The great majority of people with insulin resistance fall into the acquired categories.
Acquired
Excess dysfunctional adipose tissue Aging Physical inactivity Nutritional imbalance Medications (glucocorticoids, anti-adrenergic, protease inhibitors, atypical antipsychotics, and some exogenous insulin) Increased sodium diets Glucose toxicity Lipotoxicity from excess circulating free fatty acids