Preventing insulin resistance is essential in achieving optimal health. Scientists have discovered more than a dozen genes related to blood sugar control. Certain population groups have a strong genetic disposition for this silent killer.

Insulin resistance causes your body’s cells to become tone deaf to insulin’s glucose-regulating signals. It is called a Silent Killer due to the chronic inflammation it causes and because it is a strong predictor for the development of Type 2 diabetes. Insulin resistance is typically present in people who are overweight or obese; however, insulin resistance is silently present in a much larger group of the population. It can be diagnosed from an oral glucose tolerance test, which is seldom requested by physicians.

Scientists have discovered more than a dozen genes related to blood sugar control that, in certain groups of people, are faulty. Your chances of developing insulin resistance go up the more of those faulty genes you have (1). However, not everyone who receives a diagnosis of Type 2 diabetes is overweight and some who are overweight do not develop diabetes. So, where does the truth lie?

The Genetic Connection

A strong genetic predisposition to insulin resistance exists among certain population groups. For example, African Americans develop insulin resistance at a higher rate than European Americans when matched for age, gender and body mass index. This is due to variations in genes that regulate cellular energy production as well as genes that increase inflammation and initiate arterial plaque formation (2, 3).

Certain Asian women populations have a higher susceptibility to insulin resistance when consuming a low carbohydrate and high saturated fat diet due to a gene variant that carries a protein for fatty acids. The women with this gene variant are more prone to developing insulin resistance and diabetes (4).

A genetic variation in women increases insulin resistance and elevates cholesterol in association with a condition known as polycystic ovary syndrome. This genetic mutation results in a substitution of the amino acids arginine to glutamine. In these instances, high levels of insulin resistance have been reported (5).

Environmental Triggers

But, it doesn’t stop there. There are many epidemiologic studies on exposures to pesticides, polychlorinated biphenyls (PCBs), flame retardant chemicals and polycyclic aromatic hydrocarbons such as charbroiled meat that show an association with insulin resistance and related metabolic disorders like obesity, diabetes and metabolic syndrome (6). These negative environment factors can damage otherwise healthy genes.

So, while you can’t change your genetic makeup or undo your past exposures, having this knowledge can help you make the best lifestyle and health decisions going forward to mitigate your chances of developing insulin resistance or, if you currently have the condition, for it to progress to diabetes.

Nutrigenetics to the Rescue

You can control the genes that control your blood sugar and insulin levels with your food choices. Known as nutrigenetics or nutrigenomics, this burgeoning new science is providing us with mountains of evidence on how genes are turned on or off by foods, nutrients, and medicinal herbs. Dietary changes can suppress the activity of those gene variants that can cause insulin resistance.

The Power of Fats

Much has been written about the Paleo diet and its benefits for metabolic healing. Your intake of good fats and low carbohydrates can be a powerful tool in your insulin resistance arsenal depending upon your genetic profile (7, 9). Studies have shown for the general population that diets high in saturated fats will worsen insulin resistance and while diets high in intake of monounsaturated and polyunsaturated fats will improve it (8, 9). There have been studies using diet to change gene expression in which changes in dietary intake of polyunsaturated and monounsaturated fats and antioxidant-containing foods changed the expression of genes for inflammation, immunity and lipid metabolism (10). Olive oil would be an example of a monounsaturated fat and sunflower and safflower oils would be examples of polyunsaturated fats.

Diets rich in unsaturated fats improve insulin sensitivity by improving the structure of cell membranes, where insulin receptors are located. The quality of dietary fat can be so powerful in some people that it affects insulin resistance regardless of body weight. Metabolic syndrome promotes high blood pressure, high cholesterol and triglycerides, all of which promote insulin resistance. Preventing metabolic syndrome by losing weight, reducing fat intake and replacing saturated fat with mono- and polyunsaturated fats reverses and prevents insulin resistance.

Fruits and Veggies

Flavonoid antioxidants in fruits and vegetables can help regulate carbohydrate digestion, insulin secretion and insulin sensitivity by influencing the genes that control these activities and thereby lower the risk of type 2 diabetes (11, 12). The green tea flavanol epigallocatechin gallate (EGCG) has been proposed to improve insulin secretion and protect the insulin producing cells of the pancreas when blood glucose levels are high, a condition that is known to result in damage to these cells. Overall, EGCG exerts nutrigenetic effects on insulin secretion, glucose uptake, insulin resistance, glucose tolerance, oxidative stress, inflammation and cellular energy production (13).

Naringen and hesperidin, flavonoids found in citrus fruits, tweak a gene that senses blood glucose levels and controls insulin secretion (14). Quercetin, one of the most prevalent and important flavonoid compounds in plants, has been shown to influence genes in the liver and pancreas that control blood sugar and insulin concentrations (15).

Celery, parsley and other herbs contain flavonoid compounds that protect insulin-producing cells of the pancreas (16). Soy flavonoid compounds genistein and daidzein increase activity of genes that promote production of insulin-producing cells, improve glucose tolerance and control insulin levels (17).

Medicinal Herbs

Olive leaf extract contains a compound called oleanolic acid that improves insulin response and preserves the health of insulin-producing cells by inducing the expression of certain genes and other important activation factors (18). Berberine, found in barberry, goldenseal and Oregon grape, significantly improved high blood sugar by acting on pancreatic beta cell gene expression (19, 20, and 21).

Vitamins

Vitamin D protects the cells of the pancreas from cell-damaging inflammation. In total, vitamin D modifies the activity of many different genes related to inflammation, immune function and pancreatic function, all of which influence insulin response (22).

Low doses of vitamins C, E, and beta-carotene have been found to have antioxidant effects on genes in all groups. Although for diabetics, high doses of these same vitamins can have damaging pro-oxidant effects (23).

Amino Acids

The amino acids taurine (24) and leucine (25) have been shown to activate genes essential for insulin secretion. In addition, the amino acid glutamine not only activates these genes but also regulates genes in the liver, kidney and muscle cells (26).

Take Action

Preventing insulin resistance is essential in achieving optimal health. KlothoGenics can help you to prevent or fight this silent killer by determining from your genetic profile the tools your body needs to beat insulin resistance. Call us to see how we can assist you in your journey to optimal health.

Reference List

  • http://www.ncbi.nlm.nih.gov/pubmed/18719881
  • http://www.ncbi.nlm.nih.gov/pubmed/26789776
  • http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351975/
  • http://www.ncbi.nlm.nih.gov/pubmed/16732014
  • http://www.ncbi.nlm.nih.gov/pubmed/26662654
  • http://www.ncbi.nlm.nih.gov/pubmed/26670033
  • http://www.ncbi.nlm.nih.gov/pubmed/26848765
  • http://www.ncbi.nlm.nih.gov/pubmed/15297079
  • http://www.ncbi.nlm.nih.gov/pubmed/10889805
  • http://www.ncbi.nlm.nih.gov/pubmed/26667694
  • http://www.ncbi.nlm.nih.gov/pubmed/24029069
  • http://www.ncbi.nlm.nih.gov/pubmed/22357723/
  • http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3298777/
  • http://www.ncbi.nlm.nih.gov/pubmed/16427799
  • http://www.ncbi.nlm.nih.gov/pubmed/19496084/
  • http://www.ncbi.nlm.nih.gov/pubmed/18090225/
  • http://www.ncbi.nlm.nih.gov/pubmed/20484465/
  • http://www.ncbi.nlm.nih.gov/pubmed/23704520/
  • http://www.ncbi.nlm.nih.gov/pubmed/23118793/
  • http://www.ncbi.nlm.nih.gov/pubmed/14749281/
  • http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4116378/
  • http://www.ncbi.nlm.nih.gov/pmc/articles/2879406/
  • http://www.ncbi.nlm.nih.gov/pubmed/23861227/
  • http://www.ncbi.nlm.nih.gov/pubmed/18708284/
  • http://www.ncbi.nlm.nih.gov/pubmed/11272147/
  • http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.336.59