Metabolic syndrome is called a syndrome rather than a disease because it refers to a group of risk factors that occur together and which increase the risk for coronary artery disease, peripheral artery disease, type 2 diabetes and stroke. It is believed to effect approximately 25% or 47 million of the US population. Risk factors for metabolic syndrome include: genetics, hypertension, insulin resistance, hyperlipidemia and obesity, especially increased abdominal girth.
Epigenetics is now considered an important mechanism in the evolution of metabolic syndrome. One theory among many regarding the possible genetics behind insulin resistance was “The Thrifty Gene” proposed by geneticist James Neel in 1962. Thrifty genes are genes which enable individuals to efficiently collect and process food to deposit fat during periods of food abundance. Those carrying the thrifty gene survived when food was scarce. The Thrifty Gene historically was advantageous in times of famine, but has become detrimental in the modern world.
The exact epigenetic explanation of insulin resistance is unclear, but what is clear is that genetics play a key role. Research shows that those with a genetic predisposition have a slowed metabolic rate. The mitochondria in people with metabolic syndrome produces up to 70% less ATP, or energy, than controls. Ethnic groups where metabolic syndrome runs rampant are; African Americans (50%), Pima Indians (nearly 100%), Polynesians, and Mexican Americans (50%)
To better understand metabolic syndrome, one must understand the basics of glucose metabolism. When food is eaten, carbohydrates are broken down to the end product of glucose. This stimulates the release of insulin which the body needs to absorb glucose into fat, heart, liver and muscle cells. Over time, if insulin is secreted in high amounts due to high carbohydrate intake, the cells begin to ignore the insulin messenger. When that signal is ignored, the body’s insulin producers—beta cells of the pancreas—have to work harder and harder, overproducing insulin to get the job done, causing insulin resistance.
In addition, insulin promotes the conversion of glucose to fat for storage in adipocytes (fat cells). If we overeat and don’t exercise enough, the supply of fat will exceed the demand for energy. That can lead to obesity, the main cause of insulin resistance.
It is now known that there is a link between obesity and inflammation. Many of the inflammatory markers found in plasma of obese individuals appear to originate from adipose tissue. In other words, fat cells are little “hotbeds of inflammation”. Therefore excess belly fat is a great source of inflammation. Inflammatory chemicals released, such as TNF-alpha and IL-6, directly interfere with insulin signaling pathways making cells more insulin resistant. Therefore being obese can cause insulin resistance and insulin resistance can cause obesity. The oxidative effects of insulin depletes our glutathione, vitamin C, vitamin E and other antioxidants.
Insulin’s role in cardiovascular disease and stroke risk is due to the damaging effects insulin has on the endothelium or cells lining our blood vessels. Endothelium dysfunction reduces nitric oxide production needed for healthy blood vessels. It also reduces blood flow by causing vascular smooth muscle contraction and the growth of vascular smooth muscle cells. As a result, the blood vessels are thicker with a smaller lumen; blood flow is slower and there is increased risk of clotting inside the vessels (thrombosis) and stroke. Concurrently, insulin stimulates the sympathetic nervous system increasing norepinephrine which contributes to high blood pressure. Insulin resistance significantly increases the risk of ischemic stroke in non-diabetic adults, independent of traditional vascular risk factors or metabolic syndrome, “October 2010 issue of Archives of Neurology”. Individuals in the top quarter of insulin resistance had a 45 percent greater risk of any type of vascular event.
Insulin has detrimental effects on our sex hormones. Aromatization occurs when testosterone is chemically converted to estrogen. The conversion of testosterone to estrogen occurs mostly in fat tissue which has a high level of the aromatase enzymes. Unfortunately, in people with excess fat and especially abdominal fat, this production of estrogen from testosterone occurs at an abnormally high rate. High insulin levels will contribute further to increased aromatization. Insulin increases lutenizing hormone (LH) which blocks testosterone production. In men this process can causes low testosterone and high estrogen levels.
Aromatization in women causes a disorder called PCOS – Polycystic Ovarian Syndrome. A woman’s body converts androgens to estrogens and levels of both testosterone and estrogens can significantly exceed that of progesterone. The ovaries are strongly effected by high insulin levels, increasing Lutenizing Hormone (LH), preventing ovulation and causing production of multiple small cysts beneath the ovarian capsule. These insulin-damaged ovaries act like testicles making excessive androgens, from DHEA to testosterone. Symptoms of PCOS include: heavy periods, painful periods, irregular or absent periods, acne or oily skin, depression or mood swings, excess facial hair and lack of ovulation.
Fatty liver, also known as fatty liver disease (FLD), is a reversible condition where fat accumulates in liver cells due to obesity. Despite the strong association between insulin resistance and dyslipidemia/fatty liver, the precise mechanism linking these conditions is unclear.
Insulin resistance may evolve to type 2 diabetes. A pre-diabetes state occurs when insulin becomes elevated and borderline high fasting glucose levels reach 100. In time, elevated insulin will stress the beta cells, which will wear out and type 2 diabetes will occur. At this point, the pancreas has already lost some of it’s ability to make insulin. Insulin resistance can also result in dermatological effects such as skin tags, acne and acne rosacea.
The goal for treating Metabolic Syndrome is to reduce obesity and improve insulin sensitivity. Dietary modification is crucial to healing. There are various diets being touted for metabolic syndrome including raw, vegan and the Paleolithic diet approach. In my experience as an ND, I believe if there was a one size fits all diet (which there isn’t) the, “Hunter Gatherer” diet would be my choice. Based on human evolutionary history the “Paleo Diet” reflects what our Paleolithic ancestors (i.e., before agriculture) evolved eating over a million years.
Carbohydrates: Avoid white Foods with a low glycemic index and fast foods. Complex carbohydrates in moderation.
Non-Starchy Vegetables –should be the majority of carbohydrates.
Protein – Beans, Legumes, Fish, Free Range Animal Protein. Grass fed beef. Protein at each meal preferred.
Healthy fats – avocado, organic butter, olive oil, coconut. Avoid hydrogenated oils and fried foods. Nuts in moderation.
Fruit – moderate consumption. Only in season. Small amounts of fruit are OK but eat it with protein meals and not alone. Berries are best. No dried fruit.
Reduction or elimination of sweeteners (including artificial and stevia which can elevate insulin)
Dairy – whole milk is best. But the best is no milk, as it raises the blood sugar.
Dietary fiber promotes improved post-prandial glucose and insulin responses. Guar gum, glucomannan and oat fiber have shown best results.
Exercise may be the single most important factor for reversing insulin resistance. Exercise improves insulin sensitivity, lowers fasting glucose, lowers fat mass, and improves fat metabolism. Stress reduction and quality sleep are other important lifestyle factors. Sleep deficiency significantly worsens insulin resistance, with a nearly 40% decrease in glucose tolerance. Sleep apnea may cause metabolic changes that increase insulin resistance, according to researchers from the University of Pittsburgh Medical Center. In a study that addressed the issue of insulin sensitivity with respect to sleep disordered breathing (SDB), SDB was strongly associated with a decrease in insulin sensitivity, glucose effectiveness, and pancreatic cell function – independent of obesity. During times of stress, both cortisol and catecholamine stress hormones are capable of elevating blood sugar and chronic elevation of cortisol results in increased plasma insulin levels.
Since lifestyle factors – diet, exercise, sleep and stress reduction – play the pivotal role in metabolic syndrome, they should be considered a priority in the management of insulin resistance. Supplements found to be helpful include, berberine, alpha lipoic acid, chromium, vanadium, cinnamon, fish oil and fiber. The drug, Metformin is also effectively used in treating insulin resistance along with the lifestyle changes mentioned. If you are concerned about stroke or heart disease risks, your doctor may want to run the following tests:
Remember metabolic syndrome is an outcome of our sedentary, fast-food oriented modern lifestyle. With a commitment to healthy eating, daily exercise and your doctor’s support, metabolic syndrome can be reversed.
This Power Point presentation by Elizabeth Large ND covers information on the effect Metabolic Syndrome and Insulin Resistance have on inflammation.
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