If you are one of the many North Americans who fear high-carbohydrate foods, you may be moving to a diet lower in carbohydrates and higher in fats and proteins. It may even be your own physician who is sending you in this direction.
When blood glucose (sugar) levels rise, you are said to be prediabetic. The higher your blood sugar levels become, the closer you are edging to full-blown diabetes. The rate of prediabetes and diabetes is steadily increasing in the developed world. At the present time, one in three Canadians are already suffering from one of these conditions and people who are twenty years old today face a 50% chance of developing diabetes in their lifetime (1). Unfortunately, conventional dietary guidelines, based on a misunderstanding of the mechanism that causes increasing blood sugar levels, still often recommend a carbohydrate-restricted diet to slow down the advent of type-2 diabetes (once known as adult-onset diabetes). You will discover, as you keep reading on, that altering your diet towards a lower carbohydrate content is a dangerous step to take.
Metabolic Syndrome is Associated With Insulin Resistance. What is Metabolic Syndrome?
Metabolic syndrome is a collection of risk factors that together unequivocally raise the risks of developing many chronic diseases. The risk factors that make up metabolic syndrome are high blood sugar, increased blood pressure, excess body fat around the waist and abnormal cholesterol or triglyceride levels. Having three or more of these factors is considered a diagnosis of metabolic syndrome (2,3,4). There are few symptoms of metabolic syndrome. You may notice that you have a large waist circumference and, if your blood sugar is high, you might suffer the symptoms of diabetes – increased thirst, increased urination, fatigue and blurred vision (2). The Public Health Agency of Canada, using statistics from the Canadian Health Measures Survey 2007-2009, determined that, at that time, 14.9% of Canadian adults had metabolic syndrome. Incidence in the US during the same time period was more than twice as high at 34.4% (4).
What is Insulin Resistance?
Insulin resistance lies at the heart of metabolic syndrome. It is the dysfunction in glucose absorption and metabolism within the cells themselves that leads to high blood sugar levels and is key to the development of type-2 diabetes. Insulin resistance is the inability of cells to communicate with insulin, leaving glucose particles, the preferred fuel for the human body, unable to enter cells. Glucose then accumulates in the blood vessels resulting in ever-increasing blood sugar levels (5).
You may also hear the term insulin sensitivity. Insulin sensitivity and insulin resistance are two sides of the same situation. A person with insulin resistance has low insulin sensitivity while a person with high insulin sensitivity does not have insulin resistance.
Insulin resistance is more prevalent in those with obesity (6,7). In the US, the incidence of insulin resistance in overweight and obese women without any diagnosed disease is 70.6% (8).
Insulin resistance is strongly associated with other diseases and conditions besides obesity and diabetes. People with insulin resistance and/or metabolic syndrome have up to a 93% greater risk of heart disease (9,10). Other illnesses in which insulin resistance may play a causative role are non-alcoholic fatty liver disease (NAFLD) (11), chronic kidney disease (12), polycystic ovarian syndrome (PCOS) (13), Parkinson’s disease (14,15), cancer (16), Alzheimer’s disease (17,18), and impaired cognition (19,20).
What is the Cause of Insulin Resistance?
The cause of insulin resistance was not understood until Magnetic Resonance Imaging (MRI) machines were developed in the late 1970s and early 1980s. MRI machines allow researchers to actually observe what is happening inside the tissues of a living body. What was discovered within people with insulin resistance was excessive amounts of fat inside the cells of their muscles and liver compared to levels in healthy people (21).
Subsequent studies found that healthy adults who ate a single meal high in fat showed increased fat absorption into their muscle tissue along with the development of insulin resistance within hours of eating the meal. Rates of glucose entering muscle cells were cut in half in those eating the fatty meal while no changes in insulin sensitivity or level of fat in muscle tissues occurred after the consumption of a low-fat meal (22). Additionally, when high-fat intake continued regularly over a period of weeks or months, fat in muscle tissue accumulated and insulin resistance increased (23).
More recent research has further added to the understanding of this process. A review from 2012 illustrated the link between visceral adipose tissue (fat surrounding the organs in the abdomen) and insulin resistance. The human body has a highly evolved ability to store fat in adipose tissue. However, this storage capacity is finite. Once the adipose tissue is full, any excess fat is left in the blood vessels and ends up being absorbed by the liver, muscles and sometimes other organs as well. These tissues are not designed to store fat and excess lipid accumulation in them induces insulin resistance (24).
There are a variety of different factors that can impair one or more steps of the insulin signalling process and the pathways it regulates thus leading to insulin resistance. Saturated fats can increase the production of ceramide which contributes to insulin resistance. Triacylglycerols (aka triglycerides), another lipid type, appear to be metabolized into products that deposit in skeletal muscle and interfere with insulin signalling (24,25,26,27). The damaging effects of free radicals can also disrupt cell metabolism and signalling pathways and have been said to be one of the major pathological factors responsible for disturbances in glucose and lipid metabolism (28).
Regardless of the exact mechanism(s), it is now recognized that the main cause of insulin resistance and metabolic syndrome is diet, specifically one that is high in fat and combined with obesity and lack of physical activity (29). The problematic fat that ends up accumulating in blood vessels and ultimately stored in places not meant for fat storage can originate from the diet or from a person’s own body fat spilling out of adipose tissue that is overfull (30).
What is happening in muscle and liver tissues as insulin resistance develops?
When you eat a carbohydrate-containing food, it is digested into smaller particles such as disaccharides and monosaccharides. Fiber, which is not digestible in the small intestine will move on into the colon for further processing with help from the gut microbiome. Monosaccharides, the smallest carbohydrate molecules, easily pass through the walls of the digestive tract to enter the bloodstream. Glucose is the most important monosaccharide found in the human body and is the prime energy source for humans and animals. These “sugar” molecules however cannot enter body tissues without the help of the hormone, insulin. The pancreas, a small organ that sits behind the stomach, senses any increase in blood sugar levels and reacts by producing insulin and secreting it into the bloodstream. Though insulin has several actions in the human body, its main one is to promote the entrance of glucose into body cells. It does this by attaching to an insulin receptor on the outside of a cell which starts a cascade of enzyme activation within the cell that results in glucose being allowed to pass through the cell membrane into the cell (5).
In type-1 diabetes, the pancreas is no longer able to produce insulin. This is why a type-1 diabetic must inject insulin several times a day. In type-2 diabetes and prediabetes, the situation is quite different. In this case, the pancreas can produce insulin, at least for awhile. This insulin will attach to insulin receptors on the cells but, because the cell is clogged with fat, insulin’s message does not get through. The required enzymes are not activated and little to no glucose is able to enter the cell. Inevitably, blood sugar levels begin to rise even further (21,31,27). Such flaws in the action of insulin occur even before prediabetes is detected.
This is the essence of insulin resistance. Insulin is present but it is unable to promote the absorption of glucose into cells. Consequently, the pancreas keeps on creating more and more insulin in an effort to correct the rising blood sugar levels. Unfortunately, all that results is increasing levels of insulin in the blood along with continuing high levels of sugar. Sadly, the pancreas cannot keep up this elevated rate of insulin production forever. Eventually, its beta cells, the ones that produce the insulin, wear out and begin to die, leading eventually to the necessity of injecting insulin in a type-2 diabetic (33).
The communication problem between insulin and the cell is caused by fat stored in the cells, producing toxic metabolites and inflammatory free radicals that block the insulin signalling pathway. When this happens, it doesn’t matter how much insulin is produced, its message will not be received and glucose absorption will be minimal. There is considerable scientific evidence supporting the role of excess fatty acids as the main cause of insulin resistance both in the muscles and the liver (34,35). Long-chain saturated fatty acids such as palmitic and stearic acids are particularly potent inducers of insulin resistance (36,37).
What is the evidence that a high-fat diet leads to insulin resistance?
Ingestion of any type of fat, including polyunsaturated fat, monounsaturated fat and saturated fat, causes increased fatty acid levels in the bloodstream. High total fat ingestion is associated with increased levels of fasting insulin and decreased insulin sensitivity. Saturated fat is especially potent in these effects, likely because it creates more toxic breakdown products and increased oxidative stress (38,39,40).
Research in healthy, non-diabetics shows that saturated fat ingestion causes insulin resistance
Eating a high-fat diet has become a good predictor for the development of insulin resistance in healthy people. It can also predict the progression of insulin resistance into type-2 diabetes (38).
Evidence for the blood sugar increasing effect of high total dietary fat and high saturated fat in non-diabetics is plentiful and consistent (41,42,43,44). In research on non-diabetic people, saturated fat ingestion can cause reduced insulin sensitivity within hours (45). Even though subjects were not diabetic and should have been able to boost their insulin secretion from the pancreas to reduce blood sugar levels, the insulin produced did not prevent blood sugar levels from rising (39). Even a modest increase in fat in the blood has shown inhibition of insulin signalling (46). Researchers calculate that increases in the intake of fat of 40 gm/day is associated with increasing insulin resistance and a 3.4-fold increase in risk for type-2 diabetes (42). Other studies have infused free fatty acids directly into the leg veins of healthy adolescent volunteers and reported a 50% increase in the fat content of their muscle cells and the development of insulin resistance (47).
High-fat diets weaken the gut immune system. A type of antibody known as IgA is produced naturally in the gut. This antibody plays a crucial role in regulating the bacterial species that live in the gut, selecting for healthy ones and neutralizing potentially dangerous bacteria. Animal studies have shown that a high-fat diet reduces IgA resulting in a significant shift in the gut microbial population towards unhealthy species of bacteria and a compromised intestinal immune system. The result is that bacteria begin to leak through the lining of the gut into the bloodstream, causing inflammation and insulin resistance (48).
Low-carb diets are high in protein. It may be surprising to learn that eating a single high-protein meal can also dramatically increase blood sugar levels, especially 3 to 5 hours after consuming the meal. This delayed rise is additive to the rise in blood sugar caused by fat (49). In addition, if a person loses 10% of their body weight on a high-protein diet, the expected benefit on blood glucose levels usually seen after losing weight does not occur (49,50).
High saturated fat intake can cause defects in insulin production and secretion as well as insulin action. Beta cells are the insulin-producing cells in the pancreas. Saturated fats appear to be much more harmful to beta cells than are unsaturated fats (51,39).
The Nitty Gritty on Low-Carb Diets
When you eat a diet low in carbohydrates, you inevitably consume mostly fats and proteins. You have essentially removed carbohydrates from your diet, severely lowering the nutrient that shows up as high blood sugar. However, the replacement nutrients you are eating are the very ones that cause insulin resistance. Sugar, a carbohydrate, is not the cause of this problem; it is only the symptom.
Unless you are intentionally eating a plant-based low-carb diet, you will be consuming high amounts of saturated fats from foods such as meats, eggs, butter, dairy products and coconut oil. These are the very fats that build up inside your muscle and liver cells and cause insulin resistance. Because you are eating only a few carbohydrates, you can indeed lower and stabilize your blood glucose levels. But if you then eat extra carbohydrate-containing foods once in awhile, say an orange or a slice of bread or two, your blood sugar will soar. This does not mean that you shouldn’t eat carbohydrates; it means that you have made yourself insulin resistant. Many people are simply happy to be losing weight and plan to continue to avoid carbohydrates for the rest of their lives. Sadly, this is a mistake.
The conundrum here is that the healthiest foods in the world are the foods avoided when restricting carbohydrates. There is abundant evidence to show that people who eat low-carb diets are at significantly higher risk for early death from all causes and increase their risks for many chronic diseases including the big three; cardiovascular disease including high blood pressure, coronary artery disease, atherosclerosis and stroke; diabetes; and cancer (52). In addition, weight loss, the main benefit of eating a low-carb diet, can also be accomplished on a high-carb diet with the bonus of optimizing total body health and preventing many chronic diseases (53,54,61).
How Can Insulin Resistance be avoided?
Perhaps by now the answer to this question is obvious. Go back to the cause of insulin resistance. Elevated fat storage in tissues not intended to store fat and being overweight comes from eating too many fats in the diet (55,56). Excess dietary protein and lack of exercise also have their own roles to play.
Many studies have shown that blood sugar control is improved by eating diets higher in carbohydrate and naturally-occurring fiber and lower in fat (38). Increasing dietary fiber is associated with greater insulin sensitivity (57). Weight loss improves insulin sensitivity (58). Higher daily physical activity is associated with better insulin sensitivity (59).
The vast majority of available scientific evidence regarding the health of different diets clearly shows that a diet high in whole food carbohydrates** from plants is the most effective way to prevent and reverse many chronic diseases including insulin resistance, metabolic syndrome and diabetes (60).
** Carbohydrates found in whole plants are complex carbohydrates, high in fiber and other healthful nutrients such as vitamins, phytochemicals and antioxidants, unlike refined carbohydrates such as refined sugar and white flour that have been stripped of their beneficial components.
Eating a diet based on whole plant foods (legumes, whole grains, vegetables, fruits, nuts and seeds) is a high carbohydrate, high fiber diet that is low in fat and completely adequate in protein. Such a diet prevents obesity and fosters weight loss. Add to this some daily physical activity and you have yourself a lifestyle that enhances insulin sensitivity. This way of life also promotes increased lifespan AND increased healthspan. In other words, it is a pathway toward excellent health throughout a lifetime and enjoyment of life into old age (60).
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