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From the Townsend Letter
June 2015

Insulin Resistance: The Unintended Consequence of Fat Phobia and the Case for Ketosis
by Sara Wood, ND
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Insulin resistance (IR) is a condition wherein cellular receptors become less sensitive to insulin, causing an inability for glucose to enter the cell and glucose buildup in the bloodstream.1 IR leads to a prediabetic elevation of blood glucose and, eventually, to type 2 diabetes (T2D) if there is no intervention. Between 1980 and 2011, the number of US adults diagnosed with diabetes more than tripled, leaving 9% of the population with diagnosed type 2 diabetes and more than twice that with insulin resistance.2 This epidemic is the 7th leading cause of death in the US and costs an estimated $245 billion a year.3 Though insulin resistance is present in nonobese individuals and not all obese people exhibit IR, obesity and insulin resistance are almost inextricably linked: excess glucose in circulation is stored as fat, and fat tissue is an endocrine organ that promotes insulin resistance through the release of hormones and cytokines.4,5 It can be assumed that one without the other is simply a matter of time and, consequently, suggested lifestyle modifications for IR patients focus primarily on weight loss. Additionally, insulin resistance and heart disease are intimately connected. IR is a key component of metabolic syndrome: a cluster of physiologic changes that includes elevated serum triglyceride levels, hypertension, abdominal obesity, and changes in cholesterol profiles.6 Recommended strategies for both weight loss and reduction in serum lipids typically include the avoidance of fat, which has led to widespread replacement of dietary fat with carbohydrates, consequent elevations in glucose and insulin, and ironically to further an insulin resistance and diabetes epidemic. In short, treatment for obesity and cardiovascular risk significantly contributes to diabetes, which in turn leads to increased cardiovascular disease and obesity.

Led Astray
Of all the "nutritional myths" that have been propagated over the past few decades, one of the most harmful has been the idea that dietary fat, and specifically saturated fat, is responsible for weight gain and increased cardiovascular risk. This erroneous idea has driven many people to choose a "low-fat" diet with higher carbohydrate intake and has contributed to the epidemic of blood sugar dysregulation, insulin resistance, and type 2 diabetes.7,8 In 1977, the initial Dietary Goals for Americans proposed an increase in carbohydrates and a decrease in consumption of saturated fat and cholesterol.9 These guidelines were based on studies that suggested that diets high in these elements increased the risk of coronary artery disease (an idea that has since been repeatedly debunked).10,11 The theory that dietary fat contributes to obesity has evolved because fat contains more calories per gram than either protein or carbohydrates (9 compared with 4); however, this assumption has been discredited several times over.12-14 Decrease in the consumption of one macronutrient requires caloric compensation from another: a reduction in dietary fat typically results in increased carbohydrate intake. Correlation does not prove causation; however, levels of obesity as well as insulin resistance and type 2 diabetes have increased dramatically since the beginning of the low-fat diet trends, indicating that efforts to improve cardiovascular health and treat obesity have seemingly made things worse.15 It has repeatedly been shown that the reduction of sugar is more effective at improving insulin sensitivity, weight loss, and cardiovascular risk than avoidance of fat.16,17 Yet current dietary guidelines still recommend that Americans consume the majority of their calories from carbohydrates and reduce saturated fat to 7% to 10% of total calories.18 Dietary modifications are difficult for many people to implement, as there are many social, environmental, and emotional associations with food that can be difficult to overcome. In addition to having lifelong habits and biochemical cravings, patients are confused about conflicting medical information and ill informed by outdated nutritional guidelines.

If Fat Doesn't Make People Fat, What Does?
Insulin controls the admission of glucose into cells for immediate use, and the presence of insulin indicates a fed state, which facilitates the production of glycogen (stored glucose) in the liver and muscle as well as triglycerides in adipose cells.19 The capacity for glycogen storage is limited to approximately 500 grams (although this varies with muscle mass).20 When glycogen stores are saturated, excess glucose is stored as triglycerides. Additionally, insulin inhibits the mobilization of fatty acids in adipose tissue. Insulin causes the creation of fat, but prevents the breakdown; therefore the key to fat loss (and the prevention of fat accumulation) is controlling insulin, and insulin production is stimulated by the presence of glucose in the blood. There are several proven ways to lower serum glucose and insulin levels, and though their mechanisms are nuanced and efficacies variable, any effort to control insulin is worthwhile in the prevention or treatment of insulin resistance and diabetes.

Spoonful of Sugar
A common place to start with the reduction of carbohydrates is the removal of "added sugar" (sugar that doesn't occur naturally in a given food) from the diet. This is an idea with merit, as Americans (and the rest of the world) are consuming more sugar than ever before, including a dramatic increase in added sweeteners.21,22 Added sugar, and especially high-fructose corn syrup (HFCS), has been especially implicated in contributing to obesity, insulin resistance, and type 2 diabetes.23

Good Carbs vs. Bad Carbs
Many physicians and diabetic associations are counseling their patients on the benefits of a low glycemic index (GI) or low glycemic load (GL) diet, wherein rate of digestion, protein, and fiber content of a food cushion the absorption of sugar into the bloodstream and attenuate the glucose and insulin spike.24-26 The glycemic index is a way to categorize food in relation to its effect on blood sugar and is standardized using glucose as the comparison at a value of 100. This is especially useful in helping patients understand that many foods which they may not consider "sugar," such as grains, potatoes, fruit juices, or baked goods, have a profound impact on blood sugar levels, sometimes equal to or greater than pure glucose. In observational studies, consumption of high-GI foods has been correlated with the incidence of type 2 diabetes and cardiovascular disease.27 A low glycemic index is typically defined as <70.28 The glycemic index doesn't take into account the quantity of a food being consumed, although glycemic load does incorporate average serving size. Low-GI and -GL diets change the way that ingested carbohydrates affect blood sugar levels, but they do not necessarily involve a reduction in total carbohydrates.

Cut Out the Carbs
Low-GI diets have a positive effect on blood sugar markers (fasting glucose, insulin, and hemoglobin A1c), serum lipid levels, and weight; however, they are less efficient than low-carbohydrate diets.29 Carbohydrate is a term for one of the three primary macronutrients consumed in food (the other two being protein and fat). Depending on the size of the carbohydrate molecule, it may be classified as a sugar, starch, or cellulose (fiber); and as the glycemic index shows, these do not have equal impact on physiology. The Institute of Medicine currently recommends that adults consume at least 130 grams of carbohydrates/day, although the average consumption is nearly double that.30 There is no official or regulated definition of "low-carb"; however some consider anything less than the recommended carbohydrate intake (50%–65% of calories or 130 grams/day) to be low. Another commonly used guideline is the restriction of carbohydrates to 20% of total caloric intake. How "low-carb" is defined does matter, as there is a stepwise improvement in risk of diabetes and heart disease for metabolic syndrome patients that correlates with the reduction in dietary carbohydrates.31 When it comes to restrictive diets, most regulatory organizations and dietary guidelines favor a low fat diet; however, the low-fat vs. low-carb debate has been well researched, and data overwhelmingly support the benefits of reducing carbohydrates to improve cardiovascular risk markers and reduce excess weight.32-37

Fat Friendly
Taking the low-carb diet one step further: if carbohydrates are restricted to a level below the requirements of ongoing metabolic need, the liver releases glucose from its glycogen stores until depleted and then begins to break down fat (from the diet as well as body storage) into ketone bodies which can be used as an alternative source of cellular energy. The three primary ketones produced are B-hydroxybutyrate (BHB), acetoacetate, and acetone, which can be measured in serum, urine, and breath respectively. This is a normal adaptive physiologic response, called ketosis, which has historically enabled humans to survive periods of famine. The human body, and especially the brain, requires either glucose or ketones to produce energy, and we can only store about 24 hours' worth of glucose (glycogen). Without the ability to use fat and protein to produce fuel for brain tissue, our ability to survive even short periods of time without dietary carbohydrates would be severely compromised.

Unfortunately, ketones are perhaps best known in medicine for their role in diabetic ketoacidosis (DKA), a dangerous consequence of uncontrolled diabetes caused by a buildup of ketone bodies in the blood that disrupts the serum acid/base balance. In the presence of insulin, ketone production is regulated and toxic levels do not occur. During nutritional ketosis, the serum concentration of BHB (the primary ketone in serum) is typically between 0.5 and 3 mM, whereas the serum levels of a ketoacidotic patient can approach 15 to 25 mM.38 This is a very important distinction to make, as many people confuse the terminology and this mistake has contributed greatly to the condemnation of this diet by many. In small quantities, ketones are not only not dangerous but also provide significant benefit to a variety of conditions, including obesity, insulin resistance, diabetes, cancer, and epilepsy.39-43

The positive effects of nutritional ketosis have been reported for over 80 years, though the name that most people associate with a low-carb, high-fat diet is Dr. Robert Atkins, who brought the ketogenic diet into the mainstream in the 1970s and continued to be a proponent until his death in 2003.44 Atkins's popular diet includes an induction phase that is ketogenic, followed by incremental increases in carbohydrates. The level of carbohydrate restriction required to maintain ketosis is individually variable and many people remain in a state of nutritional ketosis beyond the induction phase. The Atkins diet has been immensely popular despite coinciding with the peak of the low-fat craze. Because the fundamentals of a ketogenic diet (high fat and low-carbohydrate) directly contradict the nutritional guidelines, there has been widespread criticism on the safety of ketosis and carbohydrate restriction.45 To induce nutritional ketosis, not only do carbohydrates need to remain sufficiently low (<50g/day), but adequate dietary fat is required to provide alternative energy. The popular (yet unsubstantiated) idea that dietary fat causes weight gain is often one of the biggest obstacles that patients must overcome when adopting this diet.

With each study published debunking the idea that dietary fat causes obesity and heart disease, the case for a low-carbohydrate, high-fat, ketogenic diet is stronger.46-49 Not all low-carb diets are ketogenic; however, ketogenic diets are all low carb (by definition). Consequently, research that supports the general reduction in carbohydrates further bolsters the case for ketosis. A low-carbohydrate diet reduces insulin resistance, obesity, and cardiovascular risk, and dietary fat (even saturated) does not raise serum lipid levels. The remaining arguments against a ketogenic diet center on the risk of ketones themselves; however, since ketogenic diets have been used for nearly 100 years to treat epilepsy in children, and more recently in adults as well, we do have examples of populations who have safely maintained a state of nutritional ketosis for long periods of time with limited side effects.50-52 In addition to the general benefits of a low-carb diet, a ketogenic diet offers several supplementary advantages: during the catabolism of triglycerides and fatty acids to create ketone bodies in substitution for glucose, the liver will convert glycerol (the backbone of the triglyceride) and protein into glucose through a process called gluconeogenesis, which requires a significant amount of energy (increased caloric expenditure).53 Fat and protein (compared with carbohydrates) have a higher satiety effect, and ketone bodies have been shown to directly suppress hunger.54 So patients on a ketogenic diet increase their metabolic rate and often experience less hunger than on other diets.55 Lipid profiles do not get worse with the ingestion of high fat (as has long been asserted) on a ketogenic diet; rather total cholesterol and LDL levels actually decrease, serum triglycerides decrease, and HDL levels increase: all improvements in cardiovascular risk markers.56 Diabetic patients on a ketogenic diet should be closely monitored, as a reduction in medications may be required as insulin levels decrease.57

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