The New Atkins For A New You Part 23

JUST TO BE CLEAR.

We've packed a lot of information into the plans. Here's how to read them: - Recipes that appear in this book are in boldface. See the recipe index on page 203 for page numbers.- Meals and snacks show the carb content of each item and a subtotal.- When a meal or snack includes an incremental food for the higher level of Net Carbs, it appears in bold italics.- When a meal or snack includes an incremental food the higher level of carb content in the subtotal follows the lower level and is in parentheses.- The day's total appears at the bottom of each day. In the case of two-tiered plans, the higher level of carb intake appears in parentheses.- Foundation vegetables are also listed in the day's tally.

Finally, a daily variance at any carb level is natural and fine as long as you don't consistently overshoot your carb tolerance level, as you'll see in the daily totals.

INDEX OF MEAL PLANS.

Phase 1, Induction 20 grams of Net Carbs 24647 Phase 2, ongoing Weight Loss 25 and 30 grams of Net Carbs 24849 35 and 40 grams of Net Carbs 25051 45 and 50 grams of Net Carbs 25253 Phase 3, Pre-Maintenance, and Phase 4, Lifetime Maintenance 55 and 65 grams of Net Carbs 25455 75 and 85 grams of Net Carbs 25657 95 grams of Net Carbs 25859 VEGETARIAN AND VEGAN MEAL PLANS.

Phase 2, Ongoing Weight Loss Vegetarian at 30 and 35 grams of Net Carbs 26061 Vegetarian at 40 and 45 grams of Net Carbs 26263 Vegetarian at 50 and 55 grams of Net Carbs 26465 Vegan at 50 grams of Net Carbs 27273 Phase 3, Pre-Maintenance, and Phase 4, Lifetime Maintenance Vegetarian at 60 and 70 grams of Net Carbs 26667 Vegetarian at 80 and 90 grams of Net Carbs 26869 Vegetarian at 100 grams of Net Carbs 27071

Phase 1, Induction

Phase 2, Ongoing Weight Loss, at 25 and 30 Grams of Ongoing Weight Loss, at 25 and 30 Grams of Net Carbs (30-gram additions in bold italics) Net Carbs (30-gram additions in bold italics)

Phase 2, Ongoing Weight Loss, at 35 and 40 Grams of Net Carbs (40-gram additions in bold italics)

Phase 2, Ongoing Weight Loss, at 45 and 50 Grams of Net Carbs (50-gram additions in bold italics)

* www.atkins.com/Recipes/showRecipe884/Atkins-Cuisine-waffles.aspx.

Phase 3, Pre-Maintenance, and Phase 4, Lifetime Maintenance, at 55 and 65 Grams of Net Carbs (65-gram additions in bold italics)

*www.atkins.com/Recipes/showRecipe884/Atkins-Cuisine-waffles.asp, **www.atkins.com/Recipes/showRecipe883/Atkins-Cuisine-Pancakes.aspx.

Phases 3, Pre-Maintenance, and 4, Lifetime Maintenance, at 75 and 85 Grams of Net Carbs (85-gram additions in bold italics)

* www.atkins.com/Recipes/showRecipe884/Atkins-Cuisine-waffles.aspx, **www.atkins.com/Recipes/showRecipe883/Atkins-Cuisine-Pancakes.aspx.

Phases 3, Pre-Maintenance, and 4, Lifetime Maintenance, at 95 Grams of Net Carbs

* www.atkins.com/Recipes/showRecipe884/Atkins-Cuisine-waffles.aspx, **www.atkins.com/Products/productdetail.aspx?productID=36, ***www.atkins.com/Recipes/showRecipe883/Atkins-Cuisine-Pancakes.aspx.

Phase 2, Ongoing Weight Loss, Vegetarian, at 30 and 35 Grams of Net Carbs (35-gram additions in bold italics)

Phase 2, Ongoing Weight Loss, Vegetarian, at 40 and 45 Grams of Net Carbs (45-gram additions in bold italics)

Phase 2, Ongoing Weight Loss, Vegetarian, at 50 and 55 Grams of Net Carbs (55-gram additions in bold italics)

Phase 3, Pre-Maintenance, and Phase 4, Lifetime Maintenance, Vegetarian, at 60 and 70 Grams of Net Carbs (70-gram additions in bold italics)

* www.atkins.com/Recipes/showRecipe883/Atkins-Cuisine-Pancakes.aspx, **www.atkins.com/Recipes/showRecipe884/Atkins-Cuisine-waffles.aspx Phase 3, Pre-Maintenance, and Phase 4, Lifetime Maintenance, Vegetarian, at 80 and 90 Grams of Net Carbs (90-gram additions in bold italics)

* www.atkins.com/Recipes/showRecipe883/Atkins-Cuisine-Pancakes.aspx, **www.atkins.com/Recipes/showRecipe884/Atkins-Cuisine-waffles.aspx Phase 3, Pre-Maintenance and Phase 4, Lifetime Maintenance, Vegetarian, at 100 Grams of Net Carbs

*www.atkins.com/Recipes/showRecipe883/Atkins-Cuisine-Pancakes.aspx, **www.atkins.com/Recipes/showRecipe884/Atkins-Cuisine-waffles.aspx Phase 2, Ongoing Weight Loss, Vegan, at 50 Grams of Net Carbs

Part IV

A DIET FOR LIFE: The Science of Good Health

Chapter 13 METABOLIC SYNDROME AND CARDIOVASCULAR HEALTH.

The words healthy healthy and and low fat low fat seem inextricably linked, but the rationale for a low-fat diet is based on two overly simplistic ideas that we now understand to be incorrect. seem inextricably linked, but the rationale for a low-fat diet is based on two overly simplistic ideas that we now understand to be incorrect.

In this and the following chapter, we'll highlight how carbohydrate-restricted approaches can address cardiovascular disease (and metabolic syndrome) and diabetes and look at the impressive body of research in both these areas. (You may want to share these chapters with your health care professional.) One in four deaths in the United States stems from heart disease, making it the leading cause of death for both women and men. Heart disease develops over decades, and a poor diet can aggravate and accelerate its progression. Whether you have a strong family history of heart disease or you're blessed with cardioprotective genes, you can improve your quality of life by adopting a healthy diet that targets some of the known modifiable risk factors.

Although the majority of the medical establishment has focused on LDL cholesterol, an increased understanding of the progression of heart disease has directed attention and appreciation toward other risk factors. For example did you know that LDL cholesterol is actually a family of particles of various sizes and that the smallest particles are the most dangerous ones? The Atkins Diet eradicates small LDL particles like a strategic missile defense system. You'll soon understand the significance of this fact for both cardiovascular disease and metabolic syndrome.

Before we go any further, two brief definitions are in order. In simple terms, metabolic syndrome is a collection of markers that amplifies your risk for heart disease, including high blood triglyceride level, low HDL cholesterol level, and elevated glucose and insulin levels. Likewise, in simple terms, inflammation is a catchall word that encompa.s.ses the processes by which your body protects you from unfamiliar and potentially damaging substances. As part of your body's natural defense system, a certain amount of inflammation is healthy, especially when it responds to infection, irritation, or injury. But once the battle has been fought, inflammation should return to normal levels. Unchecked inflammation, which can be detected during the early phases of heart disease by elevated levels of C-reactive protein (CRP), is now understood to be one of the best predictors of future heart problems. Levels of triglycerides, HDL cholesterol, glucose, and insulin are also important markers that provide a complete picture of your overall risk status. We'll explore both conditions in detail below.

This chapter will explore the ascendancy of scientific studies supporting the effectiveness of diets low in carbohydrate as a way to achieve cardiovascular heath. This is true even though you'll be eating plenty of fat. If you've read the rest of this book, we can a.s.sume that you've put aside any fear of fat. In case you still have any lingering anxiety, however, the following pages will convince you otherwise. First, however, let's consider the rationale for a low-fat diet and issue a report card.

ARE LOW-FAT DIETS A MAJOR SUCCESS OR A SERIOUS DISTRACTION?.

Most of you know that for the last few decades, the government agencies concerned with health care have beamed forth a strong and unwavering message: reduce your total fat, saturated fat, and cholesterol intake to achieve a healthy weight and decrease heart disease. The message has been so unrelenting that the terms "healthy" and "low fat" seem inextricably linked, but the rationale for a low-fat diet is based on two overly simplistic ideas that we now understand to be incorrect.

First, fat contains 9 Calories per gram, more than twice the 4 Calories per gram of both protein and carbohydrate. Since fat is more calorically dense, reducing intake of it should be the easiest way to promote weight loss, while still allowing you to eat a greater total volume of food and thus feel satisfied. This logic is expressed in the axiom "You are what you eat." In other words, if you eat fat, you must get fat. The corollary is that if you eat less fat, then you'll easily lose body fat. Many Americans have embraced this seemingly intuitive strategy hook, line, and sinker, only to find themselves drowning in disappointment.

As a nation, our consumption of total fat and saturated fat has remained relatively steady and even trended slightly downward over the last two decades. So why are we experiencing frightening twin epidemics of obesity and diabetes? And why has metabolic syndrome become a significant health threat to tens of millions of Americans? Not because we failed to pay attention to dietary recommendations focused on lowering fat. Rather, we replaced fat calories with an abundance of carbohydrate calories, without understanding that many people have a metabolism that cannot process the additional carbohydrate. Basically, the low-fat approach has backfired.

A second reason for the major emphasis on reducing dietary fat, saturated fat, and cholesterol is based on the belief that consumption of fatty foods will lead to increased blood cholesterol levels, which, in turn, will increase the incidence of heart disease. This belief system, often called the "diet-heart hypothesis," has shaped nutrition policy in this country for the last forty years. Despite decades of research and billions of taxpayer dollars earmarked to prove this hypothesis, there's little evidence to support its basic premise.

The largest and most expensive study on the role of fat in the diet was the Women's Health Initiative, a randomized, controlled trial in which almost 50,000 postmenopausal women aged 50 to 79 were tracked for an average of eight years. Researchers a.s.signed partic.i.p.ants either to a low-fat diet that reduced total fat intake and increased the intake of vegetables, fruits, and grains, or to a control group who could eat whatever they wanted. Multiple research papers reported on the results of this colossal experiment, which can be summarized as nothing short of a major public health disappointment. A low-fat eating pattern revealed no significant effect on weight loss or the incidence of heart disease, diabetes, or cancer.1 You can see why the low-fat dietary approach to weight control gets a failing grade. You can see why the low-fat dietary approach to weight control gets a failing grade.

METABOLIC SYNDROME.

As waistlines expand, so does the epidemic of metabolic syndrome. It's estimated that nearly one of every four American adults has this condition,2 which puts them on the fast track to developing type 2 diabetes and triples their risk for developing heart disease. The identification of metabolic syndrome two decades ago which puts them on the fast track to developing type 2 diabetes and triples their risk for developing heart disease. The identification of metabolic syndrome two decades ago3 is now recognized as a turning point in our understanding of metabolism as it plays out in the clinical states of obesity, diabetes, and cardiovascular disease. As a theory, metabolic syndrome represents an alternative and conflicting paradigm to the diet-heart hypothesis because elevated LDL cholesterol is typically not a problem in metabolic syndrome. More important, the most effective treatment for metabolic syndrome is restriction of carbohydrate, not fat. Restricting dietary fat and replacing it with carbohydrate actually exacerbates many of the problems of metabolic syndrome. The metabolic syndrome paradigm has therefore caused a great deal of distress-and pushback-among those advocating low-fat diets. is now recognized as a turning point in our understanding of metabolism as it plays out in the clinical states of obesity, diabetes, and cardiovascular disease. As a theory, metabolic syndrome represents an alternative and conflicting paradigm to the diet-heart hypothesis because elevated LDL cholesterol is typically not a problem in metabolic syndrome. More important, the most effective treatment for metabolic syndrome is restriction of carbohydrate, not fat. Restricting dietary fat and replacing it with carbohydrate actually exacerbates many of the problems of metabolic syndrome. The metabolic syndrome paradigm has therefore caused a great deal of distress-and pushback-among those advocating low-fat diets.

Metabolic syndrome involves a cl.u.s.ter of markers that predispose people to diabetes and heart disease. Because metabolic syndrome includes the presence of more than one of several potential markers, the public health community has struggled with the decision of how best to define, diagnose, and treat it. Obesity is a common characteristic, particularly excessive fat in the waist and stomach area, which makes a person look "apple-shaped." Problems with fat metabolism manifest as high plasma levels of triglycerides, and although a patient's LDL cholesterol is usually within the normal range, the size size of the LDL particles tends to be the small, more dangerous type. High blood pressure is another common marker, as is elevated blood glucose. Additional markers include chronically elevated inflammation and abnormal blood vessel function (see the sidebar "Do You Have Metabolic Syndrome?"). of the LDL particles tends to be the small, more dangerous type. High blood pressure is another common marker, as is elevated blood glucose. Additional markers include chronically elevated inflammation and abnormal blood vessel function (see the sidebar "Do You Have Metabolic Syndrome?").

DO YOU HAVE METABOLIC SYNDROME?.

A person is defined as having metabolic syndrome if he or she has three or more of the following markers. 4 4

Men Women 1 Waist Circ.u.mference 40 inches 35 inches Triglycerides 150 mg/dL*

150 mg/dL HDL cholesterol 40 mg/dL 50 mg/dL Blood pressure 130/85 mm Hg or use of medication for hypertension 130/85 mm Hg or use of medication for hypertension Fasting glucose 100 mg/dL or use of medication for high blood glucose 100 mg/dL or use of medication for high blood glucose *Milligrams per deciliter.

Why do the diverse problems that characterize metabolic syndrome tend to show up? The prevailing opinion is that all of them are signs of insulin resistance, which is defined as the diminished ability of a given concentration of insulin to exert its normal biological effect. When insulin resistance develops, it has broad effects on a variety of metabolic pathways that can lead to the specific markers for metabolic syndrome. But not everyone responds to insulin resistance in the same way; moreover, the time frame in which certain signs develop varies. This variability makes defining-and treating-metabolic syndrome tricky.

Treatment of metabolic syndrome is controversial, with nutritional approaches generally downplayed in favor of multiple medications that target the individual components. Conventional recommendations tend to emphasize caloric restriction and reduced fat intake, even though metabolic syndrome can best be described as carbohydrate intolerance. Think of it as the first signs of the metabolic bully leaving marks. Low-carbohydrate diets therefore make intuitive sense as a first-line treatment. Let's take a closer look at how they impact the various features of both metabolic syndrome and heart disease.5 GLUCOSE AND INSULIN.

Increased glucose levels are a signal that the body may be having trouble processing dietary carbohydrate. High insulin levels usually go hand in hand with elevated fasting glucose levels. (See "Understanding Blood Sugar Readings" on page 297.) Dietary carbohydrate contributes directly to blood glucose levels and is well accepted as the major stimulator of insulin secretion. Lowering carbohydrate intake is the most direct method to achieve better control of both glucose and insulin levels. Could it really be that simple? Yes, it is. The insulin resistance of metabolic syndrome is characterized by intolerance to carbohydrate. If you have lactose intolerance, you avoid lactose. If you have gluten intolerance, you avoid gluten. You get the idea.

Not surprising, many studies of low-carbohydrate diets have shown that glucose levels improve significantly in subjects following them.6 Insulin levels also decrease, regardless of glucose tolerance status and even in the absence of weight loss. Insulin levels also decrease, regardless of glucose tolerance status and even in the absence of weight loss.7 The reduction in insulin levels throughout the day, even after meals, is crucial to promoting a metabolic environment that favors fat burning. In this way, controlling carbohydrate intake has an important effect on the way the body handles fat, along with profound effects on lipid and cholesterol levels. But before we discuss the research on lipids, a quick tutorial on insulin is in order. The reduction in insulin levels throughout the day, even after meals, is crucial to promoting a metabolic environment that favors fat burning. In this way, controlling carbohydrate intake has an important effect on the way the body handles fat, along with profound effects on lipid and cholesterol levels. But before we discuss the research on lipids, a quick tutorial on insulin is in order.

HOW INSULIN WORKS.

The pancreas makes and releases the hormone insulin in response to increases in blood glucose. Its most recognized function is to restore glucose levels to normal by facilitating the transport of blood glucose into (mainly) muscle and fat cells. However, insulin has a mult.i.tude of other effects and is generally described as the "storage hormone" because it promotes the storage of protein, fat, and carbohydrate. For example, insulin facilitates the conversion of amino acids into protein and also promotes the conversion of dietary carbohydrate into either glycogen (the storage form of carbohydrate in the body) or fat. While insulin promotes the storage of nutrients, it simultaneously blocks the breakdown of protein, fat, and carbohydrate in the body. Put another way, when insulin is increased, it puts the brakes on burning fat for fuel and at the same time encourages storage of incoming food, mostly as fat. But when you limit your carbohydrate consumption, you stimulate increased fat burning and decreased fat synthesis.

In fact, fat breakdown and fat burning are exquisitely sensitive to changes in the amount of insulin released in response to dietary carbohydrate.8Small decreases in insulin can almost immediately increase fat burning severalfold. Insulin also increases glucose uptake and activates key enzymes that transform glucose into fat. Because low-carbohydrate diets significantly blunt insulin levels throughout the day, the Atkins Diet is a.s.sociated with significant changes in fat metabolism that favor decreased storage and increased breakdown. Translation: you burn more body fat and store less. This is an important adaptation that contributes to a decreased risk for heart disease with better lipid profiles and improvement in all features of metabolic syndrome. This is why dietary fat is your friend and consuming carbohydrate above your tolerance level acts as a metabolic bully.

CONTROL CARBS TO BURN FAT.

Controlling carbohydrate intake and the subsequent decline in insulin levels permits most of the body's cells to use fat almost exclusively for energy, even while an individual is exercising.9 During Induction and OWL, body fat provides a large share of that energy. During Pre-Maintenance and Lifetime Maintenance, the diet provides most of the needed fuel. Either way, the final effect of the core principle of the Atkins Diet, keeping carb intake at or just below one's individual carb threshold, is the creation of a metabolic state characterized by enhanced mobilization and utilization of both dietary and body fat. Many of the beneficial effects of the Atkins Diet on risk factors for metabolic syndrome and heart disease are extensions of this powerful transformation. During Induction and OWL, body fat provides a large share of that energy. During Pre-Maintenance and Lifetime Maintenance, the diet provides most of the needed fuel. Either way, the final effect of the core principle of the Atkins Diet, keeping carb intake at or just below one's individual carb threshold, is the creation of a metabolic state characterized by enhanced mobilization and utilization of both dietary and body fat. Many of the beneficial effects of the Atkins Diet on risk factors for metabolic syndrome and heart disease are extensions of this powerful transformation.

THE SATURATED FAT PARADOX.

Now that you know that you shouldn't avoid dietary fat on a low-carbohydrate diet, you might still have some skepticism about eating saturated fat. After all, just about every health expert would advise you to limit it, and one of the major criticisms of the Atkins Diet is that it contains more saturated fat than is currently recommended. Let us put your mind at rest.

When one nutrient in the diet decreases, usually one or more other nutrients replace it. In fact, researchers have explored the question of what happens when you reduce saturated fat in the diet and replace it with carbohydrate. A recent metastudy made up of eleven American and European cohort studies that followed more than 340,000 subjects for up to ten years came to the conclusion that replacing saturated fat with carbohydrate increases the risk of coronary events.10 Yes, according to the best scientific evidence, the very recommendation made by most health experts to reduce saturated fat actually Yes, according to the best scientific evidence, the very recommendation made by most health experts to reduce saturated fat actually increases increases your chances of having heart disease. Yet this is the same dietary pattern adopted by many Americans. your chances of having heart disease. Yet this is the same dietary pattern adopted by many Americans.11 The failure of low-fat dietary approaches is partially explained by the lack of understanding that many people consume more carbohydrates when they lower their saturated fat intake. The culprit is not saturated fat per se. If your carbohydrate intake is low, there's little reason to worry about saturated fat in your diet. The failure of low-fat dietary approaches is partially explained by the lack of understanding that many people consume more carbohydrates when they lower their saturated fat intake. The culprit is not saturated fat per se. If your carbohydrate intake is low, there's little reason to worry about saturated fat in your diet.

However, if your carbohydrate intake is high, increasing the levels of saturated fat in your diet may become problematic. Higher levels of saturated fatty acids in the blood have been shown to occur in individuals with heart disease.12 As you now know, the Atkins Diet is all about controlling your carbohydrate intake to ensure that fat remains your body's primary fuel. This explains why, on Atkins, saturated fat intake is not a.s.sociated with harmful effects. Two of the authors of this book explored what happens to saturated fat levels in subjects who were placed on the Atkins Diet. As you now know, the Atkins Diet is all about controlling your carbohydrate intake to ensure that fat remains your body's primary fuel. This explains why, on Atkins, saturated fat intake is not a.s.sociated with harmful effects. Two of the authors of this book explored what happens to saturated fat levels in subjects who were placed on the Atkins Diet.13 In this experiment, the Atkins subjects consumed three times the levels of saturated fat as did subjects consuming a low-fat diet. Both diets contained the same number of calories, meaning that all the subjects were losing weight. After twelve weeks, the Atkins group subjects showed consistently greater reductions in the relative proportion of saturated fat in their blood. In this experiment, the Atkins subjects consumed three times the levels of saturated fat as did subjects consuming a low-fat diet. Both diets contained the same number of calories, meaning that all the subjects were losing weight. After twelve weeks, the Atkins group subjects showed consistently greater reductions in the relative proportion of saturated fat in their blood.

This inverse a.s.sociation between dietary intake and blood concentrations of saturated fat prompted further experiments to validate the effect under controlled conditions. The additional study involved weight-stable men who habitually consumed a typical American diet. They followed a low-carbohydrate diet akin to the Lifetime Maintenance Phase, which contained more saturated fat than did their regular diet. All foods were prepared and provided to the subjects during each feeding period. Enough food was provided to maintain their weight. After six weeks on the diet, despite consuming more saturated fat, the men showed a significant reduction in their blood levels of saturated fat. They also improved their triglyceride and HDL cholesterol levels, LDL particle size, and insulin level. This study further supports the conclusion that low dietary carbohydrate is a key stimulus positively impacting the metabolic processing of ingested saturated fat.14 These studies clearly show that low-carbohydrate diets high in saturated fat show effects that are very different from results in studies of individuals following a moderate- to high-carbohydrate diet. The likely cause is a combination of less storage and greater burning of saturated fat. This research supports the conclusion that dietary fat, even saturated fat, isn't harmful in the context of a low-carbohydrate diet.15 A LONG HISTORY OF SAFE USE.

An equally valid indication of the long-term safety of low carbohydrate diets can be found in the doc.u.mented experience of Europeans as they explored the North American continent and its established cultures. Very often, the most successful explorers were those who adopted the diet of the indigenous cultures, which in many regions consisted mostly of meat and fat with little carbohydrate. Examples of explorers who doc.u.mented such experiences include Lewis and Clarke, John Rae,16 Frederick Schwatka, Frederick Schwatka,17and even Daniel Boone.

The explorer whose experience living as a hunter was the most carefully doc.u.mented was the controversial anthropologist Vilhjalmur Stefansson. After spending a decade in the Arctic among the Inuit in the early 1900s, he wrote extensively about their diet around the same time that scientists discovered the existence of vitamins. Challenged to prove that he could remain healthy on a diet of meat and fat, he ate an Inuit diet under close medical observation for a year. The result, published in a prestigious scientific journal,18 demonstrated that Stefansson remained well and physically capable while consuming a diet of more than 80 percent animal fat and about 15 percent protein. demonstrated that Stefansson remained well and physically capable while consuming a diet of more than 80 percent animal fat and about 15 percent protein.

In addition to recounting some remarkable stories of physical stamina and courage, the reports of these explorers provide valuable insight into the dietary practices of aboriginal hunting societies that lived for millennia on little or no dietary carbohydrate. Of particular importance was the practice of valuing fat over protein, so that the preferred mix of dietary energy was high in fat and moderate in protein. Also of note: Rae, Boone, and Stefansson all lived into their eighties, despite eating mostly meat and fat for years.

Though these historical lessons don't, in and of themselves, prove the long-term safety of low-carbohydrate diets, they const.i.tute strong supporting evidence. When this acc.u.mulated history of safe use is combined with our recent research into the effects of carbohydrate restriction on blood lipids and indicators of inflammation, the inescapable conclusion is that a properly formulated low-carbohydrate diet can be safely utilized for months or even years.

RESEARCH ON SEIZURE CONTROL.

In the early 1920s, physicians observed that people subject to epileptic seizures experienced relief when they were placed on a total fast for two weeks. However the benefits of this treatment didn't continue when eating resumed, and a complete fast causes muscle wasting, so this was obviously not a sustainable treatment. But in a series of reports, a Minnesota physician, Mynie Peterman, demonstrated that a very-low-carb diet produced a similar effect in children, reducing or stopping their seizures, and that this diet could be effectively followed for years. 19 19 In 1927, Dr. Henry Helmholz reported on more than one hundred cases of childhood seizures treated with Dr. Peterman's ketogenic diet.20 His results indicated that about one-third of the children were cured of seizures, one-third improved, and one-third didn't respond to the treatment. A ketogenic diet remained the "standard of care" for seizure disorders until effective antiseizure drugs were developed in the 1950s. Between 1922 and 1944, doctors at the Mayo Clinic in Minnesota prescribed the ketogenic diet to 729 seizure patients, with success rates similar to those originally reported by Dr. Peterman. His results indicated that about one-third of the children were cured of seizures, one-third improved, and one-third didn't respond to the treatment. A ketogenic diet remained the "standard of care" for seizure disorders until effective antiseizure drugs were developed in the 1950s. Between 1922 and 1944, doctors at the Mayo Clinic in Minnesota prescribed the ketogenic diet to 729 seizure patients, with success rates similar to those originally reported by Dr. Peterman.21 Most of these patients stayed on the diet for a year or two, but some continued it for more than three decades. Most of these patients stayed on the diet for a year or two, but some continued it for more than three decades.The development of antiseizure drugs with similar efficacy rates superseded the ketogenic diet between 1960 and 1980. Although the diet is equally effective, it's far easier for a doctor to write a prescription for a drug than to educate and motivate an individual or family to make a major dietary change. In the 1990s, Dr. John Freeman at Johns Hopkins University revived the ketogenic diet and reported that many children whose seizures didn't respond to drugs did respond to the low-carb diet. With Dr. Eric Kossoff, Dr. Freeman also noted that children experienced fewer side effects from the low-carbohydrate diet than they did from the antiseizure drugs. For example, not surprisingly, their school performance was better when they were off the drugs. These observations have led to a resurgence of interest in low-carbohydrate diets to treat both children and adults suffering from seizures.22 Today, more than seventy clinics in the United States report the use of this dietary treatment for seizures. Today, more than seventy clinics in the United States report the use of this dietary treatment for seizures.

INDICATORS OF IMPROVEMENT.

Now let's take a closer look at some of the most common markers improved by low-carbohydrate diets.

TRIGLYCERIDES.

Much of the fat circulating in your blood, and much of that available to be burned as fuel, is in the form of triglycerides. Increased blood levels of triglycerides are a key feature of metabolic syndrome and have been shown to be an independent risk factor for heart disease. One of the most dramatic and consistent effects of lowering carbohydrate consumption is a reduction in triglyceride levels. In fact, the decline rivals that produced by any current drugs. Most studies focus on fasting levels of triglycerides, but after a meal, fat is packaged into triglycerides within the gastrointestinal tract that are dumped into your blood. The liver can also pump out triglycerides after a meal, especially one high in carbohydrate. People who have an exaggerated and prolonged elevation of blood triglycerides, whether from a high-fat or high-carbohydrate meal, have been shown to be at increased risk for heart disease. The good news is that low-carbohydrate diets consistently decrease triglycerides both in the fasting state and and in response to meals. in response to meals.23 Interestingly, this beneficial effect occurs even when weight loss is minimal. Interestingly, this beneficial effect occurs even when weight loss is minimal.24 HDL CHOLESTEROL.

The clinical significance of increased HDL levels is well established as an important target for good health.25 Higher levels are desirable because this lipoprotein offers protection against heart disease. Typical lifestyle changes such as exercise and weight loss are often recommended to increase HDL, but their effects are small compared to those achieved by following a low-carbohydrate diet, which consistently outperform low-fat diets in raising HDL levels. Higher levels are desirable because this lipoprotein offers protection against heart disease. Typical lifestyle changes such as exercise and weight loss are often recommended to increase HDL, but their effects are small compared to those achieved by following a low-carbohydrate diet, which consistently outperform low-fat diets in raising HDL levels.26 The effects are prominent in men and even more so in women. The effects are prominent in men and even more so in women.27 Dietary saturated fat and cholesterol are actually important nutrients that contribute to an increase in HDL cholesterol levels. Replacing carbohydrate with fat has also been shown to increase HDL. Dietary saturated fat and cholesterol are actually important nutrients that contribute to an increase in HDL cholesterol levels. Replacing carbohydrate with fat has also been shown to increase HDL.

KETONES: WHAT ARE THEY, AND WHAT DO THEY DO?.

Antiseizure diets are often referred to as ketogenic diets because restricting carbohydrates requires that the body use an alternative to glucose (blood sugar) as the brain's primary fuel. In place of glucose, the liver uses fat molecules to make acetoacetate and hydroxybutyrate, two compounds known as ketones. The body adopts this same fuel strategy during a total fast of more than a few days. Ketones have gotten a bad name because they can rise to very high levels in individuals with uncontrolled type 1 diabetes, a state known as diabetic ketoacidosis. However, there is more than a tenfold difference between the ketone levels seen in ketoacidosis and those achieved with a carbohydrate-restricted diet, which we call nutritional ketosis. Equating the two is comparable to confusing a major flood with a gentle shower. Far from overwhelming the body's acid-base defenses, nutritional ketosis is a completely natural adaptation that is elegantly integrated into the body's energy strategy whenever carbs are restricted and fat becomes its primary fuel.

LDL CHOLESTEROL.

The main aim of low-fat diets and many drugs such as statins is to lower concentrations of LDL cholesterol. On average, low-fat diets are more effective at lowering LDL cholesterol levels than are low-carbohydrate diets. But before you chalk up this marker to low fat, consider that simply lowering LDL cholesterol by restricting dietary fat doesn't reduce your risk of developing heart disease.28 Why? An obvious reason is that low-fat diets exacerbate other risk factors; they increase triglycerides and reduce HDL cholesterol. But there's another explanation that relates to the LDL particles themselves. Not all forms of LDL particles share the same potential for increasing heart disease. Within the category labeled LDL, there is a continuum of sizes, and research shows that smaller LDL particles contribute more to plaque formation in arteries (atherosclerosis) and are a.s.sociated with a higher risk for heart disease. Although low-fat diets may decrease total LDL concentration, they tend to Why? An obvious reason is that low-fat diets exacerbate other risk factors; they increase triglycerides and reduce HDL cholesterol. But there's another explanation that relates to the LDL particles themselves. Not all forms of LDL particles share the same potential for increasing heart disease. Within the category labeled LDL, there is a continuum of sizes, and research shows that smaller LDL particles contribute more to plaque formation in arteries (atherosclerosis) and are a.s.sociated with a higher risk for heart disease. Although low-fat diets may decrease total LDL concentration, they tend to increase increase the proportion of small particles, the proportion of small particles,29 making them more dangerous. However, going in the other direction, numerous studies indicate that replacing carbohydrate with fat or protein leads to increases in LDL size. making them more dangerous. However, going in the other direction, numerous studies indicate that replacing carbohydrate with fat or protein leads to increases in LDL size.30 Therefore, it's clear that carbohydrate intake is strongly and directly related to promoting the forms of LDL that contribute to arterial plaque formation, Therefore, it's clear that carbohydrate intake is strongly and directly related to promoting the forms of LDL that contribute to arterial plaque formation,31 whereas replacing carbohydrates in the diet with fat, even saturated fat, seems to promote the forms of LDL that are harmless. whereas replacing carbohydrates in the diet with fat, even saturated fat, seems to promote the forms of LDL that are harmless.

INFLAMMATION.

As discussed above, when inflammation stays elevated because of a repeated insult such as a poor diet, it spells bad news. Researchers now appreciate the importance of this ongoing low-grade condition in contributing to many chronic health problems, including diabetes, heart disease, and even cancer. We typically think of inflammation in respect to fighting off bacteria and viruses. However, other substances, including excess carbohydrates and trans fats, can contribute to inflammation. A single high-carbohydrate meal can lead to increased inflammation.32 Over time, eating a high-carbohydrate diet can lead to increased markers of inflammation. Over time, eating a high-carbohydrate diet can lead to increased markers of inflammation.33 What about low-carbohydrate diets? Levels of CRP, a cytokine marker for inflammation, have been shown to decrease by approximately one-third on the Atkins Diet.34 In subjects with higher levels of inflammation, CRP levels decreased more in response to a low-carbohydrate diet than to a fat-restricted diet. In subjects with higher levels of inflammation, CRP levels decreased more in response to a low-carbohydrate diet than to a fat-restricted diet.35 A recently published study compared subjects with metabolic syndrome on a low-fat diet to those who were consuming a very-low-carbohydrate diet. The low-carb group showed a greater decrease in eight different circulating inflammatory markers compared to the low-fat group. A recently published study compared subjects with metabolic syndrome on a low-fat diet to those who were consuming a very-low-carbohydrate diet. The low-carb group showed a greater decrease in eight different circulating inflammatory markers compared to the low-fat group.36 These data implicate dietary carbohydrate rather than fat as a more significant nutritional factor contributing to inflammation, although the combination of both increased fat and a high carbohydrate intake may be particularly harmful. These data implicate dietary carbohydrate rather than fat as a more significant nutritional factor contributing to inflammation, although the combination of both increased fat and a high carbohydrate intake may be particularly harmful.

The anti-inflammatory effects of the omega-3 fats EPA and DHA have been shown in cell culture and animal studies, as well as in trials using humans.37 These effects partially explain why these fats appear to have widespread health-promoting effects, especially in reducing the risk of heart disease and diabetes. Several hundred studies have demonstrated the cardioprotective effects of fish oil, and numerous review studies have summarized this body of work. These effects partially explain why these fats appear to have widespread health-promoting effects, especially in reducing the risk of heart disease and diabetes. Several hundred studies have demonstrated the cardioprotective effects of fish oil, and numerous review studies have summarized this body of work.38 That's why we recommend regular consumption of fatty fish or use of a supplement containing EPA and DHA. That's why we recommend regular consumption of fatty fish or use of a supplement containing EPA and DHA.