THE NEW ATKINS FOR A NEW YOU
Page 29
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 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.
Metabolic syndrome involves a cluster 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 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
Men
Women 1
Waist Circumference
≥ 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.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.
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 multitude 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 associated 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.
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 increases 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.
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 associated 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.
This inverse association 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 documented 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 documented such experiences include Lewis and Clarke, John Rae,16 Frederick Schwatka,17and even Daniel Boone.
The explorer whose experience living as a hunter was the most carefully documented 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.
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 constitute strong supporting evidence. When this accumulated 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
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.21 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.
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, fa
t 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 in response to meals.23 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.26 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.
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.