Clinical guide

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WHITE PAPER January 2010 UNDERSTANDING THE ATKINS DIET Information for the Practicing Clinician Dr. Stephen D. Phinney and Dr. Jeff S. Volek The Atkins Diet, also known as the Atkins Nutritional Approach, has attracted millions of followers. As Kleenex is to facial tissue, Atkins has become synonymous with low- carbohydrate diets. Not all low-carbohydrate diets are the same, however; among this class of diet, only the Atkins Diet is grounded in science. The introduction of the Atkins Diet in 1972 occurred at approximately the same time as the institution of low-fat recommendations, which may partially explain the historical resistance to the approach by many health professionals. Despite this combination of inopportune timing and underappreciation of the scientific evidence supporting low-carbohydrate diets, the Atkins Diet has nonetheless enjoyed enduring popularity for nearly four decades. The relative ease of use and prompt weight loss associated with the Atkins Diet represent the tip of the iceberg, as new evidence supports the effectiveness of controlling carbohydrates for a variety of clinical conditions. The scientific method is a process, and over the past decades the nuances of the Atkins Diet have evolved, based on findings from a multitude of new studies that have validated previous work and made new discoveries. The updated Atkins perspective paints a promising picture of efficient and sustained weight loss and robust health improvements. The objective of this white paper is to present the Atkins Diet to healthcare practitioners as a science-based therapeutic tool, sharing new information that will instill confidence and assurance that the Atkins Diet is safe and effective. This guide will: 1) provide a clear physiological explanation of how and why the Atkins Diet works, 2) review the science supporting the Atkins Diet and 3) outline key aspects of the Atkins Diet in practice. The Atkins Diet: How and Why It Works After three decades, the obesity epidemic in the United States and much of the developed world remains unchecked(1). At its most basic level, obesity is a problem of excess storage of body fat, which is often accompanied by other metabolic disturbances. The solution logically involves biasing a person’s metabolism toward oxidizing fat rather than carbohydrate as the body’s primary fuel. The essence of the Atkins Diet is to provide that stimulus by means of reducing dietary carbohydrate and insulin to the point at which the person is able to preferentially oxidize body fat (Fig 1). Finding this point is a unique process, and the updated Atkins Diet provides individualized guidance through its four Low High Insulin Concentration Fat Breakdown Maximum Minimum High Carbohydrate Diet Fig 1. Decreases in plasma insulin, that occur with the Atkins Diet, result in large increases in fat breakdown and oxidation.

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Low carb studies

Transcript of Clinical guide

Page 1: Clinical guide

WHITE PAPER

January 2010

UNDERSTANDING THE ATKINS DIET Information for the Practicing Clinician

Dr. Stephen D. Phinney and Dr. Jeff S. Volek

The Atkins Diet, also known as the Atkins Nutritional Approach, has attracted millions of followers. As Kleenex is to facial tissue, Atkins has become synonymous with low-carbohydrate diets. Not all low-carbohydrate diets are the same, however; among this class of diet, only the Atkins Diet is grounded in science. The introduction of the Atkins Diet in 1972 occurred at approximately the same time as the institution of low-fat recommendations, which may partially explain the historical resistance to the approach by many health professionals. Despite this combination of inopportune timing and underappreciation of the scientific evidence supporting low-carbohydrate diets, the Atkins Diet has nonetheless enjoyed enduring popularity for nearly four decades. The relative ease of use and prompt weight loss associated with the Atkins Diet represent the tip of the iceberg, as new evidence supports the effectiveness of controlling carbohydrates for a variety of clinical conditions. The scientific method is a process, and over the past decades the nuances of the Atkins Diet have evolved, based on findings from a multitude of new studies that have validated previous work and made new discoveries. The updated Atkins perspective paints a promising picture of efficient and sustained weight loss and robust health improvements. The objective of this white paper is to present the Atkins Diet to healthcare practitioners as a science-based therapeutic tool, sharing new information that will instill confidence and assurance that the Atkins Diet is safe and effective. This guide will: 1) provide a clear physiological explanation of how and why the Atkins Diet works, 2) review the science supporting the Atkins Diet and 3) outline key aspects of the Atkins Diet in practice. The Atkins Diet: How and Why It Works After three decades, the obesity epidemic in the United States and much of the developed world remains unchecked(1). At its most basic level, obesity is a problem of excess storage of body fat, which is often accompanied by other metabolic disturbances. The solution logically involves biasing a person’s metabolism toward oxidizing fat rather than carbohydrate as the body’s primary fuel. The essence of the Atkins Diet is to provide that stimulus by means of reducing dietary carbohydrate and insulin to the point at which the person is able to preferentially oxidize body fat (Fig 1). Finding this point is a unique process, and the updated Atkins Diet provides individualized guidance through its four

Low HighInsulin Concentration

Fat Breakdown

Maximum

Minimum

HighCarbohydrate

Diet

Fig 1. Decreases in plasma insulin, that occur with the Atkins Diet, result in large increases in fat breakdown and oxidation.

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phases—in essence, functioning as a turn-by-turn metabolic GPS. The power of the Atkins Diet rests on the fact that carbohydrate, in addition to being an energy source, has a potent effect on fat metabolism. Carbohydrate is the major stimulus for insulin release, and consistent with its general anabolic functions, insulin potently inhibits the breakdown(2) and promotes the storage of fat. In this way, dietary carbohydrate-induced increases in circulating glucose and insulin block access to body fat—exactly the opposite metabolic outcome desired if body fat mobilization and weight loss are the desired outcomes. However, by reducing carbohydrate intake below a level where the insulin response blockades stored body fat, the Atkins Diet enables a unique metabolic state characterized by increased fat oxidation and decreased fat synthesis.

As one example of this principle that dietary carbohydrate restriction results in more efficient fat metabolism, we have demonstrated a reduction in plasma-saturated fatty acids in subjects following the Atkins Diet. This occurred despite the fact that this group of subjects consumed three times as much saturated fat as the comparison group of subjects consuming a low-fat diet(3). Increased utilization of fat for fuel has a profound impact on a range of metabolic processes such as cholesterol metabolism, glucose control, appetite regulation, inflammation and oxidative stress. For many patients, particularly those with pre-existing insulin resistance, the cellular conversion to burning fat has a global effect to enhance weight loss, allow for sustained weight management and improve metabolic health (Fig 2).

• Humans have a remarkable capacity to adapt to low carbohydrate intake.

• The reduction in carbohydrate provides the ‘cellular trigger’ to switch the fuel mix from predominately carbohydrate to mainly fat.

• Enhanced cellular fat oxidation facilitates weight loss and broad spectrum health benefits.

Fat LossImproved Health

50:50(RQ 0.85)

+ Insulin

Fig 2. The Atkins Diet puts people in the fat burning zone.

100% Carbs (RQ 1.0)

- Insulin

100% Fat (RQ 0.7)

Fuel Mix Being Burned in the Body

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The Atkins Diet: A Valuable Tool Backed by Science Weight loss. Published dietary recommendations imply that a low-fat/high-carbohydrate diet is the accepted standard for weight loss. However, a careful review of the current literature indicates that this “traditional diet” has a poor track record in experimental trials. Most recently, for example, is its rather poor showing in the Women’s Health Initiative(4). Several dozen studies have examined low-carbohydrate and low-fat diets over the last decade. Results from a sampling of that large body of work are shown in Tables 1 and 2. Studies published since 2003 of more than six-months duration are presented in Table 1(5-14); those of less than six-months duration are shown in Table 2(15-22). Although there is great variability in the comparison of diets of any duration, low-carbohydrate diets do at least as well and usually better than low-fat diets. It is generally agreed that the major effect of a low-carbohydrate diet is a spontaneous reduction in calories. The greater and lasting weight loss in so many trials of low-carbohydrate diets is clear evidence they should no longer be dismissed. Although the studies were relatively consistent in terms of design and nutritional composition, there were differences in patient populations, target carbohydrate levels in the low-carbohydrate groups, macronutrient percentages and total daily calorie consumption. There were also differences in the level of dietetic involvement and compliance to dietary protocols. However, the uniformity of the conclusions from these studies with regard to weight loss and improvement in established risk factors across these varied conditions supports the use of the Atkins Diet as a potent clinical tool in the long-term management of obesity. The greater weight loss is not simply due to water loss. The studies that measured fat mass always show a similar or greater loss of body fat in subjects on a low-carbohydrate diet than those on a low-fat diet. In fact, a comprehensive metaregression of 87 diet trials concluded that diets lower in carbohydrate were associated with greater fat loss during weight loss(23). Some evidence indicates that abdominal fat may be targeted(24).

Dyslipidemia.

Although weight loss is a major benefit, the Atkins Diet also results in profound positive changes in lipoprotein metabolism [reviewed in(25)]. The reduced conversion of carbohydrate to fat in the liver (lipogenesis) and the low insulin state enabling fat oxidation are major factors contributing to the improvements in processing of lipoproteins commonly observed in patients following the Atkins Diet. The most consistent response is a decrease in plasma triglycerides, most dramatically in those with pre-existing hypertriglyceridemia. This decrease in plasma triglycerides is so dependable that if a study purporting to examine a low-carbohydrate diet does not report a decrease in this lipoprotein, the level of dietary adherence must be suspect. The Atkins Diet also demonstrates a striking reduction in the postprandial lipemic

• Results from clinical trials are overwhelmingly in favor of low carbohydrate diets for weight loss.

• The Atkins Nutritional Approach maximizes fat loss while preserving lean body mass.

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response to a high-fat meal(26) and has positive effects on postabsorptive and postprandial vascular function(27). The decrease in hepatic production of large triglyceride-rich VLDL particles is mechanistically linked to favorable changes in other lipoproteins. Most notably, the Atkins Diet leads to a consistent shift from smaller, more atherogenic LDL particles to larger, less dense LDL particles(22,28). Low-carbohydrate diets are also one of few interventions that consistently raise HDL cholesterol. Importantly, these beneficial effects on lipoprotein metabolism are evident independent of weight loss. The replication of these effects across studies performed at different institutions shows how robust and consistent the favorable effects of the Atkins Diet are on important risk factors of cardiometabolic disease.

Glucose Control and Glycemic Index. Dietary carbohydrate is a direct source of blood glucose and driver of insulin secretion. Therefore, restriction in dietary carbohydrate intuitively leads to fewer fluctuations in blood glucose and more stable insulin levels. Indeed studies consistently show better glucose and insulin control and increased insulin sensitivity, both in healthy populations and especially in patients with pre-existing metabolic syndrome or type 2 diabetes [reviewed in(29)]. Given the widespread interest in diets with a low glycemic index (GI) or low glycemic load (GL), it is necessary to put into context how these approaches relate to the Atkins Diet. Glycemic index scores foods based on their acute glycemic impact relative to a standardized amount of carbohydrate, and are considered a measure of the quality of carbohydrate consumed. The term is somewhat misleading, however, in that even a low glycemic index carbohydrate still causes excursions in serum insulin and glucose levels. In contrast, it is noteworthy that, in response to normal meals consumed using the Atkins Diet, postprandial glucose and insulin values rise minimally(30). In this regard, the Atkins Diet can be considered the definitive low glycemic index diet, that is, one that reduces the quantity of glucose in the first place. Nonetheless, the concepts of GI and GL—the latter corrects for total carbohydrate consumption—have become part of the political controversies surrounding diet; proponents usually urge a low GI diet as an alternative rather than a variation of low-carbohydrate diets(31).

• The Atkins Nutritional Approach improves postprandial metabolism of fat and has beneficial effects on lipoprotein metabolism.

• The most consistent effects are decreased triglycerides, increased HDL, and transition to larger less atherogenic LDL particles.

• Humans have a remarkable capacity to adapt to low carbohydrate intake.

• The reduction in carbohydrate provides the ‘cellular trigger’ to switch the fuel mix from predominately carbohydrate to mainly fat.

• Enhanced cellular fat oxidation promotes weight loss and broad spectrum health benefits.

• The Atkins Diet is a potent tool to control blood glucose, reduce insulin levels, and improve insulin sensitivity.

• Dietary strategies based on GI have the same rationale as the Atkins Diet: reduce fluctuations in insulin.

• A potentially beneficial alternative to low fat recommendations, low GI diets would seem to be more accurately a variation of carbohydrate restriction than an alternative.

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Table 1. Effects of low-carbohydrate versus low-fat diets on weight loss and metabolic syndrome in studies lasting six months to two years.

Reference Subjects Length Diets Carb PERCENT CHANGEg/day Weight HDL TAG Glucose Insulin

Brehm et al . 2003

Obese Women 6 mo Low Carb 41-97 -9.3 13.4 -23.4 -9.1 -14.8

Low Fat 163-169 -4.2 8.4 1.6 -4.0 -23.0

Sondike et al . 2003

Overweight Adolescents

12 wk Low Carb 37 -10.7 8.7 -40.5

Low Fat 154 -4.1 4.2 -5.4

Samaha et al . 2003

Obese Men/Women

6 mo Low Carb 150 -4.5 0.0 -20.2 -8.6 -27.3

Low Fat 201 -1.4 -2.4 -4.0 -1.6 5.6

Foster et al . 2003

Obese Men/Women

1 yr Low Carb na -7.3 18.2 -28.1

Low Fat na -4.5 1.4 0.7

Stern et al . 2004

Obese Men/Women

1 yr Low Carb 120 -3.9 -2.8 -28.6

Low Fat 230 -2.3 -12.3 2.7

Yancy et al . 2004

Obese Men/Women

24 wk Low Carb 30 -12.3 9.8 -47.2

Low Fat 198 -6.7 -2.9 -14.4

Seshadri et al . 2004

Obese Men/Women

6 mo Low Carb 113 (-8.5) -2.4 -7.4 -40.0

Low Fat 198 (-3.5 kg) -2.4 -2.3 11.2

McAuley et al . 2006

Overweight Insulin Resistant

1 yr Low Carb 50 -5.6 10.5 -25.1 2.0 -26.0

Low Fat -4.5 -1.7 -16.5 -2.0 -36.1

Gardner et al . 2007

Obese Women 1 yr Low Carb 61-138 -5.5 9.2 -23.4 -2.0 -18.0

Low Fat 197-222 -3.0 0.0 -12.6 -0.9 -2.0

Shai et al . 2008

Obese Men/Women

2 yr Low Carb -5.5

Low Fat -3.3

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Table 2. Effects of low-carbohydrate versus low fat diets on weight loss and metabolic syndrome in studies lasting one to four months.

Reference Subjects Length Diets Carb PERCENT CHANGEg/day Weight HDL TAG Glucose Insulin

Volek et al . 2004

Overweight Women

4 wk Low Carb 29 -3.9 1.3 -23.0 -3.8 -8.8

Low Fat 186 -1.4 -8.6 -11.2 1.3 23.2

Sharman et al . 2004

Overweight Men 6 wk Low Carb 36 -5.6 -3.3 -44.1 -5.8 -41.5

Low Fat 224 -3.6 -6.6 -15.0 -5.2 -28.1

Brehm et al . 2004

Obese Women 4 mo Low Carb 69 -10.8 16.3 -37.3

Low Fat 174 -6.8 4.5 -10.3

Meckling et al . 2004

Obese Men/Women

10 wk Low Carb 59 -7.7 12.2 -29.4 -8.0 -28.7

Low Fat 225 -7.4 -15.4 -25.4 -10.2 -3.3

Aude et al . 2004

Obese Men/Women

12 wk Low Carb na -6.2 -2.6 -23.2

Low Fat na -3.4 -7.0 -10.5

Dansinger et al . 2005

Obese Men/Women

2 mo Low Carb 103 -4.7 8.8 -27.6 -10.0 -29.5

Low Fat 183 -4.3 -0.6 -7.1 -5.7 -11.0

Daly et al . 2006

Diabetic Men/Women

3 mo Low Carb 110 -3.5 -27.0

Low Fat 169 -0.9 -9.7

Volek et al . 2009

Men/Women w/ MetSyn

12 wk Low Carb 45 -10.5 12.8 -50.8 -11.9 -49.5

Low Fat 208 -5.5 -0.8 -19.2 -2.1 -18.6

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Metabolic Syndrome. Metabolic syndrome (insulin resistance syndrome) represents a group of seemingly disparate physiologic signs that indicate a predisposition to obesity, diabetes and cardiovascular disease. Metabolic syndrome is generally treated with combinations of drugs that target the individual markers: overweight, hypertension and atherogenic dyslipidemia, low HDL-C, high triglycerides and the so-called pattern B (high levels of small dense LDL-C). Insulin-sensitizing drugs (e.g., thiazolidinediones) have the potential for broad spectrum effects, but treatment is associated with significant weight gain and edema(32), and there is concern regarding cardiovascular safety (33) that often necessitates combination therapy to counteract these medication risks(34). Nutritional approaches are generally downplayed, perhaps because the traditional low-fat diet actually raises serum triglycerides in many patients. Official recommendations nonetheless tend to emphasize caloric restriction and reduced fat intake, even though the state can best be described as carbohydrate intolerance. Consistent with the idea that a relative intolerance to carbohydrate is a common underlying feature of metabolic syndrome, we have shown that reduction in dietary carbohydrate results in global improvement in traditional and emerging markers associated with metabolic syndrome (Fig 3). For example, in a recently published study(3,22), outpatients with metabolic syndrome were randomized to a traditional low-fat, energy-restricted diet or to the Atkins Diet for 12 weeks. Both groups lost weight, but both weight loss and fat loss were greater with the Atkins Diet. In addition, abdominal adipose losses, serum triglyceride reductions and HDL cholesterol increases, as well as several other markers associated with insulin resistance syndrome, were improved more with the Atkins Diet compared to the low-fat diet. Furthermore, evaluation of serum triglyceride fatty acid composition revealed greater reductions in both relative and absolute amounts of saturated fats in the subjects following the Atkins Diet. In contrast, as demonstrated in the Tables 1 and 2 above, control diets restricted in fat are consistently reported to be less effective. These experimental results point to carbohydrate restriction using the Atkins Diet as an effective alternative to the pharmaceutical approach that generally requires multiple drugs (“polypharmacy”), for the diverse manifestations of metabolic syndrome.

• Humans have a remarkable capacity to adapt to low carbohydrate intake.

• The reduction in carbohydrate provides the ‘cellular trigger’ to switch the fuel mix from predominately carbohydrate to mainly fat.

• Enhanced cellular fat oxidation promotes weight loss and broad spectrum health benefits.

• Low carbohydrate diets are more likely than low fat diets to effect global improvement in markers associated with metabolic syndrome.

• Treating any of the individual metabolic syndrome markers with carbohydrate restriction holds promise to benefit the others.

• Low carbohydrate diets are therefore the preferred primary intervention when >1 sign of insulin resistance is observed.

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Type-2 Diabetes. Diabetes is essentially a disease of advanced carbohydrate intolerance that afflicts about 10 percent of adults in the United States. In type I diabetes, there is an inability to produce insulin in response to glucose, whereas type 2 diabetes (90–95 percent of cases) is characterized by an inability to respond to insulin (i.e., insulin resistance). The goal for type 2 diabetes is better control of blood glucose and insulin levels. Historically, dietary carbohydrate restriction was a major therapeutic approach before the discovery of insulin. Dietary carbohydrate (sugar and starch) is the main stimulator of insulin in the body, and elevated blood insulin is the driving force behind the multitude of metabolic problems that accompany type 2 diabetes. Intuitively, this suggests that both the amount and the quality of dietary carbohydrate should be monitored and managed carefully. A number of recent studies have evaluated the response of groups with type 2 diabetes to carbohydrate-restricted diets over short- or long-term time periods. Boden et al.(35) observed 10 obese diabetics as inpatients for two weeks on a low-carbohydrate diet, and noted dramatic reductions in blood glucose and insulin levels, as well as improved dyslipidemia. Similar results have been reported by Bistrian et al.(36) and Dashti et al.(37) over longer periods in outpatients. All three of these studies demonstrated that carbohydrate restriction could improve glucose control, reduce serum insulin levels and reduce or obviate medication requirements in patients with type 2 diabetes.

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AbFat TG

TGAUC Glu

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Insulin HOMA LeptinTotalSFA

Fig 3. Results after 3 months in 40 subjects with metabolic syndrome randomized to either the Atkins Diet or a low fat calorie restricted diet (Forsythe et al. 2008).

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Why Do Some Physicians Shy Away from Using Atkins? The Atkins Diet is built upon sound biochemical and physiologic principles, but some misconceptions about the program have resulted in confusion among healthcare professionals and the public.

Misconception Atkins is a gustatory free-for-all that permits patients to gorge on huge portions of a limited selection of high-fat foods.

Reality Because both protein and a modicum of fat have potent satiating effects, most patients are satisfied with moderate portions, including salads and cooked vegetables from the first day of Phase 1, Induction.

Misconception Atkins is a red-meat-only plan that does not include vegetables and fruits.

Reality While red meat is allowed, so is a wide range of healthy protein sources, including vegetarian options. The result is a diet that is moderate in its protein content, while consisting of plenty of vegetables and fruits.

Misconception Atkins is a diet for short-term weight loss. Reality While many patients experience rapid weight loss in Phase 1,

Induction, and Phase 2, Ongoing Weight Loss (OWL), most revert to their prior unhealthy weight IF they resume their prior poor quality diet. The Atkins Diet provides patients with a personalized “roadmap” to follow through all four phases, enabling them to find a healthy maintenance diet within the limits of their personal carbohydrate tolerance that can be followed for years.

Misconception Dietary carbohydrates are required for exercise. Reality The body has a remarkable capacity to adapt to using fat for

fuel while sparing carbohydrate. In fact, exercise scientists have explored the effects of low-carbohydrate/high-fat diets on athletes for decades since they consistently augment the body’s use of fat and thereby spare glycogen. Following a week or two for the body’s metabolism to adjust to fat-burning, both endurance and resistance exercise capacity rebound to normal(38,39). A modicum of salt intake is also an important adjunct to allow the circulatory response to exercise or heat exposure.

Misconception Initially, restricting carbohydrates causes some people to feel faint, lethargic and fatigued.

Reality This is true for some people, but it can be easily avoided. Carbohydrate restriction increases salt excretion by the kidneys, so again a modest daily intake of salt is necessary to maintain hydration and electrolyte balance. This almost always alleviates

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any of the above signs. Misconception The relatively high intake of dietary fat, especially saturated fat,

is dangerous. Reality Fat, including saturated fat, is processed very efficiently when

carbohydrates are restricted. Simply put, when the metabolic roadblock of carbohydrate-induced hyperinsulinemia is removed, saturated fats are preferentially and rapidly oxidized to CO2 and water. The preferred form of fat to consume when following the Atkins Diet is monounsaturated. However, even when saturated fat intake is not restricted, tests on both animals and humans demonstrate that blood triglyceride levels of saturated fats actually decline more during the Atkins Diet than during a low-fat/high-carbohydrate weight loss diet. And as a final note, a recent comprehensive meta-analysis of long-term studies of diet and heart disease finds no correlation between saturated fat intake and actual coronary disease risk(40).

Misconception Ketones are dangerous. Reality Nutritional ketosis is a sign of accelerated fatty acid oxidation

and ketones are a preferred fuel for nearly all extrahepatic cells. The nutritional ketosis induced by the Atkins Diet results in serum ketones 10-20 fold lower than levels in diabetic ketoacidosis.

Misconception Atkins is high in protein and causes bone loss and kidney problems.

Reality Atkins is not a high-protein diet, providing levels that are only slightly higher than the RDA but well within ranges shown to be optimal for human wellbeing. New research indicates that moderate protein intake actually protects bones.

Misconception Caffeine is harmful. Reality Caffeine in moderation may improve health and assist in fat

burning/fat loss. Coffee and tea are major sources of antioxidants.

Misconception The majority of weight loss comes from water and lean body mass.

Reality In head-to-head comparisons, the Atkins Diet consistently outperforms other diets in terms of fat loss. The majority of studies indicate that when carbohydrates are reduced, there is a greater percentage of fat loss and better retention of lean body mass. It is true that the first few days of the Atkins Diet may increase water loss, which is why drinking plenty of water and ensuring adequate electrolyte intake (sodium, potassium, magnesium) is important.

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The Obesity Epidemic: How Bad Is It? Obesity is now considered one of the nation’s leading health issues; the American Cancer Society, the American Diabetes Association and the American Heart Association have all taken positions that excess weight is associated with increased risk of cancer, diabetes, heart disease and stroke. Such well-publicized concerns have maintained public awareness of overweight and obesity, and an increasing number of Americans are now concerned about the impact of their body weight on their overall health. The prevalence of obesity and overweight has increased dramatically over the last several decades. Estimates from the 2007–2008 NHANES indicate that 72.3 percent of adult men and 64.1 percent of adult women are overweight (BMI ≥ 25 kg/m2) and approximately one-third of adults are obese (Fig 4)(1). While recent data suggest that the rising prevalence of obesity among adults has plateaued, there is much to be done to reverse the damage of the last three decades. An alarming four out of five Hispanic and Mexican-American men and black women are overweight. High BMI is linked to the risk of type 2 diabetes, cholelithiasis, hypertension, coronary heart disease (CHD) and increased morbidity. The Atkins Diet: Part of the Solution

The unremitting high prevalence of obesity in the United States coupled with the very limited efficacy of traditional restricted diets has led to considerable frustration among physicians and patients. As a result, there has been a continual interest and, more recently, an acceptance of the Atkins Diet as an alternative dietary/lifestyle approach to obesity and its related diseases. In fact, the American Diabetes Association recently listed a low-carbohydrate diet as an alternate dietary approach(41). Of their own volition, millions of Americans are following, or considering starting, the Atkins Diet to manage their weight, improve their health or both. However, transient success at weight loss confers little long-term benefit unless the diet can be transitioned into a sustainable lifestyle. This is why the Atkins Diet consists of four phases, leading to an individualized program of Lifetime Maintenance. Progress through these phases over a number of months benefits from support by healthcare practitioners, yielding particularly positive effects in patients with pre-existing conditions such as metabolic syndrome or type 2 diabetes. For these individuals, rapid improvements often mandate reductions in medications, following which active monitoring of blood lipids, hemoglobin A1c or blood pressure may be indicated during the transition to Lifetime Maintenance.

Fig 4. Prevalence of overweight (BMI ≥ 25 kg/m2) in adult men and women. Data from 2007-2008 National Health and Nutrition Examination Survey (Flegal et al. 2010).

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• The promise of never feeling hungry and enjoying copious amounts of delicious food while knowing you are continuing to burn fat, lose weight and improve your health is absolutely empowering.

Why Do Patients Consider the Atkins Diet? In 2004, according to a survey conducted by The Valen Group, a strategy consulting firm, 59 million American adults were controlling their intake of carbohydrates, and more than 40 million others said they were considering adopting a low-carbohydrate diet in the next 12 months. Collectively, those figures approach half of all American adults. This indicates a broad-based unmet need among patient groups that would best be satisfied by a coordinated effort of the patient and his or her healthcare provider, rather than leaving the patient to self-manage the long-term process of finding a safe and sustainable weight management program. The Atkins Diet has been in the public eye for many years, during which its popularity has grown, due to its appeal to those trying to manage their weight. Many people are drawn to the Atkins Diet because they find the simple task of counting grams of carbohydrates more appealing than counting calories or fat grams. For many people, their metabolism is simply not responsive to restricting fat. Despite heroic efforts of willpower, the end result is often disappointing. Atkins represents an evidence-based, commonsense alternative that is behaviorally and metabolically well tolerated by most patients, and preferable for some. Once a person successfully navigates the initial few weeks of metabolic transition, he or she usually experiences a reduction in appetite and cravings. As a result, the Atkins Diet offers a lifestyle people can stay with long enough to see dramatic results.

Up until the recent wave of clinical studies supporting the safety and efficacy of the Atkins Diet, its popularity was primarily spread by word-of-mouth. However since 2002, the several clinical trials and metabolic studies summarized above have garnered a great deal of positive press. Such media attention has not only helped Americans to focus on the fact that obesity is a clear and present danger to their own health and that of the nation, but also on the fact that there are nutritional approaches that can help them to lose weight. On a more emotional level, recognition and appreciation of the Atkins Diet’s benefits gives many Americans renewed hope that they can take charge of not only their weight but some of their cardiovascular risk factors and their overall health.

Why Healthcare Professionals Should Be Familiar with the Atkins Diet Though the Atkins Diet is not appropriate for every overweight patient in every medical practice, it can be an effective program for many patients in a general medical setting. In particular, individuals with metabolic syndrome, insulin resistance and type 2 diabetes (all diseases of carbohydrate intolerance) are likely to see symptomatic as well as objective improvements in biomarkers of disease risk.

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From the patient’s perspective, the Atkins Diet may be appropriate for those who have struggled with weight loss in the past and have been unsuccessful with the recommendation to eat less and exercise more. It can also provide an option for those whose lifestyles or preferences suggest that the Atkins Diet strategy may be more likely to produce successful outcomes than conventional regimens. As the popularity of this approach increases, patients who perceive that it may help them to lose weight and to moderate cardiovascular and/or metabolic risk factors may ask their physicians for permission to try it.

In the absence of contraindications, patients who ask permission to try the Atkins Diet may view their physicians’ receptivity to it as a first step in establishing that level of physician-patient communication that is essential to the success of health-improvement programs.

Due to the proliferation of medical and quasimedical advice available to the public on a variety of media levels, including print, television, radio, the Internet and word-of-mouth, today’s overweight individuals hear about a bewildering, if not overwhelming, number of alternative diets, nutritional approaches and lifestyle programs, all of which focus on losing weight or improving health. In contradistinction to the Atkins Diet, most of these have not been subjected to clinical trials and metabolic studies that demonstrate safety and efficacy. There are actually many popular versions of low-carbohydrate diets and ways to translate low-carbohydrate eating into practice. Most individuals are poorly equipped to separate fact from fiction and to make choices appropriate for their individual healthcare requirements.

Patients look to their healthcare professionals to provide guidance in health-maintaining strategies such as immunizations, preventive care, management of risk factors and areas of special concern such as healthful diet and weight management. In the past, directing a patient to conventional calorie restriction has not yielded the desired results for many, if not most, who follow this advice. With the new foundation of science supporting the Atkins Diet, this diet/lifestyle alternative now offers the physician a superior tool in his or her arsenal of tools to control obesity and its related risks.

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The Atkins Diet The basic concept of the Atkins Diet is to reduce dietary carbohydrates to the point that the patient is able to preferentially oxidize stored body fat. The degree of carbohydrate restriction necessary to achieve this goal varies considerable among individuals. However highly refined carbohydrates and simple sugars are particularly potent blockers of fat oxidation, due to their exaggerated effect on serum insulin. The Atkins Diet removes all simple sugars and refined carbohydrates, as well as reducing overall carbohydrate, while focusing instead on a balanced consumption of nutrient-dense whole foods. The Atkins Diet consists of a four-phase program whose components have been developed specifically to ensure patient success and safety (Fig 5).

• Goal: Find Carb Level for Losing (CLL)• Start at 25 net carbs• ↑ net carbs 5 g increments (explore new

foods)• Stay here until <15 lbs from goal weight

• Goal: Find Atkins CarbEquilibrium (ACE)• ↑ net carbs in 5-10 g increments until goal

weight is reached• Stay here until weight stabilized for 1 mo

• Goal: Train the body to burn fat• 20 g net carbs from salad and non-

starchy vegetables• Stay here at least 2 weeks

• Goal: Adhere to ACE while selecting from a wide variety of foods to ensure weight maintenance.

• 51 to 100 g carbs/day depending upon the carbohydrate tolerance of the individual

• Goal: Adhere to ACE while selecting from a wide variety of foods to ensure weight maintenance.

• 20 to 50 g carbs/day depending upon the carbohydrate tolerance of the individual

Fig 5. Preview the phases of the Atkins Diet.

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Atkins Diet Information Resources The Atkins Diet can be a useful tool for clinicians whose patients express an interest in losing weight through adherence to a low-carbohydrate diet.

Additional materials and resources for clinicians and patients including a more extended listing of scientific studies and patient-oriented materials and tools can be found at www.atkins.com. We need to give the URL for the health professional portal but still supply other for patients. An updated version of the Atkins Diet appears in The New Atkins for a New You, by Dr. Stephen D. Phinney, Dr. Jeff S. Volek and Dr. Eric C. Westman (Fireside/Simon & Schuster, NY, NY, 2010), which provides an excellent guide for patients and clinicians to get started. Works Cited 1. Flegal KM, Carroll MD, Ogden CL, Curtin LR. Prevalence and trends in obesity

among US adults, 1999-2008. Jama;303:235-41. 2. Jensen MD, Caruso M, Heiling V, Miles JM. Insulin regulation of lipolysis in

nondiabetic and IDDM subjects. Diabetes 1989;38:1595-601. 3. Forsythe CE, Phinney SD, Fernandez ML, et al. Comparison of low fat and low

carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids 2008;43:65-77.

4. Howard BV, Manson JE, Stefanick ML, et al. Low-fat dietary pattern and weight change over 7 years: the Women's Health Initiative Dietary Modification Trial. Jama 2006;295:39-49.

5. Brehm BJ, Seeley RJ, Daniels SR, D'Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab 2003;88:1617-23.

6. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003;348:2082-90.

7. McAuley KA, Hopkins CM, Smith KJ, et al. Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese women. Diabetologia 2005;48:8-16.

8. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003;348:2074-81.

9. Seshadri P, Iqbal N, Stern L, et al. A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. Am J Med 2004;117:398-405.

10. Sondike SB, Copperman N, Jacobson MS. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr 2003;142:253-8.

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11. Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med 2004;140:778-85.

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18. Sharman MJ, Gomez AL, Kraemer WJ, Volek JS. Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men. J Nutr 2004;134:880-5.

19. Volek JS, Sharman MJ, Gomez AL, et al. Comparison of a very low-carbohydrate and low-fat diet on fasting lipids, LDL subclasses, insulin resistance, and postprandial lipemic responses in overweight women. J Am Coll Nutr 2004;23:177-84.

20. Daly ME, Paisey R, Paisey R, et al. Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes--a randomized controlled trial. Diabet Med 2006;23:15-20.

21. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. Jama 2005;293:43-53.

22. Volek JS, Phinney SD, Forsythe CE, et al. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids 2009;44:297-309.

23. Krieger JW, Sitren HS, Daniels MJ, Langkamp-Henken B. Effects of variation in protein and carbohydrate intake on body mass and composition during energy restriction: a meta-regression American Journal of Clinical Nutrition 2006;83:260-274.

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25. Volek JS, Fernandez ML, Feinman RD, Phinney SD. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res 2008.

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33. Devchand PR. Glitazones and the cardiovascular system. Curr Opin Endocrinol Diabetes Obes 2008;15:188-92.

34. Boden G, Homko C, Mozzoli M, Zhang M, Kresge K, Cheung P. Combined use of rosiglitazone and fenofibrate in patients with type 2 diabetes: prevention of fluid retention. Diabetes 2007;56:248-55.

35. Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med 2005;142:403-11.

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37. Dashti HM, Al-Zaid NS, Mathew TC, et al. Long term effects of ketogenic diet in obese subjects with high cholesterol level. Mol Cell Biochem 2006;286:1-9.

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