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Clinical guide


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Clinical guide

  1. 1. WHITE PAPER January 2010 UNDERSTANDING THE ATKINS DIET Information for the Practicing Clinician Dr. Stephen D. Phinney and Dr. Jeff S. VolekThe Atkins Diet, also known as the Atkins Nutritional Approach, has attracted millions offollowers. As Kleenex is to facial tissue, Atkins has become synonymous with low-carbohydrate diets. Not all low-carbohydrate diets are the same, however; among thisclass of diet, only the Atkins Diet is grounded in science. The introduction of the AtkinsDiet in 1972 occurred at approximately the same time as the institution of low-fatrecommendations, which may partially explain the historical resistance to the approachby many health professionals. Despite this combination of inopportune timing andunderappreciation of the scientific evidence supporting low-carbohydrate diets, theAtkins Diet has nonetheless enjoyed enduring popularity for nearly four decades. Therelative ease of use and prompt weight loss associated with the Atkins Diet representthe tip of the iceberg, as new evidence supports the effectiveness of controllingcarbohydrates for a variety of clinical conditions. The scientific method is a process, andover the past decades the nuances of the Atkins Diet have evolved, based on findingsfrom a multitude of new studies that have validated previous work and made newdiscoveries. The updated Atkins perspective paints a promising picture of efficient andsustained weight loss and robust health improvements. The objective of this white paperis to present the Atkins Diet to healthcare practitioners as a science-based therapeutictool, sharing new information that will instill confidence and assurance that the AtkinsDiet is safe and effective. This guide will: 1) provide a clear physiological explanation ofhow and why the Atkins Diet works, 2) review the science supporting the Atkins Dietand 3) outline key aspects of the Atkins Diet in practice.The Atkins Diet: How and Why It WorksAfter three decades, the obesity epidemic Maximumin the United States and much of thedeveloped world remains unchecked(1). At Fat Breakdownits most basic level, obesity is a problem ofexcess storage of body fat, which is oftenaccompanied by other metabolicdisturbances. The solution logicallyinvolves biasing a person’s metabolismtoward oxidizing fat rather thancarbohydrate as the body’s primary fuel.The essence of the Atkins Diet is to Highprovide that stimulus by means of reducing Carbohydrate Dietdietary carbohydrate and insulin to thepoint at which the person is able to Minimumpreferentially oxidize body fat (Fig 1). Low HighFinding this point is a unique process, andthe updated Atkins Diet provides Insulin Concentrationindividualized guidance through its four Fig 1. Decreases in plasma insulin, that occur with the Atkins Diet, result in large increases in fat breakdown and oxidation.
  2. 2. P age |2phases—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 anenergy source, has a potent effect on fat metabolism. Carbohydrate is the majorstimulus for insulin release, and consistent with its general anabolic functions, insulinpotently inhibits the breakdown(2) and promotes the storage of fat. In this way, dietarycarbohydrate-induced increases in circulating glucose and insulin block access to bodyfat—exactly the opposite metabolic outcome desired if body fat mobilization and weightloss are the desired outcomes. However, by reducing carbohydrate intake below a levelwhere the insulin response blockades stored body fat, the Atkins Diet enables a uniquemetabolic state characterized by increased fat oxidation and decreased fat synthesis.As one example of this principle that dietary carbohydrate restriction results in moreefficient fat metabolism, we have demonstrated a reduction in plasma-saturated fattyacids in subjects following the Atkins Diet. This occurred despite the fact that this groupof subjects consumed three times as much saturated fat as the comparison group ofsubjects consuming a low-fat diet(3). Increased utilization of fat for fuel has a profoundimpact on a range of metabolic processes such as cholesterol metabolism, glucosecontrol, appetite regulation, inflammation and oxidative stress. For many patients,particularly those with pre-existing insulin resistance, the cellular conversion to burningfat has a global effect to enhance weight loss, allow for sustained weight managementand 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. 50:50 (RQ 0.85) Fuel Mix Being Burned in the Body + Insulin - Insulin 100% Carbs (RQ 1.0) 100% Fat (RQ 0.7) Fat Loss Improved HealthAtkins Nutritionals White Paper Fig 2. The Atkins Diet puts people in the fat burning zone.
  3. 3. P age |3The Atkins Diet: A Valuable Tool Backed by ScienceWeight loss. Published dietary recommendations imply that a low-fat/high-carbohydratediet is the accepted standard for weight loss. However, a careful review of the currentliterature indicates that this “traditional diet” has a poor track record in experimentaltrials. Most recently, for example, is its rather poor showing in the Women’s HealthInitiative(4). Several dozen studies have examined low-carbohydrate and low-fat dietsover the last decade. Results from a sampling of that large body of work are shown inTables 1 and 2. Studies published since 2003 of more than six-months duration arepresented in Table 1(5-14); those of less than six-months duration are shown in Table2(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 isgenerally agreed that the major effect of a low-carbohydrate diet is a spontaneousreduction 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 thestudies were relatively consistent in terms of design and nutritional composition, therewere 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 todietary protocols. However, the uniformity of the conclusions from these studies withregard to weight loss and improvement in established risk factors across these variedconditions supports the use of the Atkins Diet as a potent clinical tool in the long-termmanagement of obesity. The greater weight loss is not simply due to water loss. Thestudies that measured fat mass always show a similar or greater loss of body fat insubjects on a low-carbohydrate diet than those on a low-fat diet. In fact, acomprehensive metaregression of 87 diet trials concluded that diets lower incarbohydrate were associated with greater fat loss during weight loss(23). Someevidence indicates that abdominal fat may be targeted(24). • Results from clinical trials are overwhelmingly in favor of low carbohydrate diets for weight loss. Dy • The Atkins Nutritional Approach maximizes fat loss while slip preserving lean body mass. ide mia .Although weight loss is a major benefit, the Atkins Diet also results in profound positivechanges in lipoprotein metabolism [reviewed in(25)]. The reduced conversion ofcarbohydrate to fat in the liver (lipogenesis) and the low insulin state enabling fatoxidation are major factors contributing to the improvements in processing oflipoproteins commonly observed in patients following the Atkins Diet. The mostconsistent response is a decrease in plasma triglycerides, most dramatically in thosewith pre-existing hypertriglyceridemia. This decrease in plasma triglycerides is sodependable that if a study purporting to examine a low-carbohydrate diet does notreport a decrease in this lipoprotein, the level of dietary adherence must be suspect.The Atkins Diet also demonstrates a striking reduction in the postprandial lipemicAtkins Nutritionals White Paper
  4. 4. P age |4response to a high-fat meal(26) and has positive effects on postabsorptive andpostprandial vascular function(27). The decrease in hepatic production of largetriglyceride-rich VLDL particles is mechanistically linked to favorable changes in otherlipoproteins. Most notably, the Atkins Diet leads to a consistent shift from smaller, moreatherogenic LDL particles to larger, less dense LDL particles(22,28). Low-carbohydratediets are also one of few interventions that consistently raise HDL cholesterol.Importantly, these beneficial effects on lipoprotein metabolism are evident independentof weight loss. The replication of these effects across studies performed at differentinstitutions shows how robust and consistent the favorable effects of the Atkins Diet areon important risk factors of cardiometabolic disease. • 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.Glucose Control and Glycemic Index. Dietary carbohydrate is a direct source of bloodglucose and driver of insulin secretion. Therefore, restriction in dietary carbohydrateintuitively leads to fewer fluctuations in blood glucose and more stable insulin levels.Indeed studies consistently show better glucose and insulin control and increasedinsulin sensitivity, both in healthy populations and especially in patients with pre-existingmetabolic syndrome or type 2 diabetes [reviewed in(29)]. Given the widespread interestin diets with a low glycemic index (GI) or low glycemic load (GL), it is necessary to putinto context how these approaches relate to the Atkins Diet. Glycemic index scoresfoods based on their acute glycemic impact relative to a standardized amount ofcarbohydrate, and are considered a measure of the quality of carbohydrate consumed.The term is somewhat misleading, however, in that even a low glycemic indexcarbohydrate still causes excursions in serum insulin and glucose levels. In contrast, itis 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 Dietcan be considered the definitive low glycemic index diet, that is, one that reduces thequantity of glucose in the first place. Nonetheless, the concepts of GI and GL—the lattercorrects for total carbohydrate consumption—have become part of the politicalcontroversies surrounding diet; proponents usually urge a low GI diet as an alternativerather than a variation of low-carbohydrate diets(31). • The Atkins Diet is a potent tool to control blood glucose, reduce • Humans have a remarkable capacity to adapt to low carbohydrate insulin levels, and improve insulin sensitivity. intake. • Dietary strategies based on GI have the same rationale as the • The reduction in carbohydrate provides the ‘cellular trigger’ to Atkins Diet: reduce fluctuations in insulin. switch the fuel mix from predominately carbohydrate to mainly fat. • A potentially beneficial alternative to low fat recommendations, low • Enhanced cellular fat oxidation promotes weight loss and broad GI diets would seem to be more accurately a variation of spectrum health benefits. carbohydrate restriction than an alternative.Atkins Nutritionals White Paper
  5. 5. P age |5Table 1. Effects of low-carbohydrate versus low-fat diets on weight loss and metabolicsyndrome in studies lasting six months to two years. Reference Subjects Length Diets Carb PERCENT CHANGE g/day Weight HDL TAG Glucose InsulinBrehm et al . Obese Women 6 mo Low Carb 41-97 -9.3 13.4 -23.4 -9.1 -14.82003 Low Fat 163-169 -4.2 8.4 1.6 -4.0 -23.0Sondike et al . Overweight 12 wk Low Carb 37 -10.7 8.7 -40.52003 Adolescents Low Fat 154 -4.1 4.2 -5.4Samaha et al . Obese 6 mo Low Carb 150 -4.5 0.0 -20.2 -8.6 -27.32003 Men/Women Low Fat 201 -1.4 -2.4 -4.0 -1.6 5.6Foster et al . Obese 1 yr Low Carb na -7.3 18.2 -28.12003 Men/Women Low Fat na -4.5 1.4 0.7Stern et al . Obese 1 yr Low Carb 120 -3.9 -2.8 -28.62004 Men/Women Low Fat 230 -2.3 -12.3 2.7Yancy et al . Obese 24 wk Low Carb 30 -12.3 9.8 -47.22004 Men/Women Low Fat 198 -6.7 -2.9 -14.4Seshadri et al . Obese 6 mo Low Carb 113 (-8.5) -2.4 -7.4 -40.02004 Men/Women Low Fat 198 (-3.5 kg) -2.4 -2.3 11.2McAuley et al . Overweight 1 yr Low Carb 50 -5.6 10.5 -25.1 2.0 -26.02006 Insulin Resistant Low Fat -4.5 -1.7 -16.5 -2.0 -36.1Gardner et al . Obese Women 1 yr Low Carb 61-138 -5.5 9.2 -23.4 -2.0 -18.02007 Low Fat 197-222 -3.0 0.0 -12.6 -0.9 -2.0Shai et al . Obese 2 yr Low Carb -5.52008 Men/Women Low Fat -3.3Atkins Nutritionals White Paper
  6. 6. P age |6Table 2. Effects of low-carbohydrate versus low fat diets on weight loss and metabolicsyndrome in studies lasting one to four months. Reference Subjects Length Diets Carb PERCENT CHANGE g/day Weight HDL TAG Glucose InsulinVolek et al . Overweight 4 wk Low Carb 29 -3.9 1.3 -23.0 -3.8 -8.82004 Women Low Fat 186 -1.4 -8.6 -11.2 1.3 23.2Sharman et al . Overweight Men 6 wk Low Carb 36 -5.6 -3.3 -44.1 -5.8 -41.52004 Low Fat 224 -3.6 -6.6 -15.0 -5.2 -28.1Brehm et al . Obese Women 4 mo Low Carb 69 -10.8 16.3 -37.32004 Low Fat 174 -6.8 4.5 -10.3Meckling et al . Obese 10 wk Low Carb 59 -7.7 12.2 -29.4 -8.0 -28.72004 Men/Women Low Fat 225 -7.4 -15.4 -25.4 -10.2 -3.3Aude et al . Obese 12 wk Low Carb na -6.2 -2.6 -23.22004 Men/Women Low Fat na -3.4 -7.0 -10.5Dansinger et Obese 2 mo Low Carb 103 -4.7 8.8 -27.6 -10.0 -29.5al . 2005 Men/Women Low Fat 183 -4.3 -0.6 -7.1 -5.7 -11.0Daly et al . Diabetic 3 mo Low Carb 110 -3.5 -27.02006 Men/Women Low Fat 169 -0.9 -9.7Volek et al . Men/Women w/ 12 wk Low Carb 45 -10.5 12.8 -50.8 -11.9 -49.52009 MetSyn Low Fat 208 -5.5 -0.8 -19.2 -2.1 -18.6Atkins Nutritionals White Paper
  7. 7. P age |7Metabolic Syndrome. Metabolic syndrome (insulin resistance syndrome) represents agroup of seemingly disparate physiologic signs that indicate a predisposition to obesity,diabetes and cardiovascular disease. Metabolic syndrome is generally treated withcombinations of drugs that target the individual markers: overweight, hypertension andatherogenic 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 withsignificant weight gain and edema(32), and there is concern regarding cardiovascularsafety (33) that often necessitates combination therapy to counteract these medicationrisks(34). Nutritional approaches are generally downplayed, perhaps because thetraditional low-fat diet actually raises serum triglycerides in many patients. Officialrecommendations nonetheless tend to emphasize caloric restriction and reduced fatintake, even though the state can best be described as carbohydrate intolerance.Consistent with the idea that a relative intolerance to carbohydrate is a commonunderlying feature of metabolic syndrome, we have shown that reduction in dietarycarbohydrate results in global improvement in traditional and emerging markersassociated with metabolic syndrome (Fig 3). For example, in a recently publishedstudy(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, butboth weight loss and fat loss were greater with the Atkins Diet. In addition, abdominaladipose losses, serum triglyceride reductions and HDL cholesterol increases, as well asseveral other markers associated with insulin resistance syndrome, were improvedmore with the Atkins Diet compared to the low-fat diet. Furthermore, evaluation ofserum triglyceride fatty acid composition revealed greater reductions in both relative andabsolute 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 areconsistently reported to be less effective. These experimental results point tocarbohydrate restriction using the Atkins Diet as an effective alternative to thepharmaceutical approach that generally requires multiple drugs (“polypharmacy”), forthe diverse manifestations of metabolic syndrome. • Low carbohydrate diets are more likely than low fat diets to effect • Humans have a remarkable capacity to adapt to low carbohydrate global improvement in markers associated with metabolic intake. syndrome. • The reduction in carbohydrate provides the ‘cellular trigger’ to • Treating any of the individual metabolic syndrome markers with switch the fuel mix from predominately carbohydrate to mainly fat. carbohydrate restriction holds promise to benefit the others. • Enhanced cellular fatdiets are therefore the preferred and broad • Low carbohydrate oxidation promotes weight loss primary spectrum health benefits. intervention when >1 sign of insulin resistance is observed.Atkins Nutritionals White Paper
  8. 8. P age |8 Atkins Low Fat HDL ApoB/ 10 ApoA-1 Small Body Ab TG TG/ LDL Total Mass Fat TG AUC HDL ApoB Glu Insulin HOMA Leptin SFA 0 Percent Change -10 -20 -30 -40 -50 -60 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).Type-2 Diabetes. Diabetes is essentially a disease of advanced carbohydrateintolerance that afflicts about 10 percent of adults in the United States. In type Idiabetes, there is an inability to produce insulin in response to glucose, whereas type 2diabetes (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 glucoseand insulin levels. Historically, dietary carbohydrate restriction was a major therapeuticapproach before the discovery of insulin. Dietary carbohydrate (sugar and starch) is themain stimulator of insulin in the body, and elevated blood insulin is the driving forcebehind the multitude of metabolic problems that accompany type 2 diabetes. Intuitively,this suggests that both the amount and the quality of dietary carbohydrate should bemonitored and managed carefully. A number of recent studies have evaluated theresponse of groups with type 2 diabetes to carbohydrate-restricted diets over short- orlong-term time periods. Boden et al.(35) observed 10 obese diabetics as inpatients fortwo weeks on a low-carbohydrate diet, and noted dramatic reductions in blood glucoseand insulin levels, as well as improved dyslipidemia. Similar results have been reportedby Bistrian et al.(36) and Dashti et al.(37) over longer periods in outpatients. All three ofthese studies demonstrated that carbohydrate restriction could improve glucose control,reduce serum insulin levels and reduce or obviate medication requirements in patientswith type 2 diabetes.Atkins Nutritionals White Paper
  9. 9. P age |9Why Do Some Physicians Shy Away from Using Atkins?The Atkins Diet is built upon sound biochemical and physiologic principles, but somemisconceptions about the program have resulted in confusion among healthcareprofessionals 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 alleviatesAtkins Nutritionals White Paper
  10. 10. P a g e | 10 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.Atkins Nutritionals White Paper
  11. 11. P a g e | 11The Obesity Epidemic: How Bad Is It?Obesity is now considered one of the nation’s leading health issues; the AmericanCancer Society, the American Diabetes Association and the American HeartAssociation have all taken positions that excess weight is associated with increased riskof cancer, diabetes, heart disease and stroke. Such well-publicized concerns havemaintained public awareness of overweight and obesity, and an increasing number ofAmericans are now concerned about the impact of their body weight on their overallhealth. The prevalence of obesity and overweight has increased dramatically over thelast several decades. Estimates fromthe 2007–2008 NHANES indicate that 8072.3 percent of adult men and 64.1 70percent of adult women are Percent Overweight 60overweight (BMI ≥ 25 kg/m2) andapproximately one-third of adults are 50obese (Fig 4)(1). While recent data 40suggest that the rising prevalence ofobesity among adults has plateaued, 30there is much to be done to reverse Obese: 20 32.2% 35.5% BMI ≥ 30the damage of the last three decades. 10An alarming four out of five Hispanicand Mexican-American men and 0 Men Womenblack women are overweight. HighBMI is linked to the risk of type 2 Fig 4. Prevalence of overweight (BMI ≥ 25 kg/m2) in adultdiabetes, cholelithiasis, hypertension, men and women. Data from 2007-2008 National Healthcoronary heart disease (CHD) and and Nutrition Examination Survey (Flegal et al. 2010).increased morbidity.The Atkins Diet: Part of the SolutionThe unremitting high prevalence of obesity in the United States coupled with the verylimited efficacy of traditional restricted diets has led to considerable frustration amongphysicians and patients. As a result, there has been a continual interest and, morerecently, an acceptance of the Atkins Diet as an alternative dietary/lifestyle approach toobesity and its related diseases. In fact, the American Diabetes Association recentlylisted a low-carbohydrate diet as an alternate dietary approach(41). Of their ownvolition, millions of Americans are following, or considering starting, the Atkins Diet tomanage their weight, improve their health or both. However, transient success at weightloss confers little long-term benefit unless the diet can be transitioned into a sustainablelifestyle. This is why the Atkins Diet consists of four phases, leading to an individualizedprogram of Lifetime Maintenance. Progress through these phases over a number ofmonths benefits from support by healthcare practitioners, yielding particularly positiveeffects in patients with pre-existing conditions such as metabolic syndrome or type 2diabetes. For these individuals, rapid improvements often mandate reductions inmedications, following which active monitoring of blood lipids, hemoglobin A1c or bloodpressure may be indicated during the transition to Lifetime Maintenance.Atkins Nutritionals White Paper
  12. 12. P a g e | 12Why Do Patients Consider the Atkins Diet?In 2004, according to a survey conducted by The Valen Group, a strategy consultingfirm, 59 million American adults were controlling their intake of carbohydrates, and morethan 40 million others said they were considering adopting a low-carbohydrate diet inthe 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 besatisfied by a coordinated effort of the patient and his or her healthcare provider, ratherthan leaving the patient to self-manage the long-term process of finding a safe andsustainable weight management program.The Atkins Diet has been in the public eye for many years, during which its popularityhas grown, due to its appeal to those trying to manage their weight. Many people aredrawn to the Atkins Diet because they find the simple task of counting grams ofcarbohydrates more appealing than counting calories or fat grams. For many people,their metabolism is simply not responsive to restricting fat. Despite heroic efforts ofwillpower, the end result is often disappointing. Atkins represents an evidence-based,commonsense alternative that is behaviorally and metabolically well tolerated by mostpatients, and preferable for some. Once a person successfully navigates the initial fewweeks of metabolic transition, he or she usually experiences a reduction in appetite andcravings. As a result, the Atkins Diet offers a lifestyle people can stay with long enoughto see dramatic results. • 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.Up until the recent wave of clinical studies supporting the safety and efficacy of theAtkins Diet, its popularity was primarily spread by word-of-mouth. However since 2002,the several clinical trials and metabolic studies summarized above have garnered agreat deal of positive press. Such media attention has not only helped Americans tofocus on the fact that obesity is a clear and present danger to their own health and thatof the nation, but also on the fact that there are nutritional approaches that can helpthem to lose weight. On a more emotional level, recognition and appreciation of theAtkins Diet’s benefits gives many Americans renewed hope that they can take charge ofnot only their weight but some of their cardiovascular risk factors and their overallhealth.Why Healthcare Professionals Should Be Familiar with the Atkins DietThough the Atkins Diet is not appropriate for every overweight patient in every medicalpractice, 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 asobjective improvements in biomarkers of disease risk.Atkins Nutritionals White Paper
  13. 13. P a g e | 13From the patient’s perspective, the Atkins Diet may be appropriate for those who havestruggled with weight loss in the past and have been unsuccessful with therecommendation to eat less and exercise more. It can also provide an option for thosewhose lifestyles or preferences suggest that the Atkins Diet strategy may be more likelyto produce successful outcomes than conventional regimens. As the popularity of thisapproach increases, patients who perceive that it may help them to lose weight and tomoderate cardiovascular and/or metabolic risk factors may ask their physicians forpermission to try it.In the absence of contraindications, patients who ask permission to try the Atkins Dietmay view their physicians’ receptivity to it as a first step in establishing that level ofphysician-patient communication that is essential to the success of health-improvementprograms.Due to the proliferation of medical and quasimedical advice available to the public on avariety 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 ofalternative diets, nutritional approaches and lifestyle programs, all of which focus onlosing weight or improving health. In contradistinction to the Atkins Diet, most of thesehave not been subjected to clinical trials and metabolic studies that demonstrate safetyand efficacy. There are actually many popular versions of low-carbohydrate diets andways to translate low-carbohydrate eating into practice. Most individuals are poorlyequipped to separate fact from fiction and to make choices appropriate for theirindividual healthcare requirements.Patients look to their healthcare professionals to provide guidance in health-maintainingstrategies such as immunizations, preventive care, management of risk factors andareas 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 resultsfor many, if not most, who follow this advice. With the new foundation of sciencesupporting the Atkins Diet, this diet/lifestyle alternative now offers the physician asuperior tool in his or her arsenal of tools to control obesity and its related risks.Atkins Nutritionals White Paper
  14. 14. P a g e | 14The Atkins Diet The basic concept of the Atkins Diet is to reduce dietary carbohydrates to the point thatthe patient is able to preferentially oxidize stored body fat. The degree of carbohydraterestriction necessary to achieve this goal varies considerable among individuals.However highly refined carbohydrates and simple sugars are particularly potentblockers of fat oxidation, due to their exaggerated effect on serum insulin. The AtkinsDiet removes all simple sugars and refined carbohydrates, as well as reducing overallcarbohydrate, while focusing instead on a balanced consumption of nutrient-densewhole foods. The Atkins Diet consists of a four-phase program whose components havebeen developed specifically to ensure patient success and safety (Fig 5). • Goal: Train the body to burn fat • 20 g net carbs from salad and non- starchy vegetables • Stay here at least 2 weeks • 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: Adhere to ACE while selecting from a • Goal: Adhere to ACE while selecting from a wide variety of foods to ensure weight wide variety of foods to ensure weight maintenance. maintenance. • 51 to 100 g carbs/day depending upon the • 20 to 50 g carbs/day depending upon the carbohydrate tolerance of the individual carbohydrate tolerance of the individual Fig 5. Preview the phases of the Atkins Diet.Atkins Nutritionals White Paper
  15. 15. P a g e | 15Atkins Diet Information ResourcesThe Atkins Diet can be a useful tool for clinicians whose patients express an interest inlosing weight through adherence to a low-carbohydrate diet.Additional materials and resources for clinicians and patients including a more extendedlisting of scientific studies and patient-oriented materials and tools can be found We need to give the URL for the health professional portal but stillsupply 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 cliniciansto get started.Works Cited1. 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 Womens Health Initiative Dietary Modification Trial. Jama 2006;295:39-49.5. Brehm BJ, Seeley RJ, Daniels SR, DAlessio 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.Atkins Nutritionals White Paper
  16. 16. P a g e | 1611. 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;140:778-85.12. Yancy WS, Jr., Olsen MK, Guyton JR, Bakst RP, Westman EC. A low- carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004;140:769-77.13. Gardner CD, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. Jama 2007;297:969-77.14. Shai I, Schwarzfuchs D, Henkin Y, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008;359:229-41.15. Aude YW, Agatston AS, Lopez-Jimenez F, et al. The national cholesterol education program diet vs a diet lower in carbohydrates and higher in protein and monounsaturated fat: a randomized trial. Arch Intern Med 2004;164:2141-6.16. Brehm BJ, Spang SE, Lattin BL, Seeley RJ, Daniels SR, DAlessio DA. The role of energy expenditure in the differential weight loss in obese women on low-fat and low-carbohydrate diets. J Clin Endocrinol Metab 2004.17. Meckling KA, OSullivan C, Saari D. Comparison of a low-fat diet to a low- carbohydrate diet on weight loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. J Clin Endocrinol Metab 2004;89:2717-23.18. 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- 274.24. Volek JS, Sharman MJ, Gomez AL, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutr Metab (Lond) 2004;1:13.Atkins Nutritionals White Paper
  17. 17. P a g e | 1725. 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 2008.26. Volek JS, Gomez AL, Kraemer WJ. Fasting lipoprotein and postprandial triacylglycerol responses to a low-carbohydrate diet supplemented with n-3 fatty acids. J Am Coll Nutr 2000;19:383-91.27. Volek JS, Ballard KD, Silvestre R, et al. Effects of dietary carbohydrate restriction versus low-fat diet on flow-mediated dilation. Metabolism 2009;58:1769-77.28. Volek JS, Sharman MJ, Forsythe CE. Modification of lipoproteins by very low- carbohydrate diets. J Nutr 2005;135:1339-42.29. Volek JS, Feinman RD. Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab (Lond) 2005;2:31.30. Noakes M, Foster PR, Keogh JB, James AP, Mamo JC, Clifton PM. Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Nutr Metab (Lond) 2006;3:7.31. Ludwig DS, Jenkins DJ. Carbohydrates and the postprandial state: have our cake and eat it too? Am J Clin Nutr 2004;80:797-8.32. Richter B, Bandeira-Echtler E, Bergerhoff K, Clar C, Ebrahim SH. Rosiglitazone for type 2 diabetes mellitus. Cochrane Database Syst Rev 2007:CD006063.33. 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;142:403-11.36. Bistrian BR, Blackburn GL, Flatt JP, Sizer J, Scrimshaw NS, Sherman M. Nitrogen metabolism and insulin requirements in obese diabetic adults on a protein-sparing modified fast. Diabetes 1976;25:494-504.37. 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;286:1-9.38. Phinney SD, Bistrian BR, Evans WJ, Gervino E, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism 1983;32:769-76.39. Phinney SD, Horton ES, Sims EA, Hanson JS, Danforth E, Jr., LaGrange BM. Capacity for moderate exercise in obese subjects after adaptation to a hypocaloric, ketogenic diet. J Clin Invest 1980;66:1152-61.40. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr.Atkins Nutritionals White Paper
  18. 18. P a g e | 1841. Bantle JP, Wylie-Rosett J, Albright AL, et al. Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care 2008;31 Suppl 1:S61-78.Atkins Nutritionals White Paper