The document is a white paper that summarizes the scientific evidence supporting the Atkins Diet. It finds:
1) Clinical trials show the Atkins Diet results in greater weight loss than low-fat diets, especially in studies over 6 months. It maximizes fat loss while preserving muscle mass.
2) The Atkins Diet improves cardiovascular disease risk factors like triglycerides, HDL cholesterol, and LDL particle size. These benefits occur independently of weight loss.
3) The diet controls blood glucose and insulin levels better than low-fat diets due to very low carbohydrate intake. It reduces glycemic fluctuations more effectively than low glycemic index diets.
Russian Call Girls in Jaipur Riya WhatsApp ❤8445551418 VIP Call Girls Jaipur
Clinical guide
1. 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
Maximum
in the United States and much of the
developed world remains unchecked(1). At Fat Breakdown
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 High
provide that stimulus by means of reducing Carbohydrate
Diet
dietary carbohydrate and insulin to the
point at which the person is able to Minimum
preferentially oxidize body fat (Fig 1). Low High
Finding this point is a unique process, and
the updated Atkins Diet provides Insulin Concentration
individualized 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. P age |2
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.
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 Health
Atkins Nutritionals White Paper
Fig 2. The Atkins Diet puts people in the fat burning zone.
3. P age |3
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).
• 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 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
Atkins Nutritionals White Paper
4. P age |4
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.
• 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 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 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. P age |5
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 CHANGE
g/day Weight HDL TAG Glucose Insulin
Brehm et al .
Obese Women 6 mo Low Carb 41-97 -9.3 13.4 -23.4 -9.1 -14.8
2003
Low Fat 163-169 -4.2 8.4 1.6 -4.0 -23.0
Sondike et al . Overweight
12 wk Low Carb 37 -10.7 8.7 -40.5
2003 Adolescents
Low Fat 154 -4.1 4.2 -5.4
Samaha et al . Obese
6 mo Low Carb 150 -4.5 0.0 -20.2 -8.6 -27.3
2003 Men/Women
Low Fat 201 -1.4 -2.4 -4.0 -1.6 5.6
Foster et al . Obese
1 yr Low Carb na -7.3 18.2 -28.1
2003 Men/Women
Low Fat na -4.5 1.4 0.7
Stern et al . Obese
1 yr Low Carb 120 -3.9 -2.8 -28.6
2004 Men/Women
Low Fat 230 -2.3 -12.3 2.7
Yancy et al . Obese
24 wk Low Carb 30 -12.3 9.8 -47.2
2004 Men/Women
Low Fat 198 -6.7 -2.9 -14.4
Seshadri et al . Obese
6 mo Low Carb 113 (-8.5) -2.4 -7.4 -40.0
2004 Men/Women
Low Fat 198 (-3.5 kg) -2.4 -2.3 11.2
McAuley et al . Overweight
1 yr Low Carb 50 -5.6 10.5 -25.1 2.0 -26.0
2006 Insulin Resistant
Low Fat -4.5 -1.7 -16.5 -2.0 -36.1
Gardner et al .
Obese Women 1 yr Low Carb 61-138 -5.5 9.2 -23.4 -2.0 -18.0
2007
Low Fat 197-222 -3.0 0.0 -12.6 -0.9 -2.0
Shai et al . Obese
2 yr Low Carb -5.5
2008 Men/Women
Low Fat -3.3
Atkins Nutritionals White Paper
6. P age |6
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 CHANGE
g/day Weight HDL TAG Glucose Insulin
Volek et al . Overweight
4 wk Low Carb 29 -3.9 1.3 -23.0 -3.8 -8.8
2004 Women
Low Fat 186 -1.4 -8.6 -11.2 1.3 23.2
Sharman et al .
Overweight Men 6 wk Low Carb 36 -5.6 -3.3 -44.1 -5.8 -41.5
2004
Low Fat 224 -3.6 -6.6 -15.0 -5.2 -28.1
Brehm et al .
Obese Women 4 mo Low Carb 69 -10.8 16.3 -37.3
2004
Low Fat 174 -6.8 4.5 -10.3
Meckling et al . Obese
10 wk Low Carb 59 -7.7 12.2 -29.4 -8.0 -28.7
2004 Men/Women
Low Fat 225 -7.4 -15.4 -25.4 -10.2 -3.3
Aude et al . Obese
12 wk Low Carb na -6.2 -2.6 -23.2
2004 Men/Women
Low Fat na -3.4 -7.0 -10.5
Dansinger et Obese
2 mo Low Carb 103 -4.7 8.8 -27.6 -10.0 -29.5
al . 2005 Men/Women
Low Fat 183 -4.3 -0.6 -7.1 -5.7 -11.0
Daly et al . Diabetic
3 mo Low Carb 110 -3.5 -27.0
2006 Men/Women
Low Fat 169 -0.9 -9.7
Volek et al . Men/Women w/
12 wk Low Carb 45 -10.5 12.8 -50.8 -11.9 -49.5
2009 MetSyn
Low Fat 208 -5.5 -0.8 -19.2 -2.1 -18.6
Atkins Nutritionals White Paper
7. P age |7
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.
• 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. 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 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.
Atkins Nutritionals White Paper
9. P age |9
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
Atkins Nutritionals White Paper
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. P a g e | 11
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 80
72.3 percent of adult men and 64.1 70
percent of adult women are
Percent Overweight
60
overweight (BMI ≥ 25 kg/m2) and
approximately one-third of adults are 50
obese (Fig 4)(1). While recent data 40
suggest that the rising prevalence of
obesity among adults has plateaued, 30
there is much to be done to reverse Obese:
20 32.2% 35.5% BMI ≥ 30
the damage of the last three decades.
10
An alarming four out of five Hispanic
and Mexican-American men and 0
Men Women
black women are overweight. High
BMI is linked to the risk of type 2 Fig 4. Prevalence of overweight (BMI ≥ 25 kg/m2) in adult
diabetes, cholelithiasis, hypertension, men and women. Data from 2007-2008 National Health
coronary heart disease (CHD) and and Nutrition Examination Survey (Flegal et al. 2010).
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.
Atkins Nutritionals White Paper
12. P a g e | 12
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.
• 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 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.
Atkins Nutritionals White Paper
13. P a g e | 13
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.
Atkins Nutritionals White Paper
14. P a g e | 14
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: 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. P a g e | 15
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.
Atkins Nutritionals White Paper
16. P a g e | 16
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.
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, D'Alessio 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, O'Sullivan 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. P a g e | 17
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.
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. P a g e | 18
41. 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