The Diet ar y Treatment

of Obesity
Gal Dubnov-Raz, MD, MSca,*, Elliot M. Berry, MD, FRCPb

KEYWORDS
 Diet  Weight  Obesity  Glycemic index  Fat  Calcium

Talking of a man who was grown very fat, so as to be incommoded by corpulency,

Dr. Johnson said, ‘‘He eats too much, Sir.’’
BOSWELL: ‘‘I don’t know, Sir, you will see one man fat who eats moderately,
and another lean who eats a great deal.’’
JOHNSON: ‘‘Nay, Sir, whatever may be the quantity that a man eats, it is plain
that if he is too fat, he has eaten more than he should have done.’’
[Boswell’s Life of Samuel Johnson. Part IX, 1782–1783]

The obesity epidemic is a ‘‘huge’’ reality. For centuries, mankind has known that
eating too much and/or exercising too little is hazardous to one’s health. This fact
was even known in times when infectious diseases and malnutrition took their toll
and reduced human lifespan to nearly a half what it is today. For example, 800 years
ago, Maimonides asserted that one should never eat unless hungry, the stomach
should only be filled to three-quarters full, and when one exercises and works, he
will not become sick and his strength will increase. As early as the 6th century, the
Roman Catholic Church included gluttony and sloth among the seven deadly sins.
During the past decades, a dramatic increase in the rate of obesity occurred
throughout the Western world.1–5 This rapid increase cannot be explained through
changes in metabolism or genetics, pace the ‘‘thrifty’’ genotype,6 and must necessar-
ily be caused by an obesogenic or toxic environment promoting a positive energy
balance.
The burden of obesity-associated diseases paralleled this increase,7 and occurred
despite numerous studies, national statements, and position stands of professional
organizations stating that obesity must be addressed seriously, prevented, and
treated.8 More than ever, multilevel, multidisciplinary strategies seem to be needed,
with combined forces of the major stakeholders, including governments,

a
Pediatric Obesity, Exercise and Sport Medicine, Department of Pediatrics, Mount Scopus,
Hadassah-Hebrew University Medical Center, Jerusalem, Israel 91120
b
Department of Human Nutrition and Metabolism, The Braun School of Public Health and
Community Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel 91120
* Corresponding author.
E-mail address: gal-d@bezeqint.net (G. Dubnov-Raz).

Endocrinol Metab Clin N Am 37 (2008) 873–886

doi:10.1016/j.ecl.2008.08.002 endo.theclinics.com
0889-8529/08/$ – see front matter ª 2008 Elsevier Inc. All rights reserved.
874 Dubnov-Raz & Berry

communities, health care services, medical societies, industry, and media, and of
course obese individuals.9,10
Treatment of obesity obviously must lead to a negative energy balance, preferably
through both reducing food intake and increasing energy expenditure. Even though
this strategy sounds simple in theory (according to the first law of thermodynamics),
decades of advocating weight loss have failed to stop the obesity epidemic. This
article discusses contemporary issues in the dietary treatment of obesity and future
research directions.
Because of the numerous medical complications of obesity (eg, diabetes, hyperten-
sion, hypercholesterolemia, cardiovascular disease, cancer) and the profound effect
that many nutrients have on all of them, this discussion must be narrowed to weight
loss per se in adults.

INCREASING PHYSICAL ACTIVITY OR DECREASING FOOD INTAKE?

A negative energy balance can be attained through either eating less, exercising more,
or both. A deficiency of 500 kcal/d is recommended to achieve a weight loss rate of
approximately 1 lb (w 0.5 kg) per week.8,11,12 However, the major question arises
whether it matters if this energy deficit comes from decreasing food intake or increas-
ing physical activity. Several studies have addressed this question. The same energy
deficit obtained through either increased exercise or a dietary restriction seems to
yield similar changes in body weight, but the composition of lost tissue differs. On av-
erage, the composition of weight loss is approximately 70% fat and 30% lean body
mass, whereas loss of the latter causes a decrease in the resting metabolic rate.
Exercise aids in minimizing the loss of lean body mass, thereby reducing the decrease
in metabolic rate (for increased efficiency) that accompanies any loss in body
weight.13,14
Several investigators examined the differences between two methods of energy
deficit: diet restriction or increased exercise. In the first study, 52 obese men were ran-
domly assigned to one of four study groups (diet-induced weight loss, exercise-
induced weight loss, exercise without weight loss, and control).15 After 3 months,
weight decreased by 8% in the diet-induced and exercise-induced weight loss
groups, and changes in abdominal obesity, visceral fat, and insulin resistance were
also comparable (because of a higher unplanned energy deficit in the exercise group,
these values were corrected for energy deficit). A second, similar study was con-
ducted among 54 premenopausal women using a similar protocol.16 This study
showed that the exercise-induced weight loss group had a greater reduction in total
and abdominal fat compared with the diet-induced group.
A recent, randomized controlled trial tested the effect of 6 months of a 25% energy
deficit through diet alone or diet plus exercise (12.5% reduction of intake, 12.5% in-
crease in energy expenditure) on body composition and fat distribution in 35 over-
weight individuals.17 The calculated energy deficit across the intervention was not
different between the groups, as opposed to many of the previous studies. Study par-
ticipants lost approximately 10% of body weight, 24% of fat mass, and 27% of ab-
dominal visceral fat in both groups.
Finally, a 1-year randomized trial comparing the effects of increased energy expen-
diture of approximately 300 kcal/d (equivalent to walking 60 minutes) with an isocaloric
deficit of energy intake found a similar fat mass loss of 25% and comparable
reductions in heart disease risk factors, namely plasma low-density lipoprotein
(LDL) C concentration, total cholesterol/high-density lipoprotein (HDL) C ratio,
C-reactive protein (CRP) concentrations, and insulin resistance.18 The concept that
 The Dietary Treatment of Obesity 875

exercise in obese patients is beneficial even without weight loss has also been shown
in type 2 diabetics.19
Collectively, these randomized, well-controlled studies suggest that, when compar-
ing the effects of an energy deficit through increased physical activity or decreased
dietary intake on body fat, ‘‘a calorie is a calorie,’’ whether burned by increased phys-
ical activity or never consumed at all.
However, physical activity exerts additional health benefits other than pure physical
weight loss. Physical activity seems to be able to improve the metabolic complications
of obesity even without weight loss,15,16 while also preventing numerous chronic dis-
eases, such as heart disease,20 cancer,21 obesity,22 and diabetes,23 and improving
mood through many mechanisms.24 Many metabolic effects are independent of
body composition,25,26 and therefore it may be said that ‘‘fat and fit may be better
than being lean and lazy.’’
Furthermore, adding physical activity to weight loss programs is crucial to maintain
the reduced weight, and therefore the authors firmly believe it must be an integral part
of any weight-loss diet (see article elsewhere in this issue). However, to obtain the de-
sired energy deficit for weight loss under normal circumstances, caloric intake must be
reduced; it is much easier to reduce caloric intake by 500 kcal/d, for example, than to
increase expenditure of that magnitude. Examples of activities that use approximately
500 kcal of energy, for a person weighing approximately 80 kg, are an hour of jogging
at 5 km/h, or 35 minutes of jump-rope. Given that dietary intervention is a crucial part
of weight loss, the question now arises whether some diets are more effective in
weight loss than others.

ARE ALL DIETS CREATED EQUAL?

For many years, researchers and clinicians debated what the optimal diet for weight
loss is, and if such a diet actually exists. The fundamental question is again, ‘‘is
a calorie a calorie?’’; that is, do different compositions of isocaloric diets have different
effects on weight loss. The major controversy seems to be between low-fat (LF) and
low-carbohydrate (LC) diets. Two additional contemporary issues concern the bene-
fits of using a diet with a low glycemic index or a diet rich in dairy products and
calcium.

Low-Fat Versus Low-Carbohydrate Diets

LF diets are those that restrict fat intake to less than 25% to 35% of daily energy
intake.12,27,28 LC diets are those that advocate minimizing carbohydrate intake
(w20–100 g/d, depending on the type of diet and its stage), with the additional calories
needed originating from protein and fat. An in-depth review of the constituents of com-
mon diets is available.29
The first man to undergo an LC diet and report its success, nearly 150 years ago,
seemed to be William Banting,30 a relative of Sir Frederick Banting, the codiscoverer
of insulin. In 1972, Robert Atkins published his book ‘‘Dr. Atkins’ Diet Revolution,’’31
which widely publicized the concept of LC diets for weight loss, but was also imme-
diately criticized.32 Studies showing either superiority or inferiority over LF diets
sparked decade-long disputes between promoters of both nutrition regimens.33
Numerous studies comparing the two approaches for weight loss have been
conducted, accompanied by many editorial comments, reviews, and meta-
analyses.34–48 This article focuses on the larger longer-term, randomized trials. Recent
systematic reviews and meta-analyses42–44 summarized the conclusions from the
many papers comparing the two diet types. Apparently in the long-term (at least 1
876 Dubnov-Raz & Berry

year), LC diets do not induce more weight loss than LF diets, and no difference occurs
in blood pressure, lipid profile, or glucose/insulin changes; attrition rates are also
similar. Only the meta-analysis of the more recent randomized controlled trials44 con-
cluded that total cholesterol and LDL levels decreased more after LF diets, but HDL
and triglyceride values changed more after LC diets.
Four studies comparing various diet regimens for weight loss are of particular inter-
est. Dansinger and colleagues45 randomized 160 overweight participants to one of
four diets for 1 year: Atkins (carbohydrate restriction), Zone (macronutrient balance),
Weight Watchers (calorie restriction), or Ornish (fat restriction). All diets resulted in
modest weight loss at 1 year, with no statistically significant differences among diets,
and no meaningful differences in heart disease risk factors and insulin resistance. No
adverse effects or deterioration of heart disease risk factors were noted. Of the
subjects, 60% completed the study year, but compliance decreased significantly
and similarly between the diet groups.
In a similar study, Truby and colleagues46 randomized 293 overweight participants
to one of five diet groups for a 6-month trial: Atkins, Slim-Fast plan, Weight Watchers,
a precooked meal program (Rosemary Conley’s), and a control group. All diets re-
sulted in significant but similar loss of body fat and weight at the end, despite lack
of control of total energy intake by the researchers. Fasting glucose levels and choles-
terol improved only in the Weight Watchers group. Adherence to the diet for another 6
months (total of 1 year) resulted in a similar approximately 10% weight loss in all diets.
Gardner and colleagues47 randomized 311 overweight women to follow the Atkins,
Zone, LEARN (LF diet, based on national guidelines), or Ornish diets. At 12 months,
weight loss was greater in the Atkins diet group compared with the other diet groups
(–4.7 kg, –1.6 kg, –2.6 kg, and –2.2 kg, respectively), but significantly different only
from the Zone diet. The lipid profile and blood pressure changes were better in the
Atkins group. Attrition rate was relatively low at 20%.
Finally, a recent workplace-based study conducted in Israel among 322 overweight
and obese employees compared the effect of an LC, an LF, or a Mediterranean-style
diet on weight loss and cardiovascular risk factors.48 After 2 years, among the 272 par-
ticipants who adhered with the program (85%), the LC and Mediterranean diets were
associated with greater weight loss than the LF ( 0.5 body mass index [BMI] units in
LC and Mediterranean diets versus LF). In addition, beneficial changes were seen in
some metabolic markers: lipid profile improved best in the LC group; the inflammatory
marker CRP decreased by more than 20% only in the LC and Mediterranean diet
groups; and among the subgroup of diabetics, only the Mediterranean diet decreased
plasma glucose levels. This study suggests that LC and Mediterranean diets can be
beneficial over an LF diet in some circumstances, and emphasizes the ability of the
workplace in promoting lifestyle changes.
These four studies stand out because they used several diet compositions, as
opposed to those comparing LC and LF alone. The discrepancies in results between
the study by Gardner and colleagues47 and that by Shai and colleagues,48 which found
the Atkins diet to be superior to three other nutritional regimens, can be explained by
either the population studied or the higher support provided by the study staff or
spouse, as reflected in the high adherence rate. Nevertheless, these studies continue
to maintain the ongoing debate over whether LC diets are superior to the nationally
recommended LF diets.
Several mechanisms have been suggested for the possible added value of LC diets
in promoting weight loss, including (1) higher amounts of protein, which promotes sa-
tiety more than carbohydrates, (2) ongoing gluconeogenesis to compensate for the
body’s carbohydrate needs, which is an energy-consuming process, (3) increased
 The Dietary Treatment of Obesity 877

diuresis, (4) loss of glycogen stores and their associated water, (5) high levels of circu-
lating ketones, which suppress appetite, (6) limited food choices, or (7) underreporting
of food intake by the LF group.49–53
A final issue is safety. A systematic review of more than 100 studies identified no ad-
verse effects or unwarranted metabolic changes, especially renal function.43 Recently,
a life-threatening complication of an Atkins diet, in the form of severe ketoacidosis,
was described.54 Because most studies were conducted among healthy volunteers,
and only a few among diabetics, insufficient data exists on LC diets in populations
with underlying diseases.
In summary, despite several beneficial properties of LC over LF diets, even the high-
quality studies continue to generate conflicting results. Future studies will surely help
identify the best proportions between macronutrients for weight loss and metabolic
improvements. A recent summary that attempted to define the optimum dietary com-
position for a weight-loss diet suggested moderate carbohydrate (35%–50%) and fat
intake (25%–35%), with protein contributing the remainder at 25% to 30% (which is
relatively high).52 One wonders whether this is a variation of the adage ‘‘Moderation
in all things, including moderation.’’ However, the overriding factor determining the
success of any diet is long-term compliance, which is an individual choice that cannot
be manipulated easily by investigators.

Low Glycemic Index Diets

The glycemic index is a measure of glucose availability in food,55 and is calculated
as the percentage of the area under the plasma glucose response curve measured
during the 2 hours after ingestion of the food in question, relative to the same amount
of carbohydrate taken as glucose/white bread. Foods with a high glycemic index (HGI)
(>70), such as white bread, potatoes, or corn flakes, whose glucose is readily digested
and absorbed, cause a rapid increase in plasma glucose levels. Foods with a low
glycemic index (LGI) (<50), such as pasta, fruits, and beans, cause a much slower in-
crement in plasma glucose levels.
Experts have postulated that fat reduction has failed to combat the current obesity
epidemic because of the carbohydrate content: substitution of fat with HGI foods
merely causes increased hunger, anabolism of adipose tissue, and weight gain.56
The rapid absorption of sugar from an HGI causes a large surge in insulin secretion,
which then exerts its anabolic effects. In addition, the high insulin levels decrease
blood glucose levels, causing more hunger in the few hours after an HGI meal.
In an insulin-resistant person, this high demand from the b cell might potentially re-
sult in b-cell secretion defects and apoptosis, leading to type 2 diabetes. In an LGI
diet, the ambient insulin secretion is lower, without large swings, and these unwanted
effects are moderated. Therefore, it is better to eat little and often than to fast and
feast – nibbling is preferable to gorging, despite a similar total daily energy intake.
A prospective cohort study of 6-year follow-up was conducted among 185 men and
191 women, examining the role of glycemic index in future weight and fat-mass
changes.57 Using questionnaires for food frequency and various confounders, the au-
thors concluded that, in women only, an HGI diet was associated with increases in
BMI and fat mass. Another observational study among 572 healthy adults also showed
that changes in BMI were positively associated with dietary intake of carbohydrates
and the glycemic index.58
However, as in most fields of medicine, this concept is controversial. Advocates of
using an LGI diet for weight loss59 and their opponents60 both raise convincing
explanations supporting their views. In light of the existing, although not unanimous,
observational evidence that HGI diets can increase weight gain, several interventional
878 Dubnov-Raz & Berry

studies have examined whether lowering the glycemic index can affect weight loss.
This article focuses on data from the longer-term randomized trials.
A recent review of the highest-quality randomized studies examining the effect of
LGI diets on weight loss concluded that they produce larger decreases in BMI, fat
mass, and total and LDL cholesterol.61 Because studies were generally short-term,
further research with longer-term follow-up was recommended.
Results of a large 18-month study comparing weight loss effects of LGI versus HGI
diets was published concurrently.62 This study, conducted in Brazil where beans are
a common food (very low GI), randomized 203 healthy women who had a BMI ranging
from 23 to 30 kg/m2 to an LGI or HGI diet, differing by 40 glycemic index points. Intake
was high in carbohydrates (60% of energy) and low in fat (26%–28% of energy), and
individuals were given a small energy restriction ( 100–300 kcal/d). Outcome mea-
sures were weight change during 18 months, hunger, and fasting serum insulin and
lipids. Although the LGI group showed a slightly greater weight loss in the first 2
months of follow-up, both groups began to regain weight after 12 months, and at
18 months, the small weight change maintained ( 260 and 400 g for LGI and HGI)
was not significantly different between groups. A greater reduction was observed in
the LGI diet group for triacylglycerol and very low-density lipoprotein (VLDL) choles-
terol, with no differences in measures of hunger. Hence, this study did not support
the benefit of an LGI diet for weight loss.
In another recent study, researchers randomized 34 healthy overweight adults to di-
ets with 30% caloric deficiency and either an HGI or an LGI.63 All food was provided for
6 months, and subjects self-administered the diet plans for another 6 months. The LGI
diet had 40% daily energy as carbohydrates (compared with 60% in the HGI) and
a glycemic index lower by 33 units. Primary and secondary outcomes included energy
intake, body weight and fatness, hunger, satiety, and resting metabolic rate, none of
which differed between the groups at end of study. An additional study, conducted
among 39 obese subjects randomized to hypocaloric diets ( 760 kcal/d) with LGI,
HGI, or high fat, concluded that the glycemic index had no effect on weight loss.64
In summary, high-quality randomized trials continue to raise conflicting results
regarding the role of the glycemic index in weight loss and maintenance. The authors
suggest that more studies be conducted in free-living conditions, where the presumed
higher satiety of an LGI diet can be translated into a lower reduction of energy intake; in
a controlled trial, holding the energy intake constant in both LGI and HGI groups might
blunt one of the possible benefits of an LGI diet. In addition, they suggest that the effect
of LGI and HGI meals on hunger and satiety be examined in the clinic on an individual
basis, to see if lowering the glycemic index may assist in the reduced calorie diet.

Calcium and Dairy Products

In 1984, McCarron65 reported an inverse relationship between dietary calcium intake
and body weight. Since then, several observational studies and interventions have
assessed the reproducibility, magnitude, and mechanisms of this phenomenon.
Studies conducted in this field show conflicting results regarding diets with a higher
calcium or dairy intake, showing either reduced weight or increased weight loss,66–75
no effect,75–80 or even increased weight or weight gain.80–82
A systematic review of 13 randomized trials involving supplementation of either cal-
cium or dairy products again found controversial results, and summarized that these
product had no mean effect on weight loss.83 Several differences in methodology can
explain these discrepancies. One pitfall in eating dairy products for increased weight
loss might be the increased caloric intake, should the eager weight-loser try to max-
imize this mechanism. The added energy in consuming three dairy products per day
 The Dietary Treatment of Obesity 879

averaged approximately 200 kcal/d in one study,84 a meaningful increase in the long-
term. Data from the Health Professionals Follow-Up Study showed that men who had
the largest increase in high-fat dairy products gained significantly more weight than
those who decreased their intake. Therefore, total energy consumption must be con-
sidered to prevent its counteracting of possible beneficial effects of dairy products on
weight.80 Similar findings were observed in children and older adults.79,81
Several mechanisms for the effect of calcium and dairy foods on cell metabolism
and adiposity have been identified.85,86 The major mechanism seems to be a suppres-
sion of intracellular calcium, which then enhances lipolysis, with an interesting greater
effect of dairy products than calcium supplements. Possible explanations are the
presence of additional bioactive compounds, such as angiotensin converting enzyme
inhibitors or branched chain amino acids, which act synergistically with calcium to at-
tenuate adiposity.
Increased fecal fat loss is another mechanism through which calcium may aid in
weight loss. However, in this case, further increasing calcium intake should enhance
weight loss, but a large observational study did not find any benefit in increasing the
daily intake more than 800 mg/d,87 which is even below the minimal recommended in-
take for adults. In addition, different dairy products were recently found to affect body
weight differently, thereby suggesting that pooling all ‘‘dairy products’’ in question-
naires or diet recommendations may be erroneous.88 In this large study, researchers
examined the association between changes in dairy product consumption and weight
change over 9 years among 19,352 women, while addressing differential intakes of
whole milk (3% fat), medium-fat milk (1.5% fat), low-fat milk (%0.5% fat), whole
sour milk (3% fat), low-fat sour milk (0.5% fat), cheese, and butter (80% fat). Findings
were that increasing intakes of dairy products and calcium did not universally affect
weight gain, despite whether these increases involved low-fat milk or cheese and but-
ter. Subjects who complied with their consumption of more than one dairy portion of
milk with 3% fat had a statistically significant relative risk of 0.85 for weight gain,
whereas those who maintained high cheese intake had a risk of 0.70. These results
were not affected by correction for calcium or energy intake. Therefore, not all milk
products are created equal, and future studies are needed to identify the more bene-
ficial dairy products in assisting weight loss.

WEIGHT MAINTENANCE AND THE REDUCED OBESE

Why is treating obesity so difficult, and why do so many different treatments exist?
A clue may be found when studying a ‘‘rare’’ clinical subject: a reduced obese per-
son who has succeeded in losing weight and maintaining the new body weight for
more than a year. The National Weight Control Registry documented the metabolic
and behavioral cost of maintaining a reduced obese state for more than 5 years.
The average weight loss was 30 kg and minimum maintenance 13.6 kg. The results
are instructive.89 Both men and women consumed a low-fat diet (24%) and exercised
to use 470 and 360 kcal/d, respectively. The net energy balance was 918 kcal/d for
women and 1225 kcal/d for men. These reduced obese subjects ate an average of
five meals a day and conducted a very regimented existence.
Anyone with clinical experience in weight management knows that adopting such
a lifestyle is extremely hard. which perhaps explains why combating obesity is such
a difficult task. Other studies usually show a much milder amount of weight loss. A re-
cent meta-analysis summarizing 80 clinical trials of long-term weight loss through com-
binations of diet, exercise, or medications showed that in the long-term (3–4 years),
weight loss averaged 3 kg with diet alone, or nearly 4 kg with diet and exercise.90
880 Dubnov-Raz & Berry

The importance of the reduced obese is that if one only uses an experimental par-
adigm comparing normal-weight and obese subjects, then whether any abnormal
finding such as (for example) hyperglycemia or hyperinsulinemia is either primary
(causative) or secondary to the obese state cannot be known; this may only be deter-
mined after the person loses weight. If after weight reduction the abnormalities are re-
versed (such as in the examples above), then they must be secondary; however,
parameters that are normal in the obese state but abnormal after weight reduction
may be relevant to the induction of obesity or its perpetuation.
One such finding is that reduced obese subjects have diminished energy
requirements for maintaining body weight compared with similar-weight never-obese
subjects.13 This discovery suggests that weight reduction leads to an increase in met-
abolic efficiency, perhaps mediated through altered catecholamine and thyroid sensi-
tivity.14 In the former study,13 26 obese subjects, with an average weight of 152.5 kg,
were hospitalized in a metabolic ward and fed a formula so that their weight did not
change beyond  0.5 kg over a week. Caloric requirements were then calculated to
determine how many calories per meter squared per day they required.
The same experiment was repeated in a similar number of controls to determine
how many calories were needed to keep in balance a person who was never obese.
The obese subjects had their weight brought down to an average of 100 kg and the
same calculation was performed. On average, the obese subjects required
1432 kcal/m2/d. The never-obese subjects weighing 62 kg required 1341 kcal/m2/d.
No significant difference was seen between nonobese and obese people, although
in absolute terms the obese ate more because of their larger surface areas. However,
the reduced obese at 100 kg, still obese, had a dramatic reduction in the amount of
energy for maintaining caloric requirements at 1050 kcal/m2/d. This decreased energy
expenditure continued for 1 to 2 years after weight loss. Hence, in metabolic terms, the
reduced obese were much more efficient in using less energy for weight maintenance.
The body systems responding to energy metabolism are the adrenosympathetic
system and the thyroid. This system was then investigated through testing the hemody-
namic and metabolic responses to exogenous and endogenous epinephrine after insu-
lin-induced hypoglycemia.14 Three groups were examined: obese, reduced obese, and
never-obese. In all three groups, hemodynamic and glucose responses were similar.
However, when glycerol release was recorded, the obese and never-obese were found
to react similarly, but the reduced obese responded excessively despite secreting
fewer catecholamines. The obese acted like the normal subjects, whereas the reduced
obese (who are now believed to be ‘‘normal’’), were in fact abnormal.
After endogenous epinephrine infusion, the same response profiles were recorded.
Again, the obese responded like the controls, and the reduced obese had a very at-
tenuated response but seemed to be very sensitive to the effects of catecholamines,
as shown from exaggerated glycerol release. The enhanced sensitivity to the
metabolic effects of epinephrine suggests that in the reduced obese, adrenal medul-
lary activity may be reduced, with secondary up-regulation of peripheral b receptors
(or down-regulation of a). The reduced obese also seem to have low T3 concentra-
tions, perhaps in an attempt to conserve energy. This physiologic understanding
may help in the development of new treatment modalities for weight maintenance.

FACILITATING WEIGHT LOSS AND DIETING

The roles of society, the media (targeting both adults and children), the food industry
(pricing, quality, labeling, and portion sizes), and safe community infrastructure for ex-
ercise in providing an enabling environment for weight loss are essential parts of
 The Dietary Treatment of Obesity 881

national programs in combating obesity, but are beyond the scope of this article.
These areas are extensively discussed elsewhere.9,10 All programs must include in-
creased motivation to exercise in the home, community, and workplace. Furthermore,
obesity is greater in lower socioeconomic sectors of the population, and therefore pro-
grams must be suitably tailored to the needs and economic constraints of these
groups.

SUMMARY

In no sector of therapeutics is the theory so simple as in weight control. The major gap
lies in translating this theory into practice. In the final analysis, the answer lies in per-
sonal choice, because many diets seem to work, but not universally in all studies. A
reduced calorie diet is obviously essential, although the composition remains to be in-
dividually tailored. For this, health care professionals must become ‘‘personal
trainers’’ and realize the importance of lifestyle prescriptions with regard to diet and
exercise in all consultations, fitting them to the needs of patient. It may be argued
that medical practitioners do not have the necessary time or behavioral skills for these
long-term interventions, which might be better handled by a team of other health
professionals.
Prevention is, of course, better than treatment, and therefore a major effort must be
made to target children, from breast feeding to education throughout schooling. No
more surveys are needed; ‘‘we know the enemy and it is us.’’
In the words of the Lancet editorial concerning obesity:91 ‘‘Our public health leaders
must replace prevarication with imagination.’’

REFERENCES

1. Li C, Ford ES, McGuire LC, et al. Increasing trends in waist circumference and
abdominal obesity among US adults. Obesity 2007;15:216–24.
2. Wardle J, Boniface D. Changes in the distributions of body mass index and waist
circumference in English adults, 1993/1994 to 2002/2003. Int J Obes (Lond) 2007;
32:527–32.
3. Berg C, Rosengren A, Aires N, et al. Trends in overweight and obesity from 1985
to 2002 in Goteborg, West Sweden. Int J Obes (Lond) 2005;29:916–24.
4. Bendixen H, Holst C, Sorensen TI, et al. A. Major increase in prevalence of over-
weight and obesity between 1987 and 2001 among Danish adults. Obes Res
2004;12:1464–72.
5. Koziel S, Szklarska A, Bielicki T, et al. Changes in the BMI of Polish conscripts be-
tween 1965 and 2001: secular and socio-occupational variation. Int J Obes
(Lond) 2006;30:1382–8.
6. Neel JV. Diabetes mellitus: a ‘‘thrifty’’ genotype rendered detrimental by ‘‘prog-
ress’’? Am J Hum Genet 1962;14:353–62.
7. Ford ES, Giles WH, Mokdad AH. Increasing prevalence of the metabolic syn-
drome among US adults. Diabetes Care 2004;27:2444–9.
8. National Institutes of Health. Clinical guidelines on the identification, evaluation,
and treatment of overweight and obesity in adults - The evidence report. Obes
Res 1998;6:S51–210.
9. Global strategy on diet, physical activity and health. A framework to monitor and
evaluate implementation. Geneva (Switzerland): World Health Organization;
2006.
882 Dubnov-Raz & Berry

10. Branca F, Nikogosian H, Lobstein T, editors. The challenge of obesity in the WHO
European region and the strategies for response. Copenhagen (Denmark): World
Health Organization; 2007.
11. Avenell A, Sattar N, Lean M. ABC of obesity. Management: Part I - Behaviour
change, diet, and activity. BMJ 2006;333:740–3.
12. Klein S, Sheard NF, Pi-Sunyer X, et al. Weight management through lifestyle
modification for the prevention and management of type 2 diabetes: rationale
and strategies. A statement of the American Diabetes Association, the North
American Association for the Study of Obesity, and the American Society for Clin-
ical Nutrition. Am J Clin Nutr 2004;80:257–63.
13. Leibel RL, Hirsch J. Diminished energy requirements in reduced-obese patients.
Metabolism 1984;33:164–70.
14. Leibel RL, Berry EM, Hirsch J. Metabolic and hemodynamic responses to endog-
enous and exogenous catecholamines in formerly obese subjects. Am J Physiol
1991;260:R785–91.
15. Ross R, Dagnone D, Jones PJ, et al. Reduction in obesity and related comorbid
conditions after diet-induced weight loss or exercise-induced weight loss in men.
A randomized, controlled trial. Ann Intern Med 2000;133:92–103.
16. Ross R, Janssen I, Dawson J, et al. Exercise-induced reduction in obesity and
insulin resistance in women: a randomized controlled trial. Obes Res 2004;12:
789–98.
17. Redman LM, Heilbronn LK, Martin CK, et al. Effect of calorie restriction with or
without exercise on body composition and fat distribution. J Clin Endocrinol
Metab 2007;92:865–72.
18. Fontana L, Villareal DT, Weiss EP, et al. Calorie restriction or exercise: effects on
coronary heart disease risk factors. A randomized, controlled trial. Am J Physiol
Endocrinol Metab 2007;293(1):E197–202.
19. Lee S, Kuk JL, Davidson LE, et al. Exercise without weight loss is an effective
strategy for obesity reduction in obese individuals with and without type 2 diabe-
tes. J Appl Physiol 2005;99(3):1220–5.
20. Haskell WL, Lee IM, Pate RR, et al. Physical activity and public health: updated
recommendation for adults from the American College of Sports Medicine and
the American Heart Association. Circulation 2007;116:1081–93.
21. Kushi LH, Byers T, Doyle C, et al. American Cancer Society Guidelines on Nutri-
tion and Physical Activity for cancer prevention: reducing the risk of cancer with
healthy food choices and physical activity. CA Cancer J Clin 2006;56:254–81.
22. Saris WH, Blair SN, van Baak MA, et al. How much physical activity is enough to
prevent unhealthy weight gain? Outcome of the IASO 1st stock conference and
consensus statement. Obes Rev 2003;4:101–14.
23. Sigal RJ, Kenny GP, Wasserman DH, et al. Physical activity/exercise and type 2
diabetes: a consensus statement from the American Diabetes Association. Dia-
betes Care 2006;29:1433–8.
24. Dubnov G, Berry EM. Physical activity and mood: the endocrine connection. In:
Warren MP, Constantini N, editors. Sports endocrinology. Totowa (NJ): Humana
Press; 2000. p. 421–32.
25. Lee CD, Blair SN, Jackson AS. Cardiorespiratory fitness, body composition, and
all-cause and cardiovascular disease mortality in men. Am J Clin Nutr 1999;69:
373–80.
26. Wei M, Kampert JB, Barlow CE, et al. Relationship between low cardiorespiratory
fitness and mortality in normal-weight, overweight, and obese men. JAMA 1999;
282:1547–53.
 The Dietary Treatment of Obesity 883

27. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel
on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults
(Adult Treatment Panel III) final report. Circulation 2002;106:3143–421.
28. American Heart Association Nutrition Committee. Diet and lifestyle recommenda-
tions revision 2006: a scientific statement from the American Heart Association
Nutrition Committee. Circulation 2006;114:82–96.
29. Freedman MR, King J, Kennedy E. Popular diets: a scientific review. Obes Res
2001;9(Suppl 1):1S–40S.
30. Banting W. Letter on corpulence, addressed to the public. 3rd edition. London:
Harrison; 1869.
31. Atkins RC. Dr Atkins Diet Revolution. New York: David McKay Co. NY; 1972.
32. A critique of low-carbohydrate ketogenic weight reduction regimens. A review of
Dr. Atkins’ diet revolution. JAMA 1973;224:1415–9.
33. Well-Known Diet Gurus Square off at ACC 2001. American College of Cardiology
50th Annual Scientific Session. Scientific Session News 2001;19:5.
34. Brehm BJ, Seeley RJ, Daniels SR, et al. A randomized trial comparing a very low car-
bohydrate diet and a calorie-restricted low fat diet on body weight and cardiovas-
cular risk factors in healthy women. J Clin Endocrinol Metab 2003;88(4):1617–23.
35. 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(1):8–16.
36. 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(10):778–85.
37. Yancy WS Jr, Olsen MK, Guyton JR, et al. A low-carbohydrate, ketogenic diet ver-
sus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled
trial. Ann Intern Med 2004;140(10):769–77.
38. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet
for obesity. N Engl J Med 2003;348(21):2082–90.
39. 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(21):2074–81.
40. Segal-Isaacson CJ, Johnson S, Tomuta V, et al. A randomized trial comparing
low-fat and low-carbohydrate diets matched for energy and protein. Obes Res
2004;12(Suppl 2):130S–40S.
41. 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(2):177–84.
42. Pirozzo S, Summerbell C, Cameron C, et al. Advice on low-fat diets for obesity.
Cochrane Database Syst Rev 2002;(2):CD003640.
43. Bravata DM, Sanders L, Huang J, et al. Efficacy and safety of low-carbohydrate
diets: a systematic review. JAMA 2003;289(14):1837–50.
44. Nordmann AJ, Nordmann A, Briel M, et al. Effects of low-carbohydrate vs low-fat
diets on weight loss and cardiovascular risk factors: a meta-analysis of random-
ized controlled trials. Arch Intern Med 2006;166(3):285–93.
45. Dansinger ML, Gleason JA, Griffith JL, et al. Comparison of the Atkins, Ornish,
Weight Watchers, and Zone diets for weight loss and heart disease risk reduc-
tion: a randomized trial. JAMA 2005;293(1):43–53.
46. Truby H, Baic S, deLooy A, et al. Randomised controlled trial of four commercial
weight loss programmes in the UK: initial findings from the BBC ‘‘diet trials’’. BMJ
2006;332:1309–14.
884 Dubnov-Raz & Berry

47. 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(9):969–77.
48. 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.
49. Astrup A, Meinert Larsen T, et al. Atkins and other low-carbohydrate diets: hoax
or an effective tool for weight loss? Lancet 2004;364(9437):897–9.
50. Feinman RD, Fine EJ. ‘‘A calorie is a calorie’’ violates the second law of
thermodynamics. Nutr J 2004;28(3):9.
51. Buchholz AC, Schoeller DA. Is a calorie a calorie? Am J Clin Nutr 2004;79:
S899–906.
52. Schoeller DA, Buchholz AC. Energetics of obesity and weight control: does diet
composition matter? J Am Diet Assoc 2005;105:S24–8.
53. Brehm BJ, Spang SE, Lattin BL, et al. The role of energy expenditure in the
differential weight loss in obese women on low-fat and low-carbohydrate diets.
J Clin Endocrinol Metab 2005;90(3):1475–82.
54. Chen TY, Smith W, Rosenstock JL, et al. A life-threatening complication of Atkins
diet. Lancet 2006;367:958.
55. Jenkins DJ, Wolever TM, Taylor RH, et al. Glycemic index of foods: a physiological
basis for carbohydrate exchange. Am J Clin Nutr 1981;34:362–6.
56. Brand-Miller JC, Holt SH, Pawlak DB, et al. Glycemic index and obesity. Am J Clin
Nutr 2002;76(1):281S–5S.
57. Hare-Bruun H, Flint A, Heitmann BL. Glycemic index and glycemic load in relation
to changes in body weight, body fat distribution, and body composition in adult
Danes. Am J Clin Nutr 2006;84(4):871–9.
58. Ma Y, Olendzki B, Chiriboga D, et al. Association between dietary carbohydrates
and body weight. Am J Epidemiol 2005;161(4):359–67.
59. Pawlak DB, Ebbeling CB, Ludwig DS. Should obese patients be counselled to fol-
low a low-glycaemic index diet? Yes. Obes Rev 2002;3(4):235–43.
60. Raben A. Should obese patients be counselled to follow a low-glycaemic index
diet? No. Obes Rev 2002;3(4):245–56.
61. Thomas DE, Elliott EJ, Baur L. Low glycaemic index or low glycaemic load diets
for overweight and obesity. Cochrane Database Syst Rev 2007;18(3):CD005105.
62. Sichieri R, Moura AS, Genelhu V, et al. An 18-mo randomized trial of a low-
glycemic-index diet and weight change in Brazilian women. Am J Clin Nutr
2007;86(3):707–13.
63. Das SK, Gilhooly CH, Golden JK, et al. Long-term effects of 2 energy-restricted
diets differing in glycemic load on dietary adherence, body composition, and me-
tabolism in CALERIE: a 1-y randomized controlled trial. Am J Clin Nutr 2007;
85(4):1023–30.
64. Raatz SK, Torkelson CJ, Redmon JB, et al. Reduced glycemic index and glyce-
mic load diets do not increase the effects of energy restriction on weight loss and
insulin sensitivity in obese men and women. J Nutr 2005;135(10):2387–91.
65. McCarron DA. Dietary calcium as an antihypertensive agent. Nutr Rev 1984;42:
223–5.
66. Davies KM, Heaney RP, Recker RR, et al. Calcium intake and body weight. J Clin
Endocrinol Metab 2000;85:4635–8.
67. Lin YC, Lyle RM, McCabe LD, et al. Dairy calcium is related to changes in body
composition during a two year exercise intervention in young women. J Am Coll
Nutr 2000;19:754–60.
 The Dietary Treatment of Obesity 885

68. Zemel MB, Shi H, Greer B, et al. Regulation of adiposity by dietary calcium.
FASEB J 2000;14:1132–8.
69. Pereira MA, Jacobs DR, Van Horn L, et al. Dairy consumption, obesity, and the
insulin resistance syndrome in young adults. The CARDIA study. JAMA 2002;
287:2081–9.
70. Mirmiran P, Ezmaillzadeh A, Azizi F. Dairy consumption and body mass index: an
inverse relationship. Int J Obes Relat Metab Disord 2005;29:115–21.
71. Jacqmain M, Doucet E, Despres JP, et al. Calcium intake, body composition, and
lipoprotein-lipid concentrations in adults. Am J Clin Nutr 2003;77:1448–52.
72. Shahar DR, Abel R, Elhayany A, et al. Does dairy calcium intake enhance weight
loss among overweight diabetic patients? Diabetes Care 2007;30:485–9.
73. Lovejoy JC, Champagne CM, Smith SR, et al. Ethnic differences in dietary
intakes, physical activity, and energy expenditure in middle-aged, premeno-
pausal women: the Healthy Transitions Study. Am J Clin Nutr 2001;74:90–5.
74. Loos RJ, Rankinen T, Leon AS, et al. Calcium intake is associated with adiposity in
black and white men and white women of the HERITAGE Family Study. J Nutr
2004;134:1772–8.
75. Lorenzen JK, Mølgaard C, Michaelsen KF, et al. Calcium supplementation for 1 y does
not reduce body weight or fat mass in young girls. Am J Clin Nutr 2006;83:18–23.
76. Phillips SM, Bandini LG, Cyr H, et al. Dairy food consumption and body weight
and fatness studied longitudinally over the adolescent period. Int J Obes Relat
Metab Disord 2003;27:1106–13.
77. Venti CA, Tataranni PA, Salbe AD. Lack of relationship between calcium intake
and body size in an obesity-prone population. J Am Diet Assoc 2005;105:1401–7.
78. Gunther CW, Legowski PA, Lyle RM, et al. Dairy products do not lead to
alterations in body weight or fat mass in young women in a 1-y intervention.
Am J Clin Nutr 2005;81:751–6.
79. Snijder MB, van der Heijden AA, van Dam RM, et al. Is higher dairy consumption
associated with lower body weight and fewer metabolic disturbances? The Hoorn
Study. Am J Clin Nutr 2007;85:989–95.
80. Kamycheva E, Joakimsen RM, Jorde R. Intakes of calcium and vitamin D predict
body mass index in the population of Northern Norway. J Nutr 2003;133:102–6.
81. Rajpathak SN, Rimm EB, Rosner B, et al. Calcium and dairy intakes in relation to
long-term weight gain in US men. Am J Clin Nutr 2006;83:559–66.
82. Berkey CS, Rockett HR, Willett WC, et al. Milk, dairy fat, dietary calcium, and
weight gain: a longitudinal study of adolescents. Arch Pediatr Adolesc Med
2005;159:543–50.
83. Trowman R, Dumville JC, Hahn S, et al. A systematic review of the effects of cal-
cium supplementation on body weight. Br J Nutr 2006;95(6):1033–8.
84. Hollis JH, Mattes RD. Effect of increased dairy consumption on appetitive ratings
and food intake. Obesity (Silver Spring) 2007;15(6):1520–6.
85. Zemel MB. The role of dairy foods in weight management. J Am Coll Nutr 2005;
24(Suppl 6):537S–46S.
86. Teegarden D. The influence of dairy product consumption on body composition.
J Nutr 2005;135(12):2749–52.
87. Boon N, Koppes LL, Saris WH, et al. The relation between calcium intake and
body composition in a Dutch population: The Amsterdam Growth and Health
Longitudinal Study. Am J Epidemiol 2005;162(1):27–32.
88. Rosell M, Håkansson NN, Wolk A. Association between dairy food consumption
and weight change over 9 y in 19,352 perimenopausal women. Am J Clin Nutr
2006;84:1481–8.
886 Dubnov-Raz & Berry

89. Klem ML, Wing RR, McGuire MT, et al. A descriptive study of individuals success-
ful at long-term maintenance of substantial weight loss. Am J Clin Nutr 1997;66:
239–46.
90. Franz MJ, VanWormer JJ, Crain AL, et al. Weight-loss outcomes: a systematic
review and meta-analysis of weight-loss clinical trials with a minimum 1-year
follow-up. J Am Diet Assoc 2007;107:1755–67.
91. The catastrophic failures of public health. Lancet 2004;363:745.