Nutrition in weight management and obesity:

What I have learned from my Nutrition in weight management course and its role on the epidemic, obesity! 

Objective: To review the evidence on the diet and nutrition causes of obesity and to recommend strategies to reduce obesity prevalence.

Design: The evidence for potential aetiological factors and strategies to reduce obesity prevalence was reviewed, and recommendations for public health action, population nutrition goals and further research were made.

Results: Protective factors against obesity were considered to be: regular physical
activity (convincing); a high intake of dietary non-starch polysaccharides (NSP)/fibre (convincing); supportive home and school environments for children (probable); and breastfeeding (probable). Risk factors for obesity were considered to be sedentary lifestyles (convincing); a high intake of energy-dense, micronutrient-poor foods (convincing); heavy marketing of energy-dense foods and fast food outlets (probable); sugar-sweetened soft drinks and fruit juices (probable); adverse social and economic conditions—developed countries, especially in women (probable).

A broad range of strategies were recommended to reduce obesity prevalence
including: influencing the food supply to make healthy choices easier; reducing the
marketing of energy dense foods and beverages to children; influencing urban
environments and transport systems to promote physical activity; developing
community-wide programmes in multiple settings; increased communications about healthy eating and physical activity; and improved health services to promote breastfeeding and manage currently overweight or obese people.
Conclusions: The increasing prevalence of obesity is a major health threat in both
low- and high income countries. Comprehensive programmes will be needed to turn the epidemic around.

Another difficulty in rating evidence in relation to some of the potential
environmental causes of weight gain. For environmental
factors, more associated evidence and expert opinion had
to prevail because of the absence of direct studies or trials
in the area.
It is important to note that this review on obesity has
not covered the energy expenditure side of the energy
balance equation in any depth. Physical activity is at least
as important as energy intake in the genesis of weight
gain and obesity and there are likely to be many
interactions between the two sides of the equation in
terms of aetiology and prevention. The role of physical
inactivity in the development of obesity has been well
described and a recent report from the US Center for
Disease Control and Prevention summarises the evidence
base for a variety of interventions to increase physical
activity at the population.

Also, a thorough review
of weight control and physical activity has recently been
conducted by the WHO International Agency for
Research on Cancer and was also used as a basis for
recommendations on physical activity.

Current global situation and trends

The prevalence of obesity is increasing throughout the
world’s population. But the distribution varies greatly
between and within countries. In the US, over the past 30
years, the prevalence of obesity rose from about 12–20%
of the population from 1978 to 1998. The UK has
experienced an increase in the prevalence of obesity from
7% in 1980 to 16% in 1958
. Other countries, such as The
Netherlands, have experienced much smaller increases
from a low baseline of about 5% in the 1980s to about 8%
in 1997. In Asia, the prevalence of obesity has rapidly
increased. In the last 8 years the proportion of Chinese
men with a body mass index (BMI) .25 kg/m2 has tripled
from 4 to 15% of the population and the proportion in
women has doubled from 10 to 20%. Pacific populations
have some of the world’s highest prevalence rates of
obesity. The proportion of men and women with a BMI
.30 kg/m in Nauru was 77% in 1994 and for Pacific
people living in New Zealand in the early 1990s the
prevalence rates were about 65–70%.
The obesity epidemic moves through a population in a
reasonably consistent pattern over time and this is
reflected in the different patterns in low- and high income
countries. In low income countries, obesity is more
common in people of higher socioeconomic status and in
those living in urban communities. It is often first
apparent among middle-aged women. In more affluent
countries, it is associated with lower socioeconomic
status, especially in women, and rural communities.
The sex differences are less marked in affluent countries
and obesity is often common amongst adolescents and
younger children.
Brazil is an example of a country with well documented
changes in obesity prevalence as it undergoes
rapid nutrition transition. There has been a rapid
increase in obesity where the prevalence among urban
men with high incomes is about 10%, but still only 1% in
rural areas. Women in all regions are generally more
obese than men and the prevalence for those on low
income is still increasing. However, the rate of obesity
among women with high income is becoming stable or
even declining.
The standard definitions of overweight (BMI 25
kg/m2) and obesity (30 kg/m2) have been mainly
derived from populations of European descent. However,
in populations with large body frames, such as Polynesians,
higher cut-off points have been used 16. In
populations with smaller body frames, such as Chinese
populations, lower cut-off points have been proposed
and studies are being undertaken to evaluate appropriate
cut-off points for a variety of Asian populations.
Body fat distribution (often assessed by the waist
circumference or the waist:hip ratio) is an important
independent predictor of morbidity. Although this
review focuses on weight gain and the development of
overweight and obesity, it is acknowledged that increases
in abdominal fatness (particularly, intra-abdominal fat)
pose a greater risk to health than increases in fatness
around the hips and limbs. In general, the causes of weight
gain and abdominal weight gain are the same and it is the
characteristics of the individuals (such as sex, age,
menopausal status) that influence the distribution of the
fat that is gained.

The nutrition transition

The increasing westernisation, urbanisation and mechanisation
occurring in most countries around the world is
associated with changes in the diet towards one of high fat,
high energy-dense foods and a sedentary lifestyle. This
shift is also associated with the current rapid changes in
childhood and adult obesity. Even in many low income
countries, obesity is now rapidly increasing, and often
coexists in the same population with chronic undernutrition.
Life expectancy has increased due to
advancement in nutrition, hygiene and the control of
infectious disease. Infectious diseases and nutrient
deficiency diseases are, therefore, being replaced in
developing countries by new threats to the health of
populations like obesity, cardiovascular disease and
A sharp decline in cost of vegetable oils and sugar
means that they are now in direct competition with cereals
as the cheapest food ingredients in the world. This has
caused a reduction in the proportion of the diet that is
derived from grain and grain products and has greatly
increased world average energy consumption, although
this increase is not distributed evenly throughout the
world’s population. As populations become more urban and incomes rise,
diets high in sugar, fat and animal products replace more
traditional diets that were high in complex carbohydrates
and fibre. Ethnic cuisine and unique traditional food
habits are being replaced by westernised fast foods, soft
drinks and increased meat consumption. Homogenisation
and westernisation of the global diet has increased
the energy density and this is particularly a problem for
the poor in all countries who are at risk of both obesity and
micronutrient deficiencies.

Health consequences of obesity

Mortality rates increase with BMI and they are greatly
increased above a BMI of 30.
As obesity has increased over the last 30 years, the
prevalence of type 2 diabetes has increased dramatically.
The global numbers of people with diabetes (mainly type
2) are predicted to rise by almost 50% in 10 years—151
million in 2000 to 221 million in 2025. The most potent
predictor for the risk of diabetes, apart from age, is the
BMI23. Even at a BMI of 25 kg/m2 the risk of type 2 diabetes
is significantly higher compared to BMI of less than
22 kg/m2 but at BMI over 30 kg/m2 the relative risks are
enormous. Type 2 diabetes is becoming increasingly
prevalent among children as obesity increases in those age
groups. A high BMI is associated with higher blood pressure and
risk of hypertension, higher total cholesterol, LDLcholesterol
and triglyceride levels and lower HDLcholesterol
levels. The overall risk of coronary heart
disease and stroke, therefore, increases substantially with
weight gain and obesity.Gall bladder disease and the incidence of clinically
symptomatic gallstones are positively related to BMI23.
There is evidence to suggest increased cancer risk as BMI
increases, such as colorectal cancer in men, cancer of the
endometrium and biliary passage in women, and breast
cancer in post-menopausal women. Obese people are
also at increased risk of gout, sleep apnoea, obstetric and
surgical complications.

Host issues
There are a variety of behaviours and other host factors
that have a potential effect on a population’s level of
obesity. These are, of course, closely linked to the vectors
and the environments and in many cases the issues merge
and overlap. Issues related to social aspects of eating are
not covered.

Snacking/eating frequency:

While there is no one definition of snacking, it is probably
best to consider the content of snack foods and the
increased eating frequency that snacking promotes as
separate issues. There is evidence that
snacking prevalence (i.e. occasions of snacking) is
increasing, the energy density of snack foods is increasing
and the contribution to total energy is increasing. Snacks
contribute to about 20–25% of total energy intake in
countries like the US and UK. However, there is little
evidence that a higher frequency of eating per se is a
potential cause of obesity. Cross-sectional studies tend to
show a negative relationship or no relationship between
meal frequency and BMI37. Low eating frequency may, of
course, be a response to obesity rather than a cause.
Experimental studies have found mixed results on the
degree of caloric compensation that people make at meal
time in response to a prior snack with some studies
Diet, nutrition and the prevention of excess weight gain and obesity showing more complete compensation among lean
people. There is insufficient evidence to support an
effect of a higher frequency of eating on obesity or weight
gain. If anything, it is protective against weight gain. The
high energy density of common snack foods, however,
may do the opposite and promote weight gain (see below).
Restrained eating, dieting and binge eating patterns.
While a degree of selective or restrained eating is probably
needed to prevent obesity in an environment of plenty,
some individuals (dieters and non-dieters) score highly on
the Restraint Scale and paradoxically may also exhibit
periods of disinhibited eating. Such individuals appear
to be at risk of dieting–overeating cycles. The concepts
used to define these constructs and the instruments used
to measure them continue to evolve, but the studies would
suggest that a ‘flexible restraint’ eating pattern is associated
with a lower risk of weight gain whereas a ‘rigid
restraint/periodic disinhibition’ pattern is associated with
a greater risk of weight gain. Binge eating disorder and
night eating syndrome would be examples of the latter
pattern. Binge eating disorders are significantly more
common in obesity in cross-sectional studies. The
relationships between these dietary patterns and weight
gain or obesity is complex with both cause and effect
relationships likely.

Eating out:

In western countries, the frequency of eating food
prepared outside the home is increasing and this is most
apparent and best documented in the US. In 1970, 26% of
the food dollar in the US was spent on food prepared
outside the home. By 1995, it had climbed to 39% and is
projected to rise to 53% by 2042,43. This shift towards an
increase in the frequency of eating meals and snacks away
from home and the proportion of food budget spent on
away from home foods 42,44,45 has coincided with the
increasing prevalence of obesity.

In the US, food prepared away from home is higher in
total energy, total fat, saturated fat, cholesterol and
sodium, but contains less fibre and calcium and is overall
of poorer nutritional quality than at-home food. Also, the
fat content of at-home food has fallen considerably from
41% of total energy in 1977 to 31.5%, but there has been no
change in the fat content of food prepared away from
home (37.6%)43.

These food composition differences and the increasing
portion sizes, are likely contributors to the rising
prevalence of obesity in the US. Those who eat out
more, on average, have a higher BMI than those who eat
more at home. The evidence implicating the increasing
use of food prepared outside the home as a risk for obesity
is largely limited to the US but this may be extrapolated to
other western countries. It is unknown whether a high
frequency of eating out is associated with obesity or
weight gain in other populations, for example, in Asian
countries, where eating outside the home may not be a
risk for weight gain.

Early nutrition
Birth weight is a crude indicator of intrauterine nutrition. A
systematic review of predictors of obesity by Parsons et al.
found that studies reported a consistent and positive
relationship between birth weight and BMI (or risk of
overweight) as a child or as an adult. It is possible that
low birth weights may also be associated with high adult
BMI (i.e. that the relationship is a J-shaped curve rather
than linear and positive). However, very low birth weight
is a much weaker predictor of high adult BMI than high
birth weight.
Maternal and childhood undernutrition are common in
low income countries and childhood stunting is often used
as a marker for this. A later exposure to more western-style
diets and lifestyles (such as through migration to urban
areas and/or improved economic conditions) may
promote an excessive increase in body fatness or
abdominal fatness. Popkin et al. studied 3–9-year-old
children in cross-sectional studies in four countries (China,
Russia, South Africa and Brazil) and found that stunted
children (low height-for-age z-score) were more likely
than non-stunted children to be overweight (high weight for-height
z-score) with relative risks. On the other hand, a cohort of children measured at
age 3 in Guatemala and followed into adulthood showed
that childhood stunting was associated with a low BMI and
low percent body fat in men but no such relationships
were seen in women. Only when BMI or percent body
were adjusted for, did an association between severe
stunting and high waist:hip ratio become evident.
The hypothesis that intrauterine and/or early childhood
undernutrition leads to adult obesity or abdominal obesity
is an important one that links with the other relationships
between early undernutrition and adult diseases such as
hypertension and diabetes. This could pose a major
problem for countries undergoing the economic and
nutrition transition. However, the relationships are
clearly complex and the available data were judged
insufficient to be able to make a single summary statement
in the evidence table.

Vector issues

Percent fat, percent carbohydrate and energy density
Background: Most of the debate about the fat and
carbohydrate content of the diet in relation to obesity
centres on the effects of altering the reciprocal proportions
of carbohydrate and fat in the diet on energy density, total
energy intake, body weight and lipoprotein profiles. The
debate 58–60 has become vigorous and, at times, muddled
because several issues are usually debated at the same
time. Also, the epidemiological evidence comes from
different types of studies (ecological, cross-sectional and
prospective) which suffer from multiple potential sources
of bias, the instruments used to measure dietary intake are
blunt, and there is substantial obesity-related underreporting
of energy and fat intake.

Diet, nutrition and the prevention of excess weight gain and obesity in the diet and obesity or weight gain.

Ecological studies between populations tend to show a
positive relationship between fat and obesity, especially if
populations with low fat intakes are included, but
negative relationships are also seen. Similarly, studies in
the same population over time tend to show positive
relationships between obesity and dietary fat intake in
populations undergoing nutrition transition but a negative
relationship in many westernised populations. Crosssectional
and prospective studies also show mixed
results. In light of the methodological drawbacks of
these types of studies and the mixed results they have
produced controlled trials are needed to address the

Percent fat in the diet—fixed total energy trials:
According to Reaven the simplest way to answer the
question about the impact of fat and carbohydrate in the
diet on body weight ‘is to focus on studies that vary in
macronutrient composition, but are equal in energy’.
Studies that have done this have indeed found that
‘clamping’ total energy produces similar weight changes
irrespective of the macronutrient composition. The
rationale for many of these studies was to assess the
impact of macronutrient changes independent of total
energy intake. They were not to emulate the real world
where total intake is ad libitum. The conclusion from the
fixed energy studies is that if a high percent fat diet
promotes weight gain, the mechanism appears to be
mediated by promoting a higher total energy intake.
Percent fat in the diet—ad libitum trials, covert
manipulations: Several trials have covertly manipulated
the fat and carbohydrate proportions of equally palatable
diets while allowing study participants to eat ad libitum
total intakes. Most of the studies were short term with
the longest being 11 weeks. These trials consistently
show a progressive rise in total energy intake and body
weight on the higher percent fat diets and the opposite on
the lower percent fat diets. The amount (weight) of food
eaten is similar on both types of diet. These covert
manipulation studies are central to the debate on dietary
fat and weight gain because they demonstrate that, other
things being equal, the physiological–behavioural consequence
of a high percent fat diet is a slow weight gain
through the ‘passive overconsumption’ of total energy.
Percent fat in the diet—ad libitum trials, overt
manipulation: Longer term trials of high and low percent
fat diets have generally used educational strategies to get
participants to select reduced fat food options and
compared them with standard or higher fat diets. The
diet is unrestricted in total amount (weight) and
replacement of lost energy from fat is not specifically
replaced by carbohydrate. It is important to note that,
unlike the covert manipulations, it is difficult to blind
such studies and, therefore, psychosocial effects,
personal preferences and other effects not directly related
to physiology can confound the results.

An interesting study attempting to replicate realistic
food choices randomised normal weight and overweight
participants into two groups who selected either full fat or
reduced fat foods from small, realistic ‘supermarkets’ in
the study centres. The free access to higher fat products
resulted in a significant increase in energy intake
(0.9 MJ/d) and body weight (0.7 kg) over 6 months
compared to the reduced fat group.
Reducing the fat content of the diet consistently
produces modest reductions in body weight but one
could argue that instructions to individuals to reduce other
macronutrients in the diet or to restrict the intake of certain
high volume foods (such as staple carbohydrates) would
also result in weight loss. Indeed, there are a myriad of
popular diets with a wide variety of food and drink
restrictions and all have their champions who have lost
weight. It is obvious that any such restrictions that result in
a reduction in total energy intake will produce weight loss.

The rationale for promoting a reduction in the fat content
of the diet to prevent weight gain or promote weight loss is
that it is concordant with the body’s physiological–
behavioural mechanisms regulating food intake as
evidenced by the covert manipulation studies.

Another potential criticism of promoting a reduced fat
content of the diet is that the ad libitum weight loss studies
show a modest effect (a few kilograms) with a tendency to
return towards the previous weight after the intervention
period. This rebound is common to all dietary
interventions and there are a number of potential
explanations for this. They include: a reduction in
compliance to the diet, perhaps due to an environment
that is unsupportive of healthy food choices; overeating of
foods known to be low in fat and; physiological
adaptations that attenuate the impact of negative energy
balance on weight loss.

Extremely low fat, high carbohydrate diets are also very
effective for weight loss but it must be stressed that
large reductions in total fat intake would be unattainable at
a population level. Average changes in the order of 2–3 kg
may seem small for individuals but they are important on a
population level in the context of obesity prevention. A
shift of one unit of BMI in the overall distribution in the
population is associated with a 5% point change in the

Many studies have
manipulated the macronutrient content of short term diets
under isocaloric weight stable conditions (such as reducing
saturated fat and replacing the energy with carbohydrate or
other types of fat). In many but not all such studies, the
high carbohydrate diet is associated with increased
triglycerides and decreased HDL-cholesterol (especially if
predominantly simple carbohydrates are used).
The weight loss effect of a reduced-fat diet, ad libitum
diet, however, appears to compensate for these potentially
detrimental effects. Schaefer et al. directly compared the
effects of shifting subjects from a high fat diet (35% of
energy) to a low fat diet (15% of energy) under isocaloric
(5–6 weeks) and ad libitum (10–12 weeks) conditions.
In order to achieve energy equivalence in the isocaloric
part of the study, the weight and volume of the food
consumed on the lower fat diet had to be increased by
30%. Under weight-maintenance conditions, on the low
fat diet there was a significant reduction total, LDL- and
HDL-cholesterol and an increase in total:HDL cholesterol
ratio and plasma triglyceride concentrations. At the end of
the ad libitum diet, subjects had lost an average of 3.6 kg
and achieved greater reductions in total and LDL cholesterol
compared to the low fat isocaloric diet. The
total:HDL cholesterol ratio and triglyceride levels were no
different at the end of the ad libitum period compared to

This and other studies that assess the interaction
between macronutrient composition and weight change
on blood lipids77,99,100 suggest that the effects of short
term, isocaloric manipulations under metabolic ward
conditions on lipids cannot be extrapolated to long term,
ad libitum conditions in free-living individuals.

Summary of percent fat and obesity: At a macronutrient
level, there is no evidence that energy from fat is more
fattening than the same amount of energy from
carbohydrate or protein. At a dietary level, there is still
debate about the effects of diet composition on unhealthy
weight gain, and more research is needed in this area.

However, it was considered that the overall evidence from
the randomised controlled trials was convincing that a
high intake of energy-dense foods (which are often also
micronutrient poor) promotes unhealthy weight gain. The
short term, isocaloric substitution studies were considered
far less relevant to free living individuals than the longer
term, ad libitum studies. These latter studies show a highly
consistent effect of a high fat content on promoting weight
gain. The covert manipulations of fat content show that the
effect is a physiological–behavioural one and is not
dependent on conscious reductions in food eaten. The
main mechanism for this appears to be that a diet high in
fat has a weak impact on satiety because of its high energy
density and this leads to a passive overconsumption of
total energy. The high palatability of high fat foods and the
relatively weak metabolic autoregulation in the face of a
high fat diet are also likely contributors. While most high
fat diets tend to be energy dense diets and thus weight promoting
diets, important caveats were noted. For
example, many processed low fat foods were quite
energy-dense and could promote weight gain if eaten in
large amounts and conversely vegetable-based foods were
quite energy dilute even with significant added fat and
could protect against weight gain.

Carbohydrate type (sugar, glycemic index (GI) and nonstarch
polysaccharide (NSP).

The definitions of carbohydrates are often confusin and not just to me.

Sugars are predominantly monosaccharides and disaccharides.
The term ‘free sugars’ has been defined in
relation to the sugars that promote dental caries and refers
to all mono and disaccharides added by the manufacturer,
cook or consumer plus sugars naturally present in fruit
juice, honey and syrups. Polysaccharides are either starch
or NSP, the latter having considerable commonality with
the term ‘dietary fibre’ which is still in common parlance
and was the term used in many of the studies reviewed.
Sugars, GI and NSP/fibre are considered in turn, although
of course there is significant overlap between these factors
within foods.

Sugar in foods: There is a reciprocal relationship
between the percent fat and percent carbohydrate in the
diet because these two nutrients generally contribute over
80% of total energy. Therefore, the previous section on
percent fat could also be stated as: diets with a high
carbohydrate content provide protection against weight
gain. However, if the diet is high in sugar, does the same
association apply? Large population studies have demonstrated
that those who have high total energy intakes tend
to have a high total sugar intake although in relative
terms, a reciprocal relationship is also seen between the
percent fat and percent sugar in the diet. Studies relating
sugar intake to BMI consistently show an inverse relation
between sugar intake as a percent of energy and BMI or
obesity prevalence.

It is possible that the negative relationship between
sucrose consumption and BMI is affected by confounding
factors. For example, more active people need extra
energy and this could be provided by sugar. Selective
underreporting of high sugar foods and drinks by
overweight/obese people is another possible confounder.

The high sugar content of some products with
reduced fat claims may falsely imply that the products are
low in energy as well.

Simple sugars have hedonistic value. Sweetening
increases the palatability of many foods and it has been
suggested that sweetness may lead to overconsumption.

However, there appears to be a limit to the
hedonistic response to sweetened foods. Palatability of
foods is also increased by fat and therefore processed
foods containing both high sugar and fat content may lead
to weight gain. Overall, the mixed results, especially
amongst the few available trials, does not allow a judgement to be made about the sugar content of food and obesity.

Studies have compared high fat diets with low fat diets
that are high in either sugar or starch. Raben et al. found
that similar amounts of energy were consumed on the
high fat and high sucrose diets but there was a lower
energy intake and weight loss with the high starch
diets. Saris et al. found a relative weight loss of 1.7 kg
in the high sugar diet and 2.6 kg in the high starch diet
compared to the high fat diet (both statistically
significant) but the differences between carbohydrate
types was not significant.

Sugar in drinks: The energy density of drinks such as
regular soda drinks is low because of the high water
content but physiologically the energy density of fluids
and foods may have not have comparable effects on
satiety and food consumption. It, therefore,
seems prudent to consider the impact of drinks that
contribute a significant amount to total energy intake
(such as high sugar soda drinks) separately from foods.
In a cross-over study, Tordoff and Alleva compared
the consumption of soda (1150 g/d for 3 weeks) which
had been sweetened with either a high fructose corn syrup
or aspartame on body weight. The high fructose soda
condition increased total energy intake by 335 kcal/d and
resulted in a significant mean weight gain of 0.66 kg
compared to the aspartame soda condition where total
energy intake decreased by 179 kcal/d and weight
decreased non-significantly by 0.17 kg.

Some fruit drinks and cordial drinks can also be high in
sugar and may promote weight gain if drunk in large
quantities but this has been less extensively studied than
soda drinks.

Overall, the evidence that high sugar drinks promote
weight gain is consistent and moderately strong, but is of
most relevance in those populations with a high intake
(such as children in many countries).

Glycemic index: A further mechanism by which
carbohydrates may influence energy intake and body
weight is by their GI. Different carbohydrate foods
increase blood glucose and serum insulin to varying
extents even when the same amount of carbohydrate is
eaten. The different changes in glucose and/or insulin may
have subsequent effects on food intake or the promotion
of overweight and obesity, with lower GI diets
producing greater satiety. In addition to the effects
of carbohydrates on satiety, there is a suggestion that low
GI diets may provoke greater increases in cholecystokinin
and fullness post-meal (satiation).

Ludwig et al. demonstrated that voluntary food intake
was greater after high GI meals were consumed compared
to medium and low GI meals. They found that rapid
absorption of glucose altered hormonal and metabolic
functions and promoted excessive food intake after the
ingestion of a high GI meal. Agus et al found during a
randomised cross-over trial that when the acute (9 days)
effects of energy restricted diets of high and low glycemic
loads were studied in overweight young men, the high
glycemic load diet produced a greater decline in metabolic
rate, more negative nitrogen balance and greater voluntary
food intake.

On energy restrained diets, a 12 week cross-over trial by
Slabber et al.demonstrated that a low GI diet produced
lower insulin levels and a greater weight loss than
corresponding high GI diets. Spieth et al found that
after 4 months of intervention, low GI diets may be more
effective than reduced-fat diets in treating childhood

Low GI diets may influence fuel storage by promoting
fat oxidation instead of carbohydrate oxidation,
whereas raised insulin levels in response to high GI diets
inhibit lipolysis and encourage fat storage, limiting
available fuels and encouraging overeating.
Overall, the current evidence suggests a possible
influence of GI on body weight and composition, but
long term trials with changes in body weight as an
outcome are needed before more definitive statements
can be made.

Alcohol is an energy dense nutrient (7 kcal/g) and because
of its place at the top of the oxidative hierarchy, its
potential for sparing fat oxidation and promoting fat
storage is significant. However, some metabolic studies
show that isocaloric substitution of alcohol for food energy
results in weight loss while the addition of alcohol does
not promote weight gain. There is a similar paradox
seen in epidemiological studies. Dietary intake surveys
tend to show that energy from alcohol is additive to food
energy intake such that total energy intake is higher with a
higher alcohol consumption. However, the relationships
between reported alcohol intake and BMI show a
mixed pattern. One review of the epidemiological
evidence, listed 25 studies showing a positive association,
18 showing a negative association and 11 showing no
relationship. For women, there was often a negative
relationship or possibly U-shaped relationship. For
men, the relationship tends to be slightly positive or

In an earlier review of 27 studies, seven showed a
negative relationship between adiposity and alcohol
intake, seven showed a positive relationship, nine showed
different associations for women and men, and eight
showed no relationship. Emery et al. reviewed the
epidemiological studies linking a high alcohol intake
with abdominal fat distribution (high waist circumference
or waist:hip ratio)137. They concluded that the evidence
for a relationship was moderate for men and suggestive for

The potential for confounding by concurrent lifestyle
and socioeconomic factors is substantial, as is the
tendency to underreport alcohol intake. Other factors
also confound the relationships between alcohol and
obesity: alcohol–macronutrient interactions; the possibility
that obese people have reduced their alcohol
consumption because of their obesity; metabolism
through pathways with different energetic returns (e.g.
alcohol dehydrogenase versus microsomal ethanol oxidizing
system); and the direct toxic effects of alcohol.

Overall, the epidemiological evidence is mixed and
probably highly confounded. Randomised controlled
trials on the issue are unlikely to be conducted. There is
currently insufficient evidence to support a general role for
alcohol in the development of obesity.

Portion size

The portion size in pre-packaged, ready-to-eat and
restaurant foods is increasing in the US and elsewhere,
building on the consumers’ desire for ‘value for money’. In
recent years the number of restaurants offering ‘supersize’
options on their menu has rapidly risen, and other food
items, especially snack foods, have increased package
weight. The increasing size of packaging indicates lower
unit cost and encourages use of more product than small
package size. These trends are occurring in many
western countries but are less well documented than they
are in the US.
‘Supersized’ portions potentially lead to increased
energy intakes at the time and over the day and, therefore,
could be a significant contributor to obesity, particularly in
populations with a high use of meals prepared outside the
home. Many people cannot accurately estimate portion
size, and this leads to an underestimation of intake.
The energy compensation later in the day after a high
energy meal is incomplete in many individuals. Very
few studies have examined the impact of portion size on
overall energy consumption. One of these has shown that
portion size promotes a higher total intake and that this
seems to occur in adults and in 5 year olds, but not in 3
year olds. The age at which the external cues (such as
portion size) begin to influence intake is, therefore,
appears to be between 3 and 5 years.
Overall, there is strong ecological evidence of a
concurrent increase in portion sizing and obesity in
countries such as the US. The proposition that large
portion sizes promote overconsumption is logical and
likely but the empirical studies, while supportive, are very
few in number

Food marketing sector
Fast food restaurants and energy-dense foods and drinks
are among the most advertised products on television
and children are often the targeted market. The fat, sugar
and energy content of foods advertised to children is very
high compared to their daily needs and most of the foods
advertised fall into the ‘eat least’ or ‘eat occasionally’
sections of the recommended dietary guidelines. Many
studies have documented that the overwhelmingly
dominant messages that are directed at children,
particularly through the powerful medium of television
advertising, are the antithesis of what is recommended for
a healthful diet.
The food industry (mainly fast food restaurants and
manufacturers of high fat or high sugar foods and drinks)
spends huge sums on mass media advertising, mainly
through television advertisements. In 1997, they spent 11
billion US$ in the US alone. The impact of this high
volume of advertising on directing food choices to the
products being advertised has undoubtedly been closely
researched by the companies concerned but very little of
this market research data is publicly available. The high
volume of advertising for energy dense foods and
beverages is undoubtedly fuelling the increasing consumption
of these products. 
The prevalence of overweight and obesity is higher
among children who watch more television, and the
increased energy intakes of these children may be
partly responsible. Advertised products are more often
requested for purchase and consumed by children.
Brand recognition not only encourages children to request
products more often, but also targets those with
discretionary spending money. Children’s behaviour
has been shown to reflect television advertising patterns
even when they know what they should be eating.
Young children under the age of about 6–8 cannot
distinguish regular programmes from advertisements,
nor do they understand the persuasive intent of
commercials and overweight children with low self esteem
are more susceptible to commercials that promote
consumption of foods for personal enhancement.
Overall, it is probable that the heavy advertising of fast
foods and energy dense foods and drinks increases the
consumption of those products. The evidence to support
this rested on a wide variety of publicly available (often
indirect evidence) studies and the huge advertising
investment in influencing food choice behaviours which
was based on more direct but proprietary evidence.
Nutrition claims
Nutrition claims are regulated in most countries because of
the potential for misleading information to be promoted. Over the last 10 years, 20–37% of new products
carry a nutrition claim with over half those claims in recent
years being for reduced or low fat. The claims clearly
provide information about some aspect of the content of
the food but for some restrained eaters, ‘low fat’ or ‘low
calorie’ claims can become an unconscious message to eat
more of the product or accompanying foods. In some
manufactured products, the fat content has been reduced
so that a low fat claim can be made, but the energy density
remains high negating the potential benefit for reducing
weight gain.
Overall, nutrition claims are an important influence on
the food choices of consumers and the formulation of food
by manufacturers. There can be some negative consequences
when the messages or signals are misleading or
are taken in the wrong way. The regulations for nutrition
claims need to ensure that products with claims for ‘low or
reduced fat’ also have comparable reductions in energy
density so that low fat, high energy foods are excluded
from making the claim.
Substantial proportions of the population in many parts of
the world are already overweight or obese, and therefore,
efforts to reduce obesity prevalence must not only focus
on the prevention of obesity in those who have not yet
become obese (primary prevention), but also on prevention
of further weight gain and promotion of weight loss in
those who are already obese before they develop the
complications of obesity (secondary prevention). In
contrast to the primary prevention of obesity, where
only limited evidence exists to support many of the
potential interventions, substantial data exist on efficacious
approaches to treatment. The principal setting for
weight loss is likely to be in physician offices or other
health care settings.
Approaches to weight loss and weight maintenance
have been summarised in various evidence-based reports
such as the NIH clinical guidelines on the identification,
evaluation and treatment of overweight and obesity in
adults199. In general, treatments using diet, physical
activity and medications are ‘efficacious’ (i.e. they promote
weight loss in clinical trial settings with careful patient
selection, close monitoring and high adherence rates in
the short term). Studies with long term follow up,
however, are disappointing as patients return towards
their original weights. What is, therefore, lacking are
positive ‘effectiveness’ studies whereby the efficacious
interventions are translated into practice in settings where
medical care is routinely delivered. Because primary care
settings are where most patients are seen and where most
physicians work, demonstrably effective obesity treatment
strategies are essential. Gastroplastic surgery is virtually
the only intervention with long term proven effectiveness
and cost effectiveness.
It is evident that there are a number of major barriers to
the effective management of obesity within most health
systems. It is beyond my scope of this report to detail
these, but they include a lack of effective interventions in
primary care settings, the lack of self-efficacy on the part of
physicians for managing obesity, the dearth of trained
health professionals to oversee and provide these
therapies, and in most countries, the financial reimbursement
systems that mitigate against best practice
management of obesity. The paradox is that, while there
is little investment in financing obesity management, there
are huge downstream costs associated with the management
of its complications.
Obesity is arguably the biggest challenge among the
epidemics facing the world because it is on the rise in low and
high income countries, no country has a track record
in terms of attenuating and reversing the epidemic, and it
has several major downstream health consequences in
terms of diabetes, cardiovascular diseases, some cancers
and arthritis that are very common and expensive to treat.
 The main food-related vectors that promote the passive overconsumption of total energy are: energy dense foods (principally related their fat
content but sometimes their carbohydrate content), high
energy drinks, and large portion sizes. The environmental
factors tend to be multiple in each of the settings in which
food is consumed and include physical, economic, policy
and socio-cultural dimensions. There is an urgent need to
focus attention on measuring these environmental
influences, assessing their impacts on energy intake and
testing interventions designed to make them less
obesogenic. Much more research is needed in these area.
A variety of potential interventions and their implications are needed. Overall, the level of evidence for population-based interventions is weak
either because they have been tried and shown to have
a modest impact (such as dietary guidelines and
workplace interventions) or they have not been tried
and evaluated (such as fiscal food policies and banning of products and advertising.
What we are facing here is an epidemic, on a global scale but education is our first defence. 

About Jason Allan Scott

Jason Allan Scott is a successful Serial Entrepreneur, Professional Keynote Speaker, Best Selling Author, award-winning event professional, Mentor, Podcaster and a part of Tim Ferris's NR set who travels the world educating and empowering people. Scott can show you how ordinary people can build a solid living, with passion and purpose, on their own terms. Voted Top 100 Movers and Shakers in Events by Eventbrite 2016, Voted number 1 on Double Dutch 250 people in Events and top 10% of social media in events in the world and one of the Small Business Top 100 companies 2016. Jason has started and sold several companies on three continents in his entrepreneurial journey. Tired of living someone else's life? Decided you never wanna be a boss or have a boss? Or maybe you just want to see how we can connect and work on something together? Contact me. Whether you are a wanna-preneur or seasoned entrepreneur or just a dreamer that wants to be a "do-er", I can show you how with low or no resources you can follow a passion, become your own boss, and be successful. This is not "lip service" I can follow it all up, I know how to run a business with numerous life examples from my journey and those I have met and interviewed who have achieved so much with so little to start.
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One Response to Nutrition in weight management and obesity:

  1. Pingback: Nutrition in weight management and obesity: | Lord Jason Scott's Blog

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