Feb, 27th 2018 10:45 pm, Article Recommended by Dr. J. Smith
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 torecommend 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 physicalactivity (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 conditionsdeveloped countries, especially in women (probable).
A broad range of strategies were recommended to reduce obesity prevalenceincluding: influencing the food supply to make healthy choices easier; reducing themarketing of energy dense foods and beverages to children; influencing urbanenvironments and transport systems to promote physical activity; developingcommunity-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 bothlow- 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 potentialenvironmental causes of weight gain. For environmentalfactors, more associated evidence and expert opinion hadto prevail because of the absence of direct studies or trialsin the area..It is important to note that this review on obesity hasnot covered the energy expenditure side of the energybalance equation in any depth. Physical activity is at leastas important as energy intake in the genesis of weightgain and obesity and there are likely to be manyinteractions between the two sides of the equation interms of aetiology and prevention. The role of physicalinactivity in the development of obesity has been welldescribed and a recent report from the US Center forDisease Control and Prevention summarises the evidencebase for a variety of interventions to increase physicalactivity at the population.
Also, a thorough reviewof weight control and physical activity has recently beenconducted by the WHO International Agency forResearch on Cancer and was also used as a basis forrecommendations on physical activity.
Current global situation and trendsOverview:
The prevalence of obesity is increasing throughout theworlds population. But the distribution varies greatlybetween and within countries. In the US, over the past 30years, the prevalence of obesity rose from about 1220%of the population from 1978 to 1998. The UK hasexperienced an increase in the prevalence of obesity from7% in 1980 to 16% in 1958. Other countries, such as TheNetherlands, have experienced much smaller increasesfrom a low baseline of about 5% in the 1980s to about 8%in 1997. In Asia, the prevalence of obesity has rapidlyincreased. In the last 8 years the proportion of Chinesemen with a body mass index (BMI) .25 kg/m2 has tripledfrom 4 to 15% of the population and the proportion inwomen has doubled from 10 to 20%. Pacific populationshave some of the worlds highest prevalence rates ofobesity. The proportion of men and women with a BMI.30 kg/m in Nauru was 77% in 1994 and for Pacificpeople living in New Zealand in the early 1990s theprevalence rates were about 6570%.The obesity epidemic moves through a population in areasonably consistent pattern over time and this isreflected in the different patterns in low- and high incomecountries. In low income countries, obesity is morecommon in people of higher socioeconomic status and inthose living in urban communities. It is often firstapparent among middle-aged women. In more affluentcountries, it is associated with lower socioeconomicstatus, especially in women, and rural communities.The sex differences are less marked in affluent countriesand obesity is often common amongst adolescents andyounger children.Brazil is an example of a country with well documentedchanges in obesity prevalence as it undergoesrapid nutrition transition. There has been a rapidincrease in obesity where the prevalence among urbanmen with high incomes is about 10%, but still only 1% inrural areas. Women in all regions are generally moreobese than men and the prevalence for those on lowincome is still increasing. However, the rate of obesityamong women with high income is becoming stable oreven declining.The standard definitions of overweight (BMI 25kg/m2) and obesity (30 kg/m2) have been mainlyderived from populations of European descent. However,in populations with large body frames, such as Polynesians,higher cut-off points have been used 16. Inpopulations with smaller body frames, such as Chinesepopulations, lower cut-off points have been proposedand studies are being undertaken to evaluate appropriatecut-off points for a variety of Asian populations.Body fat distribution (often assessed by the waistcircumference or the waist:hip ratio) is an importantindependent predictor of morbidity. Although thisreview focuses on weight gain and the development ofoverweight and obesity, it is acknowledged that increasesin abdominal fatness (particularly, intra-abdominal fat)pose a greater risk to health than increases in fatnessaround the hips and limbs. In general, the causes of weightgain and abdominal weight gain are the same and it is thecharacteristics of the individuals (such as sex, age,menopausal status) that influence the distribution of thefat that is gained.
The nutrition transition
The increasing westernisation, urbanisation and mechanisationoccurring in most countries around the world isassociated with changes in the diet towards one of high fat,high energy-dense foods and a sedentary lifestyle. Thisshift is also associated with the current rapid changes inchildhood and adult obesity. Even in many low incomecountries, obesity is now rapidly increasing, and oftencoexists in the same population with chronic undernutrition.Life expectancy has increased due toadvancement in nutrition, hygiene and the control ofinfectious disease. Infectious diseases and nutrientdeficiency diseases are, therefore, being replaced indeveloping countries by new threats to the health ofpopulations like obesity, cardiovascular disease anddiabetes..A sharp decline in cost of vegetable oils and sugarmeans that they are now in direct competition with cerealsas the cheapest food ingredients in the world. This hascaused a reduction in the proportion of the diet that isderived from grain and grain products and has greatlyincreased world average energy consumption, althoughthis increase is not distributed evenly throughout theworlds population. As populations become more urban and incomes rise,diets high in sugar, fat and animal products replace moretraditional diets that were high in complex carbohydratesand fibre. Ethnic cuisine and unique traditional foodhabits are being replaced by westernised fast foods, softdrinks and increased meat consumption. Homogenisationand westernisation of the global diet has increasedthe energy density and this is particularly a problem forthe poor in all countries who are at risk of both obesity andmicronutrient deficiencies.
Health consequences of obesity
Mortality rates increase with BMI and they are greatlyincreased above a BMI of 30.As obesity has increased over the last 30 years, theprevalence of type 2 diabetes has increased dramatically.The global numbers of people with diabetes (mainly type2) are predicted to rise by almost 50% in 10 years151million in 2000 to 221 million in 2025. The most potentpredictor for the risk of diabetes, apart from age, is theBMI23. Even at a BMI of 25 kg/m2 the risk of type 2 diabetesis significantly higher compared to BMI of less than22 kg/m2 but at BMI over 30 kg/m2 the relative risks areenormous. Type 2 diabetes is becoming increasinglyprevalent among children as obesity increases in those agegroups. A high BMI is associated with higher blood pressure andrisk of hypertension, higher total cholesterol, LDLcholesteroland triglyceride levels and lower HDLcholesterollevels. The overall risk of coronary heartdisease and stroke, therefore, increases substantially withweight gain and obesity.Gall bladder disease and the incidence of clinicallysymptomatic gallstones are positively related to BMI23.There is evidence to suggest increased cancer risk as BMIincreases, such as colorectal cancer in men, cancer of theendometrium and biliary passage in women, and breastcancer in post-menopausal women. Obese people arealso at increased risk of gout, sleep apnoea, obstetric andsurgical complications.
Host issuesThere are a variety of behaviours and other host factorsthat have a potential effect on a populations level ofobesity. These are, of course, closely linked to the vectorsand the environments and in many cases the issues mergeand overlap. Issues related to social aspects of eating arenot covered.
While there is no one definition of snacking, it is probablybest to consider the content of snack foods and theincreased eating frequency that snacking promotes asseparate issues. There is evidence thatsnacking prevalence (i.e. occasions of snacking) isincreasing, the energy density of snack foods is increasingand the contribution to total energy is increasing. Snackscontribute to about 2025% of total energy intake incountries like the US and UK. However, there is littleevidence that a higher frequency of eating per se is apotential cause of obesity. Cross-sectional studies tend toshow a negative relationship or no relationship betweenmeal frequency and BMI37. Low eating frequency may, ofcourse, be a response to obesity rather than a cause.Experimental studies have found mixed results on thedegree of caloric compensation that people make at mealtime in response to a prior snack with some studiesDiet, nutrition and the prevention of excess weight gain and obesity showing more complete compensation among leanpeople. There is insufficient evidence to support aneffect of a higher frequency of eating on obesity or weightgain. If anything, it is protective against weight gain. Thehigh 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 probablyneeded to prevent obesity in an environment of plenty,some individuals (dieters and non-dieters) score highly onthe Restraint Scale and paradoxically may also exhibitperiods of disinhibited eating. Such individuals appearto be at risk of dietingovereating cycles. The conceptsused to define these constructs and the instruments usedto measure them continue to evolve, but the studies wouldsuggest that a flexible restraint eating pattern is associatedwith a lower risk of weight gain whereas a rigidrestraint/periodic disinhibition pattern is associated witha greater risk of weight gain. Binge eating disorder andnight eating syndrome would be examples of the latterpattern. Binge eating disorders are significantly morecommon in obesity in cross-sectional studies. Therelationships between these dietary patterns and weightgain or obesity is complex with both cause and effectrelationships likely.
In western countries, the frequency of eating foodprepared outside the home is increasing and this is mostapparent and best documented in the US. In 1970, 26% ofthe food dollar in the US was spent on food preparedoutside the home. By 1995, it had climbed to 39% and isprojected to rise to 53% by 2042,43. This shift towards anincrease in the frequency of eating meals and snacks awayfrom home and the proportion of food budget spent onaway from home foods 42,44,45 has coincided with theincreasing prevalence of obesity.
In the US, food prepared away from home is higher intotal energy, total fat, saturated fat, cholesterol andsodium, but contains less fibre and calcium and is overallof poorer nutritional quality than at-home food. Also, thefat content of at-home food has fallen considerably from41% of total energy in 1977 to 31.5%, but there has been nochange in the fat content of food prepared away fromhome (37.6%)43.
These food composition differences and the increasingportion sizes, are likely contributors to the risingprevalence of obesity in the US. Those who eat outmore, on average, have a higher BMI than those who eatmore at home. The evidence implicating the increasinguse of food prepared outside the home as a risk for obesityis largely limited to the US but this may be extrapolated toother western countries. It is unknown whether a highfrequency of eating out is associated with obesity orweight gain in other populations, for example, in Asiancountries, where eating outside the home may not be arisk for weight gain.
Early nutritionBirth weight is a crude indicator of intrauterine nutrition. Asystematic review of predictors of obesity by Parsons et al.found that studies reported a consistent and positiverelationship between birth weight and BMI (or risk ofoverweight) as a child or as an adult. It is possible thatlow birth weights may also be associated with high adultBMI (i.e. that the relationship is a J-shaped curve ratherthan linear and positive). However, very low birth weightis a much weaker predictor of high adult BMI than highbirth weight.Maternal and childhood undernutrition are common inlow income countries and childhood stunting is often usedas a marker for this. A later exposure to more western-stylediets and lifestyles (such as through migration to urbanareas and/or improved economic conditions) maypromote an excessive increase in body fatness orabdominal fatness. Popkin et al. studied 39-year-oldchildren in cross-sectional studies in four countries (China,Russia, South Africa and Brazil) and found that stuntedchildren (low height-for-age z-score) were more likelythan non-stunted children to be overweight (high weight for-heightz-score) with relative risks. On the other hand, a cohort of children measured atage 3 in Guatemala and followed into adulthood showedthat childhood stunting was associated with a low BMI andlow percent body fat in men but no such relationshipswere seen in women. Only when BMI or percent bodywere adjusted for, did an association between severestunting and high waist:hip ratio become evident.The hypothesis that intrauterine and/or early childhoodundernutrition leads to adult obesity or abdominal obesityis an important one that links with the other relationshipsbetween early undernutrition and adult diseases such ashypertension and diabetes. This could pose a majorproblem for countries undergoing the economic andnutrition transition. However, the relationships areclearly complex and the available data were judgedinsufficient to be able to make a single summary statementin the evidence table.
Percent fat, percent carbohydrate and energy densityBackground: Most of the debate about the fat andcarbohydrate content of the diet in relation to obesitycentres on the effects of altering the reciprocal proportionsof carbohydrate and fat in the diet on energy density, totalenergy intake, body weight and lipoprotein profiles. Thedebate 5860 has become vigorous and, at times, muddledbecause several issues are usually debated at the sametime. Also, the epidemiological evidence comes fromdifferent types of studies (ecological, cross-sectional andprospective) which suffer from multiple potential sourcesof bias, the instruments used to measure dietary intake areblunt, and there is substantial obesity-related underreportingof 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 apositive relationship between fat and obesity, especially ifpopulations with low fat intakes are included, butnegative relationships are also seen. Similarly, studies inthe same population over time tend to show positiverelationships between obesity and dietary fat intake inpopulations undergoing nutrition transition but a negativerelationship in many westernised populations. Crosssectionaland prospective studies also show mixedresults. In light of the methodological drawbacks ofthese types of studies and the mixed results they haveproduced controlled trials are needed to address thequestion.
Percent fat in the dietfixed total energy trials:According to Reaven the simplest way to answer thequestion about the impact of fat and carbohydrate in thediet on body weight is to focus on studies that vary inmacronutrient composition, but are equal in energy.Studies that have done this have indeed found thatclamping total energy produces similar weight changesirrespective of the macronutrient composition. Therationale for many of these studies was to assess theimpact of macronutrient changes independent of totalenergy intake. They were not to emulate the real worldwhere total intake is ad libitum. The conclusion from thefixed energy studies is that if a high percent fat dietpromotes weight gain, the mechanism appears to bemediated by promoting a higher total energy intake.Percent fat in the dietad libitum trials, covertmanipulations: Several trials have covertly manipulatedthe fat and carbohydrate proportions of equally palatablediets while allowing study participants to eat ad libitumtotal intakes. Most of the studies were short term withthe longest being 11 weeks. These trials consistentlyshow a progressive rise in total energy intake and bodyweight on the higher percent fat diets and the opposite onthe lower percent fat diets. The amount (weight) of foodeaten is similar on both types of diet. These covertmanipulation studies are central to the debate on dietaryfat and weight gain because they demonstrate that, otherthings being equal, the physiologicalbehavioural consequenceof a high percent fat diet is a slow weight gainthrough the passive overconsumption of total energy.Percent fat in the dietad libitum trials, overtmanipulation: Longer term trials of high and low percentfat diets have generally used educational strategies to getparticipants to select reduced fat food options andcompared them with standard or higher fat diets. Thediet is unrestricted in total amount (weight) andreplacement of lost energy from fat is not specificallyreplaced by carbohydrate. It is important to note that,unlike the covert manipulations, it is difficult to blindsuch studies and, therefore, psychosocial effects,personal preferences and other effects not directly relatedto physiology can confound the results.
An interesting study attempting to replicate realisticfood choices randomised normal weight and overweightparticipants into two groups who selected either full fat orreduced fat foods from small, realistic supermarkets inthe study centres. The free access to higher fat productsresulted in a significant increase in energy intake(0.9 MJ/d) and body weight (0.7 kg) over 6 monthscompared to the reduced fat group.Reducing the fat content of the diet consistentlyproduces modest reductions in body weight but onecould argue that instructions to individuals to reduce othermacronutrients in the diet or to restrict the intake of certainhigh volume foods (such as staple carbohydrates) wouldalso result in weight loss. Indeed, there are a myriad ofpopular diets with a wide variety of food and drinkrestrictions and all have their champions who have lostweight. It is obvious that any such restrictions that result ina reduction in total energy intake will produce weight loss.
The rationale for promoting a reduction in the fat contentof the diet to prevent weight gain or promote weight loss isthat it is concordant with the bodys physiologicalbehavioural mechanisms regulating food intake asevidenced by the covert manipulation studies.
Another potential criticism of promoting a reduced fatcontent of the diet is that the ad libitum weight loss studiesshow a modest effect (a few kilograms) with a tendency toreturn towards the previous weight after the interventionperiod. This rebound is common to all dietaryinterventions and there are a number of potentialexplanations for this. They include: a reduction incompliance to the diet, perhaps due to an environmentthat is unsupportive of healthy food choices; overeating offoods known to be low in fat and; physiologicaladaptations that attenuate the impact of negative energybalance on weight loss.
Extremely low fat, high carbohydrate diets are also veryeffective for weight loss but it must be stressed thatlarge reductions in total fat intake would be unattainable ata population level. Average changes in the order of 23 kgmay seem small for individuals but they are important on apopulation level in the context of obesity prevention. Ashift of one unit of BMI in the overall distribution in thepopulation is associated with a 5% point change in the
Many studies havemanipulated the macronutrient content of short term dietsunder isocaloric weight stable conditions (such as reducingsaturated fat and replacing the energy with carbohydrate orother types of fat). In many but not all such studies, thehigh carbohydrate diet is associated with increasedtriglycerides and decreased HDL-cholesterol (especially ifpredominantly simple carbohydrates are used).The weight loss effect of a reduced-fat diet, ad libitumdiet, however, appears to compensate for these potentiallydetrimental effects. Schaefer et al. directly compared theeffects of shifting subjects from a high fat diet (35% ofenergy) to a low fat diet (15% of energy) under isocaloric(56 weeks) and ad libitum (1012 weeks) conditions.In order to achieve energy equivalence in the isocaloricpart of the study, the weight and volume of the foodconsumed on the lower fat diet had to be increased by30%. Under weight-maintenance conditions, on the lowfat diet there was a significant reduction total, LDL- andHDL-cholesterol and an increase in total:HDL cholesterolratio and plasma triglyceride concentrations. At the end ofthe ad libitum diet, subjects had lost an average of 3.6 kgand achieved greater reductions in total and LDL cholesterolcompared to the low fat isocaloric diet. Thetotal:HDL cholesterol ratio and triglyceride levels were nodifferent at the end of the ad libitum period compared tobaseline.
This and other studies that assess the interactionbetween macronutrient composition and weight changeon blood lipids77,99,100 suggest that the effects of shortterm, isocaloric manipulations under metabolic wardconditions on lipids cannot be extrapolated to long term,ad libitum conditions in free-living individuals.
Summary of percent fat and obesity: At a macronutrientlevel, there is no evidence that energy from fat is morefattening than the same amount of energy fromcarbohydrate or protein. At a dietary level, there is stilldebate about the effects of diet composition on unhealthyweight gain, and more research is needed in this area.
However, it was considered that the overall evidence fromthe randomised controlled trials was convincing that ahigh intake of energy-dense foods (which are often alsomicronutrient poor) promotes unhealthy weight gain. Theshort term, isocaloric substitution studies were consideredfar less relevant to free living individuals than the longerterm, ad libitum studies. These latter studies show a highlyconsistent effect of a high fat content on promoting weightgain. The covert manipulations of fat content show that theeffect is a physiologicalbehavioural one and is notdependent on conscious reductions in food eaten. Themain mechanism for this appears to be that a diet high infat has a weak impact on satiety because of its high energydensity and this leads to a passive overconsumption oftotal energy. The high palatability of high fat foods and therelatively weak metabolic autoregulation in the face of ahigh fat diet are also likely contributors. While most highfat diets tend to be energy dense diets and thus weight promotingdiets, important caveats were noted. Forexample, many processed low fat foods were quiteenergy-dense and could promote weight gain if eaten inlarge amounts and conversely vegetable-based foods werequite energy dilute even with significant added fat andcould protect against weight gain.
Carbohydrate type (sugar, glycemic index (GI) and nonstarchpolysaccharide (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 inrelation to the sugars that promote dental caries and refersto all mono and disaccharides added by the manufacturer,cook or consumer plus sugars naturally present in fruitjuice, honey and syrups. Polysaccharides are either starchor NSP, the latter having considerable commonality withthe term dietary fibre which is still in common parlanceand was the term used in many of the studies reviewed.Sugars, GI and NSP/fibre are considered in turn, althoughof course there is significant overlap between these factorswithin foods.
Sugar in foods: There is a reciprocal relationshipbetween the percent fat and percent carbohydrate in thediet because these two nutrients generally contribute over80% of total energy. Therefore, the previous section onpercent fat could also be stated as: diets with a highcarbohydrate content provide protection against weightgain. However, if the diet is high in sugar, does the sameassociation apply? Large population studies have demonstratedthat those who have high total energy intakes tendto have a high total sugar intake although in relativeterms, a reciprocal relationship is also seen between thepercent fat and percent sugar in the diet. Studies relatingsugar intake to BMI consistently show an inverse relationbetween sugar intake as a percent of energy and BMI orobesity prevalence.
It is possible that the negative relationship betweensucrose consumption and BMI is affected by confoundingfactors. For example, more active people need extraenergy and this could be provided by sugar. Selectiveunderreporting of high sugar foods and drinks byoverweight/obese people is another possible confounder.
The high sugar content of some products withreduced fat claims may falsely imply that the products arelow in energy as well.
Simple sugars have hedonistic value. Sweeteningincreases the palatability of many foods and it has beensuggested that sweetness may lead to overconsumption.
However, there appears to be a limit to thehedonistic response to sweetened foods. Palatability offoods is also increased by fat and therefore processedfoods containing both high sugar and fat content may leadto weight gain. Overall, the mixed results, especiallyamongst 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 dietsthat are high in either sugar or starch. Raben et al. foundthat similar amounts of energy were consumed on thehigh fat and high sucrose diets but there was a lowerenergy intake and weight loss with the high starchdiets. Saris et al. found a relative weight loss of 1.7 kgin the high sugar diet and 2.6 kg in the high starch dietcompared to the high fat diet (both statisticallysignificant) but the differences between carbohydratetypes was not significant.
Sugar in drinks: The energy density of drinks such asregular soda drinks is low because of the high watercontent but physiologically the energy density of fluidsand foods may have not have comparable effects onsatiety and food consumption. It, therefore,seems prudent to consider the impact of drinks thatcontribute a significant amount to total energy intake(such as high sugar soda drinks) separately from foods.In a cross-over study, Tordoff and Alleva comparedthe consumption of soda (1150 g/d for 3 weeks) whichhad been sweetened with either a high fructose corn syrupor aspartame on body weight. The high fructose sodacondition increased total energy intake by 335 kcal/d andresulted in a significant mean weight gain of 0.66 kgcompared to the aspartame soda condition where totalenergy intake decreased by 179 kcal/d and weightdecreased non-significantly by 0.17 kg.
Some fruit drinks and cordial drinks can also be high insugar and may promote weight gain if drunk in largequantities but this has been less extensively studied thansoda drinks.
Overall, the evidence that high sugar drinks promoteweight gain is consistent and moderately strong, but is ofmost relevance in those populations with a high intake(such as children in many countries).
Glycemic index: A further mechanism by whichcarbohydrates may influence energy intake and bodyweight is by their GI. Different carbohydrate foodsincrease blood glucose and serum insulin to varyingextents even when the same amount of carbohydrate iseaten. The different changes in glucose and/or insulin mayhave subsequent effects on food intake or the promotionof overweight and obesity, with lower GI dietsproducing greater satiety. In addition to the effectsof carbohydrates on satiety, there is a suggestion that lowGI diets may provoke greater increases in cholecystokininand fullness post-meal (satiation).
Ludwig et al. demonstrated that voluntary food intakewas greater after high GI meals were consumed comparedto medium and low GI meals. They found that rapidabsorption of glucose altered hormonal and metabolicfunctions and promoted excessive food intake after theingestion of a high GI meal. Agus et al found during arandomised cross-over trial that when the acute (9 days)effects of energy restricted diets of high and low glycemicloads were studied in overweight young men, the highglycemic load diet produced a greater decline in metabolicrate, more negative nitrogen balance and greater voluntaryfood intake.
On energy restrained diets, a 12 week cross-over trial bySlabber et al.demonstrated that a low GI diet producedlower insulin levels and a greater weight loss thancorresponding high GI diets. Spieth et al found thatafter 4 months of intervention, low GI diets may be moreeffective than reduced-fat diets in treating childhoodobesity.
Low GI diets may influence fuel storage by promotingfat oxidation instead of carbohydrate oxidation,whereas raised insulin levels in response to high GI dietsinhibit lipolysis and encourage fat storage, limitingavailable fuels and encouraging overeating.Overall, the current evidence suggests a possibleinfluence of GI on body weight and composition, butlong term trials with changes in body weight as anoutcome are needed before more definitive statementscan be made.
AlcoholAlcohol is an energy dense nutrient (7 kcal/g) and becauseof its place at the top of the oxidative hierarchy, itspotential for sparing fat oxidation and promoting fatstorage is significant. However, some metabolic studiesshow that isocaloric substitution of alcohol for food energyresults in weight loss while the addition of alcohol doesnot promote weight gain. There is a similar paradoxseen in epidemiological studies. Dietary intake surveystend to show that energy from alcohol is additive to foodenergy intake such that total energy intake is higher with ahigher alcohol consumption. However, the relationshipsbetween reported alcohol intake and BMI show amixed pattern. One review of the epidemiologicalevidence, listed 25 studies showing a positive association,18 showing a negative association and 11 showing norelationship. For women, there was often a negativerelationship or possibly U-shaped relationship. Formen, the relationship tends to be slightly positive ornon-existent.
In an earlier review of 27 studies, seven showed anegative relationship between adiposity and alcoholintake, seven showed a positive relationship, nine showeddifferent associations for women and men, and eightshowed no relationship. Emery et al. reviewed theepidemiological studies linking a high alcohol intakewith abdominal fat distribution (high waist circumferenceor waist:hip ratio)137. They concluded that the evidencefor a relationship was moderate for men and suggestive forwomen.
The potential for confounding by concurrent lifestyleand socioeconomic factors is substantial, as is thetendency to underreport alcohol intake. Other factorsalso confound the relationships between alcohol andobesity: alcoholmacronutrient interactions; the possibilitythat obese people have reduced their alcoholconsumption because of their obesity; metabolismthrough pathways with different energetic returns (e.g.alcohol dehydrogenase versus microsomal ethanol oxidizingsystem); and the direct toxic effects of alcohol.
Overall, the epidemiological evidence is mixed andprobably highly confounded. Randomised controlledtrials on the issue are unlikely to be conducted. There iscurrently insufficient evidence to support a general role foralcohol in the development of obesity.
The portion size in pre-packaged, ready-to-eat andrestaurant foods is increasing in the US and elsewhere,building on the consumers desire for value for money. Inrecent years the number of restaurants offering supersizeoptions on their menu has rapidly risen, and other fooditems, especially snack foods, have increased packageweight. The increasing size of packaging indicates lowerunit cost and encourages use of more product than smallpackage size. These trends are occurring in manywestern countries but are less well documented than theyare in the US.Supersized portions potentially lead to increasedenergy intakes at the time and over the day and, therefore,could be a significant contributor to obesity, particularly inpopulations with a high use of meals prepared outside thehome. Many people cannot accurately estimate portionsize, and this leads to an underestimation of intake.The energy compensation later in the day after a highenergy meal is incomplete in many individuals. Veryfew studies have examined the impact of portion size onoverall energy consumption. One of these has shown thatportion size promotes a higher total intake and that thisseems to occur in adults and in 5 year olds, but not in 3year olds. The age at which the external cues (such asportion size) begin to influence intake is, therefore,appears to be between 3 and 5 years.Overall, there is strong ecological evidence of aconcurrent increase in portion sizing and obesity incountries such as the US. The proposition that largeportion sizes promote overconsumption is logical andlikely but the empirical studies, while supportive, are veryfew 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. Childrens 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 68 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
Nutrition in weight management and obesity: | Neuro Nutrition