Nutrition, Physical Activity, Weight Management, and HealthBody weight, diet, and level of physical activity are important de-terminants of chronic illness, mor-bidity, and quality

Revista Colombiana de Psiquiatría, Suplemento, vol. XXXV / 2006 157 S

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

Nutrition, Physical Activity, Weight Management, and Health

Nutrition, Physical Activity, Weight Management,and Health

John E. Lewis1

Neil Schneiderman2

Abstract

Non-communicable chronic diseases, such as metabolic syndrome, cardiovascular dys-function, type 2 diabetes, and obesity, make up a large portion of total world-widemortality, and are becoming more prevalent in developing countries. These diseaseshave taken on a larger importance, as fertility rates in many developing countries arestill rising and contributing to the overall planetary population. Chronic diseases aretypically due to poor dietary habits, physical inactivity, and subsequent unhealthy bodycomposition. However, achieving a healthy weight and then sustaining weight losscan reduce obesity-related disorders and improve the risk profile for chronic disease.Weight control through an improved diet style and higher levels of caloric expenditurecan also improve the quality of life for people with diabetes, HIV/AIDS, and mentalhealth, although the specific recommendations for the disease may vary slightly. Thesebenefits will last for a long time if the modifications are sustained. Understanding theeffects that various diets and physical activity modes and patterns have on healthyweight maintenance will ultimately prove beneficial for people who are otherwise atrisk for a variety of chronic diseases.

Key words: Obesity, chronic disease, diet, exercise.

Título: Nutrición, actividad física, control de peso y salud.

Resumen

Enfermedades crónicas no transmisibles, tales como síndrome metabólico, disfuncióncardiovascular, diabetes tipo 2 y obesidad, componen una gran proporción de la mor-talidad mundial y se están volviendo más prevalentes en países en vía de desarrollo.Estas enfermedades han cobrado importancia debido a que la rata de fertilidad enmuchos países subdesarrollados continúa aumentando, contribuyendo a la poblaciónmundial. Las enfermedades crónicas se deben generalmente a la presencia de hábi-tos alimenticios deficientes e inactividad física, con una composición corporal pocosaludable como consecuencia. Sin embargo, alcanzar un peso saludable y después

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

1 Ph. D. Assistant Professor University of Miami School of Medicine.2 Ph. D. James L. Knight Professor of Health Psychology and Professor of Psychiatry, University

of Miami.

11. Nutrition.p65 16/06/2006, 14:22157

Revista Colombiana de Psiquiatría, Suplemento vol. XXXV / 2006158 S

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

Lewis J.E., Schneiderman N.

sostener la pérdida de peso puede redu-cir los trastornos relacionados con la obe-sidad y mejorar el perfil de riesgo paraenfermedad crónica. El control de peso através de un estilo dietario mejorado ymayores niveles de gasto calórico tambiénpuede mejorar la calidad de vida de per-sonas con diabetes, VIH/sida y enferme-dad mental, aunque las recomendacionesespecíficas para cada trastorno pueden va-riar levemente. Estos beneficios seránduraderos si las modificaciones se man-tienen. Comprender los efectos que tie-nen diversas dietas y patrones de activi-dad física sobre la manutención de unpeso saludable beneficiará a personas quede otro modo estarían en riesgo de sufriruna variedad de enfermedades crónicas.

Palabras clave: obesidad, enfermedadcrónica, dieta, ejercicio.

Introduction

At the beginning of this century,non-communicable chronic dis-eases contributed approximately60% of the total deaths in the worldand about 46% of the global burdenof disease (1). About half of thesechronic disease deaths are attrib-utable to cardiovascular disease(CVD), with many being related totype 2 diabetes or obesity. The prob-lem of non-infectious chronic dis-ease is not limited to the developedregions of the world, but is becom-ing a major problem in developingcountries as well (2). Thus, thelabeling of non-communicable dis-eases by previous generations as“diseases of affluence” no longer ap-pears applicable, as these diseasescontinue to emerge both in poorer

countries and in the poorer popula-tion groups of wealthier nations.This shift in disease pattern is tak-ing place at an accelerating rate andis occurring faster in developingcountries than it did in industrial-ized regions a century ago (3). Be-cause these chronic diseases for themost part are related to inadequatephysical inactivity and poor weightmanagement, we shall focus onthese issues in the present article.It should be kept in mind, however,that cigarette smoking and alcoholabuse also contribute to excess mor-tality from non-communicablechronic diseases (4).

Body weight, diet, and level ofphysical activity are important de-terminants of chronic illness, mor-bidity, and quality of life. The risksassociated with many co-morbidconditions may be reduced withmodest weight loss. Clinical stud-ies suggest that minimal, sus-tained weight loss of 5% to 10% canreduce or eliminate obesity-relateddisorders (5). Weight control meth-ods often produce short-term suc-cess, but sustained weight main-tenance is difficult to reach (6-7).Weight cycling and relapse of bodyweight are common features aftera weight loss intervention. Themaintenance of treatment-inducedweight loss thus remains a signifi-cant challenge in the managementof obesity (8).

Nutritional therapy emphasiz-ing mostly low-fat, whole plant foods

11. Nutrition.p65 16/06/2006, 14:23158


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


has been successfully utilized toachieve and maintain weight con-trol, and can also be beneficial fornormal blood glucose levels, hyper-tension, hyperlipidemia, dyslipi-demia, cardiovascular disease risk,and mental status (9-12). Thesebenefits have been found to last foryears if the diet style is maintained(13-14).

Nutrition

A large amount of researchfinds that nutrition is one of themost critical factors for health. Theaccumulation of all research to thispoint, including animal, laboratory,clinical, and epidemiological find-ings, demonstrates compelling evi-dence for the link between nutri-tional deficiencies with chronicdisease (15-16). The debate ragesregarding what is considered theoptimal diet style for preventionand/or reversal of various chronicdiseases and conditions. Particu-larly for weight loss, high-protein,low-carbohydrate, Atkins-Style di-ets have been enormously popularin the mass media. Understandingbeneficial long-term eating pat-terns is critical to minimizing therisk of unhealthy weight gain,given that the findings for the ben-efit on CVD death of weight reduc-tion alone are unclear (17-18). Re-cent findings examining thebenefits of a very low carbohydratediet (19) do not support the belief

that this style of diet is any betterthan standard diets for weight lossand CVD risk, despite other evi-dence to the contrary (20-21). Theenormous interest in diets promot-ing high protein and/or low carbo-hydrate intake is occurring, whilesome evidence suggests that eat-ing a diet high in processed sugarshas followed the similar increasingcurves of obesity and type 2 diabe-tes (22). Several studies have foundbetter results in weight loss whencomparing the effect of a free-living,very low carbohydrate diet to a low-fat, high-carbohydrate diets over aperiod of 6 months (20-21,23-27).

Adequate intake of fruits, veg-etables, and fiber-rich foods isknown to be beneficial for healthand appears to have protective ef-fects for such diseases as some can-cers (15,28-29). However, in someparts of Latin America, poor accessto clean water may influence theappropriateness of food choices rec-ommended on the basis of researchin developed countries. In addition,some controversies persist regard-ing the definitive nature of causallinks among nutrition, health, anddisease, the degree of benefits thatcan be expected with change, andoptimal quantitative advice (30-31).The exact role of dietary factors andnutritional risk in disease is stillbeing researched, but the evidenceis currently sufficient to warrant aconcerted research effort in promot-ing healthy eating behavior. The

11. Nutrition.p65 16/06/2006, 3:58159


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


potential public health benefit fromimproved eating patterns, coupledwith the low risk of adopting guide-lines for healthy eating, provides astronger foundation than ever be-fore for efforts to understand andencourage good nutrition amongthe general population, patients,and persons at high risk for disease(28,32).

Physical Activity

Running parallel to the risingepidemic of overweight and obesityis the increasing rate of physicalinactivity. Physical inactivity iswidely recognized as a major threatto public health (2). Data from SãoPaulo, Brazil indicate that 70-80%of the population are remarkablyinactive (33). A sedentary lifestylecombined with poor nutrition ac-counts for an estimated 16% of theactual causes of death and approxi-mately 24.4 billion dollars per yearin health care expenditures in theUnited States alone (4,34). In con-trast, a physically active lifestylehas been associated with healthbenefits that include improved con-trol of hypertension, diabetes, obes-ity, hyperlipidemia, and reducedoverall morbidity and mortality (35-38). An objective of Healthy People2010 is that adults exercise for atleast 30 minutes of moderate physi-cal activity for most, if not all, daysof the week (39), but more than 60%of people do not achieve this

amount and are inactive by defini-tion (38).

Several studies have shownthat people who are more physicallyactive are less likely to gain weightover time than those who are not(40-43). Others found that most peo-ple are gaining weight due to con-suming less than 100 excess calo-ries/day (44). Therefore, increasingphysical activity by 100 calories/day could theoretically preventweight gain in most people, whichaverages out to 2,000 additionalsteps each day (44). Although thisis a possible approach to prevent-ing weight gain, the amount ofphysical activity that would be re-quired for substantial weight loss isnot feasible for many people. Fur-thermore, the National Weight Con-trol Registry (NWCR), a database ofalmost 5,000 successful weight lossmaintainers, shows that 90% oftheir participants report losingweight with both food restrictionand physical activity (45).

Subjects in the NWCR who havesucceeded in long-term weight lossmaintenance report expending2,800 calories/week in physical ac-tivity (45). More than 90% are main-taining their weight loss with highlevels of regular physical activity.The amount of physical activity re-ported by the NWCR participants ispositively correlated with theamount of weight they are main-taining. A decrease in physical ac-tivity in this group has been shown

11. Nutrition.p65 16/06/2006, 3:58160


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


to be a predictor of weight gain overtime (46). Another study found thatobese subjects who had previouslylost weight and engaged in at least200 minutes/week of physical ac-tivity were less likely to regain thelost weight than those participantswho engaged in not as much physi-cal activity (47). Some argue thatusing inexpensive, electronicpedometers and providing physicalactivity goals in steps per day is ef-fective in increasing physical activ-ity over the short run (48). However,combining dietary modification withincreased physical activity will pro-duce the best results.

Obesity

During the past twenty years,the developed world and citieswithin developing countries havefallen to a pervasive health epi-demic: obesity. Approximately 1.7billion people are now obese, itsprevalence is rising in most coun-tries, and dramatically increasingamong children and adolescents(49). The incidence of overweight(defined as a body mass index [BMI]between 25 and 30 kg/m2) andobesity (defined as a BMI > 30 kg/m2) among adults is at an all timehigh and continuing to rise (50,51).More people are now overweight orobese than people who smoke, livein poverty, or drink heavily. Over-weight/obesity has become such anepidemic that it is now listed as one

of the leading health indicators inHealthy People 2010 (39) and obes-ity in the United States is secondonly to tobacco use as a publichealth threat. Obesity as a singlecausative factor now stands to ac-tually negatively impact life expect-ancy rates, which have risen forthe last 200 years (52). Obese indi-viduals and even persons with mildto moderate overweight have in-creased risk for multiple condi-tions, many of which are associatedwith a relatively high rate of mor-bidity and mortality, such as type 2diabetes, cardiovascular disease,endometrial, postmenopausalbreast, kidney, and colon cancer,musculoskeletal disorders, sleepapnea, and gallbladder disease(5,7,51,53-56). For example, type 2diabetes is directly related to bodyweight (57).

The number of overweight andobese persons is also emerging asa major financial drain, resultingin more than $70 billion a year inpublic health expenditures in theUnited States (58). Obesity also con-tributes to higher health care ex-penditures than either smoking oralcohol use (59). Overweight andobesity cost taxpayers $117 billionper year in direct health care costsand indirect costs, such as lostwages (60). One study found thatobese adults (18 to 65 years of age)have 36% higher than average an-nual medical expenditures com-pared to those of normal weight (59).

11. Nutrition.p65 16/06/2006, 3:58161


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


Malnutrition and Obesity: ADouble Burden of Disease in

Developing Countries

Almost 30% of the people on ourplanet suffer from malnutrition (61).Among children under 5 years ofage in the developing world, some60% of all deaths are related to thiscondition (1). Concurrently, an epi-demic of obesity, with its attendantco-morbidities of diabetes, stroke,and CVD, has also affected develop-ing as well as industrialized coun-tries (2). This is associated with ahigh prevalence of obesity begin-ning in youth in developing coun-tries and regions as diverse as In-dia, Nigeria, Latin America, and theCaribbean (62). Thus, beginningwith malnutrition in early child-hood, nutritional transitions mayoccur leading to relatively cheaphigh energy density diets that arebasically inadequate.

The good news about economicdevelopment is that it leads to anincreased food supply and a de-crease in dietary deficiencies ashas occurred in much of LatinAmerica. The bad news is thatsome of the shifts that have oc-curred in food availability have ledto higher energy density diets withincreases in saturated fat andsugar as well as reduced fresh fruitand vegetable intake (63). Unfortu-nately, these dietary changes haveoccurred in conjunction with otherunhealthy lifestyle changes includ-

ing reduced physical activity atwork and leisure (64). Thus, peoplewithin particular developing coun-tries may concomitantly suffer fromfood shortages, nutrient inadequa-cies, and obesity, all leading to anincrease in chronic diseases (2).

Metabolic Syndrome, Type 2Diabetes, and Cardiovascular

Risk

The worldwide increase in theprevalence of obesity in the past twodecades has been accompanied bytwo major medical developmentsthat have important consequencesfor the future prevalence of CVD.One of these has been the currentworldwide epidemic of type 2 diabe-tes (65). The second developmenthas been the recognition that obes-ity is associated with the cluster-ing of a group of CVD risk factorsthat has been termed the metabolicsyndrome (66).

Risk factors that comprise themetabolic syndrome include, butare not limited to, central obesity,high blood pressure, glucose intol-erance, elevated triglycerides, lowlevels of high density lipoprotein(HDL) cholesterol, fibrinolysis, andinsulin resistance (67-68). Diag-nostic guidelines for metabolic syn-drome have been provided by theWorld Health Organization (68) andthe National Cholesterol EducationProgram (NCEP) in the UnitedStates (67) among others. Recently,

11. Nutrition.p65 16/06/2006, 3:58162


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


using a hierarchical structureanalysis, Shen et al. showed thatfour factors, obesity, insulin resist-ance, dyslipidemia, and hyperten-sion, were all significantly associ-ated with a common metabolicsyndrome factor across gender andethnic groups (69). To the extentthat the insulin resistance factorwas made up of fasting insulin andfasting glucose, this finding of aninsulin resistance factor, helping todefine metabolic syndrome, lendssupport to the WHO working defini-tion, which specifies either glucoseintolerance or insulin resistanceas a prerequisite condition. Bothtype 2 diabetes and impaired glu-cose tolerance have previouslybeen closely associated with thesyndrome. Clustering of the syn-drome components predicts boththe development of manifest diabe-tes and CVD (70-71).

The relationship between psy-chosocial factors and metabolic syn-drome is not well understood, butthe Third National Health and Nu-trition Examination Study in theUnited States found that womenwith a history of a major depressiveepisode were twice as likely to havethe metabolic syndrome comparedwith those without a history of de-pression (72).

Type 2 diabetes accounts for thevast majority of diabetes casesworldwide and for more than 90%of cases in the United States (73).It develops when the production of

insulin by the pancreas is insuffi-cient to overcome the underlyingabnormality of increased resist-ance to its action. In its early stage,type 2 diabetes is characterized byan overproduction of insulin(hyperinsulinemia). As the diseaseprogresses, the insulin level falls,as the insulin producing cells of thepancreas begin to fail. Complica-tions of untreated type 2 diabetesinclude: blindness, kidney failure,foot ulcerations that may lead toamputation, and increased risk ofinfections, stroke, and CVD. Accord-ing to WHO, the criterion for diabe-tes is a fasting plasma glucose con-centration = 126mg/dL (68).

In the year 2000, approximately150 million people worldwide hadtype 2 diabetes and this figure isexpected to double by 2025 (74).While type 2 diabetes is the fourthor fifth leading cause of mortalityin most developed countries, it isalso reaching epidemic proportionsin many developing countries (75).It is expected that in the near fu-ture the majority of cases of type 2diabetes will occur in these devel-oping countries with India andChina having more cases than anyother country in the world (76). Peo-ple with diabetes are more likely todie from a heart attack and aremore likely than those without dia-betes to have a second event (77).Patients with diabetes, who havenever had a myocardial infarction,have as high a risk of heart attack

11. Nutrition.p65 16/06/2006, 3:58163


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


as non-diabetics who have alreadyhad a myocardial infarction (78).

Lifestyle Intervention forPrevention of Type 2 Diabetesand Cardiovascular Disease

Current evidence suggests thatmoderate weight reduction (5-10%)may reduce major risk factors fortype 2 diabetes and CVD includingobesity, elevated blood glucose, in-sulin resistance, dyslipidemia, fibri-nolysis, inflammation, and highblood pressure (79-82). Both theNCEP (67) and the WHO Expert Panel(83) have stressed the importance oflifestyle modification (including ca-loric restriction, improved nutrition,and physical activity) in the preven-tion of type 2 diabetes and CVD.

The largest and most compre-hensive study of the effect of life-style intervention in subjects atrisk for type 2 diabetes was reportedby the Diabetes Prevention Pro-gram (84). This trial randomly as-signed 3234 non-diabetic personswith elevated fasting and post-loadplasma glucose concentrations toplacebo, metformin, or a lifestylemodification program. The goalswere for participants to have 7%weight loss and 150 minutes ofphysical activity per week. Averagefollow-up was 2.8 years. The lifestyleintervention significantly reducedthe incidence of type 2 diabetes by58% and metformin by 31% as com-pared with placebo. The lifestyle

intervention was significantlymore effective than metformin. Ina similar trial carried out in Fin-land, Tuomilehto et al. randomlyassigned 522 middle-aged, over-weight men and women with im-paired glucose tolerance to eitheran intervention or a control group(85). Each subject in the interven-tion group received individualizedcounseling aimed at reducingweight and intake of total fat andsaturated fat, and increasing in-take of fiber and physical activity.Mean duration of follow-up was 3.2years. During the trial the risk ofdiabetes was significantly reducedby 58%. The reduction in the inci-dence of diabetes was directly as-sociated with changes in lifestyle.Both the DPP (84) and the Finishdiabetes prevention trial (85)showed lifestyle changes that lastedseveral years and are thus an ex-cellent model for such interven-tions. The Look AHEAD NIH trialnow is assessing the long-term ef-fects of such a program in terms ofmorbidity and mortality in type 2diabetics (86).

HIV and AIDS

With the increased survivalrate of people with HIV infection,primarily due to the use of anti-retroviral medications, the co-mor-bid prevalence and impact of disabil-ity in this population has also risen.As in the general population, exer-

11. Nutrition.p65 16/06/2006, 14:23164


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


cise is a primary managementstrategy used to ameliorate impair-ments (problems with body functionas a significant loss, such as painor weakness), activity limitations(difficulties an individual may have,such as inability to engage in mod-erate exertion), and participationrestrictions (problems, such as in-ability to work) in victims of HIV/AIDS (87). Exercise can be used toaddress unwanted increases inweight and body fat related to meta-bolic syndrome as a consequenceof the use of highly active anti-retroviral treatment (HAART) andfrom HIV infection itself (88).

Regular exercise has beenfound to slow down the progressionof HIV and increase the CD4 cellcount. The results of one studyshowed that HIV patients exercising3-4 times per week were less likelyto develop AIDS than those only car-rying out daily exercise (89), reveal-ing a need to slightly limit theamount of physical activity for peo-ple with HIV compared to otherpopulations, where the WHO recom-mends one hour of moderate exer-cise per day for the prevention ofchronic disease (90). Other improve-ments due to exercise include mus-cle strength and flexibility, cardiop-ulmonary fitness, and decreases indepression, anxiety, and anger (91-94). Progressive resistance exerciseor a combination of progressive re-sistance exercise and aerobic exer-cise at least three times a week for

at least four weeks appears to be safeand may lead to clinically importantchanges in body weight and compo-sition for adults living with HIV/AIDS who are medically stable inimmunological and virological sta-tus (95-96). These studies indicatethat moderate levels of physical ac-tivity are safe and beneficial in theshort term for individuals infectedwith HIV.

While the benefits of exercisefor the person with HIV are rela-tively straightforward, the nutri-tional recommendations havechanged from before HAART untilnow. Malnutrition, low serum levelsof micronutrients, chronic dia-rrhea, anorexia, malabsorption,impaired nutrient storage, in-creased energy demands, and al-tered metabolism were common inpersons with AIDS prior to HAARTand are still common in resource-limited countries (97). Studies con-ducted before the widespread use ofHAART suggested that HIV infectionis also associated with a proathero-genic lipid profile characterized byan increase in triglyceride levels,a decrease in HDL cholesterol le-vels, and the presence of small,dense LDL particles (98-100). Whilethe use of multivitamin or singlemicronutrient supplementationhas been modest at best (101), theuse of HAART is leading to newquestions about the importance ofmicronutrients for persons withHIV. Even though macronutrient

11. Nutrition.p65 16/06/2006, 3:58165


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


deficiencies are uncommon andless severe in developed countriestoday, HAART and HIV itself arehaving a profound affect onoxidative stress, lipodystrophy, andmetabolic syndrome (97). In par-ticular, the use of protease inhibi-tors (PI) has had further deleteri-ous effects on metabolic riskfactors. Specifically, the initiationof PI-based HAART is associatedwith the development of insulinresistance in 25% to 62% and thedevelopment of overt new-onset dia-betes mellitus in 6% to 7% (88,102-103) in persons with HIV. Increasesin LDL cholesterol and triglyceridelevels following HAART have alsobeen observed (104-105). Thus, inaddition to recommending exerciseto decrease visceral fat and improvelipid profiles, nutritional interven-tion for persons with HIV/AIDS onHAART should focus on high fiber,foods with a low glycemic index, lowsaturated fat and processed sugars,and high intake of fresh and natu-ral fruits and vegetables.

Mental Health

Approximately one-quarter of alladults are suffering from a diagnos-able mental disease (106), includingdepressive and other mood disor-ders. Nearly half (45%) of those withany mental disorder meet criteriafor two or more disorders with se-verity strongly related to co-morbid-ity (106). Major Depressive Disorder

(MDD) is the leading cause of dis-ability for persons between the agesof 15 and 44 (107). Almost 15 mil-lion adults over 18 years of age areaffected by MDD (106) and it is moreprevalent in women than in men(108). Depressive disorders often co-occur with anxiety disorders andsubstance abuse (109). Almost halfof lost employment productivity isdue to MDD at $44 billion per year(110). The WHO’s Global Burden ofDisease Study looked at disability-adjusted life years, which measurelost years of healthy life regardlessof whether the years were lost topremature death or disability forvarious diseases (111). Disabilitycaused by MDD ranks second to CVDin the magnitude of disease burdenin the developed world.

Several studies have investi-gated the effects of nutrients and/or specific components of the typi-cal diet and their impact on depres-sion. In a study of healthy collegestudents, moderate and heavy cof-fee drinkers scored higher on a de-pression scale than did low users(112). In addition, the intake of caf-feine has been linked with the de-gree of mental illness in psychiat-ric patients: the higher the intake,the more severe the depression(113). Excess intake of refined sugarfrom sweet foods can also aggravatedepression. The combination of caf-feine and refined sugar is likelyeven worse for depression than ei-ther substance consumed alone. In

11. Nutrition.p65 16/06/2006, 3:58166


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


one study, restricting sugar and caf-feine in people with depression hasbeen reported to elevate mood (114).

Low levels of folic acid have beennoted in depressed patients (115).In studies of depressed patients,15% to 38% have been shown to bedeficient in serum or red blood cellfolic acid (116-118). Depression isthe most common symptom of a folicacid deficiency. Other symptoms offolic acid deficiency are: fatigue,apathy, and dementia. Inositol is aB vitamin required for the activityof several important neurotransmit-ters, including serotonin. De-pressed people often have low levelsof inositol. In one clinical study, sub-jects were given 12 grams of inosi-tol per day and the results showedthat they had therapeutic resultssimilar to common antidepressantdrugs, but with no unwanted sideeffects (119). Additional researchhas also confirmed the value of in-ositol for treating depression (120).The results of a number of clinicalstudies suggest that S-adenosyl-L-methionine may be a useful natu-ral antidepressants (121).

While the use of these variousnutrients may be beneficial, a moreholistic approach to nutritionalmodification in depressed patientshas not been investigated. Nutri-tional therapy emphasizing mostlylow-fat, whole-plant foods, whileavoiding simple sugars and chemi-cal additives or preservatives, hasbeen successfully utilized in other

diseases and can also be beneficialfor weight control, hypertension,hyperlipidemia, dyslipidemia, CVDrisk, and mental status (9-12). Ad-ditionally, these benefits have beenfound to last for years if the diet styleis maintained (13-14). However,randomized clinical trials areneeded to establish efficacy and ef-fectiveness.

Research has shown that regu-lar exercise can improve mood incases of mild to moderate depres-sion (122). One study reported therelative risk of depression was 27percent lower for people playingthree or more hours of sport a weekcompared with those playing nosport at all (123). Another studycompared the effects of exerciseand drug therapy in treating de-pression in older people (124). The156 depressed men and womenwere divided into three groups.Over 16 weeks, one group tookantidepressants, the second groupundertook an aerobic exercise pro-gram, and the third group used bothmedications and exercise. The re-sults indicated that after 6 monthsthose patients who continued toexercise were much less likely toexperience a return of their de-pression than were the other pa-tients. Only 8 percent of patientsin the exercise group had their de-pression return, while 38 percentof the drug-only group and 31 per-cent of the exercise-plus-druggroup relapsed. Other important

11. Nutrition.p65 16/06/2006, 3:58167


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


findings included that the moreone exercised, the less likely onewould see their depressive symp-toms return and for each 50-minute increment of exercise, anaccompanying 50 percent reduc-tion in relapse risk was found.

Another study sought to exam-ine the exercise-depression linkby splitting a group of people suf-fering with MDD into two groups.One group exercised aerobically forone hour, three times a week fornine weeks while maintaining acourse of psychotherapy and medi-cation, and the other group contin-ued with psychotherapy and medi-cation only. The study showedsignificantly larger reductionscores in depression in the exer-cising group compared with thetherapy and medication group(125). The effects of aerobic exer-cise have been contrasted againstrelaxation training on depressedindividuals. Depression scoreswere reduced by both methods, al-though exercise provided greaterreductions in depressive scores(126). Exercise benefits have beendemonstrated in people who arenot clinically depressed, but whopresent some depressive symp-toms (127-128). Another study com-pared aerobic exercise, includingjogging and cycling, to non-aerobiccircuit exercise on a multi-gym.The study found both methods ofexercise to produce significant re-ductions in depressive scores (129).

Conclusions

Although medications areavailable to treat overweight, andsurgery is available for obesity, com-plex medical regimens are costly toapply over a typical lifetime, haveuntoward side effects, and patientsmay fail to achieve the treatmentgoals required to lose and/or main-tain excess fat and weight. Also,standard conventional medicaltreatment involving medications orsurgery has not been proven to un-equivocally cure or reverse the ef-fects of obesity. Potentially modifi-able environmental factors, includingpoor dietary choices and failing toengage in regular exercise, areknown to be primary contributorsto overweight and obesity and re-lated problems including high bloodpressure, CVD, stroke, diabetes,certain types of cancer, arthritis,and breathing problems. Given theenormous public health cost ofobesity, focusing on healthy eatingand a moderate and consistent ex-ercise program should be the basisof any attempt to achieve weightloss and subsequent control (16).The true impact of the public healthcosts of obesity can only be under-stood within the context of bothmental and physical health.

Reference

1. World Health Organization. Childhoodnutrition and progress in implementing the

11. Nutrition.p65 16/06/2006, 14:23168


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


international code of marketing of breast-milk substitutes. Geneva; 2002. ReportNo.: A55/14.

2. World Health Organization. Diet, nutrition,and the prevention of chronic disease.Geneva: World Health Organization; 2003.Report No.: WHO Technical Report 916.

3. Popkin BM. The shift in stages of the nu-trition transition in the developing worlddiffers from past experiences! PublicHealth Nutr. 2002 Feb;5(1A):205-14.

4. Mokdad AH, Marks JS, Stroup DF,Gerberding JL. Actual causes of death inthe United States, 2000. JAMA. 2004 Mar10;291(10):1238-45.

5. Ditschuneit HH, Flechtner-Mors M. Valueof structured meals for weight manage-ment: risk factors and long-term weightmaintenance. Obes Res. 2001 Nov;9Suppl 4:284S-9S.

6. Pasman WJ, Saris WH, Westerterp-Plantenga MS. Predictors of weight main-tenance. Obes Res. 1999 Jan;7(1):43-50.

7. Westerterp-Plantenga MS, Kempen KP,Saris WH. Determinants of weight main-tenance in women after diet-inducedweight reduction. Int J Obes Relat MetabDisord. 1998 Jan;22(1):1-6.

8. Leermakers EA, Perri MG, Shigaki CL,Fuller PR. Effects of exercise-focusedversus weight-focused maintenance pro-grams on the management of obesity.Addict Behav 1999 Mar;24(2):219-27.

9. Anderson J. Dietary fiber in nutrition ma-nagement of diabetes. In: Vahouny G,Kritchevsky D, editors. Dietary fiber: ba-sic and clinical aspects. New York: Ple-num Press; 1986. p. 343-60.

10. Anderson JW, Chen WJ, Sieling B.Hypolipidemic effects of high-carbohy-drate, high-fiber diets. Metabolism. 1980Jun;29(6):551-8.

11. Anderson JW, Gustafson NJ, Bryant CA,Tietyen-Clark J. Dietary fiber and diabe-tes: a comprehensive review and practi-cal application. J Am Diet Assoc. 1987Sep;87(9):1189-97.

12. Barnard RJ, Lattimore L, Holly RG, ChernyS, Pritikin N. Response of non-insulin-de-pendent diabetic patients to an intensive

program of diet and exercise. DiabetesCare. 1982 Jul;5(4):370-4.

13. Barnard RJ, Massey MR, Cherny S,O’Brien LT, Pritikin N. Long-term use of ahigh-complex-carbohydrate, high-fiber,low-fat diet and exercise in the treatmentof NIDDM patients. Diabetes Care. 1983May;6(3):268-73.

14. Story L , Anderson JW, Chen WJ,Karounos D, Jefferson B. Adherence tohigh-carbohydrate, high-fiber diets:long-term studies of non-obese diabeticmen. J Am Diet Assoc. 1985 Sep;85(9):1105-10.

15. National Research Council. Diet andhealth: implications for reducing chronicdisease risk. Washington: National Acad-emy Press; 1989.

16. United States Department of Agriculture.Report of the dietary guidelines advisorycommittee on the dietary guidelines forAmericans, 1995, to the Secretary ofHealth and Human Services and the Sec-retary of Agriculture. Washington: USDepartment of Agriculture; 1995.

17. Maru S, van der Schouw YT, GimbrereCH, Grobbee DE, Peeters PH. Bodymass index and short-term weight chan-ge in relation to mortality in Dutch womenafter age 50 y. Am J Clin Nutr. 2004Jul;80(1):231-6.

18. Williamson DF, Pamuk E, Thun M, Flan-ders D, Byers T, Heath C. Prospectivestudy of intentional weight loss and mor-tality in never-smoking overweight USwhite women aged 40-64 years. Am JEpidemiol. 1995 Jun 15;141(12):1128-41.

19. Dansinger ML, Gleason JA, Griffith JL,Selker HP, Schaefer EJ. Comparison ofthe Atkins, Ornish, Weight Watchers, andZone diets for weight loss and heart dis-ease risk reduction: a randomized trial.JAMA. 2005 Jan 5;293(1):43-53.

20. Brehm B, Seeley R, Daniels S, D’AlessioD. A randomized trial comparing a verylow carbohydrate diet and a calorie-re-stricted low fat diet on body weight andcardiovascular risk factors in healthywomen. J Clin Endocrinol Metab. 2003;88:1617-23.

11. Nutrition.p65 16/06/2006, 3:58169


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


21. Yancy WS, Jr., Olsen MK, Guyton JR,Bakst RP, Westman EC. A low-carbohy-drate, ketogenic diet versus a low-fat dietto treat obesity and hyperlipidemia: arandomized, controlled trial. Ann InternMed. 2004 May 18;140(10):769-77.

22. Gross LS, Li L, Ford ES, Liu S. Increasedconsumption of refined carbohydratesand the epidemic of type 2 diabetes in theUnited States: an ecologic assessment.Am J Clin Nutr. 2004 May;79(5):774-9.

23. Brehm B, Spang S, Lattin B, Seeley R,Daniels S, D’Alessio D. The role of energyexpenditure in the differential weight lossin obese women on low-fat and low-car-bohydrate diets. J Clin Endocrinol Metab.2005;90:1475-82.

24. Foster GD, Wyatt HR, Hill JO, McGuckinBG, Brill C, Mohammed BS, et al. Arandomized trial of a low-carbohydratediet for obesity. N Engl J Med. 2003 May22;348(21):2082-90.

25. McAuley KA, Hopkins CM, Smith KJ,McLay RT, Williams SM, Taylor RW, et al.Comparison of high-fat and high-proteindiets with a high-carbohydrate diet in in-sulin-resistant obese women. Diabetolo-gia. 2005 Jan;48(1):8-16.

26. Samaha FF, Iqbal N, Seshadri P, ChicanoKL, Daily DA, McGrory J, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med.2003 May 22;348(21):2074-81.

27. Sondike SB, Copperman N, JacobsonMS. Effects of a low-carbohydrate dieton weight loss and cardiovascular riskfactor in overweight adolescents. JPediatr. 2003 Mar;142(3):253-8.

28. United States Department of Health andHuman Services. The surgeon general’sreport on nutrition and health. Washing-ton: United States Govt. Printing Office;1988.

29. Block G, Patterson B, Subar A. Fruit, veg-etables, and cancer prevention: a reviewof the epidemiological evidence. NutrCancer. 1992;18(1):1-29.

30. Bal DG, Foerster SB. Changing theAmerican diet. Impact on cancer preven-tion policy recommendations and pro-

gram implications for the American Can-cer Society. Cancer. 1991 May15;67(10):2671-80.

31. Willett WC. Diet and health: what shouldwe eat? Science. 1994 Apr 22;264(5158):532-7.

32. Thomas P. Improving America’s diet andhealth: From recommendations to action.Washington: National Academy Press;1991.

33. Matsudo V, Matsudo S, Andrade D,Araujo T, Andrade E, de Oliveira LC, et al.Promotion of physical activity in a devel-oping country: the Agita Sao Paulo expe-rience. Public Health Nutr. 2002Feb;5(1A):253-61.

34. Colditz GA. Economic costs of obesityand inactivity. Med Sci Sports Exerc. 1999Nov;31(11 Suppl):S663-S667.

35. Blair SN, Kampert JB, Kohl HW, III, BarlowCE, Macera CA, Paffenbarger RS, Jr., etal. Influences of cardiorespiratory fitnessand other precursors on cardiovasculardisease and all-cause mortality in men andwomen. JAMA. 1996 Jul 17;276(3):205-10.

36. Church T, Kamper J, Gibbons L, BarlowC, Blair S. Usefulness of cardiorespira-tory fitness as a predictor of all-cause andcardiovascular disease mortality in menwith systemic hypertension. Am J Cardiol.2001;88:651-6.

37. Helmrich SP, Ragland DR, Leung RW,Paffenbarger RS, Jr. Physical activity andreduced occurrence of non-insulin-de-pendent diabetes mellitus. N Engl J Med.1991 Jul 18;325(3):147-52.

38. United States Department of Health andHuman Services. Physical activity andhealth: a report of the surgeon general.Atlanta (GA): United States Departmentof Health and Human Services, Centersfor Disease Control and Prevention, Na-tional Center for Chronic Disease Preven-tion and Health Promotion; 1996. ReportNo.: 017-023-00196-5.

39. United States Department of Health andHuman Services. Healthy people 2010:understanding and improving health.Washington: United States GovernmentPrinting Office; 2000.

11. Nutrition.p65 16/06/2006, 3:58170


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


40. Dipietro L, Dziura J, Blair S. Estimatedchange in physical activity levels (PAL) andprediction of 5-yr weight change in mid-dle-aged men: the aerobics center longi-tudinal study. International Int J Obes RelatMetab Disord. 2004;28(12):1541-7.

41. Haapanen N, Miilunpalo S, Pasanen M,Oja P, Vuori I. Association between lei-sure time physical activity and 10-yearbody mass change among working-aged men and women. Int J Obes RelatMetab Disord. 1997 Apr;21(4):288-96.

42. Schmitz KH, Jacobs DR, Jr., Leon AS,Schreiner PJ, Sternfeld B. Physical activ-ity and body weight: associations overten years in the CARDIA study. CoronaryArtery Risk Development in Young Adults.Int J Obes Relat Metab Disord. 2000Nov;24(11):1475-87.

43. Williamson DF, Madans J, Anda RF,Kleinman JC, Kahn HS, Byers T. Recrea-tional physical activity and ten-year weightchange in a US national cohort. Int J ObesRelat Metab Disord. 1993 May;17(5):279-86.

44. Hill JO, Wyatt HR, Reed GW, Peters JC.Obesity and the environment: where dowe go from here? Science. 2003 Feb7;299(5608):853-5.

45. Klem ML, Wing RR, McGuire MT, SeagleHM, Hill JO. A descriptive study of indi-viduals successful at long-term mainte-nance of substantial weight loss. Am JClin Nutr. 1997 Aug;66(2):239-46.

46. Wing RR, Hill JO. Successful weight lossmaintenance. Annu Rev Nutr. 2001;21:323-41.

47. Jakicic JM, Winters C, Lang W, Wing RR.Effects of intermittent exercise and use ofhome exercise equipment on adherence,weight loss, and fitness in overweightwomen: a randomized trial. JAMA. 1999Oct 27;282(16):1554-60.

48. Wyatt H, Peters J, Reed G, Grunwald G,Barry M, Thompson H, et al. Using elec-tronic step counters to increase lifestylephysical activity: Colorado on the move.Journal of Physical Activity and Health.2004;1:181-91.

49. Deitel M. Overweight and obesity world-wide now estimated to involve 1.7 bil-

lion people. Obes Surg. 2003 Jun;13(3):329-30.

50. Flegal KM, Carroll MD, Ogden CL,Johnson CL. Prevalence and trends inobesity among US adults, 1999-2000.JAMA. 2002 Oct 9;288(14):1723-7.

51. World Health Organization. Obesity: pre-venting and managing the global epi-demic. Report of a WHO consultation.2000. Report No.: 894.

52. Olshansky SJ, Passaro DJ, Hershow RC,Layden J, Carnes BA, Brody J, et al. Apotential decline in life expectancy in theUnited States in the 21st century. N Engl JMed. 2005 Mar 17;352(11):1138-45.

53. Burton BT, Foster WR. Health implicationsof obesity: an NIH Consensus Develop-ment Conference. J Am Diet Assoc. 1985Sep;85(9):1117-21.

54. Pasman WJ, Saris WH, Muls E, VansantG, Westerterp-Plantenga MS. Effect ofexercise training on long-term weightmaintenance in weight-reduced men.Metabolism. 1999 Jan;48(1):15-21.

55. Pi-Sunyer F, Becker D, Bouchard C,Carlton R. NHLBI obesity education ini-tiative expert panel on the identification,evaluation, and treatment of overweightand obesity in adults. Obesity Research.1998;6:51S-209S.

56. Visscher TL, Seidell JC. The public healthimpact of obesity. Annu Rev Public Health.2001;22:355-75.

57. American Diabetes Association. NationalDiabetes Fact Sheet. 2002. Ref Type: Ge-neric.

58. Wickelgren I. Obesity: how big a prob-lem? Science. 2001;280(5368):1364-7.

59. Sturm R. Datawatch: the effects of obes-ity, smoking, and drinking on medical pro-blems and costs. Health Aff.2002;21(2):245-53.

60. United States Office of the Surgeon Gen-eral. The surgeon general’s call to actionto prevent and decrease overweight andobesity. Washington: United States Officeof the Surgeon General; 2001.

61. World Health Organization. A globalagenda for combating malnutrition:Progress report. Geneva: World Health

11. Nutrition.p65 16/06/2006, 3:58171


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


Organization; 2000. Report No.: WHO/NHD/00.6.

62. Peña M, Bacallao J. Obesity among thepoor: An emerging problem in LatinAmerica and the Caribbean. In: Peña M,Bacallao J, editors. Obesity and poverty:a new public health challenge. Washing-ton: Pan American Health Organization;2000. p. 3-10.

63. Popkin BM. The shift in stages of the nu-trition transition in the developing worlddiffers from past experiences! PublicHealth Nutr. 2002 Feb;5(1A):205-14.

64. Matsudo V, Matsudo S, Andrade D,Araujo T, Andrade E, de Oliveira LC, et al.Promotion of physical activity in a devel-oping country: the Agita Sao Paulo expe-rience. Public Health Nutr. 2002Feb;5(1A):253-61.

65. Zimmet P, Alberti KG, Shaw J. Global andsocietal implications of the diabetes epi-demic. Nature. 2001 Dec 13;414(6865):782-7.

66. Grundy SM. Obesity, metabolic syn-drome, and cardiovascular disease. J ClinEndocrinol Metab. 2004 Jun;89(6):2595-600.

67. Executive Summary of the third Report ofthe National Cholesterol Education Pro-gram (NCEP) Expert Panel on Detection,Evaluation, and Treatment of High BloodCholesterol in Adults (Adult TreatmentPanel III). JAMA. 2001 May 16;285(19):2486-97.

68. World Health Organization. Definitions,diagnosis, and classification of diabetesmellitus and its complications. Report ofa WHO consultation. Part I: Diagnosis andclassification of diabetes mellitus. Geneva:World Health Organization; 1999.

69. Shen BJ, Goldberg RB, Llabre MM,Schneiderman N. Is the factor structureof the metabolic syndrome comparablebetween men and women and acrossthree ethnic groups: the Miami Commu-nity Health Study. Ann Epidemiol. 2006Feb;16(2):131-7.

70. Lakka HM, Laaksonen DE, Lakka TA,Niskanen LK, Kumpusalo E, TuomilehtoJ, et al. The metabolic syndrome and to-

tal and cardiovascular disease mortalityin middle-aged men. JAMA. 2002 Dec4;288(21):2709-16.

71. Lorenzo C, Okoloise M, Williams K, SternMP, Haffner SM. The metabolic syndromeas predictor of type 2 diabetes: the SanAntonio heart study. Diabetes Care. 2003Nov;26(11):3153-9.

72. Kinder LS, Carnethon MR, PalaniappanLP, King AC, Fortmann SP. Depressionand the metabolic syndrome in youngadults: findings from the Third NationalHealth and Nutrition Examination Survey.Psychosom Med. 2004 May;66(3):316-22.

73. King H, Aubert RE, Herman WH. Globalburden of diabetes, 1995-2025: preva-lence, numerical estimates, and projec-tions. Diabetes Care. 1998 Sep;21(9):1414-31.

74. Steyn NP, Mann J, Bennett PH, Temple N,Zimmet P, Tuomilehto J, et al. Diet, nutri-tion and the prevention of type 2 diabe-tes. Public Health Nutr. 2004 Feb;7(1A):147-65.

75. Amos AF, McCarty DJ, Zimmet P. The ris-ing global burden of diabetes and its com-plications: estimates and projections tothe year 2010. Diabet Med. 1997;14 Suppl5:S1-85.

76. King H, Aubert RE, Herman WH. Globalburden of diabetes, 1995-2025: preva-lence, numerical estimates, and projec-tions. Diabetes Care. 1998 Sep;21(9):1414-31.

77. Miettinen H, Lehto S, Salomaa V, MahonenM, Niemela M, Haffner SM, et al. Impactof diabetes on mortality after the firstmyocardial infarction. The FINMONICAMyocardial Infarction Register StudyGroup. Diabetes Care. 1998 Jan;21(1):69-75.

78. Haffner SM, Lehto S, Ronnemaa T, PyoralaK, Laakso M. Mortality from coronaryheart disease in subjects with type 2 dia-betes and in nondiabetic subjects with andwithout prior myocardial infarction. N EnglJ Med. 1998 Jul 23;339(4):229-34.

79. Pritchett AM, Foreyt JP, Mann DL. Treat-ment of the metabolic syndrome: the im-

11. Nutrition.p65 16/06/2006, 3:58172


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


pact of lifestyle modification. CurrAtheroscler Rep. 2005 Mar;7(2):95-102.

80. Park HS, Lee K. Greater beneficial effectsof visceral fat reduction compared withsubcutaneous fat reduction on param-eters of the metabolic syndrome: a studyof weight reduction programmes in sub-jects with visceral and subcutaneousobesity. Diabet Med. 2005 Mar;22(3):266-72.

81. Hong K, Li Z, Wang HJ, Elashoff R, HeberD. Analysis of weight loss outcomes us-ing VLCD in black and white overweightand obese women with and without meta-bolic syndrome. Int J Obes (Lond). 2005Apr;29(4):436-42.

82. Jellema A, Plat J, Mensink RP. Weight re-duction, but not a moderate intake of fishoil, lowers concentrations of inflammatorymarkers and PAI-1 antigen in obese menduring the fasting and postprandial state.Eur J Clin Invest. 2004 Nov;34(11):766-73.

83. Alberti KG, Zimmet PZ. Definition, diag-nosis and classification of diabetesmellitus and its complications. Part 1: di-agnosis and classification of diabetesmellitus provisional report of a WHO con-sultation. Diabet Med. 1998 Jul;15(7):539-53.

84. Knowler WC, Barrett-Connor E, FowlerSE, Hamman RF, Lachin JM, Walker EA,et al. Reduction in the incidence of type 2diabetes with lifestyle intervention ormetformin. N Engl J Med. 2002 Feb7;346(6):393-403.

85. Tuomilehto J, Lindstrom J, Eriksson JG,Valle TT, Hamalainen H, Ilanne-Parikka P,et al. Prevention of type 2 diabetes mellitusby changes in lifestyle among subjectswith impaired glucose tolerance. N Engl JMed. 2001 May 3;344(18):1343-50.

86. Ryan DH, Espeland MA, Foster GD,Haffner SM, Hubbard VS, Johnson KC,et al. Look AHEAD (Action for Health inDiabetes): design and methods for a clini-cal trial of weight loss for the preventionof cardiovascular disease in type 2 dia-betes. Control Clin Trials. 2003 Oct;24(5):610-28.

87. World Health Organization. Internationalclassification of functioning, disability, andhealth. Geneva: World Health Organiza-tion; 2001.

88. Dever LL, Oruwari PA, Figueroa WE,O’Donovan CA, Eng RH. Hyperglycemiaassociated with protease inhibitors in anurban HIV-infected minority patient popu-lation. Ann Pharmacother. 2000 May;34(5):580-4.

89. Mustafa T, Sy FS, Macera CA, ThompsonSJ, Jackson KL, Selassie A, et al. Asso-ciation between exercise and HIV diseaseprogression in a cohort of homosexualmen. Ann Epidemiol. 1999 Feb;9(2):127-31.

90. World Health Organization. The worldhealth report 2002: Reducing risks, pro-moting healthy life. Geneva: World HealthOrganization; 2002.

91. LaPerriere A, Fletcher MA, Antoni MH,Klimas NG, Ironson G, Schneiderman N.Aerobic exercise training in an AIDS riskgroup. Int J Sports Med. 1991 Jun;12Suppl 1:S53-S57.

92. MacArthur RD, Levine SD, Birk TJ. Su-pervised exercise training improves car-diopulmonary fitness in HIV-infectedpersons. Med Sci Sports Exerc. 1993Jun;25(6):684-8.

93. Rigsby LW, Dishman RK, Jackson AW,Maclean GS, Raven PB. Effects of exer-cise training on men seropositive for thehuman immunodeficiency virus-1. MedSci Sports Exerc. 1992 Jan;24(1):6-12.

94. Spence DW, Galantino ML, Mossberg KA,Zimmerman SO. Progressive resistanceexercise: effect on muscle function andanthropometry of a select AIDS popula-tion. Arch Phys Med Rehabil. 1990Aug;71(9):644-8.

95. Lox CL, McAuley E, Tucker RS. Aerobicand resistance exercise training effects onbody composition, muscular strength,and cardiovascular fitness in an HIV-1population. Int J Behav Med. 1996;3(1):55-69.

96. Roubenoff R, McDermott A, Weiss L, SuriJ, Wood M, Bloch R, et al. Short-termprogressive resistance training increases

11. Nutrition.p65 16/06/2006, 3:58173


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


strength and lean body mass in adultsinfected with human immunodeficiencyvirus. AIDS. 1999 Feb 4;13(2):231-9.

97. Tang AM, Lanzillotti J, Hendricks K,Gerrior J, Ghosh M, Woods M, et al.Micronutrients: current issues for HIV careproviders. AIDS. 2005 Jun 10;19(9):847-61.

98. Feingold KR, Krauss RM, Pang M,Doerrler W, Jensen P, Grunfeld C. Thehypertriglyceridemia of acquired immu-nodeficiency syndrome is associatedwith an increased prevalence of low den-sity lipoprotein subclass pattern B. JClin Endocrinol Metab. 1993 Jun;76(6):1423-7.

99. Grunfeld C, Kotler DP, Hamadeh R, TierneyA, Wang J, Pierson RN. Hypertriglyceri-demia in the acquired immunodeficiencysyndrome. Am J Med. 1989 Jan;86(1):27-31.

100. Shor-Posner G, Basit A, Lu Y, CabrejosC, Chang J, Fletcher M, et al. Hypocho-lesterolemia is associated with immunedysfunction in early human immunodefi-ciency virus-1 infection. Am J Med. 1993May;94(5):515-9.

101. Tang AM, Smit E. Selected vitamins in HIVinfection: a review. AIDS Patient CareSTDS. 1998 Apr;12(4):263-73.

102. Carr A, Samaras K, Thorisdottir A,Kaufmann GR, Chisholm DJ, Cooper DA.Diagnosis, prediction, and natural courseof HIV-1 protease-inhibitor-associatedlipodystrophy, hyperlipidaemia, and dia-betes mellitus: a cohort study. Lancet. 1999Jun 19;353(9170):2093-9.

103. Walli R, Goebel FD, Demant T. Impairedglucose tolerance and protease inhibitors.Ann Intern Med. 1998 Nov 15;129(10):837-8.

104. Calza L, Manfredi R, Farneti B, Chiodo F.Incidence of hyperlipidaemia in a cohortof 212 HIV-infected patients receiving aprotease inhibitor-based antiretroviraltherapy. Int J Antimicrob Agents. 2003Jul;22(1):54-9.

105. Nolan D. Metabolic complications asso-ciated with HIV protease inhibitor therapy.Drugs. 2003;63(23):2555-74.

106. Kessler RC, Chiu WT, Demler O,Merikangas KR, Walters EE. Prevalence,severity, and comorbidity of 12-monthDSM-IV disorders in the NationalComorbidity Survey Replication. ArchGen Psychiatry. 2005 Jun;62(6):617-27.

107. World Health Organization. The worldhealth report 2004: changing history, an-nex table 3: Burden of disease in DALYsby cause, sex, and mortality stratum inWHO regions, estimates for 2002. Ge-neva: The World Health Organization;2004.

108. Kessler RC, Berglund P, Demler O, Jin R,Koretz D, Merikangas KR, et al. The epi-demiology of major depressive disorder:results from the National ComorbiditySurvey Replication (NCS-R). JAMA. 2003Jun 18;289(23):3095-105.

109. Kessler RC, Berglund P, Demler O, Jin R,Merikangas KR, Walters EE. Lifetimeprevalence and age-of-onset distributionsof DSM-IV disorders in the NationalComorbidity Survey Replication. ArchGen Psychiatry. 2005 Jun;62(6):593-602.

110. Stewart WF, Ricci JA, Chee E, Hahn SR,Morganstein D. Cost of lost productivework time among US workers with de-pression. JAMA. 2003 Jun 18;289(23):3135-44.

111. Murray C, Lopez A. The global burden ofdisease and injury series. Volume I. Theglobal burden of disease: a comprehen-sive assessment of mortality and disabil-ity from diseases, injuries, and risk factorsin 1990 and projected to 2020. Geneva,World Health Organization; 1996. RefType: Generic.

112. Gilliland K, Andress D. Ad lib caffeine con-sumption, symptoms of caffeinism, andacademic performance. Am J Psychia-try. 1981 Apr;138(4):512-4.

113. Greden JF, Fontaine P, Lubetsky M,Chamberlin K. Anxiety and depressionassociated with caffeinism among psy-chiatric inpatients. Am J Psychiatry. 1978Aug;135(8):963-6.

114. Christensen L. Psychological distress anddiet-effects of sucrose and caffeine. J ApplNutr. 1988;40:44-50.

11. Nutrition.p65 16/06/2006, 3:58174


○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○


115. Alpert JE, Fava M. Nutrition and depres-sion: the role of folate. Nutr Rev. 1997May;55(5):145-9.

116. Fava M, Borus JS, Alpert JE, NierenbergAA, Rosenbaum JF, Bottiglieri T. Folate,vitamin B12, and homocysteine in majordepressive disorder. Am J Psychiatry.1997 Mar;154(3):426-8.

117. Godfrey PS, Toone BK, Carney MW, FlynnTG, Bottiglieri T, Laundy M, et al. Enhance-ment of recovery from psychiatric illnessby methylfolate. Lancet. 1990 Aug18;336(8712):392-5.

118. Reynolds EH, Preece JM, Bailey J,Coppen A. Folate deficiency in depres-sive illness. Br J Psychiatry. 1970 Sep;117(538):287-92.

119. Levine J, Barak Y, Gonzalves M, Szor H,Elizur A, Kofman O, et al. Double-blind,controlled trial of inositol treatment of de-pression. Am J Psychiatry. 1995 May;152(5):792-4.

120. Levine J, Gonzales M, Babur I, Stir S,Elizur A, Kofman O, et al. Inositol 6 gmdaily may be effective in depression butnot in schizophrenia. Hum Psychophar-macol. 1993;8:49-53.

121. Fava M, Giannelli A, Rapisarda V, PatraliaA, Guaraldi GP. Rapidity of onset of theantidepressant effect of parenteral S-adenosyl-L-methionine. Psychiatry Res.1995 Apr 28;56(3):295-7.

122. Bloch D. Healing from depression: 12weeks to a better mood. A body, mind,and spirit recovery program. Berkeley,CA: Ten Speed Press; 2002.

123. Paffenbarger RS, Jr., Lee IM, Leung R.Physical activity and personal character-istics associated with depression andsuicide in American college men. ActaPsychiatr Scand. Suppl 1994;377:16-22.

124. Babyak M, Blumenthal JA, Herman S,Khatri P, Doraiswamy M, Moore K, et al.Exercise treatment for major depression:maintenance of therapeutic benefit at 10months. Psychosom Med. 2000Sep;62(5):633-8.

125. Byrne A, Byrne DG. The effect of exerciseon depression, anxiety and other moodstates: a review. J Psychosom Res. 1993Sep;37(6):565-74.

126. McCann IL, Holmes DS. Influence of aero-bic exercise on depression. J Pers SocPsychol. 1984 May;46(5):1142-7.

127. Berger B, Owen D, Man F. A brief reviewof literature and examination of acutemood benefits of exercise in Czechoslo-vakian and United States swimmers. Int JSport Psychol. 1993;24(2): 130-150.

128. King AC, Taylor CB, Haskell WL. Effectsof differing intensities and formats of 12months of exercise training on psycho-logical outcomes in older adults. HealthPsychol. 1993 Jul;12(4):292-300.

129. Martinsen E, Medhus A. Adherence toexercise and patients’ evaluation of physi-cal exercise in a comprehensive treatmentprogram for depression. Nordic Psychi-atric Quarterly. 1989;43:411-415. Ref Type:Journal (Full).

Recibido para evaluación: 2 de mayo de 2006Aceptado para publicación: 17 de mayo de 2006

CorrespondenciaJohn E. Lewis

1400 NW 10th Ave6th Floor (D21)

Miami, FL 33136Correo electrónico: [email protected]

11. Nutrition.p65 16/06/2006, 3:58175

Documents

Nutrition, Physical Activity, Weight Management, and HealthBody weight, diet, and level of physical activity are important de-terminants of chronic illness, mor-bidity, and quality