Obesity in Older Adults:Pathophysiology and ClinicalImplications

Cynthia L. Vuittonet, Avishkar Sbharwal, and C. S. Pitchumoni

ContentsIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Definition and Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Body Mass Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Abdominal Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Defining Obesity in Older Adults . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

Etiology and Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

Comorbidities Associated with Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

Nutritional Status in Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Obesity Paradox . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Approaches to Weight Loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11Behavioral Modifications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12Medical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12Surgical Interventions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Key Points . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

Abstract

Obesity is a global problem across all agegroups in the USA during the past 30 years;the proportion of older adults who are obesehas doubled. As in the younger age group,genetic, environmental, social, as well as sev-eral other factors, are the etiological factors. Inthe USA, according to the National Institute ofHealth (NIH), poverty and lower levels of edu-cation are linked to obesity because it ischeaper to consume tons of high-calorie,

C. L. VuittonetDepartment of Medicine, Jewish Renaissance MedicalCenter, Perth Amboy, NJ, USA

A. SbharwalHackensack University Medical Center, Hackensack, NJ,USA

C. S. Pitchumoni (*)Department of Gastroenterology, Saint Peters UniversityHospital, New Brunswick, NJ, USAe-mail: pitchumoni@hotmail.com

© Springer Nature Switzerland AG 2020C. S. Pitchumoni, T. S. Dharmarajan (eds.), Geriatric Gastroenterology,https://doi.org/10.1007/978-3-319-90761-1_98-1

1

processed food than fresh fruits and vegeta-bles. According to the World Health Organiza-tion (WHO), a BMI of >30 is a marker ofobesity. BMI above 25 is considered over-weight, whereas a BMI over 30 is consideredobese. Morbid obesity is defined as a BMIabove 35 with comorbidity (diabetes, hyper-tension, or obstructive sleep apnea) or over40 without comorbidity.

The body composition of an obese olderindividual is different from their youngercounterparts.

Hormonal regulatory alterations predisposethe old to increases in fat mass. There is redis-tribution of adipose tissue throughout the bodywith an increase in intra-abdominal fat withless subcutaneous fat. Aging results in declinein the growth hormone (GH), insulin-likegrowth factor 1 (IGF-1), testosterone, andestrogen. The decrease in GH results in adecline in lean muscle mass. Sarcopenia maycoexist with obesity and may cause frailty andassociated complications. Obesity is a risk fac-tor for type 2 DM, coronary artery disease,respiratory problems, dermatological prob-lems, osteoarthritis, and above all many formsof cancer (pancreas, breast, colon, esophageal,endometrial, kidney, thyroid, liver, and gall-bladder cancer).

Management of obesity in older adults is acomplex one and has to be done with the helpof a qualified geriatrician, nutritionist, andphysical therapist. Surgical procedures areoptions for a few selected older adults.

Keywords

BMI · Obesity · Malnutrition · Sarcopenia ·Bariatric surgery · Cancers · Waistcircumference · Frailty · Cytokines ·Osteoarthritis · Osteopenia · NAFLD

Introduction

Obesity is a growing epidemic in the United Statesand throughout the world. Older adults representapproximately 20% of the US population and

22% world wide (Ogden et al. 2013). The WorldHealth Organization (WHO) estimates thatapproximately 40% of adults are overweight(BMI 25–29.9) and 30% of adults are obese(BMI over 30) (WHO 2000). The Centers forDisease Control and Prevention (CDC) estimatesthat by 2035 over one third of those over the ageof 60 will be considered obese (Rimm 2014).Diagnosis and management of obesity in the geri-atric population is a growing dilemma for physi-cians. This chapter will discuss the definition andpathophysiology of obesity as it pertains to olderadults. Furthermore, this chapter will explore thenutritional complexities, obesity paradox, andapproaches to weight loss in the obese olderpopulation.

Epidemiology

Over the past four decades, the prevalence ofoverweight and obese individuals have tripled.Obesity is now considered to reach pandemic pro-portions in many parts of the world (Rimm 2014).The WHO reports that in 2016 approximately600 million adults are considered obese world-wide, and it is expected that this number willcontinue to rise (Fig. 1) (WHO 1997).

The USA has the highest rates of obesityworldwide, but parts of the world that previouslyhad low rates of obesity are no longer immune tothe obesity epidemic. China had less than 5% ofthe population suffering from obesity; however,now it is estimated that 29% of the Chinese pop-ulation is overweight and 11% are obese (Xi et al.2012). The prevalence of obese adults in Braziltripled and now represents 22% of the Brazilianpopulation (Hu 2009).

The rates of obesity in lower to middle socio-economic groups are rapidly rising in dispropor-tionate amounts when compared to highersocioeconomic groups. In India the prevalenceof obesity is higher in areas with higher materialwealth (Amarya 2014). Within the US also, areasof lower socioeconomic status have higher ratesof obesity (Fig. 2).

Socioeconomic factors are not the only areas inwhich variations of the prevalence of obesity are

2 C. L. Vuittonet et al.

observed. In the USA, there are racial and genderdisparities related to the prevalence of obesity inthe elderly population. Elderly Non-Hispanicblack women have a significantly higher preva-lence of obesity compared to their male andNon-Hispanic white counterparts (Fig. 3)(Mathus-Vliegen 2012). This disparity is thoughtto be multifactorial and a result of both pathophys-iologic differences and socioeconomic factors(Wang and Beydoun 2007).

As the prevalence of obesity continues to rise,clinicians will see increases in comorbid diseasesassociated with obesity. In the USA, obesityhealth expenditures is between $147 billion to$210 billion annually (Finkelstein et al. 2009).On average obese adults spend 42% more ondirect healthcare costs compared to their counter-parts with healthy weight (Yang and Hall 2008).By the year 2050, the number of older individualswill more than double and reach approximately88.5 million and it is estimated that the growing

obese elderly population will continue to use morehealth care dollars (Finkelstein et al. 2009).

Definition and Diagnosis

Body Mass Index

The most common metric for defining obesity inadults is the Body Mass Index (BMI) (Erlangerand Henson 2008). BMI is calculated by dividingweight in kilograms by height in meters squared.BMI above 25 is considered overweight whereas aBMI over 30 is considered obese. Morbid obesityis defined as a BMI above 35 with a comorbidity(diabetes, hypertension, or obstructive sleepapnea) or over 40 without a comorbidity (Table 1).

The definition of obesity based on BMI is notinternationally universal. Individuals from Indiawith a BMI over 25 are considered obese, whereasindividuals from Asia are considered obese when

Fig. 1 A comparison of obesity prevalence between 1990 and 2010 according to the CDC (Ogden et al. 2013)

Obesity in Older Adults: Pathophysiology and Clinical Implications 3

their BMI is above 28 (Dudeja et al. 2001; Wu2006). In order to prevent underdiagnosing

Fig. 2 Racial and gender disparities in the obese elderly population (Mathus-Vliegen 2012)

Fig. 3 Prevalence of the obese elderly population in the United States (Mathus-Vliegen 2012)

4 C. L. Vuittonet et al.

obesity, clinicians caring for ethnic diversepopulations must be aware of the variations indefining obesity based on BMI.

Relying on BMI to define obesity can some-times falsely under or overestimate an individual’sobesity status. BMI does not differentiate betweenmuscle, fat, and bone mass, and therefore cannotdetermine obesity status in all individuals(Kramer et al. 2013).

Abdominal Obesity

BMI is not the only defining marker of obesity.The WHO defines obesity as the accumulation ofexcessive fat that presents an overall health risk(Misra and Khurana 2008). This accumulation ofexcess fat is often defined by using waist circum-ference. Waist circumference is a marker of intra-abdominal or visceral fat. Although the exactmechanism is not known, excessive adipose tissueis thought to increase inflammation and metabolicdysfunction of the organs within the abdominalregion (Klein et al. 2007). Females with a waistcircumference over 35 in. and males with a waistcircumference over 40 in. are considered to beobese (World Health Organization 2011). Theseindividuals display increased central obesity andhave a statistically higher risk of developing insu-lin resistance, hypertension and dyslipidemia(Vazquez et al. 2007).

Defining Obesity in Older Adults

Identifying and diagnosing obesity in older adultsposes a challenge to the clinician. This challengeis related to the anatomical and physiologicchanges associated with aging. The consequenceof these anatomical and physiologic changesmorph into various forms of obesity in olderadults.

Anatomic consequences of aging are in partdue to decreased bone density. The decrease inbone density results from a loss of vertebral heightdue to thinning of intervertebral discs typicallyseen in osteoporosis (Sorkin et al. 1999a). Relyingon BMI in the older population could underesti-mate the degree of adiposity due to the reductionof height (Prentice and Jebb 2001). On average,women lose 2–3 cm more in height compared totheir male counterparts which further decreasesthe validity of relying on BMI to determine obe-sity status (Sorkin et al. 1999b).

Body composition of the obese older individ-ual is different from their younger counterparts.With aging, individuals have redistribution of adi-pose tissue throughout their bodies. The olderadult has an increased amount of intraabdominalfat with less subcutaneous fat (Cesari et al. 2005).Intraabdominal fat accumulation is observed evenin individuals with stable weight (Goodpasteret al. 2001). Intrahepatic and intramuscular fatstores increase with age and is particularly preva-lent in the thighs and calves (Goodpaster et al.2001; Cree et al. 2004). Ultimately the depositionof fat into the viscera and muscles result inincreased insulin resistance that leads to a cycleof increased adipose tissue (Schwartz and Doucet2010).

Aging is associated with a decline in musclemass. Sarcopenia is defined as the loss of musclemass with increases in adipose tissue (Beaufrèreand Morio 2000). Sarcopenia is further defined ashaving decreased walking speed or grip strength(Kalinkovich and Livshits 2015; Porter Starr andBales 2015). This condition is thought to affect upto 10% in individuals aged 50 and up to 35% ofindividuals over the age of 70 (Fuggle et al. 2017).Decreased muscle mass results in a physiologicchange that decreases the resting metabolic rate.

Table 1 Classification of weight status based on bodymass index

ClassificationBMI(kg/m2)

Underweight <18.5

Normal weight 18.5–24.9

Overweight 25–29.9

Obese 30–34.9

Morbid obesity with comorbid condition 35–39.9

Morbid obesity without comorbidcondition

�40

Obesity in Older Adults: Pathophysiology and Clinical Implications 5

This change is due to decreased mitochondrialvolume and oxidative capacity resulting in a phys-iologic reduction in caloric metabolism(Baumgartner 2000; Gallagher et al. 2017). Thephysiologic changes leading to decreased muscleactivity result in fat infiltration into the musclesleading to lipotoxicity, mitochondrial dysfunc-tion, and inflammation, further perpetuatingunderlyingmuscle dysfunction, insulin resistance,and increases in adipose tissue (Kalinkovich andLivshits 2015, 2017). These physiologic changeslead to difficulties with activities of daily livingand overall increase in morbidity and mortality(Baumgartner et al. 1995; Delmonico et al. 2009;Mathus-Vliegen 2012; Studenski 2013; Chenet al. 2014; Fuggle et al. 2017).

A lower BMI in the elderly population is asso-ciated with a higher risk of frailty syndrome inolder adults (Reinders et al. 2017). Frailty syn-drome is characterized by age-related loss anddysfunction of skeletal muscle and bone (Stoeveret al. 2015). It is thought to affect multiple areas ofhuman functioning in the geriatric population.Usually unintentional weight loss is the definingfactor of frailty syndrome; however, individualswith frailty syndrome and increased abdominalobesity are at increased risk for thecardiometabolic consequences of obesity (Sundell2011).

Sarcopenia and frailty syndrome can decreasethe validity of current diagnostic measures of obe-sity in older adults. The clinician should evaluatepatients’ prior BMI trend, waist circumference,and muscle grip to determine the status of muscleloss and increased adiposity (Zamboni andMazzali 2012). Clinicians must first understandthe complexity behind diagnosing elderly individ-uals with obesity prior to initiating treatmentstrategies.

Etiology and Pathophysiology

The etiology and pathophysiology of obesity arecomplex and involve neurobiological, physio-logic, and socioeconomic factors. There are anumber of receptors in the brain that are respon-sible for the pleasurable aspect of eating (Zhang

et al. 2014). Taste is the most important factor infood consumption in older adults which leads tostimulation of multiple receptors in the brain(Jacobson et al. 2010).

Hedonic eating refers to the emotional preoc-cupation of wanting to eat and is thought to cor-relate with the effect that pleasure has on thevarious receptors in the brain (Amy Janke andKozak 2012). Neurobiological studies show thataging causes an up regulation in the pleasurecenter of the brain. This suggests that older adultsmay be more subjective to hedonic eating(Guerdjikova et al. 2012).

Physiologic changes occur within the hypo-thalamus with aging. Hormonal regulatory alter-ations predispose the old to increases in fat mass.Aging results in a decline in the growth hormone(GH), insulin like growth factor 1 (IGF-1), testos-terone, and estrogen (Baumgartner 2000). Thedecrease in GH results in a decline in lean musclemass (Lodish et al. 2016). IGF-1 decline in olderadults may impair insulin sensitivity and causehigher rates of oxidative damage (Al-Regaiey2016). Testosterone levels decline by about 1%per year with age and contributes to a decrease inlean mass and increase in adiposity with visceralfat deposition (Kadi 2008).

From a physiologic standpoint, there is aninterplay between hormone regulation and aninflammatory response. Hormonal signalingfrom the hypothalamus leading to decreased lep-tin causes an increase in adipose tissue (Kaila andRaman 2008). The increase in adipose tissue leadsto a higher expression in the adipose hormones,adipokines, which are analogues of cytokines(Zhang et al. 2014) (Fig. 4).

Additionally, there is a low grade chronicinflammatory state caused by increase in adipo-cytes due to the over expression of cytokines,tumor necrosis factor, and interleukins 1 and6 (Kaila and Raman 2008). The chronic inflam-matory state of obesity creates a catabolic effect ofcytokines on muscle resulting in a decrease inmuscle mass (Roubenoff et al. 1997). Theseinflammatory markers also lead to oxidative dam-age throughout the body, ultimately increasing therisk of comorbid complications from obesity.

6 C. L. Vuittonet et al.

In addition to hormones and the role of inflam-mation, decreased blood flow to muscles isanother cause of obesity in the aged. Many olderadults suffer from peripheral vascular and athero-sclerotic disease resulting in a reduced blood flowstate. This decreased blood flow is thought topotentiate the physiologic effects of sarcopenia(Morley et al. 2014).

Socioeconomic forces also play a crucial rolein higher obesity rates. Individuals who possessless material wealth have more access to low cost,high calorie, nutrient poor food than nutrient richfoods which cost more (States 2012). Older adultssuffer from mobility and financial constraints thatcan make access more difficult and are sometimesdependent on premade meals that are high incalories. Additionally, older adults have sensoryand oropharyngeal changes that make consump-tion of certain foods more difficult. Poor dentition,ill-fitting dentures, and decreases in saliva con-tribute to difficulties in masticating certain meats

and vegetables (Table 2). This difficulty predis-poses these older adults to consume more carbo-hydrate rich foods (Amarya et al. 2015).

Comorbidities Associated with Obesity

Obesity is associated with an increased risk ofmultiple medical conditions that increase overallrates of mortality (Table 3) (Finlayson and Dalton2012). Type 2 Diabetes Mellitus (T2DM) is one ofthe most common medical comorbidities associ-ated with obesity (Cazzo et al. 2017). The rate ofindividuals with T2DM is estimated to haveincreased 62% over the past decade (Viljoen andSinclair 2011). Approximately 50% of individualswith T2DM are 65 and older (Corriere et al.2013). The risk of death is doubled in the olderpopulation with T2DM due to a possible interplaybetween the physiologic changes from T2DM aswell as side effects of hypoglycemic therapies

Adipose Tissue

Adipocyte Fatty AcidBiding Protein

Leptin

Hypothalamic resistanceto Leptin

Adiponectin

Insulin Resistance

Expression ofadipokines

Inflammatory Cells:CytokinesTNF- a

Macrophageinfiltration

Low grade inflammatory state

Fig. 4 The pathophysiology of increased adipose tissue

Obesity in Older Adults: Pathophysiology and Clinical Implications 7

(Sloan et al. 2008). A recent change in the targetedgoals of hemoglobin A1c for older adults reflectsthe increased risk of stringent glucose control inthis population. Critics of this change favor tightglycemic control noting that hyperglycemia in thegeriatric age group can lead to dehydration, cog-nitive decline, falls, and overall functional decline(Neumiller and Setter 2009; Sjöström et al. 2015;Valencia et al. 2018). Current oral antidiabeticagents that are safer in the older population aremetformin and Sodium-glucose Cotransporter-2(SGLT-2) inhibitors (Valencia et al. 2018).

A number of studies have found a relationshipbetween hypertension, insulin resistance, anddyslipidemia with increased abdominal adipose

tissue. This constellation of biochemical andphysiologic changes is termed metabolic syn-drome. Metabolic syndrome increases the risk ofdeveloping cardiovascular complications, such asheart disease and stroke (Blazer et al. 2006).According to the World Health Organization(WHO), the prevalence of metabolic syndromein the elderly varies from 11% to 40% with higherrates of abdominal obesity and hypertension thantheir younger counterparts (Bechtold et al. 2006).

Metabolic syndrome is not the only comorbid-ity associated with obesity. There are knownincreases in certain cancers in obese individuals.The CDC reports that obesity is associated with asmany as 13 cancers (Table 4) affecting all organsystems and represents approximately 20% of allcancers (Vucenik and Stains 2012; Bilić 2014).The exact pathophysiology of cancer develop-ment in obesity is not known; however, it isthought to be multifactorial and linked to theincreased inflammatory state and disruption ofthe individual internal milieu (Calle and Kaaks2004; Bilić 2014; Jochem and Leitzmann 2016).

Table 2 Gastrointestinal co-morbidities of obesity.(Adapted from Camilleri et al. 2017)

Gastrointestinal complications of obesity

Esophagus

Dysmotility

Gastroesophageal reflux disease

Barrett’s esophagus

Erosive esophagitis

Stomach

Motility disorders

Erosive gastritis

Gastric cancer

Small intestine

Chronic diarrhea

Celiac disease

Inflammatory bowel diseases

Colon and rectum

Constipation

Diverticulosis

Colon cancer

Clostridium difficile infection

Anal canal and pelvic floor

Dys-synergic defecation

Fecal incontinence

Liver

NAFLD

Cirrhosis

Carcinoma

Gallbladder

Gallstones

Pancreas

Acute pancreatitis (an index of severity)

Pancreatic cancer

Table 3 Comorbidities in obesity

Comorbid conditions associated with obesity

Metabolic syndrome

Hypertension

Insulin resistance (T2DM)

Dyslipidemia

Elevated triglycerides

Low HDL

Cognitive impairment

Vascular dementia

Alzheimer’s disease

Cancer (see Table 4)

Pulmonary conditions

Decreased lung function

Forced vital capacity

Total lung volume

Hypoxemia

Sleep apnea

Thromboembolic disease

Gastrointestinal

Reflux disease

Fatty liver disease

Arthritis

8 C. L. Vuittonet et al.

Pulmonary complications of obesity are alsoobserved across multiple different ethnic groups.Regional body composition changes associatedwith obesity may lead to decreased lung function,particularly in the elderly population whenchanges in muscle mass are more pronounced(Rossi et al. 2008). Abdominal obesity creates aphysical resistance that results in decreased forcedvital capacity as well as total lung capacity (Para-meswaran et al. 2006). In addition to the anatom-ical changes, obese individuals also havephysiologic pulmonary changes related todecreased alveolar ventilation. Arterial blood gassamples from individuals with increased abdomi-nal obesity demonstrated decreased pulmonarygas exchange at rest, during sleep, and duringexercise (Bhasin et al. 2015). The anatomicaland physiologic changes associated with obesityresult in hypoxemia which over time worsen cog-nitive function and other metabolic derangements.

Approximately one million individuals sufferfrom a thromboembolic event annually in theUnited States (Heit et al. 2001). Pulmonary embo-lism and deep vein thrombosis comprise the mostcommon thromboembolic disease seen in obeseindividuals (Stein et al. 2005). Obese individualsare also at increased risk of developing recurringthromboembolic events. Aging is an independentrisk factor for the development of thromboem-bolic disease (Di Minno and Tufano 2004).

Although the relationship between obesity,aging, and thromboembolic disease is not wellstudied, the hypothesis is that older obese adultsare at increased risk for thromboembolic events.

Gastrointestinal manifestations of obesity areless common (Table 2). Historically obese andelderly individuals have an increased prevalenceof gastroesophageal reflux disease (GERD). Cur-rent studies demonstrate that the obese elderlyindividuals have higher rates of GERD whencompared to their normal weight counterparts(El-Serag et al. 2005; Bashashati et al. 2016).Nonalcoholic fatty liver disease (NALFD) is com-mon in the elderly population. Research suggeststhat there is a protective role of estrogen indelaying the onset of NAFLD in younger femaleindividuals; however, in the older population, thehepatic and extra-hepatic consequences ofNAFLD are worse than in younger individuals(Bertolotti et al. 2014).

Osteoarthritis is a comorbid disorder associ-ated with obesity and is the leading cause ofreported disability in the old (March et al. 2014).Approximately 12 million adults over the age of65 suffer from osteoarthritis (Hootman et al.2012). The prevalence of osteoarthritis is risingand thought to be in part to the rising obesityepidemic (Kwoh 2012). Older obese individualssuffering from osteoarthritis are less likely to wantto be physically active secondary to pain (Fig. 5).These individuals should have optimal pain con-trol to improve functional capacity and decreasethe risk to develop significant disability (Ettingerand Afable 1994; Miller et al. 2000).

Nutritional Status in Obesity

Obesity is not an indicator of good nutritionalstatus; in fact, it is considered a marker of malnu-trition. In the USA, obesity is more prevalent inareas of lower socioeconomic status (Amy Jankeand Kozak 2012). This increased prevalence isassociated with the increased availability of lowcost, high calorie, and nutrient poor food (Ogdenet al. 2010). The consumption of “fast foods,”“junk foods,” or “ultra-processed foods” in con-junctions with calorie loaded soft-drinks are to

Table 4 Cancers associated with obesity according tothe CDC

Cancers associated with obesity

Meningioma

Thyroid

Gastrointestinal

Esophagus

Gastric

Pancreatic

Colon

Rectal

Breast

Reproductive

Uterus

Ovarian

Kidney

Multiple myeloma

Obesity in Older Adults: Pathophysiology and Clinical Implications 9

blame for the higher prevalence of obesity andnutritional deficits in low socioeconomic areas(WHO 1997; Jain and Dotan 2017).

These foods are particularly poor in micro-nutrients and high in simple sugars and carbohy-drates. Deficiency in micronutrients lead toincreased insulin resistance, hypoalbuminemia,and vitamin/mineral deficiencies in the obese pop-ulation (Via 2012). These foods lack zinc, folate,and vitamins C, D, and E. Deficiencies in thesemicronutrients play a vital role in the health of theelderly population.

Vitamin D plays a key role in calcium andphosphorous metabolism. There is growing evi-dence to suggest that vitamin D deficiency, serumlevel of 25-(OH)D less than 20 ng per milliliter,may cause or be associated with a number ofdifferent medical conditions (Holick 2017). Themost well-known association is the relationshipbetween vitamin D deficiency, osteoporosis, andan increased risk of fracture (Xu et al. 2011).Other associated conditions include autoimmunediseases, various types of cancers, cardiovasculardisease, infections, type 2 diabetes, and osteoma-lacia (García et al. 2009). Vitamin D is known toimprove glycemic control by increasing hepaticand peripheral uptake of glucose, which can bebeneficial to the obese individuals who have insu-lin resistance. The major source of endogenoussynthesis of vitamin D is via skin exposure toUltraviolet B radiation waves; however; thereare important dietary sources of vitamin D (Holick2017). These sources include fortified dairy prod-ucts, egg yolk, fatty fish (such as salmon, mack-erel, and herring), fish liver oil, and beef liver(Chernoff 2005).

Overweight and obese individuals also havedecreased levels of vitamin B12 and folate whencompared to their normal weight counterparts.Obese individuals are likely to consume morecarbohydrates, fattier proteins, and less lean pro-teins that are rich in vitamin B12 (García et al.2009). Many obese individuals are on medica-tions for glycemic control which alter the absorp-tion of vitamin B12. Notably metformin is knownto cause vitamin B12 deficiency as well as anemia(Morley 1997). Folate (vitamin B9) is essential forDNA methylation, nucleic acid synthesis, cellgrowth, and division (Kerns et al. 2015). Folatedeficiency may cause insulin resistance. Serumlevels of 5-methylterahydrofolate andunmetabolized folic acid are negatively associatedwith BMI (Amarya et al. 2015).

Approximately 30–50% of adults over the ageof 80 may be adversely affected by sarcopenia(Batsis et al. 2016). Protein deficiency is a partof sarcopenic obesity. Protein plays a key role inthe growth and maintenance of the human bodyand serves as a major structural component ofseveral tissues. Protein is used to produceenzymes, hormones, and macromolecules suchas hemoglobin. Protein deficiency causesdecreased muscle mass, weakness, brittle hair,and in some severe protein deficiency there is ageneralized edema. Deficiencies in protein alsoresult in impairment of immune response, produc-tion of enzymes and hormones ultimately leadingto a myriad of symptoms.

Micronutrient deficiencies are also due in partto decreased absorption in the small bowel.Increased adipose tissue triggering increasedinflammatory markers is one of the leading theo-ries behind the decreased absorption in the small

Obesity

Functionality

Mobility

Total Body EnergyExpenditure

Worsening HealthStatus

Fig. 5 The Obesity Cycle,a depiction of the interplaybetween various factors thatcontribute to obesity and arefurther worsened by obesity

10 C. L. Vuittonet et al.

bowel (Kerns et al. 2015). Absorptive malnutri-tion contributes to chronic state of inflammationand is thought to be secondary to deficiencies ofvitamin A, C, E, D, and K. Additionally the mal-absorption leads to deficiencies in chromium, bio-tin, thiamin, zinc, and antioxidants. Albumin is abiochemical marker of protein calorie malnutri-tion; studies suggest that patients with hypo-albuminemia are at greater risk of death orserious morbidity after surgery (Fieber et al.2018). Zinc deficiency is crucial to woundhealing, and the prevalence of chronic nonhealingwounds increases with age (Amarya et al. 2015).Vitamin A is essential for vision, immune func-tion, and maintenance of the cell membrane byregulation of multiple gene expression pathwaysin the liver, adipose tissue, skeletal muscle, andretina (Aigner et al. 2014; Schiavo et al. 2018).

In addition to availability of low-cost nutrientpoor food, the elderly suffer from sensory andanatomical changes that limit consumption ofnutrient rich foods. Edentulous individuals orthose with ill-fitting dentures may have difficultyconsuming meats and raw vegetables (Amaryaet al. 2015). Individuals with decreased salivafrom either medication side effect or as a resultof aging may have difficulty consuming meats,raw vegetables, and whole grains. The end resultis a deficiency in protein, fiber, andmicronutrients.

Obesity Paradox

In younger adults, obesity is known to increase therisk of developing diabetes, hypertension, anddyslipidemia. However, in older adults there is aphenomenon observed in which obesity may havea protective role. Obese older adults undergoingsurgery or presenting with an acute critical illness,such as congestive heart failure exacerbation, hada lower mortality rate than overweight or under-weight older adults (Cetin and Nasr 2014). Thebelief is that obese older adults have increasedenergy stores that can withstand the demands ofa critical illness.

There are limitations to the obesity paradox.The mortality benefit applies to older adults with a

BMI between 30 and 35, suggesting that olderadults with a BMI categorized as morbidly obeseno longer have this benefit. Nutritional status ofthe older adult impacts mortality independent ofBMI. Obese individuals who have hypo-albuminemia have a higher 30-day mortalitythan obese individuals with a normal albumin(Xanthakos 2009). The obesity paradox does notapply to obese individuals who have experiencedunintentional weight loss. These individuals oftenhave an underlying disorder that are associatedwith higher rates of mortality and protective ben-efit may not apply (Harris et al. 2011).

Obesity in the older adult may offer a protec-tive benefit from acute critical illness; however,there are health implications that stem from theage of onset of obesity. Obesity, particularly mor-bid obesity, increases the risk of many comorbidconditions in younger adults. Younger obeseadults who age into older obese persons aremore likely to suffer from osteoarthritis, mobilityimpairments, and disabilities compared to olderobese adult counterparts who developed obesitylater in life (Zamboni et al. 2005).

Approaches to Weight Loss

The United States Preventative Services TaskForce (USPSTF) recommends that all adults bescreened for obesity and that obese persons beprovided weight loss counseling (Felix et al.2008). Approximately 44.5% of obese 60–69-year-olds and 32.4% of individuals over the ageof 70 receive weight loss counseling from theirphysician (Chernoff 2005; Felix et al. 2008). Thethreshold of when to initiate weight loss counsel-ing in the obese older population is subject todebate (Villareal et al. 2005; Zamboni et al. 2005).

Prior to counseling the obese older adult onweight loss, the risks and benefits of weight lossshould be evaluated (Fig. 6). The physicianshould obtain history regarding food shopping,preparation of meals, and any physical barriersto eating. Physical examination should includeheight, weight, and waist circumference. Obeseolder adults at risk for micronutrient deficienciesshould be identified and appropriate laboratory

Obesity in Older Adults: Pathophysiology and Clinical Implications 11

testing should follow. Clinicians should start withbehavioral modification prior to initiation of med-ications or consideration for surgery.

Behavioral Modifications

Office-based counseling and educational mate-rials are useful tools in educating obese olderadults (Kushner 2014). Education materialsshould include information on understandingnutrition labels, calorie counting, and balanceddiet. Individualized counseling should focus onbarriers to weight loss: dentition, vision loss,access to food, and financial resources.

Caloric restriction is often the first modifica-tion that individuals implement to lose weight.Caution should be exercised in promoting caloricrestriction in the old, as this can lead to increasedrisk for developing sarcopenia (Miller and Wolfe2008; Mathus-Vliegen 2012). Calorie restrictionis associated with increased anabolic resistanceand lower muscle function in the geriatric popu-lation when compared to their younger counter-parts (Chernoff 2005; Kalinkovich and Livshits2017; Schiavo et al. 2018). The older adult popu-lation benefits from portion control with adequateamounts of micronutrient consumption in combi-nation with exercise (Villareal et al. 2011;Jarolimova et al. 2013; Porter Starr and Bales2015; Jain and Dotan 2017). In order to avoidsarcopenia, the PROT-Age study provides guide-lines with regard to daily protein requirements inthe older adult (Bauer et al. 2013). Younger adultscan maintain lean body mass when consuming0.8 g/kg/day (Bauer et al. 2013; Jankovic et al.2015). Older adults require a higher amount ofdaily protein; they require 1.2–1.5 g/kg/day ofprotein to compensate for age-related metabolicregulation, immune status, and hormonal fluctua-tions (Coker and Wolfe 2018; Petroni et al. 2019).

Exercise is a reliable form of weight loss inobese older adults (Stoever et al. 2015). TheAmerican College of Sports Medicine has issuedan updated position on the benefits of exercise andphysical activity for older adults. The updatedguidelines recommend that older adults engagein 150 min of moderate intensity exercise

(Mazzeo 2001). However, these recommenda-tions are unlikely to elicit the amount of weightloss needed to improve metabolic and cardiovas-cular health (Nicklas et al. 2004; Coker and Wolfe2018). There is an emerging consensus that olderadults should be encouraged to perform resistancetraining as it improves the muscle quality of olderadults and is useful in combating sarcopenia andfrailty syndrome (Sundell 2011; Martínez et al.2014). For patients with mobility issues, formalphysical therapy programs are often useful inaiding obese older adults (Chodzko-Zajko et al.2009). Community based strength and resistancetraining programs demonstrate improvement inweight, blood pressure, and glucose readings inthe elderly population (Kushner 2014).

Medical Management

Management of obesity in the older adult is acomplex one and has to be done with the help ofa qualified geriatrician, nutritionist, and physicaltherapist. An early surgical consult isrecommended whenever a bariatric surgical pro-cedure is being contemplated.

Medications are widely available; however,over the counter supplements are not FDAapproved. Counseling regarding the safety ofsuch supplements should be addressed. Addition-ally, decreased metabolism and clearance of med-ications is a common phenomenon in older adults;therefore, caution should be used when consider-ing medications for weight loss (Porter Starr andBales 2015) (Table 5). The following areFDA-approved medications for weight loss:Phentermine, Topiramate, Naltrexone-Bupropion,Liraglutide, Lorcaserin, Orlistat, and Sibutramine(Table 3) (Erlanger and Henson 2008; Kaila andRaman 2008; Kushner 2014). Many of the cur-rently approved medications for weight loss arecontraindicated in patients with hypertension,mood disorders, or glaucoma. These contraindi-cations are clearly more prevalent in the geriatricpopulation.

12 C. L. Vuittonet et al.

Surgical Interventions

Bariatric surgical interventions are increasinglycommon to treat the morbidly obese and obeseindividuals with multiple comorbid conditionsafter those individuals who failed behavioral andmedical interventions. The indications for bariat-ric surgery in the older adult are same as those inyounger individuals. Selection for surgery has to

be made based on comorbid conditions, surgicalrisk, and life expectancy. The older literature fromthe 2000s reported significantly worse outcomesin those older adults undergoing bariatric surgerycompared with younger patients. Presently, thereis a changing trend with the outcomes of bariatricsurgery in the older adult (WHO 2000; Maggardet al. 2005; Batsis and Dolkart 2015).

Establish Obesity Status:BMI over 30Waist Circumference

Female: over 35 inchesMale: over 40 inches

Evidence of Malnutrition:BMI downtrending (muscle/bone mass loss)Low albuminMicronutrient deficiencies (ex: vitamin D, iron)

Yes No

Establish Nutritional Status:Evaluate BMI over past two yearsCheck albuminCheck for micronutrient deficiencies

Identify risks and deficiencies:Access to food:

Social services referralCommunity Food Bank resources

Correct nutritional deficiencies:Oral medicationsIntramuscular medicationsLow volume high nutrient supplements

Approaches to Weight Loss in the Elderly:Nutritional Counseling

Portion ControlNutrition Label Teaching

Exercise CounselingResistance TrainingStrength Training

Frequent Follow Up VisitsTrack WeightAssess Nutritional Status

Evaluate for surgical or endoscopic interventionsfor weight loss

Fig. 6 Approach to the elderly patient with obesity

Obesity in Older Adults: Pathophysiology and Clinical Implications 13

Table 5 Medical management options for obesity

Name Mechanism of action Contraindications Adverse effects

Phentermine Similar structure todextroamphetamine

Advanced arteriosclerosis Increased bloodpressure and heartrate

Stimulates hypothalamus to result indecreased appetite

Symptomatic cardiovascular disease Insomnia

Uncontrolled hypertension Restlessness

Hyperthyroidism Dry mouth

Glaucoma Diarrhea

History of drug abuse Tremor

Concomitant monoamine oxidaseinhibitor (MAOI) use

Topiramate Blocking of voltage-dependent sodiumand calcium channels

History of glaucoma Acute myopia

Inhibits excitatory glutamate pathway Visual field defects

Excites inhibitory effect of GABA Oligohidrosis andhyperthermia

Inhibits carbonic anhydrase activity Metabolic acidosis

Suicidal ideation

Cognitive effects

Neuropsychiatriceffects

Hyperammonemiaandencephalopathy

Kidney stones

NaltrexoneSR–bupropionSR

Stimulation of alpha-melanocyte-stimulating-hormone causing anorecticeffect

Uncontrolled hypertension Nausea

Inhibition of the autoinhibitory effectof beta-endorphin

Regulation of mesolimbic rewardpathways

ConstipationHistory of seizures

DizzinessChronic opioid use

HeadacheHistory of eating disorder

Dry mouth

Liraglutide Glucagon-like peptide (GLP-1)analogue that regulates hypothalamicresponse to appetite

History of gallstones Nausea

DiarrheaHistory of pancreatitis

ConstipationPregnancy

Family history of medullary thyroidcarcinoma or multiple endocrineneoplasia type 2

Vomiting

Hypoglycemia

Headache

DizzinessKidney disease

Lorcaserin Serotonin 2C receptor agonist Concomitant MAOI use Headache

History of mood disorder Dizziness

Diabetes Dry mouth

Selectively activates 5-HT2C receptorsin the hypothalamus to produce ananorectic effect

Heart failure Fatigue

Valvular heart disease Nausea

Driving or operating heavymachinery

Constipation

(continued)

14 C. L. Vuittonet et al.

Current surgical options include Roux-en-Ygastric bypass, sleeve gastrectomy,biliopancreatic diversion with duodenal switch,adjustable gastric banding, and intermittent vagalblockade (Maggard et al. 2005). There are newerendoscopic approaches that include an expand-able gastric balloon and gastric suturing (Kumarand Thompson 2011). Despite the numerousoptions for surgical and endoscopic therapies forweight loss, there are a small number of studiesthat focus on the outcome of bariatric surgicalprocedures in the elderly population. Retrospec-tive cohort studies demonstrate safety of bothRoux-en Y gastric bypass and sleeve gastrectomyin individuals between the age of 60 and70 (Reijntjes et al. 2015).

Key Points

• The Centers for Disease Control and Preven-tion (CDC) estimates that by 2035 over onethird of those over the age of 60 will be con-sidered obese.

• BMI of >30 is a marker of obesity. The WHOdefines obesity as the accumulation of exces-sive fat that presents an overall health risk.

• Abdominal or visceral obesity (metabolic obe-sity) is measured by waist circumference.

• Measurement of obesity is complicated byage-related anthropometric changes.

• On average, women lose 2–3 cm more inheight compared to their male counterpartswhich further decreases the validity of relyingon BMI to determine obesity status.

• The older population suffers from decreasedmuscle mass or sarcopenia that is defined asthe loss of muscle mass with an increase inadipose tissue.

• Frailty syndrome is characterized byage-related loss and dysfunction of skeletalmuscle and bone.

• Obesity is an independent risk factor for anumber of cancers.

• Elderly individuals should be cautious aboutuse of low-calorie diets as this can worsensarcopenia and other nutritional deficiencies.

• Bariatric surgery has a limited role in selectedolder obese adults.

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