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- •Preface
- •Contents
- •Introduction
- •Prevention
- •Harm Reduction
- •Decision-Making/Differential Diagnosis
- •Screening
- •Health Maintenance
- •References
- •Physical Exam
- •Vaccinations
- •Introduction
- •Symptoms
- •Other History
- •Physical Exam
- •Lab Tests
- •Differential Diagnosis
- •Treatment
- •Prevention
- •Long Covid
- •References
- •Introduction
- •Provider Perspectives
- •Portable Medical Summary
- •Education
- •Employment
- •Specialist-Dominated Care
- •Internist-Dominated Care
- •Condition-Specific Medical Knowledge
- •Medication Reconciliation/Polypharmacy
- •Secondary Medical Conditions
- •Behavioral Health
- •Health Maintenance
- •Sexual Health
- •Sexual Abuse
- •Contraception
- •Cervical Cancer Screening
- •Health Disparities
- •Ethical Considerations
- •Conclusion
- •References
- •Introduction
- •Outpatient Assessment
- •Social History
- •Medications
- •Functional Assessment
- •Geriatric Syndromes
- •Delirium
- •Confusion Assessment Method (CAM): Short version [14]
- •Delirium Evaluation
- •Depression
- •Medication Management
- •Preventing Future Falls
- •Polypharmacy
- •Sensory Loss
- •Vision
- •Hearing Loss
- •Osteoporosis
- •Sleep Disorders
- •Advanced Care Planning
- •Home Care
- •References
- •History
- •Palliative Care/Hospice Care
- •Constipation
- •Nausea/Vomiting
- •Pain
- •Conclusion
- •References
- •Introduction
- •Definitions
- •Decision-Making
- •Identification
- •Key History
- •Workup
- •Management
- •Risky or Unhealthy Alcohol Use
- •Risky Opioid Use or OUD
- •References
- •Introduction
- •History
- •Physical Exam
- •Type 1 Diabetes
- •Type 2 Diabetes
- •Lifestyle Changes
- •Metformin
- •GLP-1 Receptor Agonists (Exenatide, Liraglutide, Dulaglutide, Lixisenatide)
- •DPP-4 Inhibitors (Sitagliptin, Saxagliptin, Linagliptin, Alogliptin)
- •SGLT-2 Inhibitors (Canagliflozin, Dapagliflozin, Empagliflozin, Ertugliflozin)
- •Thiazolidinediones (Pioglitazone)
- •Alpha-Glucosidase Inhibitors (AGIs) (Acarbose, Miglitol)
- •Insulin
- •References
- •Subclinical Hypothyroidism
- •Treatment Challenges
- •Hyperthyroidism
- •Brief Introduction
- •Key H&P
- •Decision-Making/Differential Diagnosis
- •Treatment
- •Graves’ Disease
- •Hypothyroidism
- •Brief Introduction
- •Key H&P
- •Decision-Making/Diagnosis
- •Treatment
- •Overt Hypothyroidism
- •Radioactive Iodine (RAI)
- •Surgery
- •Treatment: Subclinical Hyperthyroidism
- •Thyroid Nodules
- •Brief Introduction
- •Key H&P
- •Decision-Making/Differential Diagnosis
- •Treatment
- •References
- •Introduction
- •History
- •Medical History
- •Family History
- •Social History
- •Physical Exam
- •Decision-Making/Differential Diagnosis
- •Screening Population
- •Testing Lipid Levels: Fasting vs. Non-fasting
- •Treatment
- •Treatment Strategies
- •Lifestyle Modification
- •Statins
- •Fibrates
- •Fish Oil
- •Other Non-statin Medications
- •Monitoring After Initiating Therapy
- •References
- •Introduction
- •History
- •Who Should Lose Weight?
- •Treatment
- •Diet
- •Physical Activity
- •Pharmacotherapy
- •Long-Term Follow-Up After Uncomplicated Bariatric Surgery
- •References
- •Brief Introduction
- •Decision-Making/Differential Diagnosis
- •Acute Cough
- •Subacute Cough
- •Chronic Cough
- •Evaluation/Investigation
- •Disease-Specific Features
- •Acute Cough
- •Subacute Cough
- •Chronic Cough
- •Treatment
- •References
- •Introduction
- •Sudden-Onset Dyspnea
- •Acute-Onset Dyspnea
- •Episodic Dyspnea
- •Chronic Dyspnea
- •Treatment
- •References
- •Introduction
- •Acute Sinusitis
- •Chronic/Recurrent Sinusitis
- •Physical Findings
- •Diagnosis
- •Diagnostic Tests
- •Additional Evaluation
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Key H&P
- •Rapid Antigen Detection Tests
- •Treatment
- •Symptomatic Treatment
- •References
- •Introduction
- •ICSD3 Classifies Sleep Disorders into Seven Major Categories [4]
- •Prevalence
- •Sleep History
- •STOP-Bang Questionnaire
- •Understanding ESS Score
- •Focused Physical Exam
- •Definition
- •Risk Factors
- •Pathophysiology
- •Diagnosis
- •Treatment: OSAHS/SDB (Usual Therapy)
- •References
- •Brief Introduction
- •Decision-Making/Differential Diagnoses
- •Physical Examination
- •Measuring Blood Pressure
- •Diagnostic Studies
- •Clinical Quality Measure
- •Assessment
- •Treatment
- •Lifestyle Management
- •Pharmacological Interventions
- •Refractory or Resistant Hypertension
- •References
- •Chest Pain
- •History
- •Physical Exam
- •Differential Diagnosis
- •Potentially Life-Threatening
- •Acute Coronary Syndromes
- •Aortic Dissection
- •Pulmonary Embolism
- •Pneumothorax
- •Non-Life-Threatening Causes
- •Gastroesophageal Reflux Disease
- •Pleuritic Chest Pain
- •Cervical Angina
- •Pericarditis
- •Chronic Angina
- •Herpes Zoster
- •Muscular Pain
- •Rib Fracture
- •Costochondritis
- •Esophageal Spasm
- •Diagnostic Testing
- •Electrocardiogram
- •Blood Testing
- •Imaging
- •Chest X-Ray
- •X-Ray C-Spine
- •Transthoracic Echocardiogram
- •References
- •Introduction
- •Laboratory Evaluation
- •Hypoproliferative Anemias
- •Microcytic Anemia
- •Differential Diagnosis
- •Iron Deficiency Anemia
- •Epidemiology
- •Pathophysiology
- •Key History
- •Physical Exam
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Normocytic Anemia
- •Differential Diagnosis [6]
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Macrocytic Anemia
- •Differential Diagnosis [2]
- •Megaloblastic Anemia
- •Vitamin B12 Deficiency
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Folic Acid Deficiency
- •Hyperproliferative Anemia
- •Hemolytic Anemia
- •Intrinsic Hemolytic Anemia
- •Sickle Cell Anemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Thalassemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Hereditary Spherocytosis (HS)
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD Deficiency)
- •Epidemiology
- •Pathophysiology
- •History Physical Exam
- •Laboratory Evaluation
- •Extrinsic Hemolytic Anemia
- •Autoimmune Hemolytic Anemia
- •Warm Autoimmune Hemolytic Anemia (WAHA)
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Cold Autoimmune Hemolytic Anemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Assessment
- •Conclusion
- •References
- •Introduction
- •Differential Diagnosis
- •Decision-Making/Treatment
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Papulosquamous
- •Psoriasiform
- •Pityriasiform
- •Lichenoid
- •Erythroderma
- •Eczematous
- •Dermal
- •Vascular
- •Vesiculobullous
- •Infectious
- •Autoimmune, Intraepidermal
- •Autoimmune, Subepidermal
- •Noninflammatory
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Non-scarring Alopecias
- •Androgenetic Alopecia
- •Focal Hair Loss
- •Diffuse Hair Loss
- •Scarring Alopecia
- •Lymphocytic
- •Acne Keloidalis
- •Neutrophilic
- •References
- •Introduction
- •Key H&P
- •History
- •Medications
- •Social History
- •Physical Examination
- •Differential Diagnosis
- •Decision-Making
- •Treatment
- •References
- •Introduction
- •Key H&P
- •History
- •Physical Examination
- •Differential Diagnosis
- •Intrinsic Shoulder Pain
- •Decision-Making
- •Treatment
- •Rotator Cuff Injury
- •Adhesive Capsulitis
- •References
- •Introduction
- •Key H&P
- •History
- •Medications
- •Social History
- •Physical Examination
- •Differential Diagnosis
- •Decision-Making
- •Treatment
- •Pharmacotherapy
- •Non-pharmacotherapy
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Vertigo
- •Central vs. Peripheral Vertigo
- •BPPV
- •Meniere’s Disease
- •Labyrinthitis/Vestibular Neuritis
- •Migrainous Vertigo
- •Presyncope
- •Disequilibrium
- •Lightheadedness
- •Dix-Hallpike Maneuver
- •Nystagmus
- •Hearing Evaluation
- •Romberg Testing
- •Other Diagnostic Testing
- •Treatment
- •BPPV
- •Vestibular Neuritis/Labyrinthitis
- •Meniere’s Disease
- •Disequilibrium
- •Presyncope
- •Lightheadedness
- •References
- •Introduction
- •History

208
A. Manavalan
American Heart Association task force on practice guidelines.
Circulation. 2014;129(25 Suppl 2):S1–45.
11. Eckel RH, etal. AHA/ACC guideline on lifestyle management
to reduce cardiovascular risk: a report of the American College
of Cardiology/American Heart Association task force on practice guidelines. J Am Coll Cardiol. 2014;63(25 Pt B):2960–84.
12. Fowkes FG, et al. Development and validation of an ankle
brachial index risk model for the prediction of cardiovascular
events. Eur J Prev Cardiol. 2014;21(3):310–20.
13. Polonsky TS, et al. Coronary artery calcium score and risk
classification for coronary heart disease prediction. JAMA.
2010;303(16):1610–6.
14. Ranthe MF, etal. A detailed family history of myocardial infarction and risk of myocardial infarction—a nationwide cohort
study. PLoS One. 2015;10(5):e0125896.
15. Ridker PM, et al. C-reactive protein and parental history
improve global cardiovascular risk prediction: the Reynolds
Risk Score for men. Circulation. 2008;118(22):2243–51. 4p following 2251
16. Bilheimer DW, etal. Mevinolin and colestipol stimulate receptormediated clearance of low density lipoprotein from plasma in
familial hypercholesterolemia heterozygotes. Proc Natl Acad Sci
U S A. 1983;80(13):4124–8.
1 7. Bruckert E, et al. Mild to moderate muscular symptoms with
high-dosage statin therapy in hyperlipidemic patients—the
PRIMO study. Cardiovasc Drugs Ther. 2005;19(6):403–14.
18. Finegold JA, etal. What proportion of symptomatic side effects
in patients taking statins are genuinely caused by the drug?
Systematic review of randomized placebo-controlled trials to aid
individual patient choice. Eur J Prev Cardiol. 2014;21(4):464–74.
19. Thompson PD, et al. Statin-associated side effects. J Am Coll
Cardiol. 2016;67(20):2395–410.
20. Cohen DE, etal. An assessment of statin safety by hepatologists.
Am J Cardiol. 2006;97(8A):77C–81C.
21. Swerdlow DI, etal. HMG-coenzyme A reductase inhibition, type
2 diabetes, and bodyweight: evidence from genetic analysis and
randomized trials. Lancet. 2015;385(9965):351–61.
22. Elam MB, et al. Association of fenofibrate therapy with longterm cardiovascular risk in statin-treated patients with type 2
diabetes. JAMA Cardiol. 2017;2(4):370–80.
23. Keech A, et al. Effects of long-term fenofibrate therapy on
cardiovascular events in 9795 people with type 2 diabetes mel-

Chapter 9. Lipids
litus (the FIELD study): randomized controlled trial. Lancet.
2005;366(9500):1849–61.
24. Blais JE, et al. Comparative efficacy and safety of statin and
fibrate monotherapy: a systematic review and meta- analysis
of head-to-head randomized controlled trials. PLoS One.
2021;16(2):e0246480.
25. Bhatt DL, et al. Cardiovascular risk reduction with icosapent
ethyl for hypertriglyceridemia (REDUCE-IT). N Engl J Med.
2019;380:11–22.
26. Cannon CP, et al. Ezetimibe added to statin therapy after
acute coronary syndromes (IMPROVE-IT). N Engl J Med.
2015;372(25):2387–97.
2 7. Writing C, et al. ACC expert consensus decision pathway on
the role of non-statin therapies for LDL-cholesterol lowering
in the management of atherosclerotic cardiovascular disease
risk: a report of the American College of Cardiology task force
on clinical expert consensus documents. J Am Coll Cardiol.
2016;68(1):92–125.
28. Robinson JG, et al. Efficacy and safety of alirocumab in
reducing lipids and cardiovascular events. N Engl J Med.
2015;372(16):1489–99.
29. Sabatine MS, et al. Efficacy and safety of evolocumab in
reducing lipids and cardiovascular events. N Engl J Med.
2015;372(16):1500–9.
30. Ray KK, etal. Two phase 3 trials of inclisiran in patients with
elevated LDL cholesterol. N Engl J Med. 2020;382:1507–19.
31. Goldberg AC, etal. Effect of bempedoic acid vs placebo added
to maximally tolerated statins on low-density lipoprotein cholesterol in patients at high risk for cardiovascular disease: CLEAR
wisdom randomized clinical trial. JAMA. 2019;322(18):1780–8.
209

Chapter 10
Obesity
JacinthS.Ruddock andGayotriGoswami
Introduction
Obesity is a chronic, relapsing, multifactorial, neurobehavioral disease, where an increase in body fat promotes adipose
tissue dysfunction and abnormal fat mass resulting in adverse
metabolic, biomechanical, and psychosocial health consequences [1]. Obesity is defined as having a body mass index
(BMI) of ≥30kg/m2. It is estimated that about 42.5% of the
US population are obese, and almost 10% of the country are
severely obese with a BMI >40% [2].
By 2030 it is estimated that 51% of the US population will
be obese [3]. Obesity is associated with an increased risk for
developing many common chronic medical conditions. This
significant and increasing prevalence of obesity poses public
J. S. Ruddock (*)
Department of Internal Medicine, Albert Einstein College of
Medicine, New York City Health and Hospitals/Jacobi + North
Central Bronx, Bronx, NY, USA
e-mail: Jacinth.Ruddock@nychhc.org
G. Goswami
Division of Endocrinology, Department of Medicine, Westchester
Medical Center, Valhalla, NY, USA
e-mail: Gayotri.Goswami@wmchealth.org
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_10
211

212
J. S. Ruddock and G. Goswami
health as well as economic concerns. According to data from
the 2012 National Ambulatory Medical Survey, there were 11
million visits by adults age >20 years old to a physician’s
office where obesity was listed as a primary diagnosis; this
number was up to 12.7 million by 2014, and additional
chronic medical condition was associated with 73% of these
visits [4, 5].
However there has not been an equivalent increase in the
proportion of health care visits by adults with obesity that
include counseling on weight loss, nutrition, or physical
activity or prescription of weight loss drugs [5]. Primary care
physicians are faced with the challenge of screening for and
treating obesity and its related complications. The USPSTF
recommends screening all adults for obesity and treating
those with a BMI of >30kg/m2 [6]. The primary care provider
remains integral in getting patients engaged in the conversation about weight loss. Primary care providers cite limited
time, inadequate knowledge of obesity treatment, and lack
of reimbursement as reasons obesity is not addressed [7].
New evidence suggests that under medicalization of this disease may also be a contributing barrier to appropriate obesity care [5].
This text hopes to aid in bridging the knowledge deficit
and to add to the expanding body of knowledge on obesity as
a medical condition in an effort to enhance patient access to
meaningful and successful treatment options for obesity. We
provide a review of current and updated best practices for
medical evaluation and management of patients with obesity.
Approaches to the conversation about weight management
and algorithms for treatment will be highlighted.
Key History andPhysical Exam
History
Starting the conversation about weight loss is important.
Patients considered even a brief conversation with their pri-

Chapter 10. Obesity
213
mary care provider about how weight loss may improve their
health to be motivating, helpful, and appropriate [8]. As with
most health issues, the conversation should be broached sensitively. It is recommended that the physician asks the
patients’ permission to engage in a conversation about their
weight and share their concerns regarding the impact on the
patient’s health [9]. If patients are agreeable, utilize a strategy
that focuses on information sharing rather than blaming
patients for their weight. Recognize obesity as a medical condition by using language that is agreeable, inoffensive, and
clear [10]. The terms fat, obese, and morbidly obese are most
associated with stigmatization and blaming, while the terms
excess weight, high body mass index, or unhealthy weight are
more acceptable and motivating [11]. In addition to further
medicalize the condition, it’s been recommended that physicians use phrases such as “patients with obesity” rather than
“obese patients” [9].
Taking an obesity-focused history includes assessment of
historical events surrounding weight gain or loss, paying close
attention to the patient’s own perception of weight. Major life
events that may contribute to weight gain include changes in
marital status or employment status, quitting tobacco, pregnancy, and menopause. These events can be plotted on a
weight graph to aid in presenting a visual depiction of the
trends [10]. The review of medical history should be thorough
and include any history of childhood or adolescent obesity.
Assess for any symptoms or signs suggestive of secondary
causes of weight gain. For example, a body habitus suggestive
of a specific hormone imbalance or genetic anomaly might
prompt further testing. A careful review of all medications
including all over-the-counter medications should be completed in order to identify and modify any drugs or substances
known to promote weight gain. Common weight-inducing
prescription medications include beta- blockers, oral corticosteroids, anti-epileptics, sulfonylureas, insulin, atypical antipsychotics, some SSRIs, and hormonal treatments such as
progesterone.

214
J. S. Ruddock and G. Goswami
Assessment of psychological health including a thorough
psychiatric history is essential. Assess for mood or anxiety
disorders, eating disorders, post-traumatic stress disorder,
psychotic disorders, and substance abuse disorders. Any positive findings should trigger a mental health referral for further assessment prior to initiating any weight management
treatment [10].
Assessment of readiness to engage in a weight management regimen should be evaluated. Readiness is primarily
determined by the patients’ level of motivation and the feasibility of implementing and adhering to a weight-loss plan.
Identifying and addressing patient-specific barriers are critical in order for patients to achieve their weight-loss goals.
Clarify the patient’s expectations and goals and reconcile
them with the physician’s medical recommendations. It is possible that it may not be the optimal time for the patient to
undertake a weight-loss plan. The patient may still be in the
pre-contemplative or contemplative stages of behavior
change, and physician counseling may serve to catapult them
to a stage of readiness to engage in weight-loss activities.
Physicians’ use of the 5A approach (Assess, Advise, Agree,
Assist, Arrange) has been found to lead to improved weightloss outcomes [12].
Physical Examination andDiagnostics
It has been deemed necessary in more recently developed
guidelines to improve upon the diagnosis of obesity by
requiring not only BMI calculations but also a system of indicating the degree to which excess adiposity negative affects a
patient’s health [13]. The focus should be on further assessment for objective findings to quantify and qualify obesity, to
determine if any comorbid conditions or secondary contributors to obesity exist, and to direct specific screening or diagnostic testing for obesity related health conditions.
Patients who are obese may experience a great amount of
trepidation when seeking medical care as many offices do not

Chapter 10. Obesity
215
have the appropriate instruments readily available for an
accurate and comfortable examination [14]. Always use suitable instruments for a patient’s body habitus especially when
measuring weight and blood pressure. Often examination
gowns/drapes and tables may be too small. These factors may
limit the comfort of the patient and also the usefulness and
even safety of proceeding with the exam.
Calculate BMI based on an accurate height and weight.
Measurement of waist circumference provides additional
information regarding predisposition to metabolic disease
among individuals with BMI <35kg/m2 [10, 13]. Percentage of
body fat may be more useful in patients at the extremes in
muscle mass and may be a more accurate measure of body
composition. Assess blood pressure using an appropriately
sized cuff. Examine the skin for signs suggestive of glucose
intolerance such as acanthosis nigricans. Conduct a thorough
cardiorespiratory, abdominal, and musculoskeletal exam and
observe for signs of obesity-related complications (Table10.1).
The measurement of neck circumference may be useful as
part of calculating the STOP-BANG score as a screening tool
for sleep apnea [15]. Please see Chap. 15 for more
information.
Diagnostic and screening laboratory values such as lipid
panel, hemoglobin A1c, thyroid-stimulating hormone level,
liver function tests, and an EKG should be completed in
addition to any other appropriate evaluations for associated
conditions (listed below) based on history and exam findings
[10, 13].
T . Weight
classications
based on BMI
Body mass index
Weight
Normal 18.5–24.9
Overweight 25.0–29.9
Class 1 obesity 30.0–34.9
Class 2 obesity 35.0–39.9
Class 3 obesity ≥40
(BMI) (kg/m2)

216
BMI – Body mass index in kg/m
J. S. Ruddock and G. Goswami
*prediabetes *metabolic syndrome *type 2 diabetes *dyslipid-
emia *hypertension *cardiovascular disease *nonalcoholic fatty
liver disease *polycystic ovarian syndrome *female infertility
*depression *male hypogonadism *obstructive sleep apnea
*asthma *osteoarthritis *urinary stress incontinence *gastro-
esophageal reflux disease
Who Should Lose Weight?
Results of diagnostic and laboratory testing can be one of the
key factors in determining which patients need to lose weight.
Weight loss is recommended for individuals with a BMI
≥30kg/m2 or BMI 25–29.5kg/m2 with adiposity-related com-
plications (see Fig.10.1). The Edmonton obesity staging system may offer clinical guidance in assessing obesity-related
risk and prioritizing treatment (see Table10.2) [16, 17].
1. Measure height, weight and BMI
2. Measure waist circumference for
patients with BMI 25 to <35 kg/m
3. Thorough history and physical exam
4. Laboratory evaluation
2
PHARMACOTHERAPY
BMI > 30 kg/m2 or
BMI > 27 kg/m2 + Obesity
related complications
Recommendations for waist circumference cut-offs values may vary based on ethnicity
Men > 40 in/102 cm, Women > 35 in/88 cm
F . Evaluation of a patient with increased weight
Stratify BMI Category
25 – 29.9 – overweight
30 – 34.9 – Class I Obesity
35 – 34.9 – Class II Obesity
> 40 – Class III Obesity
TREATMENT OPTIONS
COMPREHENSIVE
LIFESTYLE
INTERVENTION
2
BARIATRIC SURGERY
BMI > 40 kg/m
BMI > 35 kg/m2 + Obesity
related complications
2
or

STAGE
0 1 2 3 4
Chapter 10. Obesity
T . Edmonton staging system [16]
217
Clinical
Complications
None Mild Moderate Significant Severe or End-Stage
Treatment
Management ofObesity
Obesity is a complex chronic disease that results from the
interaction of genetic, environmental, and behavioral determinants. Adipose tissue becomes a dysfunctional endocrine organ
leading to systemic metabolic disease [13]. Therefore, the cornerstone of management of obesity lies on the importance of
weight loss which has shown to reduce morbidity (e.g., reduction in the rate of progression to type 2 diabetes, decrease in
blood pressure, and plasma lipid levels) and mortality.
Most guidelines have incorporated a “complications centric approach” for management of obesity rather than a preset decline in body weight. The therapeutic endpoint is
improvement of obesity-related complications leading to
improved patient health and quality of life [18, 19].
Initial treatment includes lifestyle therapy which is the
cornerstone of all weight-loss interventions (see Fig.10.1).
An evidence-based comprehensive lifestyle therapy for treatment of obesity includes three components provided by a
trained interventionist (e.g., exercise specialists, registered
dieticians, psychologists, health counselors). The evidence
supporting the efficacy of lifestyle intervention or behavioral
modification is supported by data from two large randomized
clinical trials which have shown that even modest weight loss
of 5–10% has a significant impact on the metabolic disturbances associated with obesity [20, 21]. The three main components are as follows:
• Reduced calorie diet
• Physical activity
• Behavior modification to facilitate adherence to diet and
activity

218
J. S. Ruddock and G. Goswami
Diet
To achieve weight loss, an energy deficit is required; therefore
current guidelines recommend reducing total energy (caloric)
intake (500–750 kcal daily deficit), and this should be the main
component of any weight-loss intervention [13]. The meal plan
should be individualized based on personal and cultural preferences. Various types of diets such as Mediterranean, DASH, lowcarb, low-fat, volumetric, high- moderate- protein, vegetarian,
macronutrient-targeted, and the AHA-style Step 1 diet have
been studied. Several randomized clinical trials have shown similar weight loss on diets with different macronutrient composition
[22–25]. Diet effectiveness is more related to adherence to the
diet than the diet composition. A very-low-calorie diet (≤800kcal)
is an option in select patients using meal replacement options
and requires medical supervision [13]. There is evidence that
individuals who consumed more calories in the morning than in
the evening lost more weight [26, 27], while food intake at night
is linked to obesity independent of energy intake [28].
Due to the limited weight loss from continuous energy
restriction (CER), there have been recent interest in newer
weight loss strategies that involve restricting energy intake to
certain periods of the day or prolonging the fasting interval
between meals. These strategies include intermittent fasting
(IMF; >60% energy restriction on 2–3days per week or on
alternate days) and time-restricted feeding (TRF; limiting the
daily period of food intake to 8–10h or less on most days of
the week). Current evidence suggests that these newer strategies produce comparable weight loss to CER [29].
With dietary intervention in overweight and obese adults,
average weight loss is maximal in 6 months, with smaller
losses maintained for up to 2years during tapering of treatment and follow-up [30].
Physical Activity
The typical prescription included in a lifestyle intervention is
as follows [13]:
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