Obesity and Malnutrition Flashcards
OBESITY
● State of excess of adipose tissue mass ● Not just the fact that you are heavy ○ Excess fat cells add to your weight ■ Can cause additional problems inside your body ● Body mass index (BMI) ○ Most widely used method ○ BMI = weight/height2 (in kg/m2) ○ ≥30 kg/m2 defines obesity ○ 25.0 to 29.9 is termed overweight
ADIPOSOPATHY
Fat itself is causing an increase in morbidity and mortality by inducing other complications that cause the other condition
EPIDEMIOLOGY
● Obesity is very common nowadays because of the
increased production of food. There is an increased
availability of food that wasn’t available in the past.
● TODAY: Tendency to become more sedentary -
classes online, can eat and drink while listening, less
time to burn off fats
PREVALENCE
● Prevalence of medically significant obesity is increasing worldwide. ● Estimates of prevalence in U.S. adults >20 years of age ○ Overweight / Obese : 70% ○ Extreme obesity (BMI >40 25 kg/m2): 5.7% ● Sex ○ More common among women (38%) ■ Maybe because of genetics ■ May accumulate fat more easily ● Socioeconomic status ○ More common among poorer populations ○ In industrial societies, obesity is more common among poor women ■ Choices for food is limited ■ Forced to take in non-healthy food ● Age ○ Prevalence is increasing in children.
BODY WEIGHT
● Regulated by both endocrine and neural
components
● Easier to gain weight than to lose it
● A complex interplay that try to maintain weight
○ Alterations:
■ Weight loss: inc.appetite, decrease energy
expenditures
■ Overfeeding: decrease appetite, increase
energy expenditures
LEPTIN
● Major regulator
● Secreted by adipose cells
● Acts through brain circuits in the hypothalamus
● Influences appetite, energy expenditures and
neuroendocrine function
● Influences how we eat, how we burn what we eat
and how the body reacts
● Obesity = Increase in leptin
○ To increase metabolism and decrease appetite
● Fasted state = Decrease in leptin
APPETITE
● Neural afferents (vagal) - secondary to distention
↑ Ghrelin
appetite is statied, you lose your
appetite
↓ Glucose
your appetite is stimulated
Leptin, Insulin, Cortisol
stimulates appetite
Cultural factors
Other cultures want more plump women/men
Psychological factors
Bulimia, Anorexia - can control appetite
Neuropeptide Y, MCH, AgRP, Orexin,
Endocannabinoid
increases appetite
𝛂-MSH (melanocyte-stimulating hormone) -
induces satiety
Serotonin
decreases your appetite depending on
the various factors that stimulate it
Resting or basal metabolic rate
○ Energy being spent just by doing nothing
○ Accounts for 70% of daily energy expenditures
○ If you want to lose weight you should eat less
than your BMR
○ The bigger you are, the higher the BMR
because the body needs more calories to
function better
2. Energy cost of metabolizing and storing food
Thermic effect of exercise
5-10% - even if you exercise for half the day
Adaptive thermogenesis
○ Mostly seen among infants
○ Occurs in brown adipose tissues (BAT)
○ Expends stored energy as heat - they induce
heat formation
○ Leptin stimulates physiologic action of BA
○ Adults - less BAT, mostly white adipose tissue
(store fat for energy)
ADIPOSE TISSUE
● Lipid storing adipose cell ● Stromal/vascular component containing preadipocyte and macrophages ● Mass increases by lipid deposition and increase in adipocyte number
ADIPOCYTE
● Storage depot of fat ● Endocrine cell ● Leptin is stored in the adipocytes ○ ↑ adipocyte ↑ leptin ↓ appetite ○ ↓adipocyte ↓ leptin ↑ appetite
Factors released by adipocyte
Complement factors- Adipisin leptin, adiponectin, Resistin TNF-a, IL6 FFA, Glycerol Aromatase PAI-1, Angiotensinogen, RBP4
ETIOLOGY
● Obesity has a multifactorial etiology
○ Genetic influences
■ If your mother is on the plus size, your
tendency will still be on the plus size
■ Monozygotic twins - almost the same BMI
■ Dizygotic twins - it would depend on the
environment
○ Environmental Influences
○ Cultural factor
○ Diet
ENVIRONMENTAL INFLUENCES
● Availability and high caloric composition of the diet
● Sedentary lifestyle
● Sleep deprivation
● Recent increase in the prevalence of obesity
worldwide is largely due to lifestyle factors (changes
in diet, physical act)
● Physiologically, obesity results from an imbalance
between energy intake and energy expenditure.
○ Increased energy intake
○ Decreased energy expenditure
○ Combination of the 2 factors
● If there is a mutation in the leptin receptor
even if
you produce the leptin you will still feel that you are
starving because you don’t receive the signal from
the leptin, because the receptor is mutated.
POMC
stimulates the
feeling of satiety. If you have a mutation here then
again it’s very similar
TrkB
if there is a mutation, there is an increase of appetite. It doesn’t deliver satiety but it increases
appetite.
Prader-Willi syndrome
“FLK”- funny looking kid, you
dont look normal.
● Cohens- no medium size
DISEASES ASSOCIATED WITH OBESITY
● Cushing’s syndrome
● Hypothyroidism
● Insulinoma
○ Secondary to the feeling of hypoglycemia.
They tend to eat in order to relieve the feeling
of being hypoglycemic
● Craniopharyngioma and other disorders involving
the hypothalamus
GENETIC SYNDROMES ASSOCIATED WITH OBESITY
● Präder–Willi syndrome ● Laurence-Moon-Biedl syndrome ● Ahlström syndrome ● Cohen syndrome ● Carpenter syndrome ● Fragile X syndrome ● Wilson–Turner syndrome ● Albright’s hereditary osteodystrophy
Cohen & Carpenter
- least noticeable
Ahlstrom & Cohen
mental retardation is normal
PATHOLOGIC CONSEQUENCE OF OBESITY
● Insulin Resistance and T2DM ● Reproductive disorders ● Cardiovascular disease ● Pulmonary disease ● Hepatobiliary disease ● Cancer ● Bone, joint and cutaneous disease
METABOLIC MANIFESTATIONS OF ADIPOSOPATHY
● High blood glucose (prediabetes mellitus, type 2
diabetes mellitus)
● High blood pressure
● Metabolic syndrome
● Adiposopathic dyslipidema
● Insulin resistance
● Hepatosteatosis (fatty liver)
● Hyperuricemia and gout
● Cholelithiasis
● Acanthosis Nigricans
● Nephrolithiasis
● Glomerulopathy
● Pro-thrombotic predisposition
● Neuropsychiatric diseases (such as worsening
depression or loss of gray matter due to
adiposopathic immune and endocrine responses)
● Asthma (due to adiposopathic immune and endocrine responses)
● Worsening of other inflammatory diseases (osteoarthritis, atherosclerosis, etc.)
WOMEN
● Hyperandrogenemia ● Hirsutism ● Acne ● Polycystic ovarian syndrome ● Menstrual disorders ● Infertility ● Gestational diabetes mellitus ● Preeclampsia ● Thrombosis
MEN
● Hypoandrogenemia ● Hyperestrogenemia ● Erectile dysfunction ● Low sperm count ● Infertility
GENITOURINARY
● Urinary stress incontinence
● Pelvic prolapse (e.g. cystocele, rectocele, uterine
prolapse, vault prolapse)
REPRODUCTIVE PRE PREGNANCY Men
● Buried or hidden penis
● Erectile dysfunction
● Psychological barriers to sexual behavior
● Infertility
Women Reproductive pre pregnancy
● Psychological barriers to sexual behavior
● Infertility, anovulation, polycystic ovary syndrome
REPRODUCTIVE PREGNANCY
● Gestational diabetes mellitus
● Preeclampsia
● Increased risk of miscarriage and stillbirth
● Overdue pregnancy
○ Increased need for induction
○ Increased need and complications of cesarean
section in women (delayed healing and wound
infection)
● Large for gestational age offspring
● Thrombosis
● Obstructive sleep apnea
OBESITY AND ADIPOSOPATHY INCREASES THE
RISK OF CANCERS
● Bladder cancer
● Brain cancer
● Breast cancer (postmenopausal)
● Cervical cancer
● Colon cancer
● Endometrial/uterine cancer
● Esophageal cancer
● Gallbladder cancer
● Head and neck cancer
● Kidney/renal cancer
● Leukemia
● Liver cancer
● Multiple myeloma
● Non-Hodgkin lymphoma
● Ovarian cancer
● Pancreatic cancer
● Prostate cancer (prognosis is worse,
not necessarily increased risk)
● Stomach cancer
● Thyroid cancerHISTORY
● Age, gender, race, ethnicity
● Fat mass disease (i.e., osteoarthritis, sleep apnea)
● Adiposopathy (i.e., type 2 diabetes mellitus, high
blood pressure)
● Eating disorders
● Mental stress
● Sleep pattern
● Other medical and surgical conditions
● Medication and food allergies
● Medications that may affect body weight
○ CNS medications can induce the development of obesity
● Cigarette smoking
● Alcohol intake
● Recreational drug use (e.g., marijuana, cocaine)
FAMILY HISTORY
● Family members affected by obesity
● Applicable familial medical diseases
SUPPORT SYSTEMS
● Person who selects and purchases food
● Availability and involvement of family and friends
● Educational access to healthy nutrition and physical
activity (e.g., current knowledge base, availability of Internet, knowledge centers, etc.)
SOCIOECONOMIC AND CULTURAL HISTORY
● Economic status ● Social status ● Cultural background ● Occupation ● Family structure ● Parenting behavior ● Marital status ● Living situation ● Abuse (physical, mental, sexual) ● Geographic location (e.g., urban food desert)
EXAMINATION OF WEIGHT PATTERN OVER
PATIENT’S LIFETIME
Is it a progressive type or a yoyo type (gain-losegain-lose)hh
VITAL SIGNS
● Height with bare or stocking feet measured with a
stadiometer
● Weight using calibrated scale and method consistent
from visit to visit (i.e., light indoor clothing or gown)
● Body mass index
● Waist circumference
○ Standing using superior iliac crest
● Blood pressure using appropriately sized cuff
● Pulse
● Neck circumference
GENERAL PHYSICAL EXAM
● Comprehensive physical exam
● Special emphasis on physical exam of the nose, throat, neck, lung, heart, abdomen
ASSESSMENTS
● A good measure (especially if you really want to get
overall fat of the body) is to get the percentage of
body fat.
● The problem with this is it needs a lot of instrumentation like DEXA scan which is a low dose radiation similar to xray where you measure overall fat percentage in the body
● Can also via electrical impedance, whole body air displacement
● For the waist circumference, it can be measured around the abdomen at the level of the anterior superior iliac crest parallel to the floor. Tape should be snug against skin without compressing.
● Based on this by correlation, you get your edmonton obesity staging system. (See stages in the table)
● Stage 2: presence of established obesity-related chronic disease (like Htn, DM), moderate psychopathology (depression), moderate functional
limitation (you can not move about)
● Stage 3: established end-organ damage (like CKD, MI, CAD)
● Stage 4: Severe one, possibly the end stage, it is the disability to everything like your cardiovascular, endocrine, etc.
BODY MASS INDEX (BMI) Advantage
● Increased BMI generally correlates with metabolic
and fat mass diseases in population studies
● Commonly used
● Reasonably reproducible
● Low cost
● Adequate measure for epidemiological studies
● Adequate screening metric for most patients
Disadvantage of BMI
● May not correlate with metabolic and fat mass
diseases in an individual patient
● Does not account for muscle mass
● May over-diagnose obesity in muscular individuals,
under-diagnose patients with sarcopenia
● BMI cut-off points do not distinguish between men
and women, nor ethnic and racial consideration
● Should be used as part of the clinical evaluation, and
not the sole measure of obesity for all patients
BMI: Increase Body Fat (Adiposity)
● BMI in kg/m2 ○ Normal weight: 18.5 - 24.9 ○ Overweight: 25.0 - 29.9 ○ Class I obesity: 30.0 - 34.9 ○ Class II obesity: 35 - 39.9 ○ Class III obesity: >40 ● Different BMI cut-off points may be more appropriate based upon gender, race, ethnicity and menopausal status
Percent Body Fat Advantages
○ More specific assessment of body fat
○ May be reasonable longitudinal measure,
especially in patients who may not be losing
weight, but engaged in resistance exercise
training, and thus may be losing body fat and
increasing muscle
Disadvantages of %body fat
○ Some measurement technique are not always accurate, nor easily reproducible (i.e., single site skinfold calipers) like skinfold calipers, some computation will require you to compute neck circumference, your waist, your wrist (gives you gross value of your body fat)
○ Electronic body fat measurements may be expensive, and as with calipers, the accuracy and reproducibility is dependent upon the equipment and software, as well as the expertise of the technician
○ Cut-off points not validated to correlate to metabolic disease
American Council on Exercise Classification
○ Essential fat: ■ Women: 10-13%; Men: 2-5% ○ Athletes ■ Women: 14-20%; Men: 6-13% ○ Fitness ■ Women: 25-31%; Men: 18-24% ○ Obesity ■ Women: >32%; Men:>25%
WAIST CIRCUMFERENCE Adv
● Well-correlated to metabolic disease (The bigger
waist circumference, greater propensity to develop
CVS disease)
● Direct anatomical measure of adipose tissue
deposition, with an increase in waist circumference
reflective of adipose tissue dysfunction
● Low cost (Just need tape measure)
WC disafv
● Measurement not always reproducible
● Waist circumference is not superior to BMI in
correlating to metabolic disease in patients with BMI
>35kg/m2 (to those extremely obese individuals)
● Racial/ethnic differences
ABDOMINAL OBESITYMEN
≥ 40 inches >40 inch: Increase risk in CVS complications (but this is American data, for Asian men it is usually 90 cm)
ABDOMINAL OBESITY -
WOMEN
≥ 35 inches
>35: Increase risk in CVS
(Asian women usually
more than 80 cm)
Population Assessment
Body mass index (BMI), waist circumference (WC),
and percent body fat (%BF) similarly correlate with
prevalence of metabolic syndrome
Individual Assessment
● BMI is a reasonable initial screening
measurement for most patients
● WC provides additional information regarding
adipose tissue function/dysfunction and
predisposition to metabolic disease among
individuals with BMI<35 kg/m2
● %BF may be more useful in patients with extremes
in muscle mass (i.e., individuals with sarcopenia or substantial increases in muscle mass), and thus may be a more accurate measure of body composition when assessing the efficacy of interventions directed
towards change in muscle mass
Cushing’s syndrome
● Central obesity, hypertension, and glucose
intolerance may be present in simple obesity, but
specific stigmata of Cushing’s syndrome are absent.
● Cortisol production and urinary metabolite levels
(17-hydroxysteroids) may be increased in simple
obesity.
● Overnight 1-mg dexamethasone suppression test is
normal in 90% of obese patients without Cushing’s
syndrome; standard 2-day low-dose
dexamethasone suppression test is normal in the
remaining 10%
Hypothyroidism
● Uncommon cause of obesity
● Excluded by measuring thyroid-stimulating hormone
● Weight gain in hypothyroidism is predominantly due
to myxedema.
Male hypogonadism
● May result in increased adiposity and decreased
lean tissue
● Excluded by history and laboratory investigation,
when appropriate
Growth hormone deficiency
● Results in an increased in body fat (especially
abdominal fat) and decrease in lean tissue
● Should only be suspected when accompanied by
other evidence of pituitary disease
Insulinoma
Weight gain results from overeating to prevent
hypoglycemia.
Craniopharyngioma and other disorders of
hypothalamic dysfunction
● Hypothalamic dysfunction of systems controlling
satiety, hunger, and energy expenditure (due to central nervous system tumors, trauma, or inflammatory disorders) can cause varying degrees of obesity.
● Uncommon to identify a discrete anatomic basis for these disorders.
DIAGNOSTIC APPROACH
● Calculate body mass index and measure waist circumference.
● Determine degree and rate of acquisition of obesity.
● Exclude identifiable causes of obesity.
● Assess comorbid conditions, presence of cardiovascular risk factors, and absolute risk Status.
● Conditions that indicate high absolute risk for
obesity-related disorders
○ Established coronary artery disease
○ Other atherosclerotic disease
○ Type 2 diabetes mellitus
○ Sleep apnea
● ≥3 of the following indicate high absolute risk for
obesity related disorders
○ Hypertension
○ Cigarette smoking
○ High low-density lipoprotein cholesterol
level (>160 mg/dL)
○ Low high-density lipoprotein cholesterol level (<35 mg/dL)
ADIPOSITY-RELEVANT BLOOD TESTING
● Fasting blood glucose
● Hemoglobin A1c
● Fasting lipid levels
○ Triglycerides
○ Low-density lipoprotein (LDL) cholesterol
○ High-density lipoprotein (HDL) cholesterol
○ Non-HDL cholesterol
● Liver enzymes and other liver blood tests
● Electrolytes (i.e., potassium, sodium, calcium,
phosphorus, etc.)
● Renal blood testing (i.e., creatinine, blood urea
nitrogen, etc.)
● Uric acid
● Thyroid stimulating hormone (TSH)
● Vitamin D levels
BOdy Compartment test
Calipers DEXA BOD POD Bioelectrical impedence Underwater CT Duterium dilution hydrometry
MEDICAL MANAGEMENT AND COORDINATION
- Nutrition
- Physical Activity
- Behavior Therapy
- Pharmacotherapy
- Bariatric Surger
Conditions that may promote fat mass gain:
Genetic Syndromes
● Isolated (i.e. Prader Willi) ● Familial (melanocortin 4 receptor deficiency) Medical Conditions ● Hypothalamic damage ● Immobility ● Insulinoma ● Some cases of untreated hypothyroidism ● Hypercortisolism (Cushing’s disease) ● Sleep disorders Psychological Behavioral Conditions ● Mental stress ● Depression ● Anxiety ● Post-traumatic stress syndrome ● Binge-eating disorder ● Night-eating syndrome ● Eating disorders not otherwise specified
The potency increases. the higher the risk. For
severely obesed individuals they might require a
more invasive/ a more riskier management in order
to get the maximum weight reduction.
● Lifestyle modifications- less risk, less cost
● Lifestyle modifications + Medication- middle type,
it’s potent.
Adiposopathy (Sick Fat Disease)
● Assist with weight maintenance
● Assist with weight loss
● Improve body composition
● Improve adiposopathic psychological disturbances
● Possibly improve adipocyte function (“train” fat
cells)
○ Improve insulin sensitivity
○ Increase mitochondrial biogenesis
○ Increase browning (“beiging”) of fat cells
Non-adipose Parameters
● Improve metabolic health ● Improve musculoskeletal health ● Improve cardiovascular health ● Improve pulmonary health ● Improve mental health (e.g., mood, happiness, sense of well-being) ● Improve sexual health
MEDICAL EVALUATION TO ENSURE SAFETY
BEFORE BEGINNING NEW EXERCISE PROGRAM
● Assess current physical activity level (Do they move
a lot?)
● Assess readiness (Are they motivated enough? I’m
not hehe. Are you?)
● Agree upon patient expectations and goals with
written “contract”
● Assess potential need for medical testing/evaluation
(i.e., cardiac stress testing, pulmonary function tests,
musculoskeletal assessment, etc.)
● Assess mobility, fitness, and potential equipment
needs or modifications
● Potential adjustment of medications
○ Before start of physical activity plan
○ During implementation of physical
activity plan
● Optimal default
○ Back-up plan
Unable to Walk
● Seated exercise program ● Arm exercises (i.e., arm cycling) ● Swimming/aquatic exercises (e.g., shallow or deep water exercises) ● Gravity-mediated physical activity ● Consider physical therapy evaluation ○ Recommend rehabilitation & physical therapy guided activity program ○ Set physical activity goals ○ Assess special equipment needs
Limited Mobility, Able to Walk
● Walking ● Swimming/aquatic exercises (e.g., shallow or deep water exercises) ● Gravity-mediated physical activity ● Assess for special equipment needs
No Substantial Limitations to Mobility
● Exercise/physical activity prescription plan driven
by patient and guided by clinician
● Assess for special equipment needs
Dynamic (Aerobic) Training
● Some physical activity is better than none
● At least 150 minutes (2.5 hours) per week of
moderate physical activity or at least 75 minutes
(1.25 hours) per week of vigorous intensity aerobic
exercise = most health benefits, promote modest
weight loss, and
prevent weight gain
● > 300 minutes (5 hours) per week of
moderate physical activity or 150 minutes (2.5
hours) per week of vigorous intensity aerobic
exercise = promote more robust weight loss and
prevent weight regain after weight loss
Resistive (Anaerobic) Strength Training
● Percent body fat better assessment of body
composition than BMI
● Utilize appropriate weight-lifting technique
● Emphasize “core” muscle exercises
● Using a variety of free weights, machines,
and resistance bands may elicit less boredom and
provide greater flexibility regarding scheduling and
location
● Short-term sore muscles may be expected
● Sore joints suggests poor technique, with possible
need for medical evaluation and
physical activity modification
● Prioritize muscle mass metrics (e.g.,
myotape measurements) versus amount of weight lifted
PRINCIPLES OF HEALTHY NUTRITION
Limit:
● Highly processed foods of minimal nutritional value:
sweets, “junk foods,” cakes, cookies, candy, pies,
chips
● Energy-dense beverages: sugar-sweetened
beverages, juice, cream
Encourage:
● Consumption of healthy proteins and fats,
vegetables, leafy greens, fruits, berries, nuts,
legumes, whole grains
● Complex carbohydrates over simple sugars: Low
glycemic index over high glycemic index foods
● High-fiber foods over low-fiber foods
● Reading labels rather than marketing claims
● Managing the quality of calories is important when
reducing the quantity of calories, such as during
weight loss
NUTRITIONAL THERAPY FOR OBESITY
- Evidence-based
- Quantitative
- Patient adherence
- Patient preference
- Qualitative
Choosing Nutritional Therapy for Obesity
The most appropriate nutritional therapy for weight loss
should be safe, effective, and one to which the patient can
adhere.
● Encourage foods that result in a negative caloric
balance to achieve and maintain a healthy weight
● Consider the following:
○ Individual food preferences, eating
behaviors, and meal patterns
○ Cultural background, traditions, and food
Availability
○ Time constraints and financial issues
○ Nutritional knowledge and cooking skills
● Nutritional approaches for weight loss typically focus on the caloric manipulation of the three macronutrients: carbohydrate, fat, or protein
● Very low-calorie diets contain less than 800 kcal/day and require close medical supervision for safety reasons
○ Like you are taking just enough to maintain you, not enough to feed you.
● Low calorie diets range from 1200-1800 kcal/day (1200-1500 for women, 1500-1800 for men)
● Restricting dietary fat leads to a greater reduction in total and LDL cholesterol, whereas restricting dietary carbohydrate leads to a greater reduction in
serum triglycerides and an increase in HDLcholesterol
● Reduction of carbohydrates can lead to a greater reduction in serum glucose and hemoglobin A1C.
Restricted Fat Diet:
● Low-fat diet: <30% fat calories
● Very low-fat diet: <10% calories
*Restricted CHO Diet:
● Low-glycemic diet
● Low-carbohydrate diet: 50-150 grams/day
● Very low carbohydrate diet: <50 grams/day (with or without nutritional ketosis)
LOW-CALORIE DIETS: RESTRICTEDCARBOHYDRATE DIET
● Low-carbohydrate diet defined as 50-150 grams of
carbohydrates per day.
● Very low-carbohydrate diet defined as <50 grams of
carbohydrates per day
Weight Loss
● May produce modestly greater weight loss
compared to fat-restricted dietary intake for the first
6 months, wherein afterwards, the net weight loss
may be similar to other calorie restricted nutritional
interventions
● May assist with reducing food cravings
Metabolic Effects
● Reduces fasting glucose, insulin and triglycerides
● Modestly increases high-density lipoprotein
cholesterol levels
● May increase low-density lipoprotein cholesterol
levels
● May modestly reduce blood pressure
● The metabolic effects noted above may occur with
or without weight loss
● In patients with epilepsy, a very low carbohydrate
ketogenic diet (VLCKD) may reduce seizures
● LCKD may possibly improve diabetes mellitus
complications (i.e., nephropathy)
Risk of low carbs
● May produce carbohydrate cravings within the first
few days of implementation, which may be mitigated
by adding low-glycemic-index carbohydrate foods.
● May induce gout flare if history of gout
● May present challenges in patients undergoing
dietary protein restriction (severe kidney disease)
LOW-CALORIE DIETS: RESTRICTED-FAT DIET
Defined as 10-30% of total calories from fat
Weight Loss low fat
After six months, fat-restrictive, low-calorie
nutritional intervention generally produces the same
amount of weight loss compared to the “low-carb
diet”
Metabolic Effects low fat
● May reduce fasting glucose and insulin levels
● Modestly decreases low-density and improves your
high-density lipoprotein cholesterol levels
● May modestly reduce blood pressure
Risks
● Hunger control may present challenges, which may
be mitigated with weight-management
pharmacotherapy
● If fat restriction results in a substantial increase in
carbohydrate consumption, and if weight loss is not
achieved, an increase in carbohydrate dietary intake
may potentially contribute to hyperglycemia,
hyperinsulinemia, hypertriglyceridemia, and reduced
levels of high density lipoprotein cholesterol
● Because of the low fat intake, you might eat more
carbohydrates, and it might be the one that’s going
to hamper you.
VERY LOW-CALORIE DIETS
Defined as less than 800 kcal/day, typically
implemented utilizing specifically formulated mealreplacement products supervised by a trained
clinician
