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BEATING OBESITY BY DEMONSTRATING MEDICAL
INFORMATION MASTERY AND POEMs
FAMILY MEDICINE
ASSIGNEMENT 1a BY SCOTT D. NEFF,
DC DABCO MPS-BT CFE DABFE FABFE FAABT FFABS FFAAJTS
OBESITY
Disease Diagnosis:
The
year 2000 was the first in recorded history in which the percentage of
people worldwide who are obese exceeded the percentage of people who are
starving or malnourished. Americans are getting heavier just as the
rest of the world. Although obesity is common in all races, ages, and
both genders, African-American women are heavier than white or
Mexican-American women, Mexican-American men are heavier than white men,
and white men are heavier than African-American men. Men, as a group,
are more overweight than women in every age group but two, the 55-64 and
65-70 year old age groups. Women however, still tend to be more obese
than men on average.
The
average weight gain for the most Americans is about 5 pounds per year
starting in the third or fourth decade of life, which amounts to about
50 extra kilocalories/day per year over the energy requirement. This
gain usually occurs during the winter and holiday season and is not
reversed during the warmer months. Thus, it means that for the
individual to lose the weight, they would have to increase their energy
output by an average of 50 kcal/day (This is the amount expended
by a 150 pound person walking 2 mph for 15 minutes/ day.).
Weight
related disease or overweight and obesity are known risk factors for
Diabetes, heart disease, stroke, hypertension, gallbladder disease,
osteoarthritis, sleep apnea and uterine, breast, colorectal, kidney, and
gallbladder cancers. Obesity is associated with High blood cholesterol,
complications of pregnancy, menstrual irregularities, hirsutism, stress
incontinence, depression and increased surgical risk.
Obese
patients require a compete physical examination to rule out signs of
secondary causes of obesity, such as Cushing’s syndrome, hypothyroidism,
or other pituitary abnormalities. Obesity is a state of excess adipose
tissue mass. Although not a direct measure of adiposity, the most
widely used method to gauge obesity is the body mass index (BMI), which
is equal to weight/height2 in (kg/m2 ). Other
approaches to quantifying obesity include anthropometry (skin-fold
thickness), densitometry (underwater weighing), computed tomography (CT)
or magnetic resonance imaging (MRI), and electrical impedance.
Measurement of the waste circumference is also important. This
measurement is made at the narrowest point between the rib cage and the
umbilicus. The waist circumference is an indirect measure of abdominal
fat. High risk levels are a waist circumference of
>102 cm (40 inches)
for men with other risk factors, and >88 cm (35 inches) for women with
other risk factors. These waist measurements are less predictive
for
risk in patients with a BMI ≥35 kg/m2.
Using
data from the Metropolitan Life Tables, BMIs for the midpoint of all
heights and frames among both men and women range form 19-26 kg/m2.
Based on unequivocal data of substantial morbidity, a BMI of 30 is most
commonly used as a threshold for obesity in both men and women. Large
scale epidemiological studies suggest that all cause, metabolic, cancer,
and cardiovascular morbidity begin to rise when BMIs are ≥ 25,
suggesting that the cut-off for obesity should be lowered. Some
authorities use the term overweight (rather than obesity) to describe
individuals with BMIs between 25 and 30. A BMI between 25-30 should be
viewed as medically significant and worthy of therapeutic intervention,
especially in the presence of risk actors, that are influenced by
adiposity, such as hypertension and glucose intolerance.
Underweight < BMI=18.5, Normal 18.5-24.9, Overweight 25.0-29.9 with an
increased risk for disease, Obesity 30.0-34.9 which is considered a
Class 1 Obesity and a high to very high risk for disease, 35.5-39.9
Class 2 Obesity with very high risk for disease across categories, and
≥40 for extreme obesity also known as a Class 3 Obesity with an
extremely high risk for diseases for both men and women.
Finally
since Obesity is a known risk factor for cardiovascular disease and
diabetes mellitus, patients should undergo serum testing for
hyperlipidemia and hyperglycemia.
It must
be noted that distribution of adipose tissue in different anatomic
depots has substantial implications for morbidity. Intraabdominal and
abdominal subcutaneous fat have more significance than subcutaneous fat
present in the buttocks and lower extremities. Many of the most
important complications of obesity, such as insulin resistance,
diabetes, hypertension, hyperlipidemia (Often
hypertension is concomitant and interlinked with hyperlipidemia), and hyperandrogenism in
women, are linked more strongly to Intraabdominal and/or upper body fat
than to overall adiposity. It is thought that Intraabdominal adipocytes
are more lipolytically active than those from other depots. Release of
free fatty acids into the portal circulation has adverse metabolic
actions, especially on the liver.
Initial Evaluation:
The
initial evaluation must include evaluation of potential obesity related
diseases noted within the history, physical examination, and laboratory
tests. Always obtain a weight history, eating and activity behaviors.
Search for triggering factors, including medications (many medications
can cause obesity!), measure weight, height, and calculate body mass
index. Please categorize obesity classifications and the patient’s
health risk. Determine the patient’s readiness to lose weight. Always
spend time discussing patient goals and expectations setting achievable
goals. The initial office visit should determine the aggressiveness and
scope of therapy by evaluating the severity of obesity, the presence of
concurrent co morbidities, and risk of future obesity-related medical
complications
As noted above, certain medications can cause weight gain and increase
body fat, thereby making weight loss more difficult. These drugs differ
in their propensity to increase body weight; some medications, such as
the anticonvulsant valproic acid, can cause considerable weight gain of
15–20 kg, whereas other medications, such as the ß-adrenergic receptor
blocker propranolol, are associated with small and probably clinically
insignificant weight gain. The mechanism responsible for
medication-induced weight gain has not been carefully studied for most
of these agents, but must be related to an increase in energy intake
(e.g. antipsychotics and steroid hormones), a decrease in energy
expenditure (e.g. ß-adrenergic receptor blockers), a decrease in energy
loss (e.g. decreased glucosuria from diabetes therapy), or a combination
of these factors. Weight loss therapy can be facilitated by decreasing
the dose or substituting the medication with another drug that has less
weight gain potential, if possible.
I n
summary, medications that can cause weight gain are Psychotropic
medications such as Tricyclic antidepressants, Monoamine oxidase
inhibitors, Specific SSRIs, Atypical antipsychotics, Lithium, Specific
anticonvulsants, ß-adrenergic receptor blockers, Diabetes medications
such as Insulin, Sulfonylureas, Thiazolidinediones, Highly active
antiretroviral therapy, Tamoxifen, and Steroid hormones such as
Glucocorticoids and Progestational steroids.
1.
Pijl H, Meinders AE. Bodyweight changes as
an adverse effect of drug treatment. Drug Safety 1996;14:329-342.
Treatment:
Patient motivation, commitment, and compliance are critical for weight
loss success. Therefore, knowledge of the patient’s readiness to lose
weight will help in developing an appropriate treatment strategy. Good
candidates for treatment are patients who decide they want to lose
weight for appropriate reasons, are not currently experiencing major
life stressors, do not have psychiatric or medical illnesses that
prevent effective weight loss, and are willing to devote the time needed
to make
lifestyle changes.
In addition, the patient’s work, social, and
family environment should be considered in deciding if it is a good time
to implement weight loss therapy. If the
patient is considered to be ready to lose weight, weight loss therapy
should be initiated. If the patient is not ready to lose weight, the
immediate goal is to prevent further weight gain and explore barriers to
weight reduction. For example the patient should be able to devote
15-30 min/day to weight control for a 26 consecutive week period.
The cornerstone of obesity treatment involves consuming fewer calories
that are expended to mobilize and oxidize endogenous triglycerides as
fuel. Approximately 75%–85% of weight that is lost by dieting is
composed of fat, and 15%–25% is fat-free mass. Most, if not all, of the
loss of fat is due to a decrease in adipocyte triglyceride content. It
is also possible that long-term weight loss can decrease the number of
fat cells by stimulating apoptosis (programmed cell death) or
morphologic reversion of mature adipocytes to preadipocytes. However,
these possibilities have not been evaluated in obese subjects. Later in
this section, an overview of the key therapeutic principles involved in
obesity management is presented.
Weight loss is associated with an increased risk of gallstones because
weight loss increases bile cholesterol super saturation, enhances
cholesterol crystal nucleation, and decreases gallbladder contractility.
The incidence of new gallstones is approximately 25%–35% in obese
patients who experience rapid weight loss after treatment with a
very-low-calorie, low-fat diet (<600 kcal/d; 1–3 g fat/d) or gastric
surgery. The risk of gallstone formation increased markedly when the
rate of weight loss exceeded 1.5 kg (~1.5% of body weight) per week.
Ursodeoxycholic acid therapy can prevent gallstone formation during
rapid weight loss. In a randomized controlled trial of 1004 patients
enrolled in a 16-week, 520 kcal/d weight loss program, ursodeoxycholic
acid caused a decrease in gallstone formation from 28% in those
receiving placebo to 3% in those receiving 600 mg/d of drug. In 233
patients who had gastric bypass surgery; 600 mg/d of ursodeoxycholic
acid decreased the incidence of new gallstones from 32% to 2%. This
data indicates that 600 mg/d ursodeoxycholic acid is the optimal dose for
effective prophylaxis of gallstone formation during rapid weight loss.
1.
Shiffman ML, Kaplan GD,
Brinkman-Kaplan V, Vickers FF.
Prophylaxis against gallstone formation with ursodeoxycholic acid in
patients participating in a very-low-calorie diet program. Ann Intern
Med 1995;122:899-905.
2.
Sugerman HJ, Brewer WH, Shiffman ML, et al.
A multicenter, placebo-controlled, randomized, double-blind, prospective
trial of prophylactic ursodiol for the prevention of gallstone formation
following gastric-bypass-induced rapid weight loss. Am J Surg
1995;169:91-96.
T he clinical
management of obesity involves identifying patients who need treatment,
developing a realistic treatment plan, and implementing a structured
treatment strategy that includes long-term surveillance and the ability
to modify therapy based on the clinical response and chronic
evaluation. It can be a life commitment to “live” for some patients.
Since the factors for weight gain can be age related concomitant with
factors discussed, those who can incorporate simple weight consciousness
to their daily lives, in time perhaps they could re-teach their children
for healthy lifestyle absent obesity based on unconsciously
bad life
habits, and thus will regain weight control
based on unconsciously good life habits.
Additional support
(such as enlistment of a family member, enrollment in a community weight
loss program, referral for behavioral therapy, or referral to a
dietician) and frequently scheduled follow-up visits should be arranged.
Diet:
D ietary fat is
composed primarily of triglycerides, which increase food palatability
and energy-density. Therefore, low-fat diets often are prescribed for
obese patients because these diets facilitate energy restriction.
The key to weight
loss is burning more calories than you consume.
It is known that a
diet with a deficit of 500-1,000 kcal/day will achieve weight loss of
1-2 lb/week. Why?
if you cut 500 calories from your
typical diet each day, you'd lose about 1 pound a week (500 calories
x 7 days = 3,500 calories). If you need to
calculate this 3,500
calories equals about 1 pound (0.5 kilogram) of fat,
thus you need to burn 3,500 calories more than you take in to
lose 1 pound.
Sound Medical Nutritional
Therapy calls for
a low calorie diet and reduced fat
for achieving the goals of reducing body
mass, waist circumference, and overall weight loss.
The MNT diet calls for begining your day correctly.
Thus begin with a healthy breakfast and try to eat at least four
servings of vegetables, three servings of fruits daily, and stick to the
healthy oils (fats) such as vegetable oil, olive oils and nut butters.
Of course sugar is reduced and meat consumption is limited to a 3- once
portion which could thus fit into the palm of your hand.
Eating a diet of fruits, vegetables and whole grains or plant-based
foods help you to lose weight while keeping you healthy and strong.
Finally, try to eat fresh fish at least twice a week again the serving
portion should fit into the palm of an average persons hand.
Most
importantly check with your Doctor of Medicine before making dietary
changes. If you have any health risks or other diseases, this may
modify any quality diet plan you undertake. Even the DASH diet
must be reviewed first by your physician to make sure it will only help
you.
Exercise:
A
good MNT eating plan combined with exercise is key to aiding weight loss
and maintaining the weight you lose. Picture in your minds eye
that there are calories you can't cut with a good MNT program, but that
exercise can help to burn off those difficult calories as well as
strengthening your heart and blood vessels while reducing your blood
pressure. What has been proven scientifically through double blind
studies are that folks who were able to maintain their weight loss over
the long term, all exercised to some degree regularly (Try to spend
25-30 minutes/day at least four days a week). Examples are
aerobic exercise which may be brisk walking. Let's say you usually
take the elevator up to your office, use the steps up and down and when
shopping don't be afraid to park at the end of the lot. Walking,
walking, walking can be a very good supplement to your MNT plans.
Behavioral Therapy
B ehavior therapy is an integral part of the overall treatment regime.
Behavior therapy acts as an adjunct to diet in promoting weight loss and
weight maintenance, assessment of the patient’s motivation and readiness
to implement a plan.
Finally, after therapy or successful weight loss, maintenance programs
consisting of low calorie diets, physical activity, and behavior
therapy, should be continued indefinitely.
Medicinal Therapeutics
R elative to medicinal therapeutics, today there are only two medications
approved for long term care and four relative to short-term care. Of
course, Orlistat-Xenical, a non schedule long term medication was
approved in 1999. Sibtramine-Meridia, a schedule 4 medication approved
in 1997, is our other long term care medication. Short term approved
medications include Diethypropion-Tenuate (1973), a schedule 4 with
adverse affects preventing long term utility. Phentermine-Adipex,
lonamin, approved in 1973, is a schedule 4 medication.
Phendimetrazine-Bontril/Prelu-2, and Benzpelamine-Didrex, are schedule 3
drugs approved in 1961 and 1980 respectively, for short term use.
In conclusion, only sibutramine (Meridia) and orlistat (Xenical) have
been approved for long-term use. All the approved medications act as
anorexiants, with the exception of orlistat, which blocks the absorption
of dietary fat. Anorexiants increase satiation (level of fullness, which
regulates the amount of food consumed during a meal) or satiety (level
of fullness after a meal, which determines frequency of eating), or
both. Methamphetamine is also approved by the FDA for short-term use,
but it is a schedule II drug and should be avoided because of its abuse
potential. Three anorexiant medications have been removed from the
marketplace because of increased risks of either valvular heart disease
(fenfluramine and dexfenfluramine) or hemorrhagic stroke
(phenylpropanolamine) associated with their use.
1.
Khan MA, Herzog CA, St Peter JV, et al. The
prevalence of cardiac valvular insufficiency assessed by transthoracic
echocardiography in obese patients treated with appetite-suppressant
drugs. N Engl J Med 1998;339:713-718.
2.
Kernan WN, Viscoli CM, Brass LM, et al.
Phenylpropanolamine and the risk of hemorrhagic stroke. N Engl J Med
2000;343:1826-1832.
L ifestyle
modifications combined with Pharmacotherapy can be a useful adjunctive
measure for properly selected patients.
Surgery:
S urgery is
considered an option for patients with a BMI of ≥ 40 kg/m2 ,
or ≥ 35kg/m2 with cardiovascular risk factors.
Two procedures available are placing a restrictive band around the
stomach in order to reduce capacity or bypassing the stomach altogether.
If medical weight loss treatment has failed and are suffering from
complications of extreme obesity, surgical procedures are a
consideration. However, absent multidisciplinary care, with
attention to diet, activity, behavioral and social supports, surgical
weight loss procedures have limited permanent success due to the bowel and stomach
stretching to the former size and absorption of food often returns to
previous quantities.
Chronic Evaluation:
Obesity is on the rise around the world. It is increasing in every
group; that it is today’s reliance on others for most everything, an
absence of control of the little things in life, out of control
overeating energy requirements above expenditure needs, absent science
defined sound life habits. Thus, to correct this mechanism, it is now
clear that a commitment for subtle changes in behavior over time, and
for life, will make all the difference in the world for those whose
lives may be cut short through obesity.
Obesity is a chronic disease that requires long-term therapy for
successful long-term weight management. Often, patients who are able to
lose weight with obesity therapy regain their lost weight after therapy
is discontinued. In a recent study, 76 obese women (mean body mass
index 39.4 kg/m2) who were randomly assigned to one of three
treatment groups: 4 months of a very-low-calorie diet (VLCD) of 400–500
kcal/d, 6 months of behavior therapy and a 1000–1200 kcal/d balanced
deficit diet, or 6 months of a combination of a VLCD and behavior
therapy. Each treatment program was effective in achieving short-term
weight loss. However, most subjects regained a considerable amount of
weight by 1 year and had returned to their pretreatment weight at 5
years.
1.
Drent ML, van der Veen EA.
Lipase inhibition: A novel concept in the
treatment of obesity. Int J Obes Relat Metab Disord 1993;17:241-244.
Thus, it has become clear that maintenance therapy is important for
long-term weight management success after initial weight loss is
achieved by diet and behavior therapy. In another recent study, Perri
and colleagues randomized obese subjects who lost weight after 5 months
of diet and behavior modification therapy to “no maintenance” or a
“maintenance program” that involved biweekly contact. At 1 year after
initial weight loss was achieved, participants who received maintenance
therapy
maintained long-term weight loss,
whereas those who did not receive maintenance therapy regained half of
their lost weight.
1.
Perri MG, McAllister DA, Gange
JJ, et al. Effects of four
maintenance programs on the long-term management of obesity. J Consult
Clin Psychol 1988;56:529-534.
I n conclusion,
after the initial treatment plan duration return for Chronic Evaluation
has been proved by the evidence to help the patient maintain their
weight loss plan, whereas absent these procedures and protocol, most
patients regained weight to their detriment.
Medical Text
References:
- Sloane, Philip D et al, Essentials of Family Medicine, 4th
Edition, Lippincott-Williams & Wilkins, pages 783-801
- Andreoli Thomas E et al, Cecil Essentials of Medicine, 4th
Saunders, pages 434-437.
- Kasper Dennis L et al, Harrison’s Principles of Internal Medicine,
16th edition, Mc Graw Hill, pages 422-429
Medical Research
References:
1.
Ballor DL, Poehlman ET. Exercise-training
enhances fat-free mass preservation during diet-induced weight loss: a
meta-analytical finding. Int J Obes Relat Metab Disord 1994;18:35-40.
2.
Knittle JL, Ginsberg-Fellner F. Effect of
weight reduction on in vitro adipose tissue lipolysis and cellularity in
obese adolescents and adults. Diabetes 1972;21:754-761.
3.
Naslund I, Hallgren P, Sjostrom L. Fat cell
weight and number before and after gastric surgery for morbid obesity in
women. Int J Obes 1988;12:191-197.
4.
Hay DW, Carey MC. Pathophysiology and
pathogenesis of cholesterol gallstone formation. Semin Liver Dis
1990;10:159-170.
5.
Broomfield PH, Chopra R, Sheinbaum RC, et
al. Effects of ursodeoxycholic acid and aspirin on the formation of
lithogenic bile and gallstones during loss of weight. N Engl J Med
1988:319:1567-1572.
6.
Liddle RA, Goldstein RB, Saxton J. Gallstone
formation during weight-reduction dieting. Arch Intern Med
1989;149:1750-1753.
7.
Shiffman ML, Sugerman HJ, Kellum JM, et al.
Gallstone formation after rapid weight loss: a prospective study in
patients undergoing gastric bypass surgery for treatment of morbid
obesity. Am J Gastroenterol 1991;86:1000-1005.
8.
Weinsier RL, Wilson LJ, Lee J. Medically
safe rate of weight loss for the treatment of obesity: a guideline based
on risk of gallstone formation. Am J Med 1995;98:115-117.
9.
Shiffman ML, Kaplan GD,
Brinkman-Kaplan V, Vickers FF.
Prophylaxis against gallstone formation with ursodeoxycholic acid in
patients participating in a very-low-calorie diet program. Ann Intern
Med 1995;122:899-905.
10.
Sugerman HJ, Brewer WH, Shiffman ML, et al.
A multicenter, placebo-controlled, randomized, double-blind, prospective
trial of prophylactic ursodiol for the prevention of gallstone formation
following gastric-bypass-induced rapid weight loss. Am J Surg
1995;169:91-96.
11.
Wadden TA, Sternberg JA, Letizia
KA, et al. Treatment of obesity by
very low calorie diet, behavior therapy, and their combination: a
five-year perspective. Int J Obes 1989;13 (suppl 2):39-46.
12.
Perri MG, McAllister DA, Gange
JJ, et al. Effects of four
maintenance programs on the long-term management of obesity. J Consult
Clin Psychol 1988;56:529-534.
13.
Khan MA, Herzog CA, St Peter JV, et al. The
prevalence of cardiac valvular insufficiency assessed by transthoracic
echocardiography in obese patients treated with appetite-suppressant
drugs. N Engl J Med 1998;339:713-718.
14.
Kernan WN, Viscoli CM, Brass LM, et al.
Phenylpropanolamine and the risk of hemorrhagic stroke. N Engl J Med
2000;343:1826-1832.
15.
Drent ML, van der Veen EA.
Lipase inhibition: A novel concept in the
treatment of obesity. Int J Obes Relat Metab Disord 1993;17:241-244.
By Scott David Neff for Family Medicine
September 25, 2006
"The most acceptable service to God is doing
good to man" Ben
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