Practical Nutrition Tips for the Primary Care Physician
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Transcript Practical Nutrition Tips for the Primary Care Physician
Hot Topics in Nutrition for the
Primary Care Physician
Phillip Snider, RD, DO
Bon Secours Medical Associates
Virginia Beach, VA
Should Vitamins be
Considered Drugs?
Medline search of 4 online databases (Medline Plus, Drug Digest,
Natural Medicine Comprehensive Database, and the database of the
University of Maryland) 1966 through October 2009
Vitamins are used by over 1/3 of North Americans
Vitamins have documented adverse effects and toxicities, and most
have documented interactions with drugs
Some vitamins (biotin, pantothenic acid, riboflavin, thiamine, vitamin
B12, vitamin K) have minor and reversible adverse effects
Others, such as fat-soluble vitamins (A, E, D), can cause serious
adverse events
Two water-soluble vitamins, folic acid and niacin, can also have
significant toxicities and adverse events
Should Vitamins be
Considered Drugs?
Vitamins A, E, D, folic acid, and niacin should be
categorized as over-the-counter medications
Labeling of vitamins, should include information on
possible toxicities, dosing, recommended upper intake
limits, and concurrent use with other products
Vitamin A should be excluded from multivitamin
supplements and food fortificants
The Annals of Pharmacotherapy: Vol. 44, No. 2, pp. 311-324
Folic Acid
Aka B9, Folacin or folate (natural form)
– Name derived “folium” - Latin for leaf
– Beans, peas, spinach, broccoli
Functions
– Synthesize, repair and methylate DNA
Deficiency
– Neural tube defects
– Pernicious anemia
– Accumulation of homocysteine
– Theoretical increased risk of cancer
Folate Metabolism
Intestinal Cells
Folate reduced to tetrahydrofolate
– Folate reductase
inhibited by methotrexate
Methylated to N5-methyl-THF
–
primary blood form
`
Risk Factors Associated with Low Folate
Genetic polymorphism MTHFR
C677T
– 7 out of 10 depressed patients
– 56% - C/T polymorphism
4 X more likely to have
depression than general
population
14% - T/T polymorphism
Lifestyle
– ETOH
– Smoking
– Poor nutrition
Alpert M, et al. Jrnl Clin Psychopharmacology. 2003;23(3):309-13.
Fava M, et al. Am J Psychiatry. 1997;154(3):426-28.
Popakostas G, et al. Psychiatry Research, 2005;140(3):301-7.
Bottigleri T. Prog Neuro-Psychopharmacology & Biol Psychiatry. 2005; 29:1103-12.
Medications
– anticonvulsants
– oral contraceptives
– lithium
– fenofibrates, niacin
– sulphasalazine
– methotrexate
– metformin
Illness
– diabetes
– atrophic gastritis
– crohn’s disease
– hypothyroid
– renal failure
Arinami T, et al. Am J Genetics. 1997;74:526-28.
Procopciuc L.M., Poster Pres. P86 presented at Biol Psych. 2005.
Bjelland I. et al. Arch Gen Psychiatry. 2003;60(6):618-26.
Kelly B J, et al. Psychopharmacol. 2004 ;18(4):567-71.
Deplin as a Trimonoamine Modulator
Stahl S.M. Novel Therapeutics for Depression: L-methylfolate as a Trimonoamine Modulator and Antidepressant Augmenting Agent. CNS Spectrums. 2007;12(10):739-744.
Bioavailability
L-methylfolate
Vs.
Folic Acid
DHF Reductase
Enzyme
Dihydrofolate
(Dietary Folate)
Tetrahydrofolate
5, 10 Methylene THF
MTHFR C>T
Polymorphism
L-methylfolate
L-methylfolate
• Folic acid requires a 4 step transformation process to be converted to the active form of
folate, L-methylfolate (5-MTHF).
• L-methylfolate is unaffected by the MTHFR CT polymorphism.
Folic Acid (FA) Benefits
Nurse’s Health Study (JAMA 1998)
–
–
–
–
–
80,000 nurses, 14 yr follow-up
Relative Risk - highest vs lowest quintile
RR = 0.69 for folate
RR = 0.67 for B-6
RR = 0.55 for folate + B-6
FA supplementation – vast majority of recent studies
– Lowers homocysteine but this has not turned out to offer any
clinical benefits
Folic Acid (FA) Benefits
Depression
– Deplin (L-methylfolatye)
Stroke
– Limited evidence shows moderate benefit
Cancer
– Complex relationship
– High folate intake may protect against early
carcinogenesis
– High FA intake may promote advanced carcinogenesis
– Dietary folate usually associated with lower risk
– FA supplementation associated with higher risk
FA and Cancer
A Finnish study
– 29,133 older male smokers
– Prostate CA risk - no relationship with serum folate
levels
Recent RCT
– FA 1 mg/day
Prostate CA increased
– Dietary folate & plasma levels increased
Prostate CA decreased
FA and Cancer
Doubles the risk of prostate cancer
2006 prospective study
– 81,922 Swedish adults
– High dietary folate
Associated with a reduced risk of pancreatic cancer
FA and Cancer
2007 RCT
– Folic acid supplements
Did not reduce the risk of colorectal adenomas
Did significantly increase the presence of advanced
adenomas by 67%
A Randomized Trial on Folic Acid Supplementation and
Risk of Recurrent Colorectal Adenoma
FA 1 mg/d (n = 338) vs placebo (n = 334) for 3-6.5 yr
Primary endpoint: Any new diagnosis of adenoma during the
study period (May 1996-March 2004)
Secondary outcomes: Adenoma by site and stage and number
of recurrent adenomas
Low plasma FA = sig decrease (RR: 0.61; P = 0.01)
Adequate plasma FA = no diff (RR: 1.28; P = 0.27)
Am J Clin Nutr. 2009 Dec;90(6):1623-31.
Dietary Factors of One-carbon Metabolism & Prostate Cancer Risk
27,111 Finnish male smokers aged 50-69
End point = Diagnosis of prostate cancer between 1985 and 2002
Vit B6 intake inversely associated with prostate cancer risk (RR for
highest versus lowest quintile: 0.88; P = 0.045)
Vit B12 intake associated with sig incr risk (RR = 1.36; P = 0.01)
FA or alcohol intake no association with prostate cancer risk
FA or alcohol intake no association with risk according to stage of dz
Am J Clin Nutr. 2006 Oct;84(4):929-35
FA and Cancer
European Journal of Gastroenterology & Hepatology
University of Chile, in Santiago
Hospital-discharge data for two 4-year periods
– before folic-acid fortification (1992–1996)
– after (2001–2004)
Significant increase colon cancer
– 162% in people 45 to 64 years
– 190% in people 65 to 79 years
FA and Cancer
Aspirin/Folate Polyp Prevention Study
J Natl Cancer Inst. 2009;101:432-435
3-fold increase in prostate cancer among
men who took the folate supplement
compared with men who took placebo
AARP Diet and Health Study
Prospective study of 295,344 men 50 to 71
and free of cancer at enrollment in 1995
Multivitamin use assessed at baseline.
5% used multivitamins > 7 times a week
36% took a multivitamin daily
5 yr follow-up: 10,241 developed prostate cancer
– 8,765 localized and
– 1,476 advanced cancers
– 179 cases of fatal prostate cancer
AARP Diet and Health Study
No association: multivitamin use and risk of prostate
cancer overall (relative risk 1.06)
No association: multivitamin use and risk of localized
prostate cancer (RR 1.02)
Increased risk of advanced prostate cancer (RR 1.32)
Elevated risk of fatal prostate cancers (RR 1.98)
The associations were strongest in men with a
family history of prostate cancer or those who took
selenium, β-carotene, or zinc.
FA and Cancer
Increased breast cancer risk at high plasma folate
concentrations among women with the MTHFR 677T
allele
Nested case-control study included 313 cases (age 55–
73 y at baseline) with invasive breast cancer and 626
control subjects
Malmö Diet and Cancer – 17,000 women followed 10 yr,
10% had mutation in MTHFR 677T allele
Significant association of high plasma folate
concentration with increased risk of postmenopausal
breast cancer in carriers of the 677T allele
Vitamins & Cancer
Norwegian Vitamin Trial and Western Norway B Vitamin
Intervention Trial
6837 patients with ischemic heart disease
1998 and 2005, and followed up through December 31, 2007
FA 0.8 mg + B12 0.4 mg + Vitamin B6 40 mg (n = 1708)
FA 0.8 mg/d + B12 0.4 mg/d (n = 1703)
B6 alone 40 mg/d (n = 1705)
Placebo (n = 1721)
Vitamins & Cancer
FA + B12
– 10.0% Dx cancer vs 8.4%
– 4.0% Died-cancer vs 2.9%
– 16.1% Died-all cause vs 13.8%
HR 1.21; P = .02
HR 1.38; P = .01
HR 1.18; P = .01
Most common cancer was lung cancer
Cancer Incidence and Mortality after Treatment with Folic Acid and Vitamin B12
JAMA. 2009 Nov 18;302(19):2119-26.
Food Fortification
FDA started FA fortification in 1996
All flour in US fortified with FA at a level
of 140 μg/100 gr
Estimated to supply an extra 100 μg daily to
the average diet
Food Fortification
Study of 1480 subjects
– FA intake actually increased by 190 µg/d
– Total folate intake increased by 323 DFE/d
Folic acid intake above the UL seen only among
those taking FA supplements as well as folic acid
found in fortified grain products
Some researchers have advocated that this be
increased to double and even four times this
amount
Folic Acid
Women
Pregnant
Women
600 DFE
Men
RDA
400 DFE
UL
1,000 DFE 1,000 DFE 1,000 DFE
400 DFE
Synthetic form ~2x bioavailable
– 1 DFE
1 mcg folate
0.5 mcg folic acid (on empty stomach)
Folic acid fortification and public health:
Report on threshold doses above which
unmetabolized folic acid appear in serum
BMC Public Health 2007,
7:41doi:10.1186/1471-2458-7-41
Electronic version of this article
http://www.biomedcentral.com/14712458/7/41
Vitamins and Cancer: Take Home Message
Hickey and Roberts’ microevolutionary model
for cancer describes how cells undergoing
carcinogenesis respond to redox
(antioxidant/oxidant) signaling and changes in
redox state
It predicts that nutritional doses of antioxidant
supplements, required daily for maintenance
of normal health, inhibit carcinogenesis
Vitamins and Cancer: Take Home Message
Once a cancer is established, however, the model
suggests that nutritional or pharmacologic doses
of antioxidants may be contraindicated as they
could accelerate tumor growth
Large pharmacologic doses of nutrients, which
produce specific physiologic or biochemical
effects, are indicated for the treatment of cancer
or other diseases
Vitamins and Cancer: Take Home Message
In the oxidizing environment of a developing
tumor, nutritional doses of antioxidants could
lower oxidation levels and inhibit cancer cell
death
By contrast, pharmacologic doses of redoxactive substances that alter the antioxidant–
oxidant balance, such as vitamin C (acting as
a pro-oxidant), have been shown to destroy
cancer cells in vitro and in animal
experiments
Vitamins and Cancer: Take Home Message
People in good health should select only highquality, natural, antioxidant supplements, or
molecularly identical counterparts avoiding
synthetic forms such as DL-alpha-tocopherol
(synthetic vitamin E)
In metastatic cancer, only those supplements that
have been shown to provoke a differential redox
response in cancer cells, are appropriate
– Vitamin C, R-alpha-lipoic acid, and Vitamin K3
Interaction b/w FA and B12
FA can correct pernicious anemia from B12
deficiency
FA does not correct the neurological impact
– 3 carbon to 2 carbon conversion affected
– MMA accumulates
– Mixed neuropathy
FA over the UL (1 mg/day) can mask B12
deficiency
Obesity and Overweight
Establish diagnosis:BMI
BMI = weight / height2
Correlates well with direct measures of
adiposity
Overweight child: BMI >85th and <95th
percentile
Obese child: BMI > 95th percentile
If child < 3 years old, use weight for height
Medical Complications of Obesity
Pulmonary disease
abnormal function
obstructive sleep apnea
hypoventilation syndrome
Nonalcoholic fatty liver
disease
Idiopathic intracranial
hypertension
Stroke
Cataracts
steatosis
steatohepatitis
cirrhosis
Coronary heart disease
Diabetes
Dyslipidemia
Hypertension
Gall bladder disease
Severe pancreatitis
Gynecologic abnormalities
Cancer
abnormal menses
infertility
polycystic ovarian syndrome
breast, uterus, cervix
colon, esophagus, pancreas
kidney, prostate
Osteoarthritis
Skin
Gout
Phlebitis
venous stasis
Complications of Childhood Obesity
Relationship Between Weight Gain in
Adulthood and Risk of Type 2 Diabetes
6
Men
Relative Risk
5
Women
4
3
2
1
0
-10
-5
0
5
10
Weight Change (kg)
Willett et al. N Engl J Med 1999;341:427.
15
20
Diagnosing the Metabolic Syndrome
Risk Factor
Abdominal obesity
Men
Women
Defining Level
>40 in
>35 in
150 mg/dL
TG
HDL-C
Men
Women
Blood pressure
Fasting glucose
<40 mg/dL
<50 mg/dL
130/85 mm Hg
110 mg/dL
Diagnosis = 3
Defining Cardiometaboilc Risk
What is Abdominal Obesity ?
Can be defined by Waist Circumference
ATP- III IDF
Male:
> 42 Inch
Male :
> 37 Inch
Female :
> 35 Inch
Female :
> 31.5 Inch
Better Method ?
Waist < ½ Height
BMI Categories
A BMI of:
–
–
–
–
–
–
–
<18.5
18.5-24.9
25-29.9
30-34.9
35-39.9
40-49.9
50 and above
Classifies one as:
Underweight
Normal weight
Overweight
Obesity Class I
Obesity Class II
Obesity Class III
Super Obesity
Morbid Obesity
BMI > 35 plus >2 Comorbidities
– HTN, DM, Lipids, OSA, CAD, CVA, OA, SUI, GERD
BMI > 40
> 100 lb over Ideal weight
Morbid Obesity Examples:
BMI > 40
5’0” person > 204 lb
5’6” person > 247 lb
6’0” person > 294 lb
Morbid Obesity Examples:
BMI > 35
5’0” person > 170 lb
5’6” person > 216 lb
6’0” person > 258 lb
Obesity is a BIG problem…
1.7 billion worldwide
are overweight or
obese
The US has a higher
percentage of
overweight and obese
people than any
country in the world
And the numbers are
growing…
US Incidence of Obesity
2/3 is overweight
– 50% are obese
5% of the US population is morbidly obese
BMI subgroups growing the fastest
– 35+ 40+
Why Are We So Fat
&
What Can We Do About It?
Obesity Treatment Pyramid
Surgery
Pharmacotherapy
Lifestyle Modification
Diet
Physical Activity
Guide for Selecting Obesity Treatment
BMI Category (kg/m2)
Treatment
25-26.9
27-29.9
30-34.9
35-39.9
>40
Diet,
Exercise,
Behavior Tx
+
+
+
+
+
With comorbidities
+
+
+
With comorbidities
+
Pharmacotherapy
Surgery
The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. October
2000, NIH Pub. No.00-4084
“Hey Doc, I am fat
because my hormones are
out of whack. I know I
don’t eat too much. Can’t
you check out what’s
wrong with me and give
me a pill to fix it?”
Hormonal Causes of Obesity
Cushings
Syndrome
Most treatments for Diabetes Mellitus
NOT Hypothyroidism
Very few (less than 1%) of patients are
obese due to hormonal problems, but a
substantial number are obese in part due to
diabetes treatment or treatment with
glucocorticoids
Medications That Can Cause Weight Gain
– Insulin
Psychotropic medications
– Sulfonylureas
– Tricyclic antidepressants
– Thiazolidinediones
– Monoamine oxidase inhibitors
Highly active antiretroviral
therapy
– Lithium
Tamoxifen
– Specific anticonvulsants
Steroid hormones
– Specific SSRIs
– Atypical antipsychotics
Diabetes medications
Older -blockers
– Glucocorticoids
– Progestational steroids
“Yea, I know about balancing
food and activity, but I don’t
don’t eat that much.”
“I don’t eat more than other
people”
“I only eat salads.”
Discrepancy Between Reported and Actual
Energy Intake and Expenditure
3000
Energy Intake
Energy Expenditure
*
2500
Kcal/d
2000
1500
*
1000
500
0
Reported Actual
*P<0.05 vs reported.
Lichtman et al. N Engl J Med 1992;327:1893.
Reported Actual
“My problem is my
metabolism is
slow. Everything
I eat turns straight
to fat.”
Relationship Between Resting Energy
Expenditure and Fat-free Mass
REE (kcal/24 h)
3000
Lean females
Obese females
Lean males
Obese males
2000
1000
0
0
30
40
50
60
70
Fat-Free Mass (kg)
REE = Resting energy expenditure
Owen. Mayo Clin Proc 1988;63:503.
80
90
100
“Any time I try to lose weight, my metabolism
slows down so much that I can’t lose weight.”
Energy Metabolism Before & After Weight Loss
Energy Expenditure (kcal/d)
Mean BMI Reduced from 31 to 23 kg/m2
3500
3000
Resting Energy
Expenditure
Total Energy Expenditure
*
*
2500
2000
1500
*
*
After
Predicted
1000
500
0
Before
*P<0.05 vs before weight loss
Amatruda et al. J. Clin Invest 1993;92:1236.
Before
After
Predicted
“So obesity is all genetic.
There’s nothing I can
do.”
Gene-Environment Interaction in the
Pathogenesis of Obesity
Body Mass Index (kg/m2)
50
40
P <0.0001
Pima Indians
30
20
10
0
Maycoba, Mexico
Ravussin E et al. Diabetes Care 1994;17:1067-1074.
Arizona
Effect of Portion Size on Energy Intake
Amount Consumed (g)
500
400
300
200
100
0
500
625
750
1000
Amount of Macaroni and Cheese Served (g)
Rolls et al. Am J Clin Nutr. 2000 Dec;76(6):1207-13.
Prevalence of Obesity by Hours of Daily TV
NHES Youth Aged 12-17 in 1967-70 and NLSY
Youth Aged 10-15 in 1990
Prevalence
(%)
40
35
30
25
20
15
10
5
0
NHES 1967-70
NLSY 1990
0-1
1-2
2-3
3-4
4-5
TV Hours Per Day (Youth Report)
>5
“I don’t think I need to
change what I am
eating.
I am going to work out
and lose it that way.”
Physical Activity Alone Results in Minimal
Weight Loss
Control Group
Stefanick 1998
Exercise Group
Stefanick 1998a
*
*
Anderssen 1995
Hammer 1989
Verity 1989
Rönnemaa 1988
Wood 1988
*
-7.0
-5.0
Wood 1983
*
-3.0
-1.0
*P<0.05 vs control group Weight loss (kg)
Duration of each study ranged from 4 to 12 months.
Wing. Med Sci Sports Exerc 1999;31(suppl):S547.
1.0
Relationship Between Physical Activity
and Maintenance of Weight Loss
P<0.001
Subjects Exercising (%)
100
80
60
40
20
0
Not Maintained
Maintained
Weight Loss Pattern
Kayman et al. Am J Clin Nutr 1990;52:800.
“Isn’t there some popular
diet I can follow? One that
makes it easy.”
Popular Diets
Succeed short term because restriction
in food choice reduces calories
Fail long term because restriction of
food choices becomes unacceptable
Promote a cycle of euphoria and despair
that discourages belief in the possibility
of success
“Why can’t I just take a pill?”
Pharmacotherapy
Used as an adjunct to diet/exercise
Reserved for those with BMI>30 or those
with BMI>27 and Comorbidities
Drugs Approved by FDA for
Treating Obesity
Trade
Names
DEA
Schedule
Approved
Use
Year
Approved
Orlistat
Xenical
None
Long-term
1999
Sibutramine
Meridia
IV
Long-term
1997
Diethylpropion
Tenulate
IV
Short-term
1973
Phentermine
Adipex,
lonamin
IV
Short-term
1973
Phendimetrazine
Bontril,
Prelu-2
III
Short-term
1961
Benzphetamine
Didrex
III
Short-term
1960
Generic Name
Additive Effects of Behavior and Diet Therapy with
Pharmacotherapy for Obesity
0
Weight Change (%)
Medication alone
-5
Medication and behavior
modification
-10
*
-15
Medication, behavior
modification and meal
replacements
-20
*
-25
0
2
4
6
8
Time (months)
*P<0.05 vs medication alone.
Wadden et al. Arch Intern Med 2001;161:218.
10
12
“What about
surgery?”
Role of Surgery
Evidence
for long term
effectiveness
Is
approved by most payers
Requires
life long committment
What are The Operative
Results?
80% excess weight loss in 18 months
Roux-en-Y Gastric bypass the most widely
accepted and best results
Higher volume centers and surgeons have best
results. Still risk and complications
10 year weight loss maintenance best with surgery
Gastric Bypass
Lap Band
Who Qualifies for Surgery?
BMI greater than 40
BMI greater than 35 with obesity co-morbidity
Attendance in a plausible structured program for
some period of time, without sustained and
significant degree of weight loss
Not impaired psychiatrically?
BMI greater than 60?
Effect on Comorbid Conditions
Diabetes
–
–
Hyperlipidemia
–
70% - Improved
HTN
–
–
76.8% - Completely resolved
86.0% - Resolved or improved
61.7% - Resolved
85.7% - Resolved or improved
Obstructive Sleep Apnea
–
–
83.6% - Resolved
85.7% - Resolved or improved
Buchwald H, et al. Bariatric Surgery:
A Systematic Review and Metaanalysis. JAMA, 14:1724-37, 2004
Long-Term Changes: Weight
Regain
One study of 342 gastric bypass pts showed
excellent long-term weight maintenance:
–
% weight loss at:
1 year (89%)
2 years (87%)
5 years (70%)
10 years (75%)
However, potential for pouch stretch, selfsabotage, etc. leading to weight regain over time.
Surgery relatively new, will have to wait and
reanalyze data in a few years.
Malabsorption
Flintstones “Complete”
Women who still have menstrual periods
need iron. All women need calcium!
Common deficiencies: Iron, Folate, B12,
Calcium, Vitamin D
Long-term implications
Patient must commit to lifetime monitoring
of height, weight, and nutritional status
Women should not become pregnant up to
18 months after surgery
Encourage patient to join a support group
to celebrate and cope with weight loss
Other issues
Depression
– Many expect things to get better post-op
– Pre-existing depression exacerbated by
stress of surgery
– Suicides increased post operatively in
some series
– Ask about mood post-op
Too much weight loss too fast
– Look for signs of volume depletion
– Puts at risk for infection
Screening Recommendations
First Year:
– @3 months: CBC, Glu, Cr
– @6 months: CMP, Ferritin, TIBC, B12, Folate, Ca
[PTH] (if Ca elevated or to ensure Ca stable)
[Vit D] (possibly to ensure adequate Ca)
Every year thereafter:
– All of the above
Postmenopausal women: BMD Screening
– Variable recommendations, probably worth screening
and ensuring maximum calcium / vit D tx if low BMD
Impact of Weight Loss on Risk Factors
~5%
Weight Loss
5%-10%
Weight Loss
HbA1c
Blood Pressure
Total Cholesterol
HDL Cholesterol
Triglycerides
1
1
2
2
3
3
3
3
4
1. Wing RR et al. Arch Intern Med. 1987;147:1749-1753. 2. Mertens IL, Van Gaal LF. Obes Res. 2000;8:270-278. 3.
Blackburn G. Obes Res. 1995;3 (Suppl 2):211S-216S. 4. Ditschunheit HH et al. Eur J Clin Nutr. 2002;56:264-270.
Conclusions
Obesity is a chronic disease
Modest weight loss (5% -10% of body weight)
can have considerable medical benefits
Lifestyle change (diet and physical activity) is
the cornerstone of therapy
Pharmacotherapy can be useful in properly
selected patients
Bariatric surgery is the most effective therapy
for obesity
Metabolic Syndrome Treatment in
the Overweight or Obese
• Weight loss induced by diet and increased physical
activity is the cornerstone of therapy
• Weight loss induced by drug therapy can also
improve specific features of the metabolic syndrome
• Bariatric surgery is the most effective weight loss
therapy for extremely obese subjects and improves
all features of the metabolic syndrome
Obesity-Related Resources
Professional Associations
North American Association for the Study of
Obesity (NAASO)
www.naaso.org
American Academy of Family Physicians (AAFP)
www.aafp.org
American College of Sports Medicine (ACSM)
www.acsm.org
American Diabetes Association (ADA)
www.diabetes.org
American Dietetic Association (ADA)
www.eatright.org
American Gastroenterological Association (AGA)
www.gastro.org
American Heart Association (AOA)
www.americanheart.org
American Obesity Association (AOA)
www.obesity.org
American Society for Bariatric Surgery (ASBS)
www.asbs.org