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Hot Topics in Nutrition for the Hot Topics in Nutrition for the Primary Care PhysicianPrimary Care Physician
Phillip Snider, RD, DO
Bon Secours Medical Associates
Virginia Beach, VA
Should Vitamins be Should Vitamins be Considered Drugs?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 Should Vitamins be Considered Drugs?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 AcidFolic AcidAka 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 MetabolismFolate MetabolismIntestinal CellsFolate reduced to tetrahydrofolate
– Folate reductase inhibited by methotrexate
Methylated to N5-methyl-THF– primary blood form
`̀
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
Medications– anticonvulsants – oral contraceptives– lithium– fenofibrates, niacin– sulphasalazine– methotrexate– metformin
Illness– diabetes– atrophic gastritis– crohn’s disease– hypothyroid– renal failure
Risk Factors Associated with Low FolateRisk Factors Associated with Low Folate
Alpert M, et al. Jrnl Clin Psychopharmacology. 2003;23(3):309-13. Arinami T, et al. Am J Genetics. 1997;74:526-28.Fava M, et al. Am J Psychiatry. 1997;154(3):426-28. Procopciuc L.M., Poster Pres. P86 presented at Biol Psych. 2005.Popakostas G, et al. Psychiatry Research, 2005;140(3):301-7. Bjelland I. et al. Arch Gen Psychiatry. 2003;60(6):618-26.Bottigleri T. Prog Neuro-Psychopharmacology & Biol Psychiatry. 2005; 29:1103-12. 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.
BioavailabilityBioavailability
MTHFR C>T Polymorphism
L-methylfolate
Vs.
5, 10 Methylene THF
L-methylfolate
Tetrahydrofolate
Dihydrofolate (Dietary Folate)
DHF Reductase Enzyme
Folic AcidL-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) BenefitsFolic 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) BenefitsFolic 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 CancerFA 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 CancerFA 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 CancerFA 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 A Randomized Trial on Folic Acid Supplementation and Risk of Recurrent Supplementation and Risk of Recurrent
Colorectal AdenomaColorectal 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 Dietary Factors of One-carbon Metabolism & Prostate Cancer RiskCancer 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 CancerFA 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 CancerFA 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 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 StudyAARP 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 CancerFA 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
Am J of Clin Nutr, Vol. 90, No. 5, 1380-1389, November 2009
Vitamins & CancerVitamins & 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 & CancerVitamins & Cancer
FA + B12 – 10.0% Dx cancer vs 8.4% HR 1.21; P = .02– 4.0% Died-cancer vs 2.9% HR 1.38; P = .01 – 16.1% Died-all cause vs 13.8% 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 FortificationFood Fortification
FDA started FA fortification in 1996All 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 FortificationFood 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 AcidFolic Acid
Synthetic form ~2x bioavailable– 1 DFE
1 mcg folate 0.5 mcg folic acid (on empty stomach)
Women Pregnant
Women
Men
RDA 400 DFE 600 DFE 400 DFE
UL 1,000 DFE 1,000 DFE 1,000 DFE
Folic acid fortification and public health: Folic acid fortification and public health: Report on threshold doses above which Report on threshold doses above which
unmetabolized folic acid appear in serumunmetabolized 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/1471-2458/7/41
Vitamins and Cancer: Take Home MessageVitamins 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 MessageVitamins 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 MessageVitamins 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 redox-active 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 MessageVitamins and Cancer: Take Home Message
People in good health should select only high-quality, 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 B12Interaction 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 OverweightObesity and Overweight
Establish diagnosis:BMIEstablish diagnosis:BMI
BMI = weight / height2
Correlates well with direct measures of adiposity
Overweight child: BMI >85th and <95th percentile
Obese child: BMI > 95th percentileIf child < 3 years old, use weight for height
Pulmonary diseasePulmonary diseaseabnormal functionabnormal functionobstructive sleep apneaobstructive sleep apneahypoventilation syndromehypoventilation syndrome
Nonalcoholic fatty liver Nonalcoholic fatty liver diseasediseasesteatosissteatosissteatohepatitissteatohepatitiscirrhosiscirrhosis
Coronary heart diseaseCoronary heart disease
DiabetesDiabetes
DyslipidemiaDyslipidemia
HypertensionHypertension
Gynecologic abnormalitiesGynecologic abnormalitiesabnormal mensesabnormal mensesinfertilityinfertilitypolycystic ovarian syndromepolycystic ovarian syndrome
OsteoarthritisOsteoarthritis
SkinSkin
Gall bladder diseaseGall bladder disease
CancerCancerbreast, uterus, cervixbreast, uterus, cervixcolon, esophagus, pancreascolon, esophagus, pancreaskidney, prostatekidney, prostate
PhlebitisPhlebitisvenous stasisvenous stasis
GoutGout
Medical Complications of ObesityMedical Complications of Obesity
Idiopathic intracranial Idiopathic intracranial hypertensionhypertension
StrokeStroke
CataractsCataracts
Severe pancreatitisSevere pancreatitis
Complications of Childhood ObesityComplications of Childhood Obesity
0
1
2
3
4
5
6
Relationship Between Weight Gain in Relationship Between Weight Gain in Adulthood and Risk of Type 2 DiabetesAdulthood and Risk of Type 2 Diabetes
Re
lativ
e R
isk
Weight Change (kg)Willett et al. N Engl J Med 1999;341:427.
-10 -5 0 5 10 15 20
MenMen
WomenWomen
Diagnosing the Metabolic SyndromeDiagnosing the Metabolic Syndrome
Diagnosis = 3
Risk Factor Defining LevelAbdominal obesity Men Women
>40 in
>35 in
TG 150 mg/dL
HDL-C
Men Women
<40 mg/dL<50 mg/dL
Blood pressure 130/85 mm Hg
Fasting glucose 110 mg/dL
Defining Cardiometaboilc RiskDefining Cardiometaboilc Risk What is Abdominal Obesity ? Can be defined by Waist Circumference
ATP- III IDFMale:
> 42 Inch
Female :
> 35 Inch
Male :
> 37 Inch
Female :
> 31.5 Inch
Better Method ?
Waist < ½ Height
BMI CategoriesBMI Categories
A BMI of: Classifies one as:– <18.5 Underweight– 18.5-24.9 Normal weight– 25-29.9 Overweight– 30-34.9 Obesity Class I– 35-39.9 Obesity Class II– 40-49.9 Obesity Class III– 50 and above Super Obesity
Morbid ObesityMorbid 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: Morbid Obesity Examples: BMI > 40BMI > 40
5’0” person > 204 lb5’6” person > 247 lb6’0” person > 294 lb
Morbid Obesity Examples: Morbid Obesity Examples: BMI > 35BMI > 35
5’0” person > 170 lb5’6” person > 216 lb6’0” person > 258 lb
Obesity is a BIG problem…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 ObesityUS 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 FatWhy Are We So Fat&&
What Can We Do About It?What Can We Do About It?
Obesity Treatment PyramidObesity Treatment Pyramid
DietDiet Physical ActivityPhysical Activity
Lifestyle ModificationLifestyle Modification
PharmacotherapyPharmacotherapy
SurgerySurgery
Guide for Selecting Obesity TreatmentGuide for Selecting Obesity Treatment
The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. October 2000, NIH Pub. No.00-4084
Treatment 25-26.9 27-29.9 30-34.9 35-39.9 >40
Diet, Exercise, Behavior Tx
+ + + + +
Pharmaco-therapy
With co-morbidities + + +
SurgeryWith co-
morbidities +
BMI Category (kg/mBMI Category (kg/m22))
“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 ObesityHormonal Causes of Obesity
Cushings SyndromeMost treatments for Diabetes MellitusNOT HypothyroidismVery 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 GainMedications That Can Cause Weight Gain
Psychotropic medications
– Tricyclic antidepressants
– Monoamine oxidase inhibitors
– Specific SSRIs
– Atypical antipsychotics
– Lithium
– Specific anticonvulsants
Older -blockers
Diabetes medications
– Insulin
– Sulfonylureas
– Thiazolidinediones
Highly active antiretroviral therapy
Tamoxifen
Steroid hormones
– 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.”
0
500
1000
1500
2000
2500
3000
Discrepancy Between Reported and Actual Discrepancy Between Reported and Actual Energy Intake and ExpenditureEnergy Intake and Expenditure
Kca
l/d
Reported*P<0.05 vs reported.Lichtman et al. N Engl J Med 1992;327:1893.
Energy Intake
Actual Reported Actual
Energy Expenditure
**
**
“My problem is my
metabolism is
slow. Everything
I eat turns straight
to fat.”
0
1000
2000
3000
Relationship Between Resting Energy Relationship Between Resting Energy Expenditure and Fat-free MassExpenditure and Fat-free Mass
REE = Resting energy expenditureFat-Free Mass (kg)
RE
E (
kcal
/24
h)
Owen. Mayo Clin Proc 1988;63:503.
30 90 1000 40 50 60 70 80
Lean females
Obese females
Lean males
Obese males
“Any time I try to lose weight, my metabolism
slows down so much that I can’t lose weight.”
0
500
1000
1500
2000
2500
3000
3500
Energy Metabolism Before & After Weight LossEnergy Metabolism Before & After Weight LossE
nerg
y E
xpen
ditu
re (
kcal
/d)
Before
*P<0.05 vs before weight lossAmatruda et al. J. Clin Invest 1993;92:1236.
Predicted
Mean BMI Reduced from 31 to 23 kg/mMean BMI Reduced from 31 to 23 kg/m22
After Before PredictedAfter
Resting Energy Expenditure
Total Energy Expenditure
**
****
**
“So obesity is all genetic.
There’s nothing I can do.”
0
10
20
30
40
50
Gene-Environment Interaction in the Gene-Environment Interaction in the Pathogenesis of ObesityPathogenesis of Obesity
Bod
y M
ass
Inde
x (k
g/m
2 )
Ravussin E et al. Diabetes Care 1994;17:1067-1074.
Pima Indians
Maycoba, Mexico Arizona
P <0.0001
0
100
200
300
400
500
Effect of Portion Size on Energy IntakeEffect of Portion Size on Energy Intake
500
Am
ount
Con
sum
ed (
g)
Amount of Macaroni and Cheese Served (g)
Rolls et al. Am J Clin Nutr. 2000 Dec;76(6):1207-13.
625 750 1000
Prevalence of Obesity by Hours of Daily TV NHES Youth Aged 12-17 in 1967-70 and NLSY
Youth Aged 10-15 in 1990
4-54-53-43-42-32-31-21-20-10-1 >5>5
“I don’t think I need to
change what I am
eating.
I am going to work out
and lose it that way.”
-7.0 -5.0 -3.0 -1.0 1.0
Physical Activity Alone Results in Minimal Physical Activity Alone Results in Minimal Weight LossWeight Loss
Wing. Med Sci Sports Exerc 1999;31(suppl):S547.
*P<0.05 vs control group
Duration of each study ranged from 4 to 12 months.
Stefanick 1998
Stefanick 1998a
Anderssen 1995
Hammer 1989
Verity 1989
Rönnemaa 1988
Wood 1988
Wood 1983
Weight loss (kg)
Control Group
Exercise Group
**
**
0
20
40
60
80
100
Relationship Between Physical Activity Relationship Between Physical Activity and Maintenance of Weight Lossand Maintenance of Weight Loss
Not Maintained
Sub
ject
s E
xerc
isin
g (%
)
P<0.001
Kayman et al. Am J Clin Nutr 1990;52:800.
Weight Loss PatternMaintained
“Isn’t there some popular
diet I can follow? One that
makes it easy.”
Popular DietsPopular 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?”
PharmacotherapyPharmacotherapy
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 Drugs Approved by FDA for Treating ObesityTreating Obesity
Generic NameTrade 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
PhentermineAdipex, lonamin
IV Short-term 1973
PhendimetrazineBontril, Prelu-2
III Short-term 1961
Benzphetamine Didrex III Short-term 1960
-25
-20
-15
-10
-5
0
Additive Effects of Behavior and Diet Therapy with Additive Effects of Behavior and Diet Therapy with Pharmacotherapy for ObesityPharmacotherapy for ObesityW
eig
ht C
ha
ng
e (
%)
Wadden et al. Arch Intern Med 2001;161:218.
*P<0.05 vs medication alone.Time (months)
0 2 4 8 12106
Medication alone
Medication and behaviormodification
Medication, behaviormodification and meal
replacements
*
*
“What about
surgery?”
Role of SurgeryRole of Surgery
Evidence for long term effectiveness
Is approved by most payers
Requires life long committment
What are The Operative What are The Operative Results?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?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 ConditionsEffect on Comorbid Conditions Diabetes
– 76.8% - Completely resolved– 86.0% - Resolved or improved
Hyperlipidemia– 70% - Improved
HTN– 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 Meta-analysis. JAMA, 14:1724-37, 2004
Long-Term Changes: Weight Long-Term Changes: Weight RegainRegain
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, self-sabotage, etc. leading to weight regain over time.
Surgery relatively new, will have to wait and reanalyze data in a few years.
MalabsorptionMalabsorption
Flintstones “Complete”
Women who still have menstrual periods need iron. All women need calcium!
Common deficiencies: Iron, Folate, B12, Calcium, Vitamin D
Long-term implicationsLong-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 issuesOther 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 RecommendationsScreening 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 FactorsImpact of Weight Loss on Risk Factors
~5%Weight Loss
5%-10%Weight Loss
HbA1c
Blood Pressure
Total Cholesterol
HDL Cholesterol
Triglycerides
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.
1
2
3
3
1
2
3
3
4
ConclusionsConclusionsObesity 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 Metabolic Syndrome Treatment in the Overweight or Obesethe 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 ResourcesObesity-Related ResourcesProfessional AssociationsProfessional Associations
North American Association for the Study of Obesity (NAASO)
American Academy of Family Physicians (AAFP)
American College of Sports Medicine (ACSM)
American Diabetes Association (ADA)
American Dietetic Association (ADA)
American Gastroenterological Association (AGA)
American Heart Association (AOA)
American Obesity Association (AOA)
American Society for Bariatric Surgery (ASBS)
www.naaso.org
www.aafp.org
www.acsm.org
www.diabetes.org
www.eatright.org
www.gastro.org
www.americanheart.org
www.obesity.org
www.asbs.org
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