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