A Case of ComorbiditiesSTEPHANIE RICHARDSON, DIETETIC INTERN

Picturing the Patient

58 yo female 5’1” (1.54 m) 245 #, baseline 180# + 65# fluid overload Admitted for systolic HF and uncontrolled DM

Admitted in September and October 2015 for CHF exacerbation. Hx of multiple hospital admissions for HF Hx of noncompliance with heart meds

PMH: CAD, IBS, HTN, Hyperlipidemia, Diabetic Neuropathy, GERD

Current Medical Conditions: Obesity Class 3, Uncontrolled DMT2, systolic HF

Physical Findings

Cognitive Status: Somnolent Skin Condition: Intact Other: +1-2 pitting edema to bilateral lower

extremities

24 h recall

Food Consumption

Sister prepares with no added salt. Knowledgeable about CHO counting and eats q 3-4 h. Recall high in processed/cured meats, refined grains, some

convenience food. Low F/V intake. Drinks 3-4 sodas q day. Drinks 2 glasses of milk q day + tea/water.

Abnormal Labs

Lab Normal Pt ExplanationGlucose 70-100 mg/dL 174 mg/dL (H) T2DMHbA1C 4-5.6% 12% (H) T2DMBUN/Creatinine 10:1-20:1 36 (H) Fluid Overload

BUN 7-20 29 Fluid OverloadLDL-C <100 mg/dL 110 mg/dL (H) Hyperlipidemia

Diet Order/ Nutrition Prescription

1665-2220 kcal/kg (15-20 kcal/kg —current body wt) 50-60 g/kg (1-1.2 g/kg IBW) Low Fat diet, 2 g Na restriction, 1.5 L fluid restriction

PES

Food and nutrient knowledge deficit related to lack of understanding of how to apply information as evidenced by A1C of 12.1% and pt stating uncertainty of what constitutes good snacks for a diabetic.

F/U

Pt had difficulty recalling what foods are high in CHO and needed prompting.

Pt’s goal upon discharge is to limit soda intake to maximum of 1 per day.

Third time’s the charm: Pt finally seems ready to make dietary changes.

Obesity to DMT2

Obesity creates lipotoxic environment due to excessive adipose tissue

Adipose tissue = metabolically active organ Controls FFA levels Contributes to metabolic homeostasis by

secreting adipokines Obesity causes recruitment of immune

cells and promotes inflammation = local insulin resistance Uncontrolled release of FFA Altered balance of adipokines

Secretion of pro-inflammatory cytokines

Obesity to CHF

Obesity promotes CVD b/c excessive adipose tissue releases pro-inflammatory adipokines + renin, angiotensinogen, & angiotensin 2

These metabolites promote HTN Inflammation + HTN put extra stress on

heart muscle Result = weakness + reduced function, and

finally CHF

Heart Ed: Salt AND Sugar

CVD = leading cause of premature mortality in developed world HTN = major risk factor; usually treated with low sodium diet Noted contributor= processed foods

High in sodium High in added sugar, especially fructose

Should cardiac nutrition education evolve to specifically address added sugar (sucrose)?

Study (Yang et al, 2014)

Added Sugar Intake and Cardiovascular Diseases Mortality NHANES trend analysis from 1988-1994 (n=11,733), 1999-2004

(n=8,786), and 2005-2010 (n=10,628) ~15% kcal from added sugar = average intake Majority consumed 10%+ kcal from added sugar 10% consumed 25%+ kcal from added sugar 8% of kcal vs 17-21% of kcal >> latter had a 38% higher risk of

CVD mortality #1 source: SSB (37%); #2: grain-based desserts (13.7%); #3:

fruit drinks (8.9%)

Study

Overall diet quality did not change association between added sugar/CVD mortality Healthy Eating Index

Biological mechanisms still being understood High added sugar >> HTN, increased TG, increased LDL-C, decreased HDL-C High added sugar >> associated with inflammatory markers

Limitations: 2nd day 24 h recalls; added sugar baseline assessment; observational study

Conclusion: positive association between added sugar & CVD mortality Significant AFTER adjusting for CVD risk factors (BP, total serum cholesterol) Observations observed across age groups, sex, race, education, PA, BMI

Study (Yang et al, 2014)

Review (Malik et al, 2010) Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and

Cardiovascular Disease Risk Large epidemiological studies show high added sugar intake =

Wt gain >> obesity High dietary glycemic load from fructose >> insulin resistance, impaired B-

cell function >> T2DM & CVD DM: 50,00 women over 8 y. period consuming ≥ 1 SSB/day had 83%

greater risk of developing T2DM vs those consuming <1 SSB/month (+ more studies)

CVD: 6,154 adults over 4 y. period consuming ≥ 1 soft drink/day had 22% higher incidence of HTN vs nonconsumers (+ more studies)

Inflammation: Positive associations between SSBs and high CRP levels FYI: caramel coloring in Cola = high in advanced glycation end

products >> can increase insulin resistance and inflammation

Review (Malik et al, 2010)

Sucrose (added sugar) = Fructose + Glucose Fructose

More adverse effects than glucose d/t different metabolic pathway Fructose + Glucose = power combo

Fructose alone = poorly absorbed>> absorption enhanced by glucose Added sugar (sucrose) & HFCS } both combos of F+G

Liver Fructose preferentially metabolized to lipid Causes increased TG >> associated with insulin resistance & CVD

Conclusion: SSB intake is increasing; sig. to wt gain + T2DM + CVD

References

Yang Q, Zhang Z, Gregg EW, Flanders W, Merritt R, Hu FB. Added Sugar Intake and Cardiovascular Diseases Mortality Among US Adults. JAMA Intern Med. 2014;174(4):516-524. doi:10.1001/jamainternmed.2013.13563.

Malik  VS, Popkin  BM, Bray  GA, Després  JP, Hu  FB.  Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk. Circulation. 2010;121(11):1356-1364.