Compromised Nutritional Status in Pulmonary Disease Nutritional status reflects balance

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2 Introduction Awareness of the impact that dietary habits, nutritional status and nutritional interventions have upon COPD incidence, progression and outcome is an important component of multifactorial health care in Pulmonary Rehabilitation (PR)

3 Compromised Nutritional Status in Pulmonary Disease Nutritional status reflects balance Nutritional Status nutrient demand nutrient supply

4 Compromised Nutritional Status in Pulmonary Disease Pulmonary Disease Nutrient Supply Limited by breathing status & changes in appetite Nutrient Demand Changes in metabolism, energy expenditure and pulmonary disease process

5 Compromised Nutritional Status in Macronutrient: Pulmonary Disease Protein: LBM, albumin, hemoglobin, organs, etc. Carbohydrate: glycogen Fat: adipose tissue, myelin sheath Body Composition is reflection of Macronutrient status

6 Compromised Nutritional Status in Pulmonary Disease Micronutrients Vitamins, Minerals Other phytochemicals Demand heightened by disease process Unlikely deficiencies Adequate diet sources can decrease risk

7 Body Composition and Macronutrient Status Pathophysiology/Interrelatedness of muscle loss and adiposity Yields types of Metabolic Phenotypes Classifications based upon varying degrees deficit/excess For example:» Low LBM= Sarcopenia» Low LBM + High FM = Sarcopenic Obesity More to come Understand phenotype- Increased risk Targeted Nutritional Therapy

8 Low Body Weight The normal adaptive response energy deficit Preferential loss of FM to spare loss FFM I.e. lose adipose to save muscle

9 Low Body Weight COPD patients respond metabolically differently Weight loss = loss fat-free mass out of proportion to the loss of fat mass I.e. lose muscle > adipose loss Unintended weight loss not an adaptive mechanism found in advanced COPD Disease process leads to increase in RMR Whole body protein turnover In fact, adequate or excessive caloric intake has been observed in underweight pulmonary patients. Goris AH. Br J Nutr ;89 ( 5 ):

10 Low Body Weight Weight loss is not only terminal consequence of disease process. But is an independent determinant of survival. i.e. Not an endpoint but continuous consequence that can be managed Filley GF, Beckwitt HJ, Reeves JT, et al. Chronic obstructive bronchopulmonary disease. II. Oxygen transport in two clinical types. Am J Med 1968; 44:

11 Low Body Weight Increase/Change energy demands in COPD altered inefficient breathing mechanics Note weight gain after lung reduction surgery mechanical efficiency of lower limb exercise Peripheral skeletal muscle: A slow-twitch type 1 fibers and fast-twitch type 2 fibers Relative shift from oxidative to glycolytic capacity Glycolytic produces less ATP per molecule higher ATP cost of muscular contraction

12 Low Body Weight Prioritize weight maintenance throughout the care process >5% weight loss over 6 months Increased clinical risk BMI < 25 associated with morbidity and mortality bone mineral loss fractures and falls

13 Diminished Fat Free Mass Loss of FFM is an independent predictor of mortality irrespective of fat mass Impairs physical performance muscle protein degradation and while musclebuilding pathways are stable or even increased plasma AA Poor diet Diminished absorption Schols AM, Am J Clin Nutr 2005;82:53 9 Rutten EP, Am J Clin Nutr 2006; 83(4):

14 Excess Body Weight The prevalence of obesity in COPD populations is variable and ranges from 18-54% globally Obese (>30 kg/m 2 ) More dyspnea More exercise intolerance with same airflow limitations Use more medications Fatigue increases Greater M/M due to CVD

15 Excess Body Weight BUT!!!!!! Higher survival rates Lower hospitalization rates The obesity paradox relative reduction in static lung volumes Increase in LBM because of girth? What is a PRP to do???

16 Advanced COPD Excess Body Weight May protect against mortality Earlier stages of COPD, low grade inflammation and metabolic syndrome accentuate CV risk and increase CV and all cause mortality Rutten, E Clinical Nutrition and Metabolism, ESPEN. Accessed August 30, 2017 from

17 Micronutrient Status Sustain metabolism and maintain tissue function. Vitamins-organic compounds Co-enzymes Anti-oxidants Hormone like regulators Nutritive minerals Structural and Functional roles Electrolytes.

18 Micronutrient Status Phytochemicals = organic compounds Carotenoids (some of which are plant precursors of Vitamin A and E) Polyphenols (including phenolic acids, flavonoids and stilbenes/ligans). Anti-oxidant activity in homeostatic response to inflammation.

19 Micronutrient Status Serum levels of micronutrients reflect diet intake confounded by age, gender, smoking alcohol intake and race heightened local demand Thus need assessed by diet as well as lab tests

20 Micronutrient Status Direct positive relationships between lung function and micronutrient status Higher serum values associated with FEV1 values Vitamin A, Vitamin C, and E, calcium and iron Lowest serum values associated with FEV1, FVC Vitamin C, E, B-carotene Vitamin D/calcium deficiency associated with disease severity Negatively affects muscle contractility impairs calcium uptake down regulates protein synthesis increases cell death

21 Calcium at risk Micronutrient Status Steroid therapy Poor diet (dairy) Decreased FFM, Cachexic Poor Vitamin D status Iron at risk malabsorption of iron from the gut renal failure medications

22 Micronutrient Status Confounded by smoking Smokers need more micronutrients in diet E.g. High baseline intakes/serum levels of Vitamin E in male smokers associated with a low incidence of bronchitis and dyspnea E.g. more rapid rates of decline in FEV1 per pack year of smoking in Vitamin D deficient individuals compared to those who were not deficient

23 Diet Intake and COPD At risk!!! 75% PR patients low in Vit D and calcium >33% PR patients low in protein, Vitamins A, E and C Low fat-free mass index (FFMI) low in protein High waist circumference (WC) low in protein and micronutrients Low FFMI and high WC most often had low quality diet. van de Bool C, et. al. European Journal of Clinical Nutrition (2)

24 Diet Patterns and COPD Epidemiological evidence Fruit vegetable then less decline in FEV1 Decrease risk of COPD (35% less) Decreased risk in smokers and non smokers Frt, veg, oily fish whole grains then low FEV1 54% more likely to have COPD Poor diet quality Increased risk of COPD

25 Impediments Upon Healthy Eating Behavior Breathlessness and fatigue reduce appetite and meal duration Postprandial shortness of breath limits the volume of food Swallowing problems limit food choices soft, tender, homogenous, liquid foods are best Limited knowledge and reduced motivation Fatigue Changes in taste acuity

26 Assessment of Nutritional Status Evaluation of nutritional status Analysis of body composition Diet intake Then, if at risk the further testing

27 Assessment of Nutritional Status Schols and others identified different metabolic phenotypes Associated with increased risk Patient counseling Follow-up

28 Assessment of Nutritional Status Schols and others identified different metabolic phenotypes Associated with increased risk Patient counseling Follow-up

29 Assessment of Nutritional Status Table 2 Metabolic Phenotype and Clinical Risk Metabolic Phenotype Definition Clinical Risk Obesity BMI>30 kg/m2 é CV Risk Morbid Obesity Sacropenic Obesity Sarcopenia Precachexia BMI>35 kg/m2 BMI kg/m2 and MAMC < 15 SMI <2* MAMC < 15 SMI <2* Unintended weight loss >5% over 6 months and BMI WNL é CV Risk Impaired physical performance é CV risk Impaired physical performance é Mortality Risk Impaired physical performance é Mortality Risk Cachexia Unintended weight loss >5% over 6 months and FFMI <18.s kg/m2 (men) < 15 kg/m2 (women) é Mortality Risk Impaired physical performance * below mean of young men and wom en reference groups refer to Ref 55. Adapted from Schols 1

30 Body Composition Assessment Height weight weight history specific anthropometric measurements Skinfolds- Pros and Cons Hronek M, Kovarik M, Aimova P, Koblizek V, Pavlikova L, Salajka F, and Zadak Z. Skinfold Anthropometry -The Accurate Method for Fat Free Mass Measurement in COPD. COPD : More expensive methods as indicated by clinical indication

31 Variable Clinical Measurements Calculations Normal Ranges Height, Weight, BMI Fat Free Mass/Fat Mass FFMI and FMI Muscle Mass (MM) Visceral Fat Bone Mass and density Muscle strength and related physical performance Height and Weight BMI= Weight (kg)/height (m)2 20<BMI<25 Sum of four skinfolds: triceps, biceps, subscapular, suprailiac DEXA Mid-arm circumference (MAC) cm Triceps Skinfold (TSF) mm Bio markers (creatinine height index) Sum of SF then reference table FM= %fat x Weight (kg) FFM= Weight - FM FFM from scan FM= Weight - FFM FFMI=FFM (kg)/height (m) 2 FMI= FM (kg)/height (m) 2 Mid-arm Muscle Circumference=MAMC = MAC - ( TSF/10) CHI = [(measured urinary creatinine x 100) / Ideal urinary creatinine for a given height] SMI=ALM/height 2 or ASM/weight or % BF men=12-19% % BF women=16-25% 25 th and 75 th %iles: FFMI men =18.2 to 20 kg/m 2 FFMI women=15.0 to 16.6 kg/m 2 FMI men= kg/m2 FMI women= kg/m2 MAC=15-60 MAMC range=15-24cm mg/ L DEXA Appendicular lean mass (ALM) ASM/BMI Waist hip ratio (WHR) WHR= Waist (cm)/ Hip (cm) <WC men <94cm <WC women< 80 cm < WHR men<.90 < WHR women<.85 DEXA Ultrasonography -Sagittal diameter DEXA HRCT 6 minute walk (gait speed) One rep max Handgrip strength Timed up-and-go test Stair-climb power test Bold: The measurements capable to be preformed in all PRP. DEXA= Dual-energy X-ray Absorptiometry; CT=Computed Tomography; HRCT= High Resolution Computed Tomography Table adapted from Schols AM, Ferreira IM, Franssen FM, et al. Nutritional assessment and therapy in COPD: Eur Respir J 2014; 44: Cruz-Jentoft AJ, Baeyens JP, Bauer JM, et al. Sarcopenia: European consensus on definition and diagnosis: Report of the European Working Group on Sarcopenia in Older People. Age and Ageing. 2010;39(4): doi: /ageing/afq034.

32 Assessment of Nutritional Status Table 2 Metabolic Phenotype and Clinical Risk Metabolic Phenotype Definition Clinical Risk Obesity BMI>30 kg/m2 é CV Risk Morbid Obesity Sacropenic Obesity Sarcopenia Precachexia BMI>35 kg/m2 BMI kg/m2 and MAMC < 15 SMI <2* MAMC < 15 SMI <2* Unintended weight loss >5% over 6 months and BMI WNL é CV Risk Impaired physical performance é CV risk Impaired physical performance é Mortality Risk Impaired physical performance é Mortality Risk Cachexia Unintended weight loss >5% over 6 months and FFMI <18.s kg/m2 (men) < 15 kg/m2 (women) é Mortality Risk Impaired physical performance * below mean of young men and wom en reference groups refer to Ref 55. Adapted from Schols 1

33 Cachexia Chronic severe illness Increased mortality Health-related quality of life Muscle weakness FFMI= Fat Free Mass Index <10 th percentile strong predictor of mortality Men <17 kg/m2 Women < 15 kg/m2 Urgent indicator of nutrition intervention

34 Cachexia and Pre-Cachexia The pre-cachexic patient > 5% unexplained BW loss over 6 months without measurable deficits in FFM Attainable Goals in PR Weight stabilization Gains in FFM Nutrition Exercise Referral to RDN for MNT (Medical Nutrition Therapy)

35 Sarcopenia Sarcopenia = deficit in skeletal muscle Weakness No universal definition Sarcopenia may be optimally defined Combination of measures muscle mass physical performance Prevalent throughout all ranges of BMI regardless of FM status

36 Figure 1 A Suggested Algorithm for Sarcopenia Case Finding Entry to PR > 0.8m/sec Measure gait speed (measured during 6 min walk) < 0.8 m/sec Measure grip strength Low Grip Strength Estimate muscle mass with skinfolds SMI Normal Grip Strength Low Normal Not at current risk for sarcopenia At current risk for sarcopenia. Refer to physician and dietitian for follow-up Not at current risk for sarcopenia. Monitor Consider comorbidity and individual circumstances that may influence each finding. Adapted from Figure 2 from Cruz-Jenloft Age Ageing 2010 Jul; 39(4):

37 Sarcopenic Obesity Sarcopenic obese men highest risk of all-cause mortality but not nec. CVD Sarcopenia and central adiposity associated with greater CVD mortality and all-cause mortality Strength: CVD risk Endurance, MAMC: CVD and non CVD mortality Risks are independent of each But Central adiposity associated with better physical functioning

38 Normal BMI and FFM Normal-see reference ranges Still inquire re: weight history Low FFM Risk Assoc with rapid weight loss Serial measures plus diet analysis

39 Obesity and Morbid Obesity Obesity BMI > 25 kg/m2 Morbid obesity >30 kg/m2 Higher mortality and morbidity due to increase in CVD risk BUT if has moderate to severe obstruction Then risk due to pulmonary disease is the greater concern Thus, RECOMMEND WEIGHT LOSS ONLY WITH CAUTION FOCUS: QUALITY FOOD AND APPROPRIATE PORTIONS

40 Obesity and Morbid Obesity No studies have systematically investigated the effects of weight loss interventions on adiposity, functionality and systemic inflammatory profile in patients with COPD Let s get on it! Clinical common sense: Modest hypo-caloric, Moderate to high protein diet Aerobic exercise DEFINITELY: no rapid or unexplained weight loss

41 Diet Intake Assessment Diet histories, diet records, and 24-hour recalls Good for clinical assessment if used by trained (RDN) BUT: not standardized so not useable as PR outcomes or group comparisons FFQ Standardized, questions, Screeners less BUT have to be validated and reliable DRA alias New Leaf Freemium version Nutrascreen- gives Frt/Veg and HEI

42 Diet Intake Assessment Diet indexes -means to evaluate the results from FFQ HEI (intake per 1000 calories) Total HEI scores associated with FEV(1)/FVC PUFA, omega-3, animal protein, fiber associated with lung health AHEI-2010 total score associated with lower COPD risk DASH Higher Score associated with lower CVD risk. Mediterranean Associated not associated with impaired lung function Alcohol and Western associated with impaired lung function (women) Root M, et. al. Nutr Res (4): Varraso, et al BMJ 2015;350:h286 Schwingshackl L, Hoffman G. J Acad Nutr Diet. 2015;115: Sorli-Aguilar, M et al. BMC Pulmonary Medicine (2016) 16:162

43 HEI ahei DASH amed Score total = 100 points total = 100 points Fruit 10=5 (Total) + 5 (Whole) 10=10(Total) Vegetables 10= 5 (Total) + 5 (Greens and Beans) 10=10(Total) Grains 10=5 (Total) + 5 (Whole) 10=10(Total) Dairy 10= 10 (Total) total = 40 points (relative to quartile of study group) (1-5) point if = (1-5) quartile (1-5) point if = (1-5) quartile (1-5) point if = (1-5) quartile Low fat dairy (1-5) point if = (1-5) quartile total = 9 (relative to median of study group) 1 = 1 (Total> Median) 1 = 1 (Total> Median) 1 = 1 (Total Whole Grains > Median ) Meats, poultry, and fish Nuts, seeds, dry beans, and peas Fats and oils Sodium Refined Grains Sweets=Empty Calories Alcohol MultiVitamin Use 10= 5 (Total) + 5 (Seafood and Plant Proteins) 10= 5(Total Oils)+ 5(Fatty Acid Ratio) 10= 10 (Total) (1.1 gm to 2.0 gm) 10= 10 (Total) (1.8 oz to >4.3 oz) 20=10 (Added Sugars) + 10 (Saturated Fats) not in 2015 HEI 10=Ratio (White/Red meat) 10=10(Total) 20=10 (low transfat) + 10 (Fatty Acid Ratio) 10=10(Total Ideal) (ideal= svg men; women) 7.5=(Total x duration) Red meat: (1-5) point if = (5-1) quartile (1-5) point if = (1-5) quartile Sodium: (1-5) point if = (5-1) quartile Sweetened Beverages (1-5) point if= (5-1) quartile 1 = 1 (Total> Median Fish) 1 = 1 (Total< Median Red or processed meats) 1 = 1 (Total> Median Nuts) 1 = 1 (Total> Median Legumes) 1 = Ratio (Mono/ Saturated Fat) 1 = Total (5-25 gm/day)

44 Impact of nutritional support upon clinical outcomes 2003 Cochrane report = Confusion re: Nutrition support definition 2012 Cochrane report = nutritional supplementation promotes significant weight gain among malnourished patients with COPD significant improvements in respiratory muscle strength (MIP and MEP) and overall HRQoL Ferreira IM, Cochrane Database Syst Rev 2012; (12); CD DOI: / CD pub3.

45 Impact of nutritional support upon clinical outcomes Nutrition therapy for COPD has transitioned from a focus on supposed adverse effects of CHO overload high CHO intake and increased CO2 production NOT substantiated or reproduced strong rationale for prioritizing CHO oxidation during exercise training in COPD Schols AM. The 2014 ESPEN Arvid Wretlind Lecture: Metabolism & Nutrition: Shifting paradigms in COPD management. Clinical Nutrition 2015; 34 (6):

46 Rational for increased CHO intake Skeletal muscles Structural and metabolic abnormalities reductions in the proportion of type 1 fibers and mitochondrial density, in decreased fat oxidative capacity increased glucose production. Early muscle fatigue- even at the low exercise intensities Associated with early lactic acid rise Adenine nucleotide loss Provision of higher CHO/lower fat foods/beverages Beneficial as a rapid energy source for the muscle w/o satiety CHO rich supplements less post-prandial shortness of breath Steiner MC et.al. Thorax. 2003; 58( 9):

47 Impact of nutritional support upon Protein > 0.8 gm/kg BW clinical outcomes Substrate for muscle anabolism Combat catabolism due to whole body protein turnover Impaired branch chain amino acid extraction in some COPD patients. Must have adequate calories ( spare concept)

48 Impact of nutritional support upon clinical outcomes - risk High intakes whole grains, poly-unsaturated fatty acids, nuts, and omega-3 fats Low intakes red and processed meats, refined grains sugar sweetened drinks

49 Impact of nutritional support upon Fiber clinical outcomes function and risk of COPD Vitamin E Supplementation led to 10% risk in women Vitamin D supplementation in deficient mitochondrial oxidative phosphorylation, FEV1 volumes number of falls Calcium and Vitamin D (diet first) Recommended if taking steroids

50 Implications in Pulmonary Rehab Assess phenotype and document implications Add measuring anthropometric measures Guide nutritional intervention

51 Implications in Pulmonary Rehab Prevent and/or treat weight loss Medical Nutrition Therapy is standard Assess and improve diet quality All CVD risk Do not accept poor appetite Small frequent (every 2-3 hours) feedings of highly nutritious foods Liquid versions

52 Table 4 Metabolic Phenotypes and Implications In Nutrition and Lifestyle Metabolic Nutrition Recommendations Phenotype Gradual weight loss with high quality, adequate Obesity protein and modest calorie reduction. Emphasize increasing fruit, veg. and high fiber intake. Pulmonary Rehabilitation Implications Increase calorie deficit with exercise. Morbid Obesity Sacropenic Obesity Sarcopenia Gradual weight loss with high quality, adequate protein and modest calorie reduction. Emphasize increasing fruit, veg. and high fiber intake. Inquire re: recent weight loss. Ensure diet higher in protein. Postpone calorie reduction recommendations until FFM restored. Refer to dietitian for malnutrition MNT Increase caloric and high quality protein intake with diet or "whole food" supplementation. Refer to dietitian for malnutrition MNT Consider intermittent exercise +/- high intensity non weight bearing exercise Increase calorie deficit with exercise. Consider exercise that is load bearing and sarcogenic Precachexia Modest increase caloric and high quality protein intake with diet or "whole food" supplementation. Modify food format as necessary. If weight loss doesn't cease, refer to physician and dietitian. Consider exercise that is load bearing and sarcogenic Cachexia Increase caloric and high quality protein intake with diet or "whole food" supplementation. Utilize smaller frequent feedings as tolerated. MV supplement. Refer to dietitian for malnutrition MNT Consider intermittent exercise +/- high or low intensity non weight bearing exercise

53 Implications in Pulmonary Rehab Education classes Creative, fun - recipes Practical information Hands-on experiences versus you should Targeting class topics to limit embarrassment and frustration gain weight lose weight

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