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Η παρουσίαση φορτώνεται. Παρακαλείστε να περιμένετε

Άσκηση και Παχυσαρκία Φύλο, Κληρονομικότητα και Περιβάλλον Καρατζαφέρη Χριστίνα PhD Τμήμα Επιστήμης Φυσικής Αγωγής και Αθλητισμού ΠΑΝΕΠΙΣΤΗΜΙΟ ΘΕΣΣΑΛΙΑΣ.

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Παρουσίαση με θέμα: "Άσκηση και Παχυσαρκία Φύλο, Κληρονομικότητα και Περιβάλλον Καρατζαφέρη Χριστίνα PhD Τμήμα Επιστήμης Φυσικής Αγωγής και Αθλητισμού ΠΑΝΕΠΙΣΤΗΜΙΟ ΘΕΣΣΑΛΙΑΣ."— Μεταγράφημα παρουσίασης:

1 Άσκηση και Παχυσαρκία Φύλο, Κληρονομικότητα και Περιβάλλον Καρατζαφέρη Χριστίνα PhD Τμήμα Επιστήμης Φυσικής Αγωγής και Αθλητισμού ΠΑΝΕΠΙΣΤΗΜΙΟ ΘΕΣΣΑΛΙΑΣ

2 Άδειες Χρήσης Το παρόν εκπαιδευτικό υλικό υπόκειται σε άδειες χρήσης Creative Commons. Δεν επιτρέπεται η χρήση για εμπορικούς σκοπούς. Για εκπαιδευτικό υλικό, όπως εικόνες, που υπόκειται σε άλλου τύπου άδειας χρήσης, η άδεια χρήσης αναφέρεται ρητώς. 2

3 Χρηματοδότηση Το παρόν εκπαιδευτικό υλικό έχει αναπτυχθεί στο πλαίσιο του εκπαιδευτικού έργου του διδάσκοντα. Το έργο «Ανοικτά Ακαδημαϊκά Μαθήματα Πανεπιστημίου Θεσσαλίας» έχει χρηματοδοτήσει μόνο τη αναδιαμόρφωση του εκπαιδευτικού υλικού. Το έργο υλοποιείται στο πλαίσιο του Επιχειρησιακού Προγράμματος «Εκπαίδευση και Δια Βίου Μάθηση» και συγχρηματοδοτείται από την Ευρωπαϊκή Ένωση (Ευρωπαϊκό Κοινωνικό Ταμείο) και από εθνικούς πόρους. 3

4 Σκοποί ενότητας Η κριτική σύνδεση γνώσεων που αφορούν την επίδραση του φύλου, της φυλής και της κληρονομικότητας στην αιτιολογία της παχυσαρκίας – to critically associate scientific knowledge regarding the aetiology of obesity to non modifiable factors such as gender, race and family history Η αναγνώριση της κυριαρχικής επίδρασης του κοινωνικού περιβάλλοντος και του «μοντέρνου» τρόπου ζωής – to recognize the all imposing role of society and the modern way of life 4

5 Περιεχόμενα ενότητας Παχυσαρκία και διαφορές ανάμεσα στα δύο φύλα- Obesity and gender differences Φυλετικές διαφορές και παχυσαρκία – race considerations Κληρονομικότητα ή κοινωνικοοικονομικοί και πολιτισμικοί παράγοντες; Nature or Nurture? Παχυσαρκία στη νεαρή ηλικία – obesity in the young 5

6 The Problem of Obesity «Σήμερα, στον ανεπτυγμένο κόσμο, ο επιπολασμός της παχυσαρκίας είναι αυξανόμενος και υπάρχουν πια τόσοι παχύσαρκοι στον κόσμο όσο και άνθρωποι που υποφέρουν από την πείνα» Μτφρ από το πρωτότυπο: "Today, in the developed world, the incidence of obesity is rising and there are now as many obese people in the world as there are people suffering from hunger" Phillip Campbell, Editor, Nature and Ritu Dhand, Associate Editor, Nature. Nature 404 (6778): 631 April 6,

7 Πως ορίζεται η παχυσαρκία; Ως υπέρβαρο ή και παχύσαρκο ορίζεται το άτομο που παρουσιάζει μη φυσιολογική ή και υπερβολική συσσώρευση λιπώδους ιστού, σε τέτοιο βαθμό που υποφέρει η υγεία του. Χρησιμοποιώντας την απλή μέθοδο του Δείκτη Μάζας Σώματος [ΔΜΣ – αγγλιστί Body mass index (BMI)που υπολογίζεται με την σωματική μάζα σε χιλιόγραμμα δια το τετράγωνο του ύψους του σε μέτρα (kg/m 2 ) σύμφωνα με τον WHO (Fact sheet N°311, reviewed May 2014, accessed via on 27/6/2014): – Υπέρβαρος/Overweight: ΔΜΣ ≥25 kg/m 2 – Παχύσαρκος/Obese : ΔΜΣ ≥ 30 kg/m 2. Ο ΔΜΣ αποτελεί έναν πολύ χρήσιμο δείκτη για πληθυσμιακές μελέτες. όμως πρέπει να αποτελεί το πρώτο στάδιο αξιολόγησης αφού δεν αντικατοπτρίζει τις διαφορές μεταξύ των ατόμων στην σωματική σύσταση (δηλ στην άλιπη και λιπώδη μάζα). Περισσότερα … στο εργαστηριακό μάθημα (Βλ διαλεξη 9) 7

8 Επιπολασμός της παχυσαρκίας

9 Επιπολασμός του υπέρβαρου και της παχυσαρκίας στις ΗΠΑ, σε ενήλικες ηλικίας ετών -Prevalence of overweight and obesity among U.S. adults, age years 9 Redrawn based on Table from Age-adjusted* prevalence of overweight and obesity among U.S. adults, age years National Health and Nutrition Examination Survey (NHANES) *Age-adjusted by the direct method to the year 2000 U.S. Bureau of the Census estimates using the age groups 20-39, 40-59, and years.

10 Επιπολασμός της παχυσαρκίας στις ΗΠΑ, σε ενήλικες με κατηγοριοποίηση ανά πολιτιστική καταγωγή - Age-adjusted prevalence of obesity, by cultural origin, No signs of abating….but stabilising? Lowest in non-hispanic asian Highest in non-hispanic black 10 Blue bars drawn based on data from Fig 2 Odgen et al 2013, Prevalence of obesity among adults: United States , NCHS Data Brief no 131. Red bar drawn based on data from Odgen et al 2014, JAMA Vol 311, No. 8.

11 Υπέρβαρο και παχυσαρκία στην Ελλάδα -Overweight and obesity in Greece "Greece today is the EU state with the highest average body mass index and highest prevalence of overweight and obesity," according to the UN's Food and Agriculture Organisation 29/7/2008 report. Depending on reports and statistical analyses up 75% of Greek adults may be already overweight & obese! There is a clear ‘South vs North’ difference 7000 deaths/yr can be attributed to obesity in Greece (135k in the EU) 11

12 Παχυσαρκία και διαφορές ανάμεσα στα δύο φύλα Obesity and differences between the two sexes

13 What makes a man? What makes a woman? 13 «Όλα» οφείλονται στις «ορμόνες του φύλου» (sex hormones)! Η σεξουαλική διαφοροποίηση ξεκινά στο 2ο μήνα της ανάπτυξης του εμβρύου. Το φύλο συνδέεται με την παρουσία ή απουσία του γονιδίου SRY (του χρωμοσώματος Υ έτσι ώστε να αναπτυχθούν όρχεις). Από τον 3 ο μήνα με την επίδραση ορμονών τα εσωτερικά γεννητικά όργανα εξελίσσονται σε «αρσενικά» ή «θηλυκά» ( σε έμβρυα ΧΥ: τεστοστερόνη και αντιμυλλέριος ορμόνη / Mullerian Inhibiting Substance (MIS) -> αρσενικούς (Wolffian) πόρους και όχι θηλυκούς (Mullerian) πόρους, ενώ σε ΧΧ: έλλειψη τεστοστερόνης -> θηλυκούς (Mullerian) πόρους )

14 Χαρακτηριστικά του φύλου Gender Characteristics Στο αρσενικό οι όρχεις και στο θηλυκό οι ωοθήκες και παράγουν ορμόνες και γαμέτες (στα αρσενικά η γαμετογένεση ξεκινά με την αναπαραγωγική ωρίμανση, στις γυναίκες η γαμετογένεση αρχίζει in utero και συνεχίζεται κατά την εφηβεία) Κατά τη διάρκεια της εφηβείας οι γυναίκες και οι άνδρες θα αναπτύξουν μια σειρά από διακριτικά σεξουαλικά χαρακτηριστικά, όλα κάτω από την επίδραση των ορμονών του φύλου και τον έλεγχο του άξονα υποθαλάμου-πρόσθιας υπόφυσης. 14

15 Χαρακτηριστικά του φύλου Gender Characteristics 15 Πριν από την εφηβεία ένα παιδί έχει χαμηλά επίπεδα στεροειδών ορμονών και γοναδοτροπινών => η υπόφυση δεν είναι ακόμη ευαίσθητη σε επίπεδα στεροειδών στο αίμα Ακόμα δεν γνωρίζουμε πως ακριβώς ξεκινά η «εφηβεία» One theory supports a genetically pre-programmed maturation of hypothalamic neurons Μια θεωρία υποστηρίζει μια γενετικά προγραμματισμένη ωρίμανση των νευρώνων του υποθαλάμου Recent theories support the role of the adipose tissue hormone leptin Πρόσφατες θεωρίες υποστηρίζουν το ρόλο του λιπώδους ιστού και της ορμόνης λεπτίνης

16 Στον Ενήλικα -In the adult human 16 Women have: minimal facial & body hair, breasts, higher % body fat, less lean muscle mass, BMR of 0.9 kCal/hr/kg bw pear shape, estrogens (οιστρογόνα) Men have: facial & body hair, less body fat, more lean muscle mass, BMR of 1.0 kCal/hr/kg bw, broad shoulders, narrow waist and hips – inverted triangle shape, androgens (ανδρογόνα) Ιnsulin to glucagon ratio regulates metabolism ιn both sexes In the fed state insulin dominates by promoting anabolism

17 Επιπολασμός της παχυσαρκίας στην Αγγλία, κατά την δεκαετία του 90’ - Prevalence of obesity in England, in the 90s 17 Redrawn based on data approximation from Fig 1Prevalence of clinical obesity (body mass index >30) in England. Source: Office of Population Censuses and Surveys1 2 3 Prentice, A. M et al. BMJ 1995;311:

18 Επιπολασμός της παχυσαρκίας στην Αγγλία ανά φύλο κατά τα έτη Prevalence of overweight & obesity in England males and females, Scotland had even higher total age-adjusted prevalence for obesity (24,9 and 25,7% in males and females respectively) and overweight (71 and 60,6% in males and females respectively) In that same review, the lowest prevalence for overweight and obesity were: – in males (Bosnia-Herzegovina) 63,2% & 15,9%, respectively – In females 50,9% (Croatia) & 17% (Portugal), respectively Note: these data come from actual measurements. Self- reported data show lower prevalence!

19 Επιπολασμός της παχυσαρκίας στις ΗΠΑ, σε ενήλικες με κατηγοριοποίηση ανά πολιτιστική καταγωγή και φύλο - Age-adjusted prevalence of obesity, by cultural origin and sex, Lower in non-hispanic asian. Higher in non-hispanic black women vs men and vs all other women groups 19 Drawn based on Fig 2 from Odgen et al 2013, Prevalence of obesity among adults: United States , NCHS Data Brief no 131.

20 20 OBESITY AND GENDER DIFFERENCES Fat distribution differs between the sexes Η κατανομή του λίπους διαφέρει μεταξύ των δύο φύλων

21 Krotkiewski et al 1983 measured the distribution of adipose thickness, fat cell weight (FCW), and estimated number (FCN) in four regions in randomly selected middle-aged men and women (n=330) and in obese individuals (n=930). Used subcutaneous needle biopsies and ultrasound from predetermined epigastric, hypogastric, gluteal and femoral sites What do we observe? Από τους Από τους Krotkiewski et al 1983 μετρήθηκε η κατανομή του πάχους του λιπώδους ιστού, το βάρος των κυττάρων του λιπώδους ιστού (FCW), και ο προβλεπόμενος αριθμός (FCN) σε τέσσερις περιοχές σε τυχαία επιλεγμένους άνδρες και γυναίκες μέσης ηλικίας (n = 330) και σε παχύσαρκα άτομα (n = 930). Χρησιμοποιήσαν υποδόριες βιοψίες με βελόνα και υπερηχογράφημα από τις προκαθορισμένες περιοχές από το επιγάστριο, υπογαστρικά, τους γλουτούς και τον μηρό. Τι παρατηρούμε; 21 Κατανομή του λιπώδους ιστού στο σώμα - REGIONAL ADIPOSE TISSUE DISTRIBUTION KROTKIEWSKI et al 1983, J. Clin. Invest. 72:

22 22 Are there differences between obese men & women? υπάρχουν διαφορές μεταξύ των παχύσαρκων ανδρών και γυναικών; What do we observe? Do you think it’s important where the fat tissue is accumulated? Τι παρατηρούμε; Νομίζετε ότι είναι σημαντικό που συσσωρεύεται ο λιπώδης ιστός; KROTKIEWSKI et al 1983, J. Clin. Invest. 72:

23 Γιατί μας απασχολεί ο λιπώδης ιστός; Why does fat matter?  Adipose tissue is an active secretory organ producing adipocytokines, (tumor necrosis factor- alpha, interleukin-6, leptin, adiponectin, and resistin)  Ο λιπώδης ιστός είναι ένα ενεργό εκκριτικό όργανο αφού παράγει μια ποικιλία από μόρια γνωστά ως λιποκυτταροκίνες  Inflammatory markerσ and cytokine levels predict future development of glucose intolerance (Hotamisligil et al 1995 J Clin Invest 95: 2409–2415 ) and vascular events (Thompson 1995 N Engl J Med 332: 635–641)  Δείκτες φλεγμονής και επίπεδα κυτταροκινών φαίνεται ότι προβλέπουν τη μελλοντική ανάπτυξη της δυσανεξίας στη γλυκόζη (Hotamisligil et al 1995, J Clin Invest 95: ) και τα αγγειακά επεισόδια (Thompson 1995 N Engl J Med 332: ) 23

24 Γιατί μας απασχολεί ο λιπώδης ιστός; Why does fat matter? There is a close association between obesity and insulin resistance (Karter, et al. 1996Diabetes 45:1547–1555, DeFronzo 1991 Diabetes Care 14:173–194) Υπάρχει μια στενή σχέση μεταξύ της παχυσαρκίας και της αντίστασης στην ινσουλίνη (Karter, et al. 1996Diabetes 45: , DeFronzo 1991 Diabetes Care 14: ) There is a close association between obesity and the inflammatory markers fibrinogen and CRP - stronger in women (Ford & Dietz 2002 JAMA 287: 356–359, Hak et al 1999 Arterioscler Thromb Vasc Biol 19: 1986–1991) Και, μεταξύ της παχυσαρκίας και του δεικτών φλεγμονής όπως ινωδογόνου και CRP και η οποία είναι ισχυρότερη στις γυναίκες (Ford & Dietz 2002 JAMA 287: , Hak et al 1999 Arterioscler Thromb Vasc Biol 19: ) 24

25 Καρκίνος και Παχυσαρκία 25 Η παχυσαρκία συνδέεται με τον καρκίνο Για το έτος 1995 ο συνολικός αριθμός περιστατικών καρκίνου που αποδίδονται στο υπερβολικό βάρος στο Ηνωμένο Βασίλειο ήταν ( για την ΕΕ), και το ποσοστό των καρκίνων ήταν 2,7% για τους άνδρες και 4,9% για τις γυναίκες Κατανομή είδους καρκίνων στα αποδιδόμενα στο υπέρβαρο και την παχυσαρκία περιστατικά (Γράφημα με βάση στοιχεία από την Figure 2: Percent of cancers related to obesity (UK) Bergstöm et al Int J Cancer 91: – τιμές κατά προσέγγιση)

26 Σχετικός κίνδυνος για ανάπτυξη παθήσεων- relative risk for disease DiseaseWomenMenWorking days lost Diabetes type II12,75,25,960,000 Heart attack3,21,51,230,000 Osteoarthritis1,41,9950, Bergström et al Int J Cancer 91: All obesity linked secondary diseases

27 What is the importance of central adiposity in women? Ποια η σημασία της κεντρικής παχυσαρκίας; 27 Until menopause women enjoy a ‘protection’ from CAD ( possibly an estrogen mediated antioxidant effect - Vina et al 2005 FEBS Lett 579;12: ). This however disappears when women acquire central adiposity and after the menopause…

28 Whole body & abdominal lipolytic sensitivity to epinephrine may be suppressed in upper body obese women Horowitz & Klein (2000, Am J Physiol Endocrinol Metab 278: E1144-E1152) measured whole body & regional lipolytic and adipose tissue blood flow (ATBF) sensitivity to epinephrine in 8 lean [BMI: 21 ± 1 kg/m2] and 10 upper body obese (UBO) women (BMI: 38 ± 1 kg/m2; waist circumference >100 cm). It was found that whole body lipolytic sensitivity to epinephrine is blunted in women with UBO because of decreased sensitivity in upper body but not lower body subcutaneous adipose tissue. 28

29 Systemic resistance to the antilipolytic effect of insulin in black and white women with visceral obesity Albu et al 99 (Am J Physiol Endocrinol Metab 277: E551-E560) studied the role of visceral adipose tissue (VAT) accumulation in systemic fat metabolism. They compared black and white women who differed in their manifestations of upper body obesity It was found that, in both races, VAT accumulation was associated with systemic resistance to insulin 29

30 Σημασία της κατανομής του σωματικού λίπους σε υποδόριο και σπλαγχνικό – Importance of fat distribution in subcutaneous or visceral Visceral adipose tissue distribution in obesity is an important marker for an impaired systemic antilipolytic action of insulin and increased systemic FFA flux in nondiabetic, premenopausal obese women. Accurate measurements of the visceral and subcutaneous AT compartments in obese women could help predict insulin resistance of both carbohydrate and lipid metabolism. 30

31 Φυλή και Παχυσαρκία RACE AND OBESITY In the United States, African Americans, Native Americans, and Latinos have higher rates of obesity and overweight in comparison to non-Hispanic whites (Deckelbaum & Williams 2001, Obes Res 9: 239S–243S, Goran 2001 Am J Clin Nutr 73: 158–171, Goran et al 2003 Clin Endocrinol Metab 88: 1417– 1427) Any data in Greece for ethnic minorities? That would be an interesting project! 31

32 Φυλή και Παχυσαρκία RACE AND OBESITY It is conceivable that, genetic characteristics that served well tribes living in a pre-industrial environment may have now become a liability! (later on the thrifty gene theory) We should of course appreciate that while the genetic component is real, physical inactivity and overfeeding (= over-junk food-feeding) are key factors for the increasing prevalence of obesity in the US, Europe and elsewhere in the world – epigenetics 32

33 Φυλή και Παχυσαρκία RACE AND OBESITY Education and culture are also crucial Socioeconomic paradox: affluent people in the US tend to be thin and poor people tend to be fat, while affluent people in Pakistan tend to be fat and poor tend to be thin ie back to physical activity and availability/ quality of food! 33

34 Φυλή και Παχυσαρκία RACE AND OBESITY Researchers in multi-ethnic industrialized countries, investigate race differences in energy expenditure, lipid metabolism and body composition in order to specifically target preventive measures and policies. As with the family and twin studies, ‘race’ studies can provide us with clues to the factors determining adiposity and could help us tease out the biological and socioeconomic factors contributing to obesity 34

35 Genetic predisposition for obesity Κληρονομικότητα και παχυσαρκία So far, >600 genes, markers, and chromosomal regions have been associated or linked with human obesity phenotypes However, judging from similar attempts to link diseases like diabetes to genes, it appears that about genes may finally prove to be crucial in linking genetic inheritance to obesity Ίσως η εικόνα να αλλάξει ραγδαία στην επόμενη πενταετία... 35

36 Genes influencing lipid and lipoprotein levels in the Quebec Family Study. Linkage analyses were conducted for four quantitative lipoprotein/lipid traits, i.e., total cholesterol, triglyceride, HDL-cholesterol (HDL-C), and LDL-C concentrations, in 930 subjects enrolled in the Quebec Family Study. A maximum of 534 pairs of siblings from 292 nuclear families were available. The strongest evidence of linkage was found on chromosome 12q14.1 at marker D12S334 for HDL-C, with a logarithm of the odds (LOD) score of Chromosomal regions harboring quantitative trait loci (QTLs) for LDL-C included 1q43 (LOD = 2.50), 11q23.2 (LOD = 3.22), 15q26.1 (LOD = 3.11), and 19q13.32 (LOD = 3.59). For triglycerides, three markers located on 2p14, 11p13, and 11q24.1 provided suggestive evidence of linkage (LOD > 1.75). There is therefore evidence for several QTLs influencing lipid and lipoprotein levels (Bosse et al 04, J Lipid Res) 36

37 Heritability of Body Composition Measured by DEXA in the Diabetes Heart Study 292 women & 262 men (age, 38 to 86 yrs; BMI, 17 to 57 kg/m2) from 244 families. 492 white & 49 African- American sibling pairs. Adjustment for diabetes status, smoking, dietary intake, and physical activity resulted in only minor changes in the heritability estimates (all p < ). FM and LM measured by DEXA are highly heritable and can be effectively used in designing linkage studies to locate genes governing body composition. Additionaly, regional distribution of FM and LM may be genetically determined (Hsu et al 05 Obes Res 13: ) 37

38 Heritability of lean mass Twin and family studies have reported a stronger genetic component for fat-free mass, (0.56 to 0.80) in various populations (Arden & Spector 1997 J Bone Miner Res 12, , Seeman, et al 1996 Am J Physiol 270,E320-E327, Abney et al 2001 Am J Hum Genet 68, ). Monozygotic twin studies examining overfeeding and energy deficit experiments have shown that gene-environment interactions affect energy balance (Tremblay et al 04, Br J Nutr) ie that some individuals are more susceptible to body-weight gain or loss than others because of genetic differences. In the future, health professionals should be able to count on early diagnosis of individuals at risk for developing long-term metabolic problems and obesity or for not responding adequately to clinical interventions 38

39 THE ‘THRIFTY GENES THEORY’ - TO OIKONOMIKO  Some experts postulate the existence of a so- called "thrifty" gene, which regulates hormonal fluctuations to accommodate seasonal changes. 39

40 THE ‘THRIFTY GENES THEORY’ - TO OIKONOMIKO  In certain nomadic populations, hormones are released during seasons when food supplies have traditionally been low, which results in resistance to insulin and efficient fat storage. The process is reversed in seasons when food is readily available. Because modern industrialization has made high- carbohydrate and fatty foods available all year long, the gene (or group of genes) no longer serves a useful function and is now harmful because fat, originally stored for famine situations, is not used but stored 40

41 The Pima paradox Ενώ οι Tohono O'odham, και οι γείτονές τους οι Pima, τρώνε και ασκούνται περίπου το ίδιο όπως οι υπόλοιποι αμερικανοί, το % παχυσαρκίας της φυλής Pima είναι > 2x από ότι στους καυκάσιους αμερικάνους. Από το 1965 o Dr. Eric Ravussin προσπαθεί να εξηγήσει το παράδοξο των Pima. Το 1984, έστησε ένα μεταβολικό θάλαμο στο Phoenix, AZ – κοντά στον καταυλισμό των Pima. Εκεί άρχισε μελέτες σύγκρισης του μεταβολικού ρυθμού διαφορετικών εθνοτικών ομάδων. 41 "Any important behavior needs alternate pathways," λέει ο Ravussin. "When it comes to survival mechanisms, you need redundant systems."

42 THE EXPLANATION? The Pima’s survival mechanisms evolved to store fat extremely efficiently, a genetic make-up that would have served the tribe well in the harsh desert climate of the southwest U.S. However, because of the"thrifty gene" today ~ 80% of the Arizona Pima are obese! ( when the National US rate is about % ) Type II diabetes, is also epidemic in old and young Pima "The Pima have a genetic liability. But it's only a liability in our environment. It was an asset to survival in mankind's history." says Ravussin 42

43 IS PHYSICAL ACTIVITY THE KEY? The Pima of Mexico are closely related to those of Arizona However, due to their labor-intensive lives and low-fat diets, the Mexican Pima do not suffer from obesity, diabetes or other associated illnesses 43

44 PHYSICAL ACTIVITY IS THE KEY The abrupt change in the lifestyle of the Arizona Pima can be traced to an after WW2 damn, that forced them to abandon farming and to accept US gov. food and cash subsidies. Lessons learned: "There will have to be public health policies to curb the obesity epidemic, such as playgrounds and safe places to play, taxing high fat foods," says Ravussin. "We tax cigarettes because they kill- well, obesity kills, too.“ "Architects have to develop a better city. Instead of malls every ten miles, we need to return to main streets" says Ravussin. 44

45 So, what do you think? The thrifty-gene theory remains a theory In part because the culprit gene (s) has yet to be identified "About 80% of the CAD risk can be accounted for by known risk factors like smoking or obesity or blood pressure and the way we live and eat, which leaves very little room for genetic risk factors." Dr. Salim Yusuf of McMaster University in Canada, leading epidemiologist in CAD to Asia's War With Heart Disease, TIME Asia "Mankind's genes as a whole evolved across all ethnic groups similarly." 45

46 Other example of rapidly increasing obesity prevalence linked to a change in lifestyle Greeks (fattest kids in the block!) Eskimos Polynesians Indians - In India, nearly 50% of CVD-related deaths occur below the age of 70, compared with just 22% in the West. the World Health Organization estimated that 60% of the world's cardiac patients would be Indian by 2010 Chinese - by % of men and 40% of women could be overweight (no more bicycles) 46

47 Αντίσταση στον τεχνολογικό πολιτισμό: καλύτερο σωματικό βάρος, καλύτερη υγεία Resisting technology = better BW, better health The Amish in North America, display very low CVD rates despite a diet rich in fat and refined sugar (meat, potatoes, gravy, eggs, vegetables, bread, pies, and cakes, and is quite high in fat). The Amish follow rules (Ordnung) that ban the ownership of gasoline-powered transportation, electricity, and other modern conveniences 47

48 Resisting technology = better BW, better health Research in the Amish in southern Ontario found that the average Amish man took some 18,000 steps a day, compared with 3,000 to 5,000 for the average American. Also, a total of 25% of the men and 27% of the women were overweight while 0% of the men and 9% of the women were obese. (Bassett et al 2004 Med Sci Sports Exerc. 36(1):79-85). Amish at other parts of the country who did not report farming as primary occupation showed obesity rates similar to the general US population 48

49 Σωματική Αδράνεια – το «νέο κάπνισμα» Physical inactivity… the new smoking! An Australian study (Lennert Veerman et al Br J Sports Med 2012;46: ) reported that 1 hour of TV watching = -22 min of lifespan Shaw et al 2000 calculated that for 1 cigarette smoked= - 11 min of lifespan Hmmm, don’t watch TV and smoke!

50 Physical inActivity in the modern workplace Drawn based on data derived from Stand Up Australia Sedentary behaviour in workers August Accessed on 10/7/2014

51 Sitting is associated with CVD Sitting behaviors are significant cardiovascular disease (CVD) mortality predictors Using the 2003 National Death Index and data from a 1982 mail-back survey in 7744 men (20-89 yr) initially free of CVD, the association of two sedentary behaviors, car riding and TV watching with CVD mortality was examined [Aerobics Center Longitudinal Study]. These sedentary behaviors were positively (P trend < 0.001) associated with CVD death. Having >10 h·wk −1 riding in a car or >23 h·wk−1 of combined sitting caused 82% and 64% greater risk of dying from CVD than having <4 or <11 h·wk −1, respectively. Warren et al 2010 Sedentary Behaviors Increase Risk of Cardiovascular Disease Mortality in Men Med Sci Sports Ex Vol 42 - Issue 5 - pp

52 Πως μας αρρωσταίνει το «καθισιό»; How is sitting making us ill? It alters a variety of cellular processes that impact on overall metabolism Evidence on the cellular regulation of skeletal muscle lipoprotein lipase (LPL) : experimentally reducing normal spontaneous standing and movement time affected LPL regulation more than adding intense exercise training on top of the normal level of nonexercise activity. Inactivity initiateds unique cellular processes that are qualitatively different from the exercise responses. The emergence of inactivity physiology? Hamilton et al 2007 Role of low energy expenditure and sitting in obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease Diabetes 56(11):

53 How is sitting making us ill? Lowering energy expenditure METs for sitting down range between depending of actual activity (thinking, watching tv, sitting in class, taking notes) So less muscle activity = less energy used Less energy used = fat storage Weight gain Weight loss +

54 Could be sitting be making us ‘locally’ fat? Mechanical stress on our posterior!! Shoham et al (Am J Physiol Cell Physio 2011) attempted to mimic the stress experienced by fat cells when people sit or lie down (however it was applied continuously for three to four weeks). Results: mouse precursor fat cells were stimulated to form fat cells that produced fat at a faster rate when under static mechanical stretching. It remains to be seen if this is relevant to the human condition!

55 Κοινωνικοοικονομικοί παράγοντες NATURE OR NURTURE? Obesity and social class In Western societies, higher rates of obesity are mostly to be found in those with the lowest incomes and the least education, particularly among women and certain ethnic groups. Also true in some Greek studies (e.g. Loukas et al) Some authors have viewed this association, with hunger and obesity co-existing side-by-side, as something of a paradox. 55

56 NATURE OR NURTURE? Obesity and social class 56 This apparent paradox may be explained by: – the relatively low cost of energy dense foods, – the high palatability of sweets and fats associated with higher energy intakes, and – the association of lower incomes and food insecurity with lower intakes of fruit and vegetables.

57 Παχυσαρκία στη νεαρή ηλικία -Obesity and young age: children and adolescents Among US children aged 6 through 19 years in , 31.0% were at risk for overweight or overweight and 16.0% were overweight ( Hedley et al 04 JAMA.291: ). Among Greek periadolescent children aged 12 to 14 years adverse changes in physical activity could predict changes in adiposity ( Koutedakis et al 05 ) A follow up of the Harvard Growth Study of 1922 to 1935 by Must et al 92 ( NEJM 327: ), reported that being overweight in adolescence predicted a broad range of adverse health effects that were independent of adult weight after 55 years of follow-up! –Obese adolescents that become obese adults have an increased risk of metabolic and cardiovascular complications, possibly related to the central deposition of fat that occurs in adolescence 57

58 Effect of insulin on glycerol production in obese adolescents Impaired stimulation of glucose metabolism and reduced suppression of lipolytic activity have both been suggested as important defects related to the insulin resistance of adolescent obesity Robinson et al 98 ( Am J Physiol Endocrinol Metab 274: E737-E743 ) : 7obese and 7 lean adolescents aged yr vs 9 lean adults during a two-step euglycemic- hyperinsulinemic clamp in combination with 1) a constant [2H5]glycerol (1.2 mg · m 2 · min 1) infusion to quantify glycerol turnover and 2) indirect calorimetry to estimate glucose and net lipid oxidation rates. They reported that, lipolysis was increased in obese adolescents as a consequence of an enlarged adipose mass rather than altered sensitivity of adipocytes to the suppressing action of insulin. 58

59 Σημεία προσοχής Obesity and young age considerations Children and adolescents, depending on their biological age, exhibit variability in adiposity, size and shape (fat distribution) Chronological age is not ‘predictive’ of biological age –Thus a 9-year old may biologically be a 12-year old and vice versa It is not logical nor fair nor safe to use the ‘adult’ criteria to categorize adiposity (see lab exercise lect 9) 59

60 Obesity and young age considerations It is imperative to consider biological age when measuring children –Important to use growth charts Similarly, it is imperative to appreciate the metabolic differences that could exist between young and adult The lack of data can be attributed at least partly to the ethical considerations on involving underage persons in basic research. 60

61 Σύγχρονα προβλήματα- νέες ερ. κατευθύνσεις Current problems- Research Directions The prevalence of obesity is steadily increasing in adolescents (Gortmaker et al 1987 Am. J. Dis. Child. 141: ) and, according to the National Health and Nutrition Examination Survey (NHANES) III, ~20% of US adolescent males and females are obese (Troiano et al 1995, Arch. Pediatr. Adol. Med. 149: ). Obese adolescents that become obese adults have an increased risk of metabolic and cardiovascular complications, possibly related to the central deposition of fat that occurs in adolescence 61

62 Current problems- Research Directions Most studies on the interactions between glucose and lipid metabolism have been performed in obese adults, most of whom have had long-lasting obesity therefore, any metabolic defect detected in adult obesity may represent an adaptation to the long-term obesity rather than being causally related. Childhood obesity & adolescent obesity represent ideal models to elucidate early metabolic defects occurring at the time of excessive fat accumulation It is still unclear how lipolysis is altered in obesity during adolescence, a developmental stage that appears to be of crucial importance in adipose tissue cellular proliferation 62

63 Τι πρέπει να γίνει; What needs to be done? The International Obesity TaskForce (European Congress on Obesity May, 2004), proposed a number of measures which follow the precautionary principle of promoting health while being unlikely to increase the risk of harm: –healthy school policies involving school cafeterias, vending machines and snack bars, –plentiful school-based physical activity classes and recess activities; –classroom health education linked to the school's food and activity practices; 63

64 What needs to be done? –links between school practice and home and community activities; –prolonged interventions rather than short-term ones, involving adults and children, at school and at home; –the involvement of all children, not just some, using techniques sensitive to the cultural, ethnic and gender characteristics of the children. 64

65 What needs to be done? For the realities of Greece you were informed by Prof. Koutedakis. –P.E. is only 2 ‘hours’ per week, and –there is no integrated national body (and policy maker) monitoring the anthropometric characteristics and tracking childhood pathology. –All efforts are by individual researchers and research groups usually based in academia –None or fragmented ‘transfer’ or research findings to education establishments (e.g. school system, policies) 65

66 What needs to be done? Will a Greek physician-nurse-teacher- exercise specialist ever tell parents that –cutting down on physical activity compromises the health, quality of life and life span of their children? –it may be better to pay for a sports’ club subscription than an extra class on Latin or math? –It’s not how you look but how healthy you are? (Healthy at Any Size) Or even better, that parents should play with their children and engage in physical activities together instead of watching TV together? If s/he will, would the parents follow the advice of an obese, unfit, chain smoking physician-nurse-teacher-exercise specialist? 66

67 HEALTHY AT ANY SIZE! Η κα Nelson ζυγίζει 110 κιλά, με μέτριο ύψος Κάνει 10 ώρες άσκηση την εβδομάδα Είναι δασκάλα αεροβικής γυμναστικής Έχει αρκετά καλό λιπιδαιμικό προφίλ Δεν καπνίζει ΥΓΕΙΑ ΣΕ ΟΛΑ ΤΑ ΜΕΓΕΘΗ! 67

68 Credits Γενικές φωτογραφίες φαγητού από το 68

69 Τέλος Ενότητας Ευχαριστώ για την προσοχή σας! ΠΑΝΕΠΙΣΤΗΜΙΟ ΘΕΣΣΑΛΙΑΣ


Κατέβασμα ppt "Άσκηση και Παχυσαρκία Φύλο, Κληρονομικότητα και Περιβάλλον Καρατζαφέρη Χριστίνα PhD Τμήμα Επιστήμης Φυσικής Αγωγής και Αθλητισμού ΠΑΝΕΠΙΣΤΗΜΙΟ ΘΕΣΣΑΛΙΑΣ."

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