ΠΑΝΕΠΙΣΤΗΜΙΟ ΘΕΣΣΑΛΙΑΣ
Άσκηση και Παχυσαρκία
Φύλο, Κληρονομικότητα και Περιβάλλον
Καρατζαφέρη Χριστίνα PhD
Τμήμα Επιστήμης Φυσικής Αγωγής και Αθλητισμού
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
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
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
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
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, 2000
6
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/m2)
σύμφωνα με τον WHO (Fact sheet N°311, reviewed May 2014, accessed
via http://www.who.int/mediacentre/factsheets/fs311/en/ on 27/6/2014):
– Υπέρβαρος/Overweight: ΔΜΣ ≥25 kg/m2
– Παχύσαρκος/Obese : ΔΜΣ ≥ 30 kg/m2.
• 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
Επιπολασμός της παχυσαρκίας
Επιπολασμός του υπέρβαρου και της παχυσαρκίας στις ΗΠΑ, σε ενήλικες ηλικίας
20-74 ετών -Prevalence of overweight and obesity among U.S. adults, age 20-74
years
Obese (BMI ≥30 kg/m2)
NHANES (1999-2002)
n=7494
NHANES III (1988-1994),
n=14468
NHANES II (1976-1980),
n=11207
Overweight or Obese (BMI
≥25kg/m2)
0
20
40
60
80
Redrawn based on Table from Age-adjusted* prevalence of overweight and obesity among U.S.
adults, age 20-74 years - 1999-2002 National Health and Nutrition Examination Survey (NHANES) *Age-adjusted
by the direct method to the year 2000 U.S.
9
Bureau of the Census estimates using the age groups 20-39, 40-59, and 60-74 years.
Επιπολασμός της παχυσαρκίας στις ΗΠΑ, σε ενήλικες με κατηγοριοποίηση ανά
πολιτιστική καταγωγή - Age-adjusted prevalence of obesity, by cultural origin,
2011-2012
All US adults
hispanic
non-hispanic asian
non-hispanic black
non-hispanic white
0
10
20
30
40
50
60
Blue bars drawn
based on data from
Fig 2 Odgen et al
2013, Prevalence of
obesity among
adults: United States
2011-2012, NCHS
Data Brief no 131.
Red bar drawn based
on data from Odgen
et al 2014, JAMA Vol
311, No. 8.
• No signs of abating….but stabilising?
• Lowest in non-hispanic asian
• Highest in non-hispanic black
10
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)
% with BMI>30 kg/m2 for
the over 15years of age, EU
25
20
Greece
15
Spain
Portugal
10
Sweden
Austria
5
0
11
Obesity and differences between the two sexes
Παχυσαρκία και διαφορές ανάμεσα
στα δύο φύλα
What makes a man?
What makes a woman?
•
•
•
«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 3ο 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)
13
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
Χαρακτηριστικά του φύλου
Gender Characteristics
•
•
•
•
•
•
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
15
Στον Ενήλικα -In the adult human
•
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
16
Επιπολασμός της παχυσαρκίας στην Αγγλία, κατά την δεκαετία του 90’ Prevalence of obesity in England, in the 90s
1991
1986
Women
Men
1980
0
5
10
15
20
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;311:437-439
17
Επιπολασμός της παχυσαρκίας στην Αγγλία ανά φύλο κατά τα έτη 2001-2005
Prevalence of overweight & obesity in England males and females, 2001-2005
25-64 yrs
•
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:
50-64 yrs
25-49 yrs
–
–
•
0
50
100
in males (Bosnia-Herzegovina)
63,2% & 15,9% , respectively
In females 50,9% (Croatia) &
17% (Portugal), respectively
Note: these data come from
actual measurements. Selfreported data show lower
prevalence!
18
Επιπολασμός της παχυσαρκίας στις ΗΠΑ, σε ενήλικες με κατηγοριοποίηση ανά
πολιτιστική καταγωγή και φύλο - Age-adjusted prevalence of obesity, by cultural
origin and sex, 2011-2012
Women
hispanic
Men
Total
non-hispanic asian
non-hispanic black
non-hispanic white
0
20
40
60
Drawn based on
Fig 2 from Odgen
et al 2013,
Prevalence of
obesity among
adults: United
States 2011-2012,
NCHS Data Brief
no 131.
• Lower in non-hispanic asian.
• Higher in non-hispanic black women vs men
and vs all other women groups
19
OBESITY AND GENDER DIFFERENCES
• Fat distribution differs between the sexes
• Η κατανομή του λίπους διαφέρει μεταξύ των δύο φύλων
20
Κατανομή του λιπώδους ιστού στο σώμα REGIONAL ADIPOSE TISSUE DISTRIBUTION
•
•
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 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;
KROTKIEWSKI et al 1983,
J. Clin. Invest. 72: 1150-1162
21
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: 1150-1162
22
Γιατί μας απασχολεί ο λιπώδης ιστός; Why
does fat matter?



Adipose tissue is an active secretory organ
producing adipocytokines, (tumor necrosis factoralpha, 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
al 1995 J Clin Invest 95: 2409–2415 ) and vascular events
et
(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: 2409-2415) και τα αγγειακά επεισόδια (Thompson 1995 N Engl J Med
332: 635-641)
23
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 45:1547-1555, DeFronzo 1991 Diabetes Care
14:173-194)
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:
356-359, Hak et al 1999 Arterioscler Thromb Vasc Biol 19: 1986-1991)
24
Καρκίνος και Παχυσαρκία
μαστός
7%
παχύ
έντερο
10%
προστατης
4%
ενδομήτριο
36%
νεφρός
21%
χοληδόχος
κύστη
22%
• Η παχυσαρκία
συνδέεται με τον
καρκίνο
• Για το έτος 1995 ο
συνολικός αριθμός
περιστατικών καρκίνου
που αποδίδονται στο
υπερβολικό βάρος στο
Ηνωμένο Βασίλειο
ήταν 9.000 (70.000 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. 2001 Int J Cancer 91: 421-430 – τιμές κατά
προσέγγιση)
25
Σχετικός κίνδυνος για ανάπτυξη
παθήσεων- relative risk for disease
Disease
Women
Men
Working days lost
Diabetes type II
12,7
5,2
5,960,000
Heart attack
3,2
1,5
1,230,000
Osteoarthritis
1,4
1,9
950,000
All obesity linked secondary diseases
Bergström et al. 2001 Int J Cancer 91: 421-430
26
What is the importance of central adiposity in
women?
Ποια η σημασία της κεντρικής παχυσαρκίας;
•
•
•
Until menopause women enjoy a ‘protection’
from CAD (possibly an estrogen mediated antioxidant
effect - Vina et al 2005 FEBS Lett 579;12: 2541-2545).
This however disappears when women acquire
central adiposity
and after the menopause…
27
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
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
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
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
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
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
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
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 20-30 genes may
finally prove to be crucial in linking genetic inheritance to
obesity

Ίσως η εικόνα να αλλάξει ραγδαία στην επόμενη πενταετία...
35
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
4.06.
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
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 AfricanAmerican sibling pairs.
Adjustment for diabetes status, smoking, dietary intake,
and physical activity resulted in only minor changes in
the heritability estimates (all p < 0.0001).
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 13:312319)
37
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 12,2076-2081, Seeman, et
al 1996 Am J Physiol 270,E320-E327, Abney et al 2001 Am J Hum
Genet 68,1302-1307) .
•
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
THE ‘THRIFTY GENES THEORY’ - TO
OIKONOMIKO GONIDIO
• Some experts postulate the existence of a socalled "thrifty" gene, which regulates
hormonal fluctuations to accommodate
seasonal changes.
39
THE ‘THRIFTY GENES THEORY’ - TO
OIKONOMIKO GONIDIO

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 highcarbohydrate 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
http://www.pbs.org/saf/1110/features/fighting.htm
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.
"Any important behavior
needs alternate pathways,"
λέει ο Ravussin. "When it
comes to survival
mechanisms, you need
redundant systems."
41
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 2530%)
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
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
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
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
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 2025 37% of men and 40% of
women could be overweight (no more
bicycles)
46
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
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
Σωματική Αδράνεια – το «νέο κάπνισμα»
Physical inactivity… the new smoking!
• An Australian study (Lennert Veerman et al Br
J Sports Med 2012;46:927-930 ) 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!
Physical inActivity in the modern
workplace
% time spent
Sitting
4%
Light
29%
Moderate to
vigorous
67%
Drawn based on data derived from Stand Up Australia Sedentary behaviour in workers
August 2009. http://www.medibank.com.au/Client/Documents/Pdfs/Stand_Up_Australia.pdf
Accessed on 10/7/2014
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 (Ptrend < 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 879-885
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):2655-67.
How is sitting making us ill?
• Lowering energy expenditure
• METs for sitting down range between 1-1.8
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
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!
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
NATURE OR NURTURE? Obesity and
social class
• 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.
56
Παχυσαρκία στη νεαρή ηλικία -Obesity and
young age: children and adolescents

Among US children aged 6 through 19 years in 1999-2002, 31.0% were
at risk for overweight or overweight and 16.0% were overweight
(Hedley et al 04 JAMA.291:2847-2850).

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 327:1350-1355), 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
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 13-15 yr vs 9 lean adults during a two-step euglycemichyperinsulinemic 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
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
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
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: 535540) 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: 1085-1091).

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
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
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
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
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
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
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!
http://www.theage.com.au/articles/2003/10/05/1065292465637.html
67
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68
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