On Sun, 5 Mar 2006 18:28:41 +0100, Renato R. wrote in
Post by Renato R. Post by Enrico C
On Sun, 5 Mar 2006 16:47:35 +0100, Renato R. wrote in
Post by Renato R. Post by Alessandro Morelli Post by Renato R.
Sbagli ad agire per convenzioni anziche' per studi clinici.
Guarda che la fisica non è una convenzione, ma uno studio molto più sicuro
che gli "studi clinici"... La caloria è un'unità di misuro del lavoro e,
quindi, di energia. Ergo, se introduco una certa quantità di energia nel
mio corpo e ne uso di più (magari con l'attività fisica) dimagrisco, se ne
uso meno ingrasso.
E' cio' che il mondo occidentale va ripetendo da decenni, con quali
Che la popolazione ingrassa sempre piu' e per l'obesita' e' ormai allarme
Tra il dire di mangiare meno calorie, e il farlo, c'è di mezzo il
Ti risulta che la popolazione ingrassi *nonostante* stia consumando
non dovrebbe risultarmi vista l'abbondanza dei prodotti light rispetto al
Se il prodotto "light" è uno yoghurt con meno grasso ma zuccherato...
Se il prodotto "light" è un formaggio con una manciata di calorie in
meno ma senza alcun sapore , che lascia insoddisfatto il palato...
Se il prodotto "light" è una merendina su cui è scritto "senza
zucchero" solo perché hanno sostituito il saccarosio con il
Se il prodotto "light" è la buona coscienza per l'abbuffata del giorno
...ovviamente no! :)
Post by Renato R. Post by Enrico C
A me risulta il contrario, cioè che la popolazione occidentale mangia
più calorie di prima, ne brucia meno per via della vita sedentaria, e
- guarda un po'! - ingrassa.
guarda che la vita sedentaria non e' nata ieri mattina ne' e' applicabile ad
I bambini fanno una vita sedentaria? Una volta avevi un'abbondanza di
bambini obesi? No, e' che una volta -guarda un po'- non avevi le merendine
light ipocaloriche ad elevato contenuto di carboidrati.
La vita sedentaria non è nata ieri mattina, ma è sotto gli occhi di
tutti il fatto che i lavori manuali di fatica sono stati rimpiazzati
dal pigiar tasti al computer comodamente seduti, che la casalinga non
deve più lavare e ramazzare perché ci sono lavatrice e aspirapolvere
che fanno il lavoro per lei, che l'Italia che andava in bici o a piedi
si è motorizzata in massa, che i bambini che giocavano per strada ora
stanno al computer o alla tivù, ecc. ecc. ecc.
Quanto alle calorie, ci sono le statistiche degli americani, uno dei
popoli più obesi del mondo, secondo cui l'introito calorico è
aumentato di addirittura il 24,5 percento (530 calorie in più al
giorno) dal 1970 al 2000.
Se anche non fossero diventati più sedentari (come invece sono
diventati) già quelle 530 calorie di troppo al giorno parlano da sole!
USDA's Economic Research Service (ERS) estimates [...] dietary intake
of calories in 2000 at just under 2,700 calories per person per day.
ERS data suggest that average daily calorie intake increased by 24.5
percent, or about 530 calories, between 1970 and 2000.
Post by Renato R. Post by Enrico C
Il problema è che si mangiano calorie poco sazianti, come per esempio
quelle dello zuccchero aggiunto dappertutto in cibi e bevande, quindi
si continua ad aver fame nonostante le calorie!
Il problema e' si vuole cercare di risolvere il problema dell'obesita' senza
prima comprendere il perche' si diventa obesi.
Certo, non ci sono *solo* le calorie. Di possibili cause dell'obesità
ce ne sono diverse. Cercando su Pubmed ho trovato persino uno studio
che collega l'uso del glutammato di sodio, quello del dado da cucina,
all'obesità. Poi ci sono le predisposizioni genetiche, chi l'ha
collegata a un eccesso di grassi, chi ai cibi ad alto indice
glicemico, chi dà la colpa alla televisione, ecc.
E i vari studi si concludono dicendo che molte cose sono ancora da
Probabilmente ci sono diverse cause, o magari motivi diversi a seconda
degli individui e delle situazioni. Pensa per esempio a chi mangia
compulsivamente per motivi psicologici, qualsiasi cosa finché non
svuota il frigo...
Però, alla fine della fiera, il mangiar troppo e muoversi poco a me
pare ancora la spiegazione di fondo, almeno nella maggior parte dei
J Am Diet Assoc. 2005 May;105(5 Suppl 1):S17-23.
Beyond energy balance: there is more to obesity than kilocalories.
Bray GA, Champagne CM.
Louisiana State University System, USA. ***@pbrc.edu
Using an epidemiologic model of the interactions between environmental
agents and human hosts to explain obesity, we explored food,
medications, physical inactivity, toxins, and viruses as environmental
agents that interact with a genetically programmed host to disturb
energy balance and cause obesity. Large portion sizes, high fat
intakes, easy access to calorically sweetened beverages, and lack of
any need to be physically active all play a role in the toxic
environment that leads to obesity. The genetic and physiologic
responses of a host determine whether or not this toxic environment
will produce obesity. Reversing the current trends of obesity requires
a new look at the limits of the energy balance concept, and a better
understanding of how environmental factors acutely and chronically
change the responses of susceptible hosts.
PMID: 15867891 [PubMed - indexed for MEDLINE]
Does high glutamate intake cause obesity?
Hermanussen M, Tresguerres JA.
Aschauhof, Altenhof, Germany. ***@t-online.de
World-wide obesity has risen to alarming levels. The average weight of
German conscripts now increases by almost 400 g/year. Similar data
were obtained in Austria, Norway and the UK. The rising prevalence of
obesity coincides with a rising popularity of protein-rich diets. On
average, Germans consume meat at 100 kg/year. Children eat some
threefold more protein than recommended; infants of 6 to 12 months
receive daily up to 5 g/kg body weight of protein. We hypothesise that
it is not the protein, but the amino acid glutamate that determines
the propensity of obesity. Chronic hyperglutamataemia may intoxicate
arcuate nucleus (AN) neurons, thereby disrupting the hypothalamic
signalling cascade of leptin action, causing hyperphagia, obesity and
hyperleptinaemia. Hyperleptinaemia also exerts sympathetic effects
including blood pressure elevation that are mediated via mechanisms
different from the hypothalamic system, and other symptoms of the
'metabolic syndrome'. This may happen even before birth when in
small-for-gestational-age foetuses with impaired umbilical plasma
flow, foetal hyperglutamataemia induces AN damage followed by later
impairment of feeding regulation, hyperleptinaemia and symptoms that
characterise the 'thrifty phenotype'. We suggest abandoning the
flavouring agent monosodium glutamate and reconsidering the
recommended daily allowances of protein and amino acids, particularly
PMID: 14513871 [PubMed - indexed for MEDLINE]
1: Minerva Gastroenterol Dietol. 2002 Dec;48(4):303-8. Related
Obesity etiology: role of leptin.
Cena H, Zaccardo A, Roggi C.
Dipartimento di Scienze Sanitarie Applicate e Psicocomportamentali,
Sezione di Scienza dell'Alimentazione, Universita degli Studi di
Pavia, Pavia, Italy.
A huge interest in the scientific community has been aroused since
leptin's discovery (from greek leptos=thin), due to its important role
in the body energetic balance regulation. This protein is synthesized
from ob gene and secreted by the adipose tissue when fat mass
increases, decreasing hunger and increasing energy expenditure in
order to restore energetic balance. In the latest years many human
genetic studies have been conducted showing that sometimes obesity may
be due to mutations of genes involved in energetic balance mediated by
leptin. These findings amplified the knowledge of obesity
etiopathogenesis, thus arousing hopes and expectations for new
therapeutic horizons in this disease. Latest researches also outlined
many other functions of leptin, some of which are presented in this
review. In this paper we collected the most significant data about
leptin's physiology and its role in body energetic homeostasis,
looking also to the effects on hypothalamus-hypophysis-endocrine axes
regulation, on body thermoregulation, on the reproductive function and
on foetus and child growth. A wide section is thus reserved to the
most recent findings about the role of leptin in obesity and about its
therapeutic applications in this field.
PMID: 16491055 [PubMed - in process]
1: Nutrition. 2004 Feb;20(2):218-24.
Effect of palatable hyperlipidic diet on lipid metabolism of sedentary
and exercised rats.
Estadella D, Oyama LM, Damaso AR, Ribeiro EB, Oller Do Nascimento CM.
Department of Physiology, Universidade Federal de Sao Paulo-EPM,
Biomedical Science Building, Rua Botucatu 862, Vila Clementino,
04023-060 Sao Paulo, SP, Brazil.
OBJECTIVE: The present study was designed to examine 1) whether
continuous feeding with a palatable hyperlipidic diet and cycling this
diet with chow diet would affect lipid and carbohydrate metabolism in
a similar way; and 2) whether the effect of chronic exercise on lipid
and carbohydrate metabolism would be modified by these diet regimens.
METHODS: Male 25-d-old Wistar rats were assigned to one of six groups:
sedentary rats fed with chow diet; exercised (swimming 90 min/d, 5
d/wk) rats fed with chow diet; sedentary rats fed with a palatable
hyperlipidic diet; exercised rats fed with the palatable hyperlipidic
diet; sedentary rats fed with food cycles (four cycles alternating the
chow and hyperlipidic diets weekly); and exercised rats fed with food
cycles. After 8 wk of treatment, the animals were killed 24 h after
the last exercise session. RESULTS: The hyperlipidic diet and food
cycles schedules caused similar increases in body weight gain, carcass
lipogenesis rate and adiposity, lipid content of the liver and
gastrocnemius muscle, and serum total lipid, triacylglycerol, insulin,
and leptin levels. The exercise attenuated body weight gain, adipose
tissue mass, and serum triacylglycerol, insulin, and leptin levels
similarly in the hyperlipidic and food cycles groups. Carcass
lipogenesis rate was not affected by exercise in any of the three
groups. CONCLUSIONS: The data showed that the continuous intake of a
hyperlipidic palatable diet for 8 wk and the alternation of the
high-fat intake with periods of chow intake cause obesity and affected
lipid metabolism in a similar way. Chronic exercise attenuated body
weight gain and adiposity and improved serum lipid concentrations in
both high-fat feeding regimens.
PMID: 14962690 [PubMed - indexed for MEDLINE]
1: JAMA. 2006 Jan 4;295(1):39-49.
JAMA. 2006 Jan 4;295(1):94-5.
Low-fat dietary pattern and weight change over 7 years: the Women's
Health Initiative Dietary Modification Trial.
Howard BV, Manson JE, Stefanick ML, Beresford SA, Frank G, Jones B,
Rodabough RJ, Snetselaar L, Thomson C, Tinker L, Vitolins M, Prentice
MedStar Research Institute, Washington, DC, USA.
CONTEXT: Obesity in the United States has increased dramatically
during the past several decades. There is debate about optimum calorie
balance for prevention of weight gain, and proponents of some
low-carbohydrate diet regimens have suggested that the increasing
obesity may be attributed, in part, to low-fat, high-carbohydrate
diets. OBJECTIVES: To report data on body weight in a long-term,
low-fat diet trial for which the primary end points were breast and
colorectal cancer and to examine the relationships between weight
changes and changes in dietary components. DESIGN, SETTING, AND
PARTICIPANTS: Randomized intervention trial of 48,835 postmenopausal
women in the United States who were of diverse backgrounds and
ethnicities and participated in the Women's Health Initiative Dietary
Modification Trial; 40% (19,541) were randomized to the intervention
and 60% (29,294) to a control group. Study enrollment was between 1993
and 1998, and this analysis includes a mean follow-up of 7.5 years
(through August 31, 2004). INTERVENTIONS: The intervention included
group and individual sessions to promote a decrease in fat intake and
increases in vegetable, fruit, and grain consumption and did not
include weight loss or caloric restriction goals. The control group
received diet-related education materials. MAIN OUTCOME MEASURE:
Change in body weight from baseline to follow-up. RESULTS: Women in
the intervention group lost weight in the first year (mean of 2.2 kg,
P<.001) and maintained lower weight than control women during an
average 7.5 years of follow-up (difference, 1.9 kg, P<.001 at 1 year
and 0.4 kg, P = .01 at 7.5 years). No tendency toward weight gain was
observed in intervention group women overall or when stratified by
age, ethnicity, or body mass index. Weight loss was greatest among
women in either group who decreased their percentage of energy from
fat. A similar but lesser trend was observed with increases in
vegetable and fruit servings, and a nonsignificant trend toward weight
loss occurred with increasing intake of fiber. CONCLUSION: A low-fat
eating pattern does not result in weight gain in postmenopausal
women. Clinical Trial Registration ClinicalTrials.gov, NCT00000611.
Randomized Controlled Trial
PMID: 16391215 [PubMed - indexed for MEDLINE]
1: Lancet. 2004 Aug 28-Sep 3;364(9436):778-85.
Lancet. 2004 Aug 28-Sep 3;364(9436):736-7.
Lancet. 2004 Dec 11-17;364(9451):2095.
Effects of dietary glycaemic index on adiposity, glucose homoeostasis,
and plasma lipids in animals.
Pawlak DB, Kushner JA, Ludwig DS.
Department of Medicine, Children's Hospital, Boston, MA, USA.
BACKGROUND: Clinical studies suggest a role for dietary glycaemic
index (GI) in bodyweight regulation and diabetes risk. However, partly
because manipulation of GI can produce changes in potentially
confounding dietary factors such as fibre content, palatability, and
energy density, its relevance to human health remains controversial.
This study examined the independent effects of GI in animals. METHODS:
Partially pancreatectomised male Sprague-Dawley rats were given diets
with identical nutrients, except for the type of starch: high-GI
(n=11) or low-GI (n=10). The animals were fed in a controlled way to
maintain the same mean bodyweight in the two groups for 18 weeks.
Further experiments examined the effects of GI in rats in a cross-over
design and C57BL/6J mice in a parallel design. FINDINGS: Despite
having similar mean bodyweight (547.9 [SE 13.4] vs 549.2 [15.2] g),
rats given high-GI food had more body fat (97.8 [13.6] vs 57.3 [7.2]
g; p=0.0152) and less lean body mass (450.1 [9.6] vs 491.9 [11.7] g;
p=0.0120) than those given low-GI food. The high-GI group also had
greater increases over time in the areas under the curve for blood
glucose and plasma insulin after oral glucose, lower plasma
adiponectin concentrations, higher plasma triglyceride concentrations,
and severe disruption of islet-cell architecture. Mice on the high-GI
diet had almost twice the body fat of those on the low-GI diet after 9
weeks. INTERPRETATION: These findings provide a mechanistic basis for
interpretation of studies of GI in human beings. RELEVANCE TO
PRACTICE: The term GI describes how a food, meal, or diet affects
blood sugar during the postprandial period. GI as an independent
factor can cause obesity and increase risks of diabetes and heart
disease in animals. Use of low-GI diets in prevention and treatment of
human disease merits thorough examination.
PMID: 15337404 [PubMed - indexed for MEDLINE]
: Pediatrics. 1985 May;75(5):807-12.
Do we fatten our children at the television set? Obesity and
television viewing in children and adolescents.
Dietz WH Jr, Gortmaker SL.
The association of television viewing and obesity in data collected
during cycles II and III of the National Health Examination Survey was
examined. Cycle II examined 6,965 children aged 6 to 11 years and
cycle III examined 6,671 children aged 12 to 17 years. Included in the
cycle III sample were 2,153 subjects previously studied during cycle
II. These surveys, therefore, provided two cross-sectional samples and
one prospective sample. In all three samples, significant associations
of the time spent watching television and the prevalence of obesity
were observed. In 12- to 17-year-old adolescents, the prevalence of
obesity increased by 2% for each additional hour of television viewed.
The associations persisted when controlled for prior obesity, region,
season, population density, race, socioeconomic class, and a variety
of other family variables. The consistency, temporal sequence,
strength, and specificity of the associations suggest that television
viewing may cause obesity in at least some children and adolescents.
The potential effects of obesity on activity and the consumption of
calorically dense foods are consistent with this hypothesis.
PMID: 3873060 [PubMed - indexed for MEDLINE]
Am J Clin Nutr. 2005 Jul;82(1 Suppl):215S-217S.
Genetics of common forms of obesity: a brief overview.
Lyon HN, Hirschhorn JN.
Children's Hospital Boston, Boston, MA 02115, USA .
The obesity epidemic is attributable to dietary and behavioral trends
acting on a person's genetic makeup to determine body mass and
susceptibility to obesity-related disease. Common forms of obesity
have a strong hereditary component, yet genetic pathways that
contribute to obesity have not yet been elucidated. Many genetic
association studies have been reported, but few have been successfully
replicated. New research tools and large studies will lead to an
understanding of genes and their interaction to cause obesity, which
may help guide successful interventions and treatments.
PMID: 16002823 [PubMed - indexed for MEDLINE]
Eur J Pediatr. 2000 Sep;159 Suppl 1:S35-44.
Aetiology of overweight and obesity in children and adolescents.
Department of Paediatrics, University of Verona, Polyclinic B Roma,
The epidemic diffusion of obesity in industrialised countries has
promoted research on the aetiopathogenesis of this disorder. The
purpose of this review is to focus mainly on the contribution that
European research has made to this field. Available evidence suggests
that obesity results from multiple interactions between genes and
environment. Parents obesity is the most important risk factor for
childhood obesity. Twin, adoption, and family studies indicated that
inheritance is able to account for 25% to 40% of inter-individual
difference in adiposity. Single gene defects leading to obesity have
been discovered in animals and, in some cases, confirmed in humans as
congenital leptin deficiency or congenital leptin receptor deficiency.
However, in most cases, genes involved in weight gain do not directly
cause obesity but they increase the susceptibility to fat gain in
subjects exposed to a specific environment. Both genetic and
environmental factors promote a positive energy balance which cause
obesity. The relative inefficiency of self-adapting energy intake to
energy requirements is responsible for fat gain in predisposed
individuals. The role of the environment in the development of obesity
is suggested by the rapid increase of the prevalence of obesity
accompanying the rapid changes in the lifestyle of the population in
the second half of this century. Early experiences with food, feeding
practices and family food choices affect children's nutritional
habits. In particular, the parents are responsible for food
availability and accessibility in the home and they affect food
preferences of their children. Diet composition, in particular fat
intake, influences the development of obesity. The high energy density
and palatability of fatty foods as well as their less satiating
properties promotes food consumption. TV viewing, an inactivity and
food intake promoter, was identified as a relevant risk factor for
obesity in children. Sedentarity, i.e. a low physical activity level,
is accompanied by a low fat oxidation rate in muscle and a low fat
oxidation rate is a risk factor of fat gain or fat re-gain after
weight loss. CONCLUSION: Further research is needed to identify new
risk factors of childhood obesity, both in the genetic and
environmental areas, which may help to develop more effective
strategies for the prevention and treatment of obesity.
PMID: 11011954 [PubMed - indexed for MEDLINE]
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