"Rudy Canoza" <pipes@[EMAIL PROTECTED]
> trying to meet
his daily posting quota on behalf of the beef industry in message
news:HK2dnVrkQq-HfIDVnZ2dnUVZ_qbinZ2d@[EMAIL PROTECTED]
some five-year-old hooey dredged up from the archives..
...
> > "swamp" <swamp@[EMAIL PROTECTED]
> wrote in message
> > news:kpaifv0q5qfllvqpbfs370ksbe0n4711mb@[EMAIL PROTECTED]
> >> You mean the Yahoo link that cited Neal Barnard? I read it, and found
> >> it and find him full of hooey. His "addiction to food" proposition is
> >> ridiculous, as his conceits usually are.
'.. consumption of high-energy sweet and fat food increases endogenous
opiates release (ie, feedforward interaction; Tanda and Di Chiara, 1998;
Colantuoni et al, 2002; Grigson, 2002)
...
... reward centers activation by high sugar and fat content palatable
foods
promotes desire 'to come back for more' (Kelley et al, 2002) by
upregulating
of hunger signaling (orexin, AgRP, and MCH) in hypothalamic orexigenic
networks and by blunting brain responses to the peripheral satiety
hormones,
insulin and leptin (Erlanson-Albertsson, 2005; Isganaitis and Lustig,
2005).
Prefrontal cortex modulates these effects via reciprocal innervation with
the
hypothalamic-limbic areas (Berthoud, 2004a) by forming subjective hedonic
perceptions and integrating them with metabolic signals and with
intrapsychic
and environmental contexts (Kringelbach, 2005).
REPETITIVE PALATABLE FOOD CONSUMPTION MAY
DYSREGULATE HOMEOSTATIC AND REWARD PROCESSES
To maintain stability of the body adipose content, energy expenditure
should
tightly match caloric intake. This is accomplished through negative
feedback
regulation exerted by the endocrine markers of body fat mass, insulin and
leptin; both are also affected by recent food intake and its macronutrient
composition (Havel, 2001; Schwartz et al, 2003). In the basal state
(Figure 1),
insulin and leptin inhibit anabolic pathways (appetite and energy
conservation)
while maintaining tonic activation of the catabolic pathways (satiety and
energy outflow).
Such regulatory system may be adequate for regular diets but is
'inherently
biased toward weight gain' (Havel, 2001; Schwartz et al, 2003; Schwartz
and
Niswender, 2004) in 'obesigenic' environments abound in 'supersized'
meals,
more than twice caloric density (energy per weight) and content of healthy
diets (Prentice and Jebb, 2003). High caloric density food contributes to
abnormally elevated total caloric intake as weight and volume of meals
ingested by humans tend to remain relatively steady (Rolls et al, 1998).
Such rich in caloric content diets robustly activate reward centers and
fail
to produce pro****tional (to the amount of ingested calories) suppression
of hunger signals, as CNS insulin and leptin stop boosting and
restraining,
respectively, already activated (in the basal state) catabolic pathways
and
already inhibited (in the basal state) anabolic pathways, that is, ceiling
effect
(Schwartz et al, 2003). Thus, metabolic restraint on reward function via
insulin/leptin mechanism becomes inefficient at about 40% fat
concentration,
typical of the Western diet (Figlewicz, 2003a, 2003b, 2004), allowing
reward
mechanisms to over-ride metabolic requirements (perhaps owing to
evolutionary pressure giving preferentiality to food intake over fasting)
and
underscoring the role of cortical cognitive control mechanisms in the
determination of the amount of eaten food.
Pleasurable hedonic impact and inefficient suppression of hunger by
palatable foods predictably brings increases in the amount of consumed
food and weight gain (in the absence of compensatory caloric loss) with
ensuing hyperinsulinemia and insulin resistance (Kahn and Flier, 2000;
Homko et al, 2003), which drive weight further upward (Sigal et al, 1997;
Odeleye et al, 1997). Moreover, weight gain and insulin resistance from
habitual consumption of palatable foods decrease insulin and leptin blood-
brain barrier (BBB) penetrability (Caro et al, 1996; Kaiyala et al, 2000;
Banks, 2003; Banks and Farrell, 2003; Woods et al, 2003) and their CNS
effects (Couce et al, 2001; Banks and Farrell, 2003; Lindqvist et al,
2005;
****te et al, 2005), albeit some homeostatic hypothalamic areas lack BBB
(Peruzzo et al, 2000; Ganong, 2000). The resultant brain insulin and
leptin
'resistance' renders normal satiety signals even more ineffective
(Erlanson-
Albertsson, 2005; Isganaitis and Lustig, 2005) leading to further
impairments in physiologic mechanisms regulating food intake (eg,
overeating) and ****fting the set point for energy homeostasis towards the
development of overweight and obesity (Levine et al, 2003; Erlanson-
Albertsson, 2005; Isganaitis and Lustig, 2005). It is quite difficult to
reverse the developing vicious cycle (schematically illustrated in Figure
4)
as attempted weight loss by caloric restriction results in insulin and
leptin
declines triggering robust activation of anabolic pathways and suppression
of catabolic pathways; the magnitude of these responses exceeds by far
that during caloric overflow (Niswender et al, 2004).
Figure 4.
Diagram describing repetitive and compulsive nature of palatable food
consumption. The figure depicts transition from occasional palatable food
intake to dysregulation of homeostatic and reward processes leading to
impairments in normal signals of hunger and satiety along with adaptations
and deviations of physiological set points (cf, Koob and Le Moal, 2001).
Full figure and legend (33K)
http://www.nature.com/npp/journal/v31/n10/fig_tab/1301051f4.html#figure-title
....'
http://www.nature.com/npp/journal/v31/n10/full/1301051a.html
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