"Mxsmanic" <[email hidden]> wrote in message
"]news:[email hidden]...
Quoted message said:Mirek Fidler said:Actually, this is what low-carbers seem to experience
quite often.
There is no "economy mode" compatible with life.
The body needs a certain amount of energy to operate,
period. While fasting and starvation can induce some energy-
sparing reactions in the body, none of them are compatible
with a normal state of health--the person is still
starving, and if food isn't forthcoming soon, death will
result. The notion that human beings can go for months or
years in some sort of magic energy-saving mode that allows
them to eat virtually nothing without losing weight is a
pure fantasy. Look at any country where people _really
aren't_ eating anything, and you'll see how quickly they
die. People in developed countries who "eat nothing but
still don't lose weight" are either very incompetent at
counting calories or are lying to themselves and everyone
else about how much they actually eat.
Quoted message said:... initially, body is not adapted to burning fat and
process is ineffective - later it becomes more effective
and advantage disappears too - it also seems that
ketosis levels drop quite fast too.
The body learns to burn fat within a couple hours, since
the alternative is death from starvation. It doesn't need
to adapt to anything over longer periods. All these
mechanisms are built in, and they work very well.
Quoted message said:Anyway, mere fact that there ARE stalls indicates that
"calorie is a calorie" concept is not universal truth.
No, it's an indication of how incompetent or dishonest
some people are when they try to count calories.
--
Transpose hotmail and mxsmanic in my e-mail address to
reach me directly.
Please reconsider your position on the body's ability to
regulate its energy homeostasis as a function of food
availability, fasting. Offering evidence below. Famine and
seasonal fluctuations have been around for most of human
existence, and the metabolic survival strategy has been to
store as much fat as possible during good times, and to
economize in bad times. I submit that 'famine' may be part
of the ideal healthy CR lifestyle. :-} (also helps to
explain why modern humans have an obesity problem.) MikeV
Physiol Behav. 2001 Nov-Dec;74(4-5):683-701. Related
Articles, Links
The hypothalamus and the control of energy homeostasis:
different circuits, different purposes.
Williams G, Bing C, Cai XJ, Harrold JA, King PJ, Liu XH.
Diabetes and Endocrinology Research Group, Department of
Medicine, University of Liverpool, Duncan Building, Daulby
Street, L69 3GA, Liverpool, UK. [email hidden]
The hypothalamus regulates many aspects of energy
homeostasis, adjusting both the drive to eat and the
expenditure of energy in response to a wide range of
nutritional and other signals. It is becoming clear that
various neural circuits operate to different degrees and
probably serve specific functions under particular
conditions of altered feeding behaviour. This review will
discuss this functional diversity by illustrating
hypothalamic neurones that express neuropeptide Y (NPY), the
melanocortin-4 receptor (MC4-R) and the orexins. NPY
neurones in the arcuate nucleus (ARC) release NPY, a
powerful inducer of feeding and obesity, in the
paraventricular nucleus (PVN) and the lateral hypothalamic
area (LHA). ARC-NPY neurones are inhibited by leptin and
insulin and become overactive when levels of these hormones
fall during undernutrition. They may function
physiologically to protect against starvation. With
disruption of the inhibitory leptin signals due to gene
mutations, the NPY neurones are overactive, which
contributes to hyperphagia and obesity in the ob/ob and
db/db mice and fa/fa Zucker rat. The MC4-R is activated by
alpha-melanocyte-stimulating hormone [alpha-MSH; a cleavage
product of pro-opiomelanocortin (POMC), which is expressed
in the other ARC neurones] and inhibits feeding. This effect
is antagonised by agouti gene-related peptide (AGRP), which
is coexpressed by the ARC-NPY neurones only. Activation of
MC4-R, possibly mediated by blockade of AGRP release,
appears to restrain overeating of a palatable diet. This
response may be programmed by a transient rise in leptin
soon after presentation of palatable food, and rats that
fail to do this will overeat and become obese. Orexin-A and
-B (corresponding to hypocretins 1 and 2) are expressed in
specific LHA neurones. These have extensive reciprocal
connections with many areas involved in appetite control,
including the nucleus of the solitary tracts (NTS), which
relays vagal afferent satiety signals from the viscera.
Orexin neurones also have close anatomical connections with
LHA glucose-sensitive neurones. Orexin-A induces acute
feeding but does not cause obesity. Orexin neurones are
stimulated by hypoglycaemia partly via the NTS and inhibited
by food ingestion. These neurones may therefore be involved
in the severe hyperphagia of hypoglycaemia and short-term
control of feeding.
Publication Types: Review Review, Tutorial
PMID: 11790431 [PubMed - indexed for MEDLINE]