I presented scientific backing for my argument. You expressed an
opinion. Who has an argument again?

TC

http://www.animal-science.org/cgi/content/full/81/13_suppl_1/E27

Physical Activity.
Except for recommendations of increasing maintenance requirements of
grazing animals (NRC, 2001), the use and variation of energy in
physical activity by cattle has been largely ignored. Thermogenesis of
individual human subjects associated with activities that are not
purposeful exercise has been shown to be highly variable, heritable,
and predictive of weight gain (Snitker et al., 2001) and low in obese
individuals (Schoeller, 2001). Snitker also found that the measurement
in respiration chambers of these "activities of daily living"
correlates (r = 0.53) to individuals' free-living activity. These
types of movements, sometimes called fidgeting, can elevate sitting or
standing thermogenesis by 50 to 80% (Levine et al., 2000) and can be
monitored in free-living individuals with inclinometers and
accelerometers (Levine et al., 2001a). General usefulness of these
monitors is apparently limited by the need to calibrate them to
individual subjects (Levine et al., 2001b).

Anatomical Variations.
Many attempts have been made to explain the anatomical, physiological,
and biochemical causes of varying FHP/BW. Variations in fat-to-lean
tissue mass have been widely ascribed to explain group or individual
heat production differences, however, not always as demonstrated by
McNiven (1984). She imposed nutritional regimens on ewes to change body
fat percentage dramatically and showed little difference in FHP or
maintenance heat production per unit of BW in these groups. Visceral
organ tissue, particularly hepatic, consumes O2 at a much higher
rate/mass than the whole animal and is positively correlated with
animals or circumstances varying from mean basal metabolic rates. The
basal metabolic rates of divergent human subjects have been
successfully regenerated from the mass of individual organs and
tissues, separately determined, multiplying by the O2 consumptions/kg
of each tissue and summing these to equal that of the whole subject.
Changes in the ratios of visceral organ to whole-body mass also
parallel changes in fasting or maintenance heat production in response
to changes in level of alimentation, stage of fetal growth, young to
old, small to large BW species, or Bos indicus vs. Bos taurus cattle
(Ferrell et al., 1986; Huntington et al., 1988; Johnson et al., 1990).

Physiological Factors.
Many "maintenance control factors" have been proposed. In addition to
the above, these include T3, Na+/K+ATPase, proton leak, uncoupling
proteins, leptin, acetyl-CoA carboxylase 2, malonyl CoA, sympathetic
tone, 2-agonists, and calcium/calmodulin-dependent muscle protein
kinase. Knowledge of these factors has not resulted in the ability to
select animals to change their maintenance cost of production. However,
this research has helped to define the general requirements of groups
of animals, and many very interesting concepts have evolved. Uncoupling
proteins (UCP) are widely distributed in tissues beyond the UCP1 found
in brown adipose of most newborn animals. These proteins facilitate a
proton leak across the inner mitochondrial membrane, estimated to be
responsible for 20 to 30% of basal metabolism oxygen consumption (Brand
2000). Those observations led to the hope that the major controller of
animal metabolic rate had been found. The excitement was quenched by
the report (Enerback et al., 1997) that UCP2 knockout mice produced no
effect on lipid stores or energy balance and that UCP may function as
regulators of reactive oxygen species (Echtay et al., 2002) rather than
as uncouplers of oxidative phosphorylation. Some enthusiasm was revived
with the reports that mice with overexpressed UCP3 were hyperphagic,
lost adipose mass, and had higher metabolic rates (Clapham et al.,
2000) and that UCP3 is a molecular determinant of T3 effects on resting
metabolic rate (deLange et al., 2001). When hypothyroid rats were given
T3, UCP3 mRNA and protein were up-regulated, resting metabolic rate was
increased 45%, and muscle mitochondrial nonphosphorylating respiration
increased 40%. Additionally, work of Lebon et al. (2001) found that T3
increased muscle tricarboxylic acid cycle flux by 70% with no increase
in ATP synthesis, indicating accelerated proton leak.

The role of UCP in the control of proton leak or conductance has again
been challenged. The mitochondria of UCP3 knockout mice showed
unchanged respiration or proton leak rates (Cadenas et al., 2002). The
mice overexpressing UCP3 did show greater proton conductance, but they
did not respond to known enhancers, or inhibitors. Analogous responses
were found by introducing human UCP3 into yeast mitochondria (Harper et
al., 2002). Uncoupling was increased, but not in proportion to
increased protein; it was responsive to neither activators nor
inhibitors.

Proton leak variation between cold-blooded and homeothermic animals, as
well as large and small species, has also been linked to membrane lipid
unsaturation, particularly to the relative content of docosahexanoic
acid (Hulbert and Else, 2000). For example, rat liver mitochondria have
a greater 22:6 fatty acid content than a similarly sized lizard along
with approximately five times greater proton leak rates. They cite
previous research showing that the heart rate of mammals ranging from
mice to whales was correlated to the 22:6 content of cardiac lipids
(Gudbjarnason et al., 1978). Attention is also given to a general
relationship in other membranes of lipid composition to Na+K+ATPase
activity.

The injection of leptin into rabbits resulted in marked increases in
stored body lipid cycling (Reidy and Weber, 2002). Lipolysis and
triacylglycerol/fatty acid cycling was increased 50%, primary cycling
85%, metabolic rate 14%, and fuel use was shifted away from
carbohydrate toward lipid. The authors postulate that the general role
of leptin secretion by adipocytes is to maintain normal body mass,
adjust lipid stores via changes in metabolic rate, fuel selection, T3
secretion, UCP levels, and diet intake. They conclude that leptin
levels function to adjust the "idling rate" of animals via substrate
cycling and UCP-induced proton leak.

*********

However defined, the determination of partial efficiencies, e.g., body
tissue energy gain/ME above maintenance, would appear to be a
straightforward, simple process. But in practice, it becomes a complex
problem with multiple levels of confounding, making it difficult, if
not impossible, to precisely define the partial efficiency or
maintenance energy requirement of the producing animal. A prime example
of this complication is the frequently observed shifting maintenance
requirements as animals adapt to changing levels of alimentation. For
example, Marston (1948) reported a shifting of fasting heat production
(FHP) of sheep in direct proportion to their prior plane of nutrition.
Additional frequent confounders include changing diet digestibility,
pattern of fermentation, microbial growth, and protein supply
concomitant with changing levels of production or alimentation. Add to
these the changing nutrient flux, metabolism, hormonal control, and
product composition likely with changing level of alimentation and the
simplicity of measuring or calculating "partial efficiency" becomes
even murkier.

****

Try reading what is presented.

Two wrongs do not make a right. It is still ineffective. Statistically
it does not work.

Nice try. You don't know that they eat less calories. You do know that
they eat way more animal fats and animal proteins and they love their
food. They do not even think about portion control or calorie
restriction. They just eat what feels good, and it is not sugary
refined processed carbs. It is real whole foods made with sauces made
from real meat juice with real butter and real cream and tons of animal
fats. They don't even *have* to think about calories. That is the
French Paradox.

Je suis Francais. Je mange Francais. Je sais qu'est-ce-que les
boulangeries ons a vendre.

European pastries are not nearly as sweet and sugar-laden as Western
sweets.

When the bulk of your food is real fresh nutrient-dense whole foods, a
few (less sweet) sweets will do little harm. But when all, or most, of
your food has added sugars and hfcs, and is not nutrient-dense, sweet
and extremely sugary sweets is adding insult to injury and you have a
problem.

TC

If you had actually read and understood what I've posted, you would
realize who really is silly and stupid.

TC