Body Temperature, Metabolism, and Obesity

Also see:
Ray Peat, PhD on Thyroid, Temperature, Pulse, and TSH
Temperature and Pulse Basics & Monthly Log
Thyroid, Temperature, Pulse
Is 98.6 Really Normal?
Metabolism, Brain Size, and Lifespan in Mammals
Promoters of Efficient v. Inefficient Metabolism
Inflammation from Decrease in Body Temperature
Melatonin Lowers Body Temperature
Menopausal Estrogen Therapy Lowers Body Temperature
Thyroid Function, Pulse Rate, & Temperature
“Curing” a High Metabolic Rate with Unsaturated Fats
Fat Deficient Animals – Activity of Cytochrome Oxidase

Metabolism. 2009 Jun;58(6):871-6. doi: 10.1016/j.metabol.2009.02.017.
Is obesity associated with lower body temperatures? Core temperature: a forgotten variable in energy balance. (full paper)
Landsberg L, Young JB, Leonard WR, Linsenmeier RA, Turek FW.
The global increase in obesity, along with the associated adverse health consequences, has heightened interest in the fundamental causes of excessive weight gain. Attributing obesity to “gluttony and sloth”, blaming the obese for overeating and limiting physical activity, oversimplifies a complex problem, since substantial differences in metabolic efficiency between lean and obese have been decisively demonstrated. The underlying physiological basis for these differences have remained poorly understood. The energetic requirements of homeothermy, the maintenance of a constant core temperature in the face of widely divergent external temperatures, accounts for a major portion of daily energy expenditure. Changes in body temperature are associated with significant changes in metabolic rate. These facts raise the interesting possibility that differences in core temperature may play a role in the pathophysiology of obesity. This review explores the hypothesis that lower body temperatures contribute to the enhanced metabolic efficiency of the obese state.

Some quotables:

Resting (or “basal”) metabolic rate (RMR) accounts for
approximately 80%of energy output. About two thirds of RMR
is for maintenance of homeothermy (warm-bloodedness); about
one third is to maintain cellular integrity, ionic gradients, protein
turnover, and the like [6-8] Resting metabolic rate is largely
regulated by thyroid hormones, with a minor contribution from
the sympathetic nervous system.
Resting metabolic rate differs
by as much as 600 kcal/d for a 70-kg man [8].
Physical activity (exercise) accounts for about 10% in
truly sedentary humans; in addition to intentional activity,
this category includes nonpurposeful motion such as
fidgeting, which may differ among lean and obese
individuals [9], as well as upright posture [10].
The remaining 10% is frequently referred to as thermogenesis,
which means heat production unrelated to physical

It should be emphasized that, for nonsedentary individuals,
the activity component may be much greater than 10%
of total energy expenditure. Evidence has been developed
indicating that the combination of activity plus adaptive
thermogenesis accounts for about 44% of total energy
expenditure on average, meaning that RMR would constitute
about 56% of total energy expenditure in normally active
humans [15], as compared with 80% in the truly sedentary.

A lesser ability to dissipate ingested calories is one
example of a thrifty metabolic trait that has evolved to
promote survival in the face of fluctuations in food
. Since the initial formulation of the “thrifty
gene” hypothesis by James Neel in 1962 [16], the nature of
thrifty traits has been the subject of considerable research
and speculation. A recent formulation [17] highlights 2
distinct components: (1) decreased metabolic rate and/or a
diminished capacity for “thermogenesis” and (2) decreased
insulin sensitivity. These 2 components address the 2 main
physiologic imperatives of starvation: energy conservation
and protein preservation. A decrease in metabolic rate would
lead to more efficient storage of calories as fat, thereby
prolonging survival during famine; during periods of
abundance and in the face of dietary excess, this trait
would predispose to obesity. Resistance to the action of
insulin would divert glucose from skeletal muscle, which can
use fat-derived substrates, to the brain, an organ almost
entirely obligated to the use of glucose. In the presence of
famine, insulin resistance would spare muscle breakdown by
lessening the need for gluconeogenesis from protein; in the
face of an abundant food supply, however, and in association
with dietary excess, insulin resistance would predispose to
type 2 diabetes mellitus.

“Both metabolic efficiency and insulin resistance, moreover,
are known to vary among different individuals in the
same population. The survival value of these thrifty traits,
embedded in our genome by natural selection, underlies the
current epidemic of obesity and type 2 diabetes mellitus.
ravages of obesity in once lean indigenous peoples, such as
the Pima Indians of the US southwest [18,19], the Aboriginal
peoples of Australia [20,21], and the Maoris of New Zealand
[22], exemplify the maladaptive side of these thrifty traits in
the presence of an abundant high-energy food supply.”

The prime importance of energy conservation is demonstrated
by the decline in metabolic rate that occurs during
, a response that involves suppression of sympathetic
nervous system (SNS) activity [23]. Body temperature
also falls [24]. This conservative response that limits weight
loss during starvation also diminishes the efficacy of low energy
diets in the treatment of obesity [12,14].

Approximately two thirds of RMR is expended in
meeting the requirement of homeothermy [6,7], the maintenance
of a constant body temperature of about 37°C
(98.6°F). In truly sedentary humans where RMR is 80% of
total energy expenditure, this means that more than 50% of
total energy expenditure is dedicated to maintaining this
constant core temperature. In normally active humans where
the RMR accounts for 56% of total energy expenditure [15],
approximately 37% of total energy output is expended in the
maintenance of homeothermy. This impressive contribution
that warm-bloodedness makes to overall energy production
is exemplified by the difference in energy output between
poikilotherms and homeotherms; a mouse has a many fold
greater metabolic rate than a lizard of the same weight [37].
This metabolic energy required for homeothermy is thyroid
dependent and apparently generated principally in mitochondria
throughout the body of warm-blooded animals.
adaptive forms of thermogenesis, in contrast, are regulated
by the sympathetic nervous system and generated, at least in
part, in brown adipose tissue (BAT) [38]. It is of interest that
recent observations using positron emission tomographic
scanning have resuscitated interest in functional BAT in adult
humans [39,40].

The important relationship of body temperature to
metabolic rate is also demonstrated by the effect of
temperature elevation on the rate of oxygen consumption.
Raising core temperature by 1°C is associated with a 10% to
13% increase in metabolic rate [41]. During starvation, a fall
in body temperature occurs, contributing to the decrease in
metabolic rate noted in this state [24].
Are differences in
body temperature responsible for interindividual variations
in RMR? Is it possible that the obese have a lower body
temperature than normal-weight persons? Or that, during
periods of low energy intake or during sleep, the obese have
an exaggerated fall in temperature?
Good data appear to be
lacking; a recent book on energy metabolism and obesity
[42], for example, fails to even mention a potential role for
core temperature. Body temperature in the obese is clearly
worthy of study given the overriding importance of core
temperature as the major factor in energy expenditure.

“Parenthetically, measurements
of core temperature can be made precisely and
are free of the conundrum imposed by differences in body
size because core temperature is regulated centrally for the
whole body.”

“10. Is core temperature lower in the obese?

Lowering body temperature is an established strategy
used by homeotherms to conserve energy. Some animal
models of obesity, including the obese (ob/ob) mouse
[52,53] and the Zucker fatty (fa/fa) rat [54], are
hypothermic compared with lean controls. Hibernation
and the lesser state of shallow torpor wherein the
temperature falls at night are energy-saving adaptations
used by a variety of mammals [55,56] and even some
human populations such as the Australian Aboriginals
[57]. A decrease in body temperature, in fact, occurs at
night in relation to the sleep cycle in human populations
[58,59]. A fall in body temperature occurs during
starvation, as noted above, and in hypoglycemia, an
acute state of energy deprivation [60-62]. Recent evidence
implicating fibroblast growth factor 21 in the metabolic
response to fasting supports the important adaptive role
that temperature plays in the adaptation to starvation.
addition to stimulating lipolysis, fibroblast growth factor
21 lowers temperature and induces torpor [63]. Lower
temperature has also been linked to obesity in mice with
BAT ablation [64].”

“11. Quantitative significance of changes in
core temperature

Some quantitative considerations, although crude, also
serve to demonstrate the potential importance of core
temperature. A positive balance of 3500 to 4000 kcal
results, theoretically, in the deposition of 1 lb of fat.
Walking 1 mile, a normal-sized individual burns about 100
kcal, the amount of energy contained in 10 potato chips
and equivalent to 5% of a total energy intake of 2000 kcal/
d. A 1°C increase in core temperature, by comparison,
would increase metabolic rate by 10% to 13% [41]. In the
example of extreme sedentary existence cited above where
metabolic rate approximates 50% of overall energy output
(or about 1000 kcal for a normal-sized person), a 1°C
increase in core temperature increases expenditure of 100
to 130 kcal/d. Such an individual could achieve energy
balance eating 100 to 130 kcal more per day than one with
a 1.0°C lower body temperature. Individuals with the 1°C
lower core temperature, thus, would have a thermogenic
handicap of about 100 to 130 kcal/d or about 3000 to 4000
kcal/mo. In 1 month, this would account for 1 lb of fat, 12
lb in 1 year, and about 120 lb in a decade, all else being
equal. In the normally active example described above
where RMR constitutes 37% of total energy expenditure,
the impact is less but still impressive. Under these
circumstances, the thermogenic handicap of a 1°C lower
core temperature might approximate 74 to 96 kcal/d or
about 2200 to 2900 kcal/mo. Greater falls in temperature,
perhaps during sleep or in response to low-energy diets,
would have correspondingly greater effects.

12. Summary

Given the importance of RMR in overall energy output
and the importance of homeothermy as the major component
of RMR, core temperature should be evaluated as a potential
cause of individual differences in metabolic efficiency in
humans. Assessing core temperature in the obese can be
done, furthermore, without the confounding need to normalize
energy expenditure per unit of body mass. In these
studies, assessment of core temperature should be done for
prolonged periods, should sample day and night temperatures,
and should assess the impact of fasting and low energy
intake on obese and lean individuals.
Cross-sectional, and
especially longitudinal, population-based studies could
define the role of core temperature in the pathogenesis of
obesity. Information gained in such studies, along with
research into the central nervous system regulation of
temperature set point and the regulation of mitochondrial
metabolism, might enable the development of new therapeutic
strategies designed to enhance energy output

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