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Physiol Rev 86: 651 667, 2006;
doi:10.1152/physrev.00019.2005.
Nutrition and Aging: Changes in the Regulation

of Energy Metabolism With Aging
SUSAN B. ROBERTS AND IRWIN ROSENBERG
The Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts
I. Introduction
II. Changes in the Regulation of Energy Intake
A. Comparisons of young and elderly adults
B. Reduced hunger and increased satiation as mediators of impaired defense
against energy imbalance
C. Glucose and insulin as potential mediators of impaired regulation of food intake
D. Other hormonal mediators of impaired regulation of food intake
E. Changes in taste and smell as potential contributors to impaired regulation of food intake
F. Reduced dietary variety as a mediator of impaired regulation of food intake
G. Medical and social factors
III. Changes in Energy Expenditure With Aging
A. Basal metabolic rate
B. The thermic effect of feeding
C. Total energy expenditure and physical activity level
D. Energy expenditure responsiveness to energy imbalance
IV. Changes in Fuel Utilization With Aging
V. Summary, Conclusions, and Future Directions
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Roberts, Susan B., and Irwin Rosenberg. Nutrition and Aging: Changes in the Regulation of Energy Metabolism
With Aging. Physiol Rev 86: 651 667, 2006; doi:10.1152/physrev.00019.2005.Changes in energy regulation occur
during normal aging and contribute to the common phenomenon of weight and fat losses late in life. This review
synthesizes data on aging-related changes in energy intake and energy expenditure and on the regulation of energy
intake and expenditure. The ability of older adults to accurately regulate energy intake is impaired, with a number
of possible explanations including delayed rate of absorption of macronutrients secondary to reductions in taste and
smell acuity and numerous hormonal and metabolic mediators of energy regulation that change with aging. There
are also changes in patterns of dietary intake and a reduction in the variety of foods consumed in old age that are
thought to further reduce energy intake. Additionally, all components of energy expenditure decrease with aging, in
particular energy expenditure for physical activity and basal metabolic rate, and the ability of energy expenditure to
increase or decrease to attenuate energy imbalance during overeating or undereating also decreases. Combined,
these changes result in an increased susceptibility to energy imbalance (both positive and negative) in old age that
is associated with deteriorations in health. Practical interventions for prevention of weight and fat fluctuations in old
age are anticipated here based on emerging knowledge of the role of such factors as dietary variety, taste, and
palatability in late-life energy regulation.
I. INTRODUCTION
The human life cycle has undergone dramatic
changes in the last century. At the beginning of the 20th
century, average life expectancy at birth in the United
States for males and females combined was a mere 50
years. Now, 100 years later, average life expectancy is 77
years and is anticipated to increase to an average of 85
years by the year 2125. This change is due primarily to
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compression in morbidity rather than to an extension of

maximum life span. As a result of this, many more individuals are now living longer during the period when they
can be classified as elderly, and the percentage of the
United States population over the age of 65 years has
increased from 4% in 1900 to 13% currently (34).
In recognition of the changing world demographics,
studies of the effects of aging on physiology and metabolism are increasingly being scrutinized for their ability to
0031-9333/06 $18.00 Copyright 2006 the American Physiological Society
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contribute to better approaches for improving the quality

of life in older individuals and preventing late-life disabilities. In this context, understanding changes in energy
regulation with aging is particularly important, because
prevention of weight loss and fat loss is an important
component of maintaining health in old age. The changing
demographics now also suggest that weight loss in older
persons may not necessarily be manifested by body mass
index in underweight ranges; indeed, in National Health
and Nutrition Survey (NHANES) II, involuntary weight
loss appeared disproportionately in older obese adults
and is associated with increased mortality (145).
This review synthesizes data and reviews changes
seen in energy regulation with aging and our emerging
understanding of underlying mechanisms.
II. CHANGES IN THE REGULATION
OF ENERGY INTAKE
A. Comparisons of Young and Elderly Adults
Several disease states common in old age, such as
cancer, are well known to be associated with body weight
and fat losses. However, there has been no general
consensus until recently over whether healthy aging is
also associated with weight loss mediated by a decreased ability to regulate energy intake (22, 24, 107,
108, 125, 132, 139).
The first study of this topic was by Roberts et al.
(132), who investigated whether older age is associated
with altered energy intake responses to imposed over-
feeding and underfeeding. Since day-to-day variability in

energy intake is typically 20 25% (4) while day-to-day
variability in energy expenditure is typically only 10%
(53), there are necessarily substantial day-to-day fluctuations in energy balance. Overfeeding and underfeeding
protocols are usually thus an attempt to examine experimentally the effects of variability in energy intake and
energy balance within magnitudes that may occur during
usual life. In the studies of Roberts et al. (132), separate
overfeeding and underfeeding studies were conducted,
with young and elderly men enrolled in each protocol.
There were clear differences between age groups in body
weight change (and energy intake) following the intervention, as summarized in Figure 1. Whereas young men
responded to overfeeding by decreasing subsequent energy intake and to underfeeding by increasing subsequent
energy intake, elderly men had neither of these responses.
In consequence, young men tended to lose all the excess
weight they gained during overfeeding, and after underfeeding gained back more weight than they had lost during the experimental period, whereas elderly men lost
only 29% of the excess weight gained during overfeeding
and gained back only 64% of the weight lost during underfeeding.
Thus, in two separate protocols involving opposite,
experimentally imposed changes in energy balance, older
men had a substantial reduction in their ability to maintain a constant long-term weight and presumably energy
balance compared with young men. The fact that the
same result was obtained under opposite experimental
conditions (overfeeding and underfeeding) suggested a
basic difference between age groups rather than an ex-
FIG. 1. Body weight change in two groups of subjects during a 21-day period of underfeeding or overfeeding and subsequent ad libitum eating.
Values are means SE for young and older men (black bars are young men, open bars are older men). Mean values were significantly different
between young and older men at the point of lowest/highest weight (P 0.05). [From Roberts et al. (132).]
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AGING AND ENERGY REGULATION
perimental artifact and implies that aging is indeed associated with an impaired ability to accurately regulate
energy balance through adjustments in energy intake.
However, an unresolved question raised by that study was
whether the weight changes persisted over an extended
period of time, because the follow-up period was relatively short (7 wk). In a separate study by the same
group (107), body weight change following experimental
underfeeding was studied for a 6-mo period. As in the first
study, young normal-weight subjects regained essentially
all the weight lost during underfeeding, but elderly subjects only gained back 20% of the weight they lost on
average. On a shorter time scale, consistent results have
also been reported by two other groups. Rolls et al. (139)
gave yogurt preloads to young and older men and measured compensation for the additional energy at the subsequent meal. They observed that young men precisely
compensated for the preload with the result that net food
intake was relatively unaffected, whereas older men did
not. Morley (108) also gave preloads to young and older
subjects and found less complete compensation in the
older subjects than the young ones.
These four studies, together with several animal studies reporting impaired regulation of food intake in old age
(11, 27, 56, 65, 70, 76, 108, 187, 194, 196), suggest markedly
impaired regulation of energy intake in late life. Moreover,
when interpreting the combined results from these investigations, it is important to recognize that, as with most
studies of human aging physiology, the subjects were
healthy older men and women who would be predicted to
be less likely to exhibit age-related decrements in function than the more typical elderly individual with multiple
health problems. Thus, although the results observed here
should not be extrapolated beyond the types of diets and
experimental conditions used in the study, they may nevertheless underestimate the true extent of energy dysregulation in more typical elderly individuals with multiple chronic diseases.
B. Reduced Hunger and Increased Satiation
as Mediators of Impaired Defense
Against Energy Imbalance
The causes of apparent dysregulation of food intake
in old age are not well understood, in large part because
the mechanisms underlying successful energy regulation
at any age are not fully understood. In young adults, it is
generally accepted that multiple overlapping mechanisms
exist to regulate energy balance within fairly narrow limits, with hunger and satiety being monitored both peripherally and centrally by several systems. These mechanisms have not proven to be resistant to environmental
pressures to overeat, as seen in secular trends of weight
gain worldwide during the past 30 years (46). However,
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there is general agreement that bodily mechanisms for

energy regulation do typically protect children and young
adults from weight loss if not weight gain. Thus there are
multiple candidates for age-related changes that could
contribute to the anorexia of aging, as outlined in several
recent reviews (8, 10, 62, 108, 111, 126, 134). It is important to recognize that redundancy in energy regulation
mechanisms is likely, because of the essentiality of maintaining energy balance within limits that do not prejudice
reproduction during young adult life and species survival
generally, and this implies that multiple pathways need to
fail in old age before a measurable impairment in energy
regulation is seen. Thus quite a large number of candidate
mechanisms may potentially be impaired in old age for
impaired regulation of energy intake to be seen, and work
is needed to identify which mechanisms are quantitatively
important. The strongest candidates based on current
knowledge are summarized below and are combined in a
suggested model in Figure 2.
Concerning evidence that the presumed intermediate
end points of energy deregulation, hunger and satiety (the
latter being defined as the sensation of fullness resulting
from eating that leads to cessation of eating), are altered
in old age, several studies have documented abnormally
low hunger following fasting or experimental induction of
negative energy balance in elderly subjects (22, 24, 58,
107, 139, 173, 194, 198). Moriguti et al. (107) reported
older subjects in an experimental underfeeding study experienced significantly less frequent symptoms of hunger
(assessed using visual analog scales) than young subjects,
despite the fact that the older subjects lost significantly
more weight and would therefore be expected to experience more frequent hunger. In addition, Clarkston et al.
(22) reported that carefully screened older persons
tended to be less hungry than younger persons after a
standardized overnight fast, and after a standard meal
they reported a greater degree of satiation than did
younger persons. Intraduodenal nutrient infusion has also
been reported to reduce hunger in young but not elderly
adults (24), while a low perception of hunger during daily
life assessed by the eating inventory questionnaire (173)
predicted a 0.5-kg weight loss per year in a group of
women with an average age of 61 at baseline (58). Sturm
and co-workers (175, 176) further suggested that both
decreased premeal hunger and increased postmeal satiation are independent contributors of impaired energy regulation in old age and that the increased satiation is
associated with increased antral area (and presumably
distension) after consumption of meals. This latter suggestion is also consistent with the animal literature suggesting that low energy intake leading to weight loss in
elderly rats is caused by consumption of smaller meals of
shorter duration, rather than normal-sized meals at reduced frequency (9). Combined, these results suggest that
a reduced perception of hunger and/or increased satiation
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FIG. 2. Suggested integrated model

of metabolic impairments in the normal
cascade of mechanisms regulating energy
intake with aging. CCK, cholecystokinin;
NPY, neuropeptide Y; FFA, free fatty acids. [Adapted from Roberts and Hays
(134).]
precede and are contributing factors to weight loss in

old age.
C. Glucose and Insulin as Potential Mediators
of Impaired Regulation of Food Intake
Alterations in glucose homeostasis in old age may
contribute to altered hunger and satiety. Blood glucose
has long been postulated to be a trigger for hunger signals
in both rodents and humans (2, 10, 17, 19, 90, 98), and
recent studies in young adults and animal models linking
transient small decreases in blood glucose to initiation of
food consumption have provided tentative data in support
of this speculation (20, 170). Also consistent are the multiple studies of the effect of dietary glycemic index1 on
hunger and energy intake (reviewed in Ref. 127), suggesting that foods with a high glycemic index, such as white
bread, breakfast cereals, and other refined carbohydrates
(which typically have a glycemic index of 100 120 when
white bread is used as the reference with a value set at
100 and which induce relative hypoglycemia 90 120 min
after food consumption) promote a more rapid return of
hunger and an increase in subsequent energy intake.
1
Glycemic index is a property of food which is defined as the area
under the glucose curve after consumption of the food in an amount
containing 50 g carbohydrate, divided by the area under the plasma
glucose concentration curve versus time over 2 h after consumption of
white bread or glucose (these are two different standards) also containing 50 g carbohydrate.
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Most young adults maintain circulating glucose

within the range of 80 140 mg/dl throughout cycles of
feeding and fasting, through balanced alterations in secretions of insulin and counterregulatory hormones that
serve to facilitate uptake and synthesis and release of
glucose under different metabolic conditions. However,
when hypoglycemia occurs, it powerfully elicits sensations of hunger in young adults. In contrast, even healthy
older adults have a broader range over which circulating
glucose is maintained and in addition have attenuated
counterregulatory responses and delayed recovery from
hypoglycemia (85, 99, 100). Melanson et al. (95) recently
reported persistently elevated postprandial glucose and
insulin in the older women following consumption of
2,092- and 4,184-kJ test meals compared with younger
women. Provided that central mechanisms for converting
a signal of low blood glucose into a sensation of hunger
are intact in older individuals, as one study (16) but not
some others (85, 99, 100) indicated, the elevated postprandial blood glucose (mean values of 120 mg/dl compared
with 100 mg/dl in young adults) observed by Melanson
et al. (95) could potentially lead to an attenuated return of
hunger in the postprandial period. The elevated circulating insulin levels (8% higher than in young adults) that
are typical of the reduced insulin sensitivity occurring in
old age and which accompanied high postprandial glucose levels in that study (95) may also contribute to a
delayed return of hunger, perhaps through a central satiety effect of high insulin levels (196) or by altering central
sensitivity to other components in the cascade of mech-
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anisms that regulate food intake such as cholecystokinin

(CCK) and neuropeptide Y (NPY) (123, 163). Consistent
with the suggestion of an important role for elevated
circulating insulin and glucose in the impaired regulation
of food intake in old age, Wolden-Hanson et al. (196)
reported a greater increase in food intake following fasting in older animals given troglitazone (an insulin sensitizer) compared with young animals.
Persistently elevated postprandial glucose and insulin levels may themselves potentially be explained by a
reduced rate of gastric emptying in old age, since delayed
gastric emptying will extend the time period over which
nutrients appear in the circulation due to extended digestion. Although this is not the only potential explanation
for high circulating glucose following meal consumption
in elderly individuals (for example, delayed uptake of
glucose by muscle and liver could also provide an explanation), most studies examining gastric emptying in relation to age have reported a decreased rate in the elderly
(22, 38, 104, 184, 190). Delayed gastric emptying in general
has been linked to reduced hunger and increased satiety
(2, 22, 61, 165, 166), and thus may potentially contribute to
increased satiety and satiation and/or decreased hunger
in elderly. Several models of energy regulation (43, 47, 90)
postulate a central role for substrate availability in energy
regulation, and recent work on blood glucose and hunger
has supported the concept of a role for low blood glucose
in initiation of hunger signals in young adults (20, 82, 98,
127). Delayed gastric emptying presumably extends the
period over which not only glucose but also other energy
substrates are absorbed. In addition to influencing hunger
and satiety through the time course of postprandial nutrient availability, alterations in gastric emptying in old age
would presumably also result in a prolonged period of
stomach distension, which could additionally prolong satiation directly through afferent vagal signals (105).
Concerning the underlying causes of delayed gastric
emptying in the elderly, several mechanisms have been
suggested including increased phasic pyloric pressure
waves in response to nutrients in the duodenum (24),
impaired autonomic nervous system function (which is
common in the elderly), and persistently elevated antral
distension (175, 176) as described above. Morley (108) has
also suggested that a reduction in nitric oxide production
by the stomach in elderly adults may increase satiation by
reducing relaxation of the fundus and accelerating movement of food to the antrum.
D. Other Hormonal Mediators of Impaired
Regulation of Food Intake
Aging is associated with impairments in numerous
hormonal systems within the body (101, 143), which may
additionally influence energy regulation and are reviewed
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in detail elsewhere [for example, Blanton et al. (8) and

Horwitz et al. (62)]. Although it is not possible to discern
which of the many impairments noted below are quantitatively significant in the dysregulation of energy balance
in old age, future studies in humans and animals may help
to dissect out the key systems and individual factors.
Glucagon is currently suggested to be one of the
signals of satiation (50, 168, 174), with its action mediated
at least in part through vagal afferent signals from the
liver and perhaps also by increasing blood glucose (which
is another postulated signal, see above). Melanson et al.
(95) reported that elderly women have significantly elevated levels of glucagon by up to 25% in response to
consumption of meals of 2,092 kJ (500 kcal) or greater,
identifying a potential role for glucagon in the apparently
enhanced satiation associated with old age.
There is also evidence of both altered synthesis
and/or secretion and impaired central responsiveness to
gut hormones in late life. For example, fasting levels of
the postulated satiety hormone CCK are typically five
times higher in elderly individuals than in young adults
(83, 87, 170, 175), rise more in response to an intraduodenal fat infusion than in young adults (83), but appear to
have a weaker effect in suppressing satiety than expected
in relation to circulating levels (84, 175). Concerning evidence for impaired detection of gut hormone signals, the
rise in CCK, glucagon-like peptide 1 (GLP-1), and polypeptide YY associated with intraduodenal lipid infusion were
significantly correlated with a decrease in hunger in
young but not older individuals in one study (84). Consistent data were also obtained in animal models, with administration of exogenous CCK, bombesin, and calcitonin
having a greater suppressing effect on food intake in
young compared with elderly mice (169). Strum et al.
(175) recently suggested that in fact higher CCK in late life
is unrelated to the anorexia of aging, based on the finding
that abnormal circulating levels exist in both underweight
elders (presumably exhibiting the anorexia of aging) and
well-nourished elders (presumably without an anorexia of
aging). However, if energy dysregulation in old age requires both underlying biological impairments and lifestyle factors that (see below) promote expression of the
biological impairments, well-nourished elders could exhibit the same biological factors while differing only in
more favorable life-style conditions. Further work is
needed to elucidate the role of different metabolic parameters including CCK in the anorexia of aging.
Leptin (57, 199) has also been proposed as a candidate hormone for the anorexia of aging, but emerging data
now suggest this is unlikely. In young adults, leptin is
secreted by fat cells and acts centrally to reduce feeding
and to increase energy expenditure through pathways
thought to involve inhibition of synthesis of NPY, which
itself stimulates feeding (see below) (8). There is a significant correlation between circulating leptin and body fat
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in young adults (23, 103, 136), but in elderly adults circulating leptin may be lower than expected for body fat
levels (8, 136). Furthermore (8, 88, 103, 136, 171, 195),
central leptin administration has relatively little effect on
food intake and thermogenesis in old, obese rats compared with substantial effects in young, lean ones (for
example, 42% reduction in food intake following central
leptin administration) (150) due to decreased leptin responsiveness in old age (149, 150, 167).
The fact that a variety of peripheral satiety signals,
including CCK, leptin, blood glucose, and the sympathetic
nervous system (70), and perhaps ghrelin (52) all appear
to be imperfectly detected in old age may be related to
impairments in one or more central mechanisms responsible for coordination of energy regulation signals. One
important potential candidate is NPY, one of the most
abundant peptides in the brain that is an integrator of
metabolic endocrine and behavioral systems (73, 74) and
acts through various hypothalamic nuclei to stimulate
feeding behavior and affect release of hormones that
modulate energy metabolism such as insulin (73, 74). The
finding of high levels of NPY in both plasma and cerebrospinal fluid of elderly anorectics provides some circumstantial evidence that NPY expression does not relate to
the anorexia of aging, since high NPY is predicted to
increase feeding in the young (87). However, the fastinginduced increases in both food intake and NPY gene
expression normally seen in young rats are consistently
attenuated in aging rats (55, 56, 76, 194), indicating that
responsiveness to NPY is impaired in old age. Consistent
with this suggestion, the feeding and drinking responses
to NPY injection in the paraventricular hypothalamic nucleus are markedly attenuated in aged rats (7, 118), with
only one-quarter to one-third of the response seen in
younger animals (7).
E. Changes in Taste and Smell as Potential
Contributors to Impaired Regulation
of Food Intake
There are well-documented age-associated declines
in taste and smell sensitivity (36, 42, 151155, 191) that
may play a more important role in the energy dysregulation of old age than currently recognized. In particular,
most studies (36, 42, 151156, 191) suggest that detection
and recognition thresholds for salt and other specific
tastes increase with age, in part because of the use of
medications that impact taste (see below) but also because of a loss of functional taste bud number and structure (1) and impaired olfaction.
Intact senses of taste and smell appear to be necessary for the cephalic phase of digestion, which includes
the initial increases in salivary, gastric, pancreatic, and
intestinal secretions that initiate digestion (148, 153). The
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cephalic phase of postprandial metabolism is initiated by

olfactory, gustatory, and cognitive stimulation by food
and includes activation of both the sympathetic and parasympathetic nervous systems, which in turn initiate and
augment multiple digestion-related processes that serve
to prepare the body to absorb nutrients (15). Cognitive,
visual, and olfactory stimulation can elicit a release of
saliva that averages between one-fourth and two-thirds of
that noted following masticating, but not swallowing,
food. Because saliva contains digestive enzymes that initiate the breakdown of starch, the increased production
of saliva following consumption of most foods (21, 197)
may actually accelerate carbohydrate digestion and absorption. Tasteless stimuli have minimal effect on gastric
acid release and pancreatic secretions, whereas palatable
foods have long been known to result in marked stimulation of secretions that may promote digestion (64, 117).
Related to this observation, there is preliminary evidence suggesting that palatability may influence the rate
of nutrient absorption and/or initiate gluconeogenesis
(147, 172). Sawaya et al. (147) observed that consumption
of bland foods decreases the glycemic response to test
meals compared with palatable meals of identical macronutrient composition, which suggests there may be a
reduced rate of gastric emptying and hence slower digestion of bland foods. Consistent results were reported by
LeBlanc and Brondel (72), and although Warwick et al.
(189) reported no differential effect of palatable versus
bland liquids on circulating glucose, liquid test meals
were used in that study. Liquids appear to have very
different effects on satiety from solids (89), which may
possibly explain the different results obtained. Teff and
Engelman (179) also found no difference in postprandial
blood glucose responses to palatable versus unpalatable
test foods, but the foods used in that study were only
chewed and not swallowed, which would be predicted to
attenuate the cephalic response.
If the losses in taste and smell associated with aging
have an equivalent effect (i.e., making food seem more
bland, as commonly reported), the anticipated decrease
in gastric emptying and likely delayed absorption of nutrients could help explain the reported increase in satiation and decrease in hunger in old age. Consistent with
this suggestion, elderly individuals eat more of individual
foods if they are flavor-enhanced (157), and in another
study smell was significantly correlated with hunger and
appetite (31). It should be noted that, in this latter study,
there was no association between smell and reported
energy intake; however, documented inaccuracies in the
measurement of reported energy intake (160) make the
validity of such correlations uncertain. Additionally reported by Schiffman et al. (152), elderly individuals have
a reduced ability to identify individual foods in blinded
tests. If foods taste more similar, the pleasure of a diverse
diet will presumably be reduced, thus tending to decrease
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dietary variety in the absence of environmental and social

factors working in the opposite direction.
F. Reduced Dietary Variety as a Mediator
of Impaired Regulation of Food Intake
Studies in laboratory rats, cats, and hamsters have
shown that energy intake is greater when a variety of
foods are provided compared with when only a single
food is provided (92, 93). Numerous single-meal studies in
humans also show this phenomenon (93, 141). While two
longer-term studies have shown that laboratory rats have
greater body fat and body fat gain when fed a variety of
foods compared with when only a single food is fed (81,
142), long-term studies in humans have been lacking until
recently. McCrory et al. (92) recently reported on the
long-term association between dietary variety and body
fatness in healthy adult men and women (92). In multiple
regression analyses controlled for age and sex, dietary
variety from a combined group of sweets, snacks, condiments, entrees, and carbohydrates was positively associated with body fatness, and in the same model dietary
variety from vegetables was negatively associated with
body fatness. In other words, individuals who consumed
a wide variety of higher energy foods coupled with a low
variety of vegetables were relatively fatter.
Self-reported records of dietary intake indicate that
dietary variety is reduced in old age (17, 39), and a recent
study also demonstrated particularly low dietary variety
among elderly adults with low body mass index (BMI)
(133). The reasons why dietary variety decreases in old
age and is particularly low in elders suffering from low
BMI are not fully understood but may potentially provide
an additional explanation for weight loss in old age. Concerning potential mechanisms, a study by Rolls and
McDermott (140) observed that older adults have reduced
sensory specific satiety, a term used to describe the
phenomenon of declining pleasantness of food as it is
consumed. The adolescent and young adult subjects of
Rolls and McDermott (140) responded in the expected
manner to a yogurt preload (i.e., decreased desire to eat
yogurt but not other offered foods), but older subjects did
not respond and in fact reported an equivalent desire to
eat yogurt and other test foods after the preload. Although
necessarily short-term and requiring confirmation in a
larger study, these data suggest that older adults lack
normal patterns of sensory specific satiety that encourage
wide dietary variety. The underlying reason for decreased
sensory specific satiety in old age may potentially be
traced back to the declines in taste and smell sensitivity
associated with aging documented above (36, 42, 151156,
191), with their predicted impact on the extent of digestion and availability of incoming substrates into the circulation.
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G. Medical and Social Factors

Many social and medical changes associated with
aging have been suggested to cause weight loss, such as
poverty, bereavement, social isolation, poor dentition,
chronic disease, and the use of multiple prescription medications (36, 54, 108 111, 157). In addition, depression has
been suggested as an important cause of weight loss
among the elderly, a finding that has been confirmed in an
analysis of cohort data (35). However, it is interesting to
note that the study of DiPietro et al. (35) showed that
depression was associated with weight loss only in individuals aged 55 years or older and was actually associated
with weight gain in younger adults. One potential explanation for this finding (132) is that psychosocial factors
are potential catalysts for weight loss only when there is
an underlying impairment in the regulation of food intake
that allows impediments to eating to be expressed.
Concerning social isolation, de Castro and de Castro
(30) reported that less energy is eaten at meals taken
alone compared with meals eaten in company, with the
difference in energy intake between the two situations
being a substantial 30%. Although such data are generally
used to suggest that social eating is disadvantageous because it promotes overeating and obesity, the opposite
(namely, that eating alone leads to undereating and
weight loss) may be an equally valid interpretation. This is
especially true when it is considered that humans are a
gregarious animal species and naturally eat in social
groups (102). This is directly relevant to the issue of low
energy intake in the older population, because bereavement and functional disabilities can limit social contact
(86). Thus an increased frequency of eating alone may be
one of the factors contributing to low energy intake in
older adults. Furthermore, there is a positive association
between the frequency of eating restaurant food and body
fatness (91) and for reasons of social isolation and functional disabilities, older adults may eat out less frequently.
In support of this suggestion, in the recently reported
NHANES 1999 2000 survey, adults younger than 45 years
of age reported meals out approximately twice as often as
those over the age of 65 years (66). The combination of
these different observations and findings suggests a potentially important role for reductions in social meals and
eating out in the low energy intake and body weight loss
of older adults, which is independent of any biological
impairments associated with aging.
III. CHANGES IN ENERGY EXPENDITURE
WITH AGING
A. Basal Metabolic Rate
Basal metabolic rate (BMR) is the energy expenditure of an individual after a 12- to 14-h overnight fast
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during a period of mental and physical rest in a thermoneutral environment and reflects energy use of the body
for such basic functions as maintenance of electrochemical gradients, transporting of molecules around the body,
and biosynthetic processes. Frequently, a resting energy
expenditure is measured in preference to a BMR. Resting
energy expenditure is quantitatively similar to the BMR,
but it is not subject to all the exacting requirements of a
BMR. In this review, measurements of resting energy
expenditure are taken to be equivalent to BMR.
Typically, BMR is the largest component of energy
expenditure and comprises 50 70% of total expenditure
in most adults. A decline in BMR with aging is well
recognized (68, 119) and is implicit in standard equations
for predicting BMR in healthy men and women of different ages (40). A longitudinal study by Keys et al. (68)
documented a decline in BMR with age of 12% per decade; based on this assessment, a reduction in BMR of
400 kJ/day can be predicted between 20 and 70 years
of age.
The question of whether the decline in BMR with
aging can be accounted for by concomitant alterations in
body composition, or whether there is also a decline in
BMR per unit of tissue, has been studied by several research groups. Many (48, 69, 116, 120, 128, 188) though
not all (26, 144, 183) cross-sectional studies reported that
BMR is lower in old age even after adjustment for lower
fat-free mass in older individuals, with adjusted BMR
values being 5% lower for elderly adults than for young
adults. However, loss of fat-free mass is not the only body
composition change that occurs during the adult human
life cycle, and in particular, there is usually a substantial
increase in fat mass from young adulthood to middle age
that often quantitatively exceeds the concomitant loss of
fat-free mass (resulting in net weight gain). Two investigations also analyzed changes in BMR with aging in relation to individual variability in both fat-free mass and fat
mass (27, 186). In both of these studies, there was a
significantly lower BMR in elderly adults compared with
young ones. Because adipose tissue is metabolically active, albeit less metabolically active than muscle and
other components of fat-free mass (40), failure to account
for the increase in fat mass through middle age in analyses of BMR could theoretically underestimate BMR adjusted for fat-free mass and help explain the conflicting
results of the earlier studies.
More recently, three additional studies have further
examined BMR in relation to compartmentalized body
composition. Roubenoff et al. (144) examined BMR in
relation to total body potassium (an indicator of metabolically active tissue independent of such compartments as
extracellular water) and found no effect of age on the
relationship between total body potassium and BMR.
Consistent with this suggestion, Kutsuzawa et al. (71)
found no effect of age on muscle energy metabolism of
Physiol Rev VOL
the forearm assessed by 31P-magnetic resonance spectroscopy, and Bosy-Westphal et al. (13) found no effect of
age on BMR when organ sizes within the free-fat mass
(assessed by magnetic resonance imaging) were taken
into account (different organs are known to have tissuespecific rates of energy expenditure). These reports, suggesting no effect of age on BMR beyond that due to the
loss of different body tissues is taken into account, would
appear to conflict with the further finding of Willis et al.
(193) that there is a significant age-associated decline in
cerebral glucose metabolism (indicating energy expenditure since glucose is the primary metabolic fuel of the
brain). However, Willis et al. (193) also quantified the
change in cerebral glucose metabolism with age, and the
estimated 5 g/day decrease in glucose use between 20 and
70 years for an adult with normal brain size would result
in an estimated decrease in BMR of only 125 kJ/day,
which is 2% BMR for most adults and would not be
detected significantly except in extremely large studies.
Taken together, these observations indicate that BMR is
indeed lower in the elderly compared with young adults
even after taking body composition changes associated
with aging into account, but the difference is so small
(2% based on changes in brain glucose metabolism) that
it can be considered insignificant.
B. The Thermic Effect of Feeding
The thermic effect of feeding, previously know as
specific dynamic action, is the increase in energy expenditure above basal that is associated with consuming,
digesting, and assimilating food. Some of the increase in
energy expenditure can be directly attributed to the metabolic costs of digestion, resynthesis of macronutrient
polymers, and related processes (termed obligatory thermogenesis), while the other component of the increase
appears to be due to concomitant activation of the sympathetic nervous system (termed facultative thermogenesis) (28).
The thermic effect of feeding is equivalent to 8 15%
of ingested metabolizable energy. Some studies report a
decrease in the thermic effect of feeding in old age (51,
106, 161, 164, 180, 185), while other studies report no
change (27, 49, 96, 121, 182, 188). To avoid the potential
concern that meal size might influence differences in TEF
between young and older individuals, Melanson et al. (96)
measured the thermic effect of feeding at three levels of
energy intake. There was no significant difference in the
thermic effect of feeding between the age groups, and
mean postprandial values for energy expenditure above
initial fasting values were actually slightly higher in the
older group than the young group. Although no conclusive
explanation can currently be given for the different results between some of the studies, a suggested explana-
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tion (96) is that the thermic effect of feeding does not

decline with aging per se, but that some studies may have
confounded age with factors that decrease thermic effect
of feeding independent of aging, such as obesity and/or
digestive problems that limit nutrient absorption. Alternatively, one recent study documented decreased -adrenergically stimulated thermogenesis in aging, seen as an
18% greater infusion of isoprenaline needed to increase
metabolic rate by 15% (67); the same group further reported diminished fat oxidation in response to isoprenaline (3). It is therefore possible that there is a small
decrease in the sympathetic nervous system component
of TEF with age but that quantitatively it is hard to detect
and has given rise to inconsistent results between studies.
C. Total Energy Expenditure and Physical
Activity Level
The third major component of energy expenditure is
the energy expenditure for physical activity and arousal
(these individual components are usually grouped together due to the difficulty of separating them experimentally). Energy expenditure for physical activity and
arousal, together with the BMR and the thermic effect of
feeding, comprise an individuals total energy expenditure, which is equivalent to dietary energy requirements
during weight maintenance. In theory, energy expenditure
for physical activity and arousal, and hence total energy
expenditure, can be determined by recording the amounts
of time devoted to different activities and the energy costs
of those activities (measured in a laboratory by respiratory gas exchange) and summing the individual components in what has been called the factorial method.
However, in practice it is difficult to avoid underestimation of energy expenditure by this method because it is
impossible to record every type of activity, and there are
nonaccountable activities such as fidgeting that tend to
get under-recorded (37, 135).
To avoid the pitfalls of the factorial method, substantial effort has been directed towards developing the doubly labeled water method as an alternative, longer term,
and more accurate technique for measurement of total
energy expenditure. This method was originally developed for use in small animals (77, 78), based on the
principle that if two isotopes of water (H218O and 2H2O)
are administered and their disappearance rates from a
body fluid such as urine monitored, the disappearance
rate of 2H2O reflects water flux and the disappearance
rate of H218O reflects water flux plus carbon dioxide
production rate (79). The difference between the two
disappearance rates can therefore be used to calculate
carbon dioxide production rate over a period of 13 wk,
from which total energy expenditure can be calculated if
information is available on respiratory quotient (177).
Physiol Rev VOL
659
Validation studies of the doubly labeled water method

have been conducted in human infants and adults of
different ages using respiratory gas exchange or dietary
energy intake as the reference method (129, 159). All
these studies showed a close agreement between total
energy expenditure determined by doubly labeled water
and total energy expenditure determined by a reference
method, with a coefficient of variation for the new
method of 2 6%. In consequence, the doubly labeled water method is now widely recognized as an accurate and
precise method for assessment of total energy expenditure in human subjects. Delayed isotopic equilibration is
recognized in elderly subjects, presumably due to the
incomplete bladder emptying that frequently occurs in old
age (6, 114, 158), but this effect has been demonstrated
only for short equilibration periods after dosing (such as
4 h); in practice, this limitation can be eliminated by
employing longer equilibration periods as recommended
by Blanc et al. (6). Because the doubly labeled water
method calculates the rate of carbon dioxide production,
rather than the rate of energy expenditure, and because
the heat equivalent of carbon dioxide varies with the
substrates being oxidized (129, 159), it is necessary to
have an estimate of the respiratory quotient (RQ) of the
subject during the measurement period. Usually, RQ is
estimated from information on the subjects dietary intake, either their reported macronutrient intakes or normative data from population surveys, and errors from
necessary assumptions and errors in dietary records are
recognized to be small and usually 2% (177).
A critical mass of doubly labeled water data has
accumulated over the past 15 years, making it possible to
evaluate typical changes in total energy expenditure and
energy expenditure for physical activity (calculated as the
difference between total energy expenditure and BMR
plus the thermic effect of feeding, or indicated by a physical activity level calculated as the ratio of total energy
expenditure to BMR). Several studies have reported lower
total energy expenditure in elderly adults compared with
young adults (116, 122, 138, 148), and the summary of data
from different adult age-groups shown in Figure 3 illustrates a progressive substantial decline in total energy
expenditure (and hence physical activity level) with age
(5). Additional studies have also investigated differences
in 24-h sedentary energy expenditure when adults are
confined to a whole body calorimeter. In these studies,
sedentary energy expenditure is lower in elderly adults
than in young adults when activity in the chamber is
flexible (186), but in whole body calorimeter protocols
that standardize 24-h activity, there has been no difference in 24-h energy expenditure between age groups
(186). Taken together, these data demonstrate declines in
both planned exercise and spontaneous physical activity
in healthy old age.
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660
small since any increase in energy expenditure associated

with training seems to be offset by decreased voluntary
energy expenditure at other times of the day (94, 192).
However small the effects on energy balance, additional
effects of exercise include positive effects on cardiovascular and bone health and prevention of falls and frailty.
D. Energy Expenditure Responsiveness
to Energy Imbalance
FIG.
3. Total energy expenditure at different ages [males are solid

lines (SD); females are dotted lines (SD)]. The graph was prepared
with data from Black et al. (5).
The causes of declining total energy expenditure and

physical activity with age are not well understood. The
declines with age are reported to parallel an increase in
body fat mass, suggesting that changes in body composition may be important (130). Regression analyses predicting energy expenditure from body fat and fat-free mass in
individuals of different ages show that there is a positive
association between fat-free mass and energy expenditure but a negative association of fat mass with energy
expenditure (130). Thus it is reasonable to speculate that
the increase in body fat mass may help promote a decrease in energy expenditure for physical activity. In
NHANES III, in those over 70 years, increased BMI or
body fat was associated with limitations in functional
living activities such as carrying groceries, suggesting that
increasing body fat may influence energy expenditure
through impairment of daily activities (29). However,
Westerterp and Meijer and co-workers (94, 192) have
pointed out that the decline in physical activity energy
expenditure with age is most strongly predicted by age
itself and not by body composition, indicating an effect of
aging on expenditure independent of the quantity of lean
tissue and fat mass. It is also noteworthy that maximal
oxygen consumption is recognized to decline progressively with age, and very active individuals have declines
of 50% between 20 and 80 years that are of similar
magnitude (albeit higher absolute values) to those experienced by sedentary individuals (33). These observations
suggest that some parallel changes in fitness, energy expenditure for physical activity, and body composition
with age are probably an inevitable consequence of the
aging process, probably due to underlying hormonal and
biochemical changes in skeletal muscle and the cardiovascular system rather than a cumulative consequence of
long-term inactivity. Further studies are needed to determine the extent to which energy expenditure for physical
activity can be maintained in old age in the general population, with the expectation based on current research
that potential specific effects on energy balance may be
Physiol Rev VOL
The concept that energy expenditure plays an important role in the regulation of energy balance has been the
subject of numerous investigations since the beginning of
the 20th century (113), and it is now widely recognized
that energy expenditure increases or decreases only to a
limited extent to match energy intake to minimize
changes in energy balance resulting from overeating or
undereating (14, 59, 137).
Several studies published over the last decade have
suggested there may be important changes in energy expenditure responsiveness to changes in energy balance
with aging. Roberts and colleagues (107, 131, 146) conducted a series of overfeeding and underfeeding studies
to examine the magnitude of changes in total energy
expenditure and components of energy expenditure to
energy imbalance in young (age 20 30 years) and elderly
(age 60 80 years) men. In a combined analysis of the first
overfeeding and underfeeding studies, a significantly attenuated resting energy expenditure response to changes
in energy balance was observed in the elderly men (Fig.
4). Thus, during positive energy balance, the increase in
FIG. 4. Relationship between energy deficit during underfeeding or

energy surplus during overfeeding and the change in resting energy
expenditure (REE) in young (closed circles) and older (open circles)
men. There was a significant age by change in energy intake interaction
(P 0.05). The overall relationship for REE vs. change in energy intake
taking age group into account was also significant (R2 0.548, P
0.001). [Adapted from Salzman and Roberts (146).]
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resting energy expenditure was lower in elderly men than

young men relative to the level of energy imbalance.
Similarly, the decrease in resting energy expenditure with
negative energy balance was reduced in the elderly subjects. These changes can be predicted to result in greater
fluctuations in body weight and fat mass with overeating
and undereating in the elderly, due to reduced compensation from adaptive changes in energy expenditure. The
differences between the age groups were statistically explained by differences in muscle mass between the
groups, suggesting that 1) muscle is an important site of
adaptive thermogenesis in humans and 2) the declines in
muscle mass with age explain the reduced capacity for
changes in energy expenditure with negative energy balance. However, when the results of these studies were
separated into those obtained during overfeeding and
underfeeding, the age-group difference in change in resting energy expenditure was only significant in the overfeeding group. Thus the question of whether alterations in
energy expenditure responsiveness to changes in energy
balance are general or specific to negative energy balance
was unresolved.
To further examine this issue, the same group conducted a second, longer study to examine changes in the
capacity for reducing energy expenditure with negative
energy balance in young and elderly subjects. The results
of this second study were consistent with the combined
overfeeding/underfeeding analysis, showing an attenuated reduction in BMR during negative energy balance in
the elderly subjects compared with young subjects (27).
One theoretical expectation from these findings is that
elderly people should lose more weight for the same
decrement in energy intake. Consistent with this prediction, the second, longer underfeeding study in the series
documented greater weight loss during underfeeding in
elderly subjects than in young subjects despite the fact
that compliance with the study diet appeared to be no
different between the age groups.
IV. CHANGES IN FUEL UTILIZATION
WITH AGING
The ability of the body to oxidize dietary fat must be
a critical determinant of the success or failure of body
energy regulation, because exogenous fat that is not oxidized must be stored (43, 44). Thus, if fat oxidation can
adapt on a meal-to-meal or even week-to-week basis to
match the fat content of the diet, there will be no net fat
deposition or loss over time, and body adipose stores will
remain constant. However, body fat stores will increase if
fat oxidation is less than fat intake, and conversely, body
fat stores will decrease if fat oxidation is greater than fat
intake. The potential role of reduced fat oxidation in the
development of obesity in adults of all ages is seen in the
Physiol Rev VOL
661
data from epidemiological studies that link consumption

of a high-fat diet to increased body fat (80) and in dietary
intervention studies that have showed higher energy intakes on high-fat diets than on low-fat diets matched for
palatability (80). More direct evidence is also seen in the
prospective studies that have demonstrated a significant
association between low fat oxidation, relative to intake,
and subsequent weight gain (200), although it is important
to note both that positive energy balance is essential for
net fat accumulation and that measurements of substrate
oxidation have a strong potential to be confounded by
uncontrolled dietary intake in the days before scientific
study.
Nevertheless, observations to date raise the question
of whether there might be age-associated alterations in fat
oxidation in the postprandial state that could help explain
age-associated changes in body fatness. In a longitudinal
24-h whole body calorimeter study, Rising et al. (124)
reported a mean 0.019 RQ increase over time in seven
Pima Indian subjects (indicating 5% greater carbohydrate oxidation and 5% less fat oxidation), and consistent
results were more recently reported in a larger population
by Levadoux et al. (75). Melanson et al. (96) used postprandial measurements of oxygen consumption and carbon dioxide production to observe that, following meals
simulating the size of a snack or a small meal (1,046 and
2,092 kJ), older women had rates of fat oxidation comparable to those in young women (Fig. 5). However, the
same elderly women had significantly lower fat oxidation
following consumption of a moderately large meal (4,184
kJ). In regression analyses, maximal oxygen consumption, lean body mass, and circulating triglycerides explained individual differences in fat oxidation. However,
the number of subjects was rather small for this type of
analysis, and there were several similar models with comparable statistical significance, so the separation of age
from body composition and fitness was not possible.
These statistical findings are consistent with known influences on fat oxidation. For example, skeletal muscle mass
is known to be the primary site for fat oxidation, and
vigorous activity influences insulin sensitivity and hence
the extent to which fat is used as a fuel source instead of
carbohydrate (60).
Concerning fat oxidation in the fasting state, there
are reports of both increased and decreased fasting fat
oxidation in elderly individuals (12, 18). In addition,
Melanson et al. (97) observed no significant effects of age
per se on fasting fat oxidation measured over 10 h, but
there was a significant negative effect of body fat in the
best-fitting multiple regression model, which was probably due to the fact that the fatter subjects were in the
older group. These latter observations appear consistent
with the data of Calles-Escandon et al. (18) and lend
weight to the suggestion that aging may also be associated
with no increase in fat oxidation, and perhaps even a
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662
FIG. 5. Individual values for fat oxidation (corrected for postprandial energy expenditure) in relation to meal size and study duration in 16
young and older women. There was a significant age group by meal size
interaction (P 0.02), and the older women had significantly lower
values for fat oxidation after consumption of the 4,148-kJ meal than did
the young women (P 0.02). [From Melanson et al. (97).]
decrease in fat oxidation after taking fat mass into account (which is positively correlated with fasting fat oxidation in younger subjects; see Ref. 162).
The fact that the apparent impairments in fat oxidation in old age are associated with reduced muscle mass
and fitness suggest that alterations in fuel availability with
age may underlie differences in fat oxidation, and therefore that exercise may help reverse or attenuate the ageassociated effects through alterations in insulin sensitivity. Consistent with this view, several previous studies,
Physiol Rev VOL
including one in elderly subjects, have reported increased

fasting fat oxidation with improved fitness, resulting from
increased muscle mass and increased activity of fat oxidative enzymes in muscle (60, 63, 181). Additional evidence comes from another study documenting impaired
fat oxidation in association with persistently high levels of
circulating glucose for several hours in the postmeal period after consumption of a moderate-large meal size (95).
The young women in that study responded to increasing
meal size with appropriately increased circulating insulin
and minimal changes in circulating glucagon, with the
result that circulating levels of glucose increased only
slightly with increasing meal size and showed the expected pattern of a small initial increase followed by a
rapid return to baseline. Appropriate patterns of insulin,
glucagon, and glucose were also seen in the older women
during the fasting experiment and after consumption of
the 1,046 kJ meal. In contrast, consumption of the
2,092-kJ meal, and to an even greater extent the 4,184-kJ
meal, caused a substantial prolonged increase in circulating levels of both insulin and glucagon (but not free fatty
acids) in the older group. The trend toward elevation in
glucagon with meal consumption is noteworthy because
it is in direct contradiction to the expected meal-induced
suppression of glucagon secretion in individuals without
non-insulin-dependent diabetes (25) and may well be a
contributor to the persistent postmeal elevation in circulating glucose. The net effect of these changes, coupled
with the expected underlying modest degree of insulin
resistance in older individuals (41), was a substantial
increase in the peak circulating glucose during the postmeal period and a persistent elevation of circulating glucose throughout the 5-h postprandial study period. Thus,
although classified as normally glucose tolerant in an oral
glucose tolerance test performed during the screening
examination, these older women did in fact exhibit abnormal glucose profiles when challenged with mixed
meals of 2,092 kJ or greater. Since fat oxidation is suppressed by high levels of circulating glucose (45), these
high levels of glucose help explain why fat oxidation was
suppressed.
V. SUMMARY, CONCLUSIONS,
AND FUTURE DIRECTIONS
Several lines of evidence demonstrate that dysregulation of energy intake occurs in old age even in apparently healthy individuals and increase the risk of energy
imbalance. There is also emerging data suggesting equivalent dysregulation of body energy expenditure and substrate oxidation in old age. The extent to which body
weight and fat increases or decreases in response to
age-related energy dysregulation will depend on the prevailing environmental circumstances and health of the
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individual. Since body weight change is associated with

such undesirable consequences as micronutrient deficiencies, frailty, increased hospital admission, an increased
risk of disability from falls, delayed recovery from injury,
and premature death (32, 112, 115, 178), further research
is clearly needed to identify the specific underlying causes
of aging-associated energy dysregulation. Current research also points to the potential for manipulation of
dietary factors such as variety, taste, and meal size for
preventing weight loss or weight gain through compensatory changes in energy intake.
ACKNOWLEDGMENTS
We thank all the members of the Energy Metabolism Laboratory at the Jean Mayer USDA Human Nutrition Research
Center on Aging at Tufts University for their invaluable contributions to the studies described in this review, in particular,
Paul Fuss, Gaston Bathalon, Nicholas Hays, Kathleen Melanson,
Megan McCrory, and Edward Saltzman. We also gratefully acknowledge the enduring inspiration of our late colleague and
friend Vernon R. Young.
Address for reprint requests and other correspondence:
S. B. Roberts, Energy Metabolism Laboratory, USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111 (e-mail: susan.roberts@tufts.edu).
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Physiol Rev 86: 651 667, 2006;

Nutrition and Aging: Changes in the Regulation

compression in morbidity rather than to an extension of

0031-9333/06 $18.00 Copyright 2006 the American Physiological Society

SUSAN B. ROBERTS AND IRWIN ROSENBERG

contribute to better approaches for improving the quality

feeding and underfeeding. Since day-to-day variability in

Physiol Rev VOL

AGING AND ENERGY REGULATION

there is general agreement that bodily mechanisms for

SUSAN B. ROBERTS AND IRWIN ROSENBERG

FIG. 2. Suggested integrated model

precede and are contributing factors to weight loss in

Physiol Rev VOL

Most young adults maintain circulating glucose

AGING AND ENERGY REGULATION

anisms that regulate food intake such as cholecystokinin

in detail elsewhere [for example, Blanton et al. (8) and

SUSAN B. ROBERTS AND IRWIN ROSENBERG

cephalic phase of postprandial metabolism is initiated by

AGING AND ENERGY REGULATION

dietary variety in the absence of environmental and social

G. Medical and Social Factors

SUSAN B. ROBERTS AND IRWIN ROSENBERG

AGING AND ENERGY REGULATION

tion (96) is that the thermic effect of feeding does not

Validation studies of the doubly labeled water method

SUSAN B. ROBERTS AND IRWIN ROSENBERG

small since any increase in energy expenditure associated

3. Total energy expenditure at different ages [males are solid

The causes of declining total energy expenditure and

FIG. 4. Relationship between energy deficit during underfeeding or

AGING AND ENERGY REGULATION

resting energy expenditure was lower in elderly men than

data from epidemiological studies that link consumption

SUSAN B. ROBERTS AND IRWIN ROSENBERG

including one in elderly subjects, have reported increased

AGING AND ENERGY REGULATION

individual. Since body weight change is associated with

SUSAN B. ROBERTS AND IRWIN ROSENBERG

AGING AND ENERGY REGULATION

SUSAN B. ROBERTS AND IRWIN ROSENBERG

125. Roberts SB. Effects of aging on energy requirements and the

mined by using the doubly labeled water method. Am J Clin Nutr

AGING AND ENERGY REGULATION

Physiol Rev VOL

distribution, and physical activity level. Am J Clin Nutr 61: 772

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