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Critical Reviews in Food Science and Nutrition

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Perception of taste and smell in elderly persons

a
Susan S. Schiffman Ph.D.
a
Department of Psychology , Duke University , Durham, NC, 27706
Published online: 29 Sep 2009.

To cite this article: Susan S. Schiffman Ph.D. (1993) Perception of taste and smell in elderly persons, Critical Reviews in Food
Science and Nutrition, 33:1, 17-26, DOI: 10.1080/10408399309527608

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 Critical Reviews in Food Science and Nutrition, 33(1): 17-26 (1993)

Perception of Taste and Smell in Elderly

Persons
Susan S. Schiffman, Ph.D.
Department of Psychology, Duke University, Durham, NC 27706

ABSTRACT: By the turn of the century, there will be considerable shifts in demographics, including a massive
increase in our aging population. As we plan for better nutrition in the twenty-first century, the special sensory
and nutritional needs of the elderly must be taken into account. Chemosensory losses, specifically decrements
in the senses of taste and smell, can lead to inadequate intake, especially in the elderly sick. These losses result
Downloaded by [New York University] at 19:33 18 May 2015

not only from anatomic changes that occur during normal aging but also from certain diseases; pharmacological
and surgical interventions, radiation, and environmental pollutants. The design of foods for the elderly that
could both compensate for these chemosensory losses and meet nutritional needs presents new challenges and
opportunities for the food industry.

KEY WORDS: aging, taste, smell, elderly.

I. INTRODUCTION pensating for these losses are described. These

By the year 2025, the number of people aged
60 years and above is expected to triple globally
from 376 million to 1.21 billion. A large pro-
portion of this population will have age-related
sensory losses that must be compensated for if
the elderly are to maintain adequate interactions
with their environments. The decrements in taste
and smell are especially troublesome because
these chemosensory losses can reduce the quality
of life, increase the risk from food poisoning,
and lead to inadequate nutrition, especially in the
elderly sick.1"4
This article describes chemosensory losses
that have been measured in older people, includ-
ing elevated thresholds as well as decrements in
discrimination and identification of chemical
stimuli. Chemosensory losses result from normal
aging, certain disease states (especially Alz-
heimer's disease), pharmacological and surgical
interventions, radiation, and environmental ex-
posure. Scientific research into methods of com-
innovations include adding commercial flavor
(odors) to increase food intake and offset poor
nutrition as well as development of chemical
models that may finally offer treatment possibil-
ities for taste and smell losses in the elderly.
II. PERCEPTUAL LOSSES IN TASTE
AND SMELL IN THE ELDERLY
A gradual loss in taste and smell perception
seems to be an inevitable part of the aging pro-
cess. Although some losses may occur earlier,
most individuals begin to suffer chemosensory
decrements by the age of 60 and more significant
losses when over the age of 70. The usual clas-
sification of chemosensory loss includes ageusia
(no taste sensation), hypogeusia (decreased taste
sensation), dysgeusia (distorted taste sensation),
anosmia (no sensation of smell), hyposmia (de-
creased sensation of smell), and dysosmia (dis-
torted smell sensation).

1040-8398/93/$.50
© 1993 by CRC Press, Inc.

17
 A. Taste
In older people, a variety of difficulties are
caused by a decreased ability to perceive taste
sensations. Elevated detection thresholds mean
that more molecules of a tastant are required be-
fore sensation occurs. Elevated recognition
thresholds mean that a greater concentration of
a tastant is required before it can be correctly
identified. Early studies done on the elderly dem-
onstrate elevated taste thresholds for sucrose,
NaCl, HC1, and quinine HC1, which were chosen
to represent sweet, salty, sour, and bitter taste
groups, respectively.2
We must mention here that current research
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does not support the position that there are only
four primary taste sensations of sweet, sour, salty,
and bitter. Those four derive from Wundt, who,
in 1893, reduced the list to four from earlier
classifications that tended toward multiplicity.5
For example, Linnaeus proposed 11 categories:
sweet, acid, astringent, sharp, viscous, fatty, bit-
ter, insipid, aqueous,.saline, and nauseous. Wundt
argued that the other qualities stemmed from sen-
sations of pain, touch, or odor. Experimental evi-
dence of the past 2 decades suggests, however,
that there are many more than four taste qualities.
In a multidimensional scaling study in which taste
stimuli were arranged in a space based on sim-
ilarity of taste quality, Schiffman and Erickson6-7
found that stimuli did not cluster into four groups;
rather, stimuli spanned the space, suggesting that
Wundt's four groups do not do justice to the
complexity of possible taste sensations. For ex-
ample, monosodium glutamate (MSG) and other
amino acids have tastes that cannot be described
by the basic four; in Japanese, there is even a
word for the taste quality of MSG ("umami"),
although no similar word exists in English.
Schiffman and colleagues have experimen-
tally determined detection thresholds for a very
broad range of sweeteners, sodium salts, acids,
bitter compounds, and amino acids that allowed
them to expand on earlier studies of loss of taste
perception in the elderly (Tables 1-6). When
they compared detection thresholds of older peo-
ple with those of young controls, they found that
the average detection threshold for elderly people
was 2.72 times higher for sweeteners, 11.58 times
18
higher for sodium salts, 4.29 times higher for
acids, 6.94 times higher for bitter compounds,
2.48 times higher for amino acids, and 5.04 times
higher for glutamate salts presented alone or when
mixed with the taste enhancer inosine-5'-mono-
phosphate. This is an average loss of 5.41 across
these qualities.
Not only do older people have difficulty de-
tecting and recognizing tastants, but at su-
prathreshold levels they also have less ability to
discriminate between different intensities of the
same tastant. Using the method of constant stim-
uli for weak and moderate concentrations of NaCl,
KC1, and CaCl2, Schiffman (previously unpub-
lished) studied the ability of the elderly to discern
the differences in concentrations of salts. Whereas
young subjects generally needed only a 6% to
12% difference in concentration to perceive a
change, the elderly subjects required an incre-
ment of 25% to distinguish a difference in
intensity.
Older people have also been found to have
different hedonic responses to food. Warwick and
Schiffman8 found that whereas young subjects
were responsive to the amount of fat in fat-salt
and fat-sucrose mixtures, the older subjects were
not.
Loss of taste perceptions can have serious
consequences for the elderly. Inability to detect
or distinguish among concentrations of sugar
makes it difficult for the elderly diabetic to con-
trol sugar consumption. Similarly, loss of ability
to accurately assess salt levels may lead hyper-
tensive patients to violate a low-sodium diet.
B. Smell
The elderly are also less sensitive to olfactory
stimuli. In studies of volatile chemicals (includ-
ing n-butanol, thiophene, pyridine, menthol, and
citralva) as well as a range of food odors, the
elderly were found to have higher detection and
recognition thresholds.3 Such tests of olfactory
ability are usually done using an olfactometer,
glass sniff bottles, plastic squeeze bottles, or strips
of blotter paper impregnated with an odorant. A
review of the literature shows that older people
 TABLE 1
Mean Detection Thresholds for Sweet Compounds

Stimulus Young(Y) Elderly (E) E/Y

Acesulfam-K 4.44 x 10~ 5 M 7.47 x 10-= M 1.68

Aspartame 2.24 x 10~ 5 M 9.13 x 10-=/W 4.07
Calcium cyclamate 2.66 x 10~*M 4.12 x 10- 4 M 1.55
Fructose 4.39 x 10~ 3 M 10.1 x 10"3/W 2.30
Monellin 1.95 x 10" 8 M 9.13 x 10- 8 M 4.67
Neohesperidin 2.20 x 10" 6 M 4.60 x 10" 6 M 2.09
dihydrochalcone
Rebaudioside 4.61 x 10"6/W 13.0 x 10" 6 M 2.82
Sodium saccharin 1.47 x 10~sM 4.24 x 10-5M 2.88
Stevioside 5.31 x 10"6/W 16.0 x 10"6/W 3.02
Thaumatin 7.16 x 10~8/W 13.3 x 10- 8 M 1.86
D-Tryptophan 1.09 x 10- 4 M 3.22 x 10-"/W 2.95
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TABLE 2 have thresholds that are 2 to 15 times higher for

Mean Detection Thresholds for Sodium most odors than young subjects.
Salts (pH 7.0) Older individuals also have reduced su-
prathreshold responses to odors as has been shown
Elderly by three different methodologies. In one exper-
Stimulus Young (Y) (E) E/Y
imental technique, subjects are asked to give
Monosodium 0.00126 M 0.00638 M 5.06 numbers to odors according to that odor's inten-
glutamate sity. Such magnitude estimation studies indicate
Na acetate 0.00242 M 0.0190 M 7.84 that for older subjects, an odor may be half as
Na ascorbate 0.00404 M 0.0250 M 6.19 intense as would be perceived by a younger per-
Na carbonate 0.00218 M 0.00829 M 3.79 son. In tests that require subjects to identify odors,
Na chloride 0.00238 M 0.01850 M 7.76
Na citrate 0.000531 M 0.0130 M 24.5
scores for elderly subjects are usually 25 to 40%
Na phosphate 0.00307 M 0.0160 M 5.21 lower than those of young people. The method
monobasic of multidimensional scaling in which subjects are
Na succinate 0.000854 M 0.0138 M 16.2 asked to rate odors based on perceived similarity
Na sulfate 0.000981 M 0.0283 M 28.8 also indicates that older people are less able to
Na tartrate 0.00151 M 0.0159 M 10.5 discriminate the amount of difference between
the odors of foods.
Although it is certainly clear that the elderly
have reduced olfactory ability, it is less certain
TABLE 3 which effect that reduced ability has on the en-
Mean Detection Thresholds for Acid
joyment of food. Some older people who com-
Compounds
plain of substantially less pleasure from their
Stimulus Young (Y) Elderly (E) E/Y meals are found to have only relatively small
threshold and suprathreshold losses (e.g., 20%).
Acetic 0.000106 M 0.000273 M 2.58 However, some individuals who report little re-
Ascorbic 0.000281 M 0.000725 M 2.58 duction in their ability to enjoy food are found
Citric 0.0000498 M 0.000375 M 7.53 to have much greater sensory losses (e.g., 50%).
Glutamic 0.0000920 M 0.000463 M 5.03
It seems likely that those individuals whose he-
Hydrochloric 0.0000179 M 0.0002 M 11.17
Succinic 0.000132 M 0.000188 M 1.42 donic response has been greatly reduced have
Sulfuric 0.0000468 M 0.000100 M 2.14 suffered concomitant losses in texture and taste
Tartaric 0.0000864 M 0.000163 M 1.89 sensitivity.

19
 TABLE 4
Mean Detection Thresholds for Bitter Compounds

Stimulus Young (Y) Elderly (E) E/Y

Caffeine 1.30 X 10~3 M 1.99 X 10~ 3 M 1.53

Denatonium benzoate 1.15 X 10~8 M 3.23 X 10" 8 M 2.81
KNO3 1.91 X 10- 3 M 3.27 X 10-2/W 17.1
MgCI2 1.02 X 10~3 M 5.20 X 10~ 3 M 5.10
MgN0 3 1.40 X 10~3 M 3.33 X 10-2/W 23.8
MgSO< 3.23 X 10- 4 M 6.08 X 10" 3 M 18.8
Naringin 4.27 X 10~5 M 1.38 X 10" 4 M 3.23
Phenylthiocarbamide 5.91 X 10- 4M 1.26 X io-3/w 2.13
Quinine HCI 3.99 X 10- 6 M 8.07 X 10-6/W 2.02
Quinine sulfate 2.04 X 10- 6 M 8.75 X 10" 6 M 4.29
Sucrose octaacetate 3.89 X 10- 6 M 5.32 X 10"6/W 1.37
Urea 1.03 X 10'1 M 1.16 X 10~1 M 1.12
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TABLE 5
Mean Detection Thresholds for Amino Acids

Stimulus Young(Y) Elderly (E]I E/Y

L-Alanine 1.62 X 10- 2 M 1.95 X 10- 2 M 1.20

L-Arginine 1.20 X 10- 3 M 1.12 X 10-3M 0.93
L-Arginine HCI 1.23 X 10- 3 M 2.39 X 10- 3 M 1.94
L-Asparagine 1.62 X 10- 3 M 9.33 X 10- 3 M 5.75
L-Aspartic acid 1.82 X 10- 4 M 5.01 X 10~4 M 2.75
L-Cysteine 6.30 X 10- 5 M 3.90 X 10- 4 M 6.19
L-Cysteine HCI 1.60 X 10- 5 M 2.00 X 10- 5 M 1.25
L-Glutamic acid 6.30 X 10-5/W 1.00 X 10~4 M 1.59
L-Glutamine 9.77 X 10" 3 M 2.69 X 10- 2 M 2.75
L-Glycine 3.09 X 10- 2 M 6.17 X 10- 2 M 2.00
L-Histidine 1.23 X 10- 3 M 6.45 X 10- 3 M 5.24
L-Histidine HCI 7.94 X 10~s M 3.89 X 10- 4 M 4.90
L-lsoleucine 7.41 X 10- 3 M 1.20 X 10" 2 M 1.62
L-Leucine 6.45 X 10- 3 M 1.29 X 10" 2 M 2.00
L-Lysine 7.08 X 10-" M 2.24 X 10- 3 M 3.16
L-Lysine HCI 4.47 X 10" 4 M 2.09 X 10- 3 M 4.68
L-Methionine 3.72 X 10"3 M 2.63 X 10- 3 M 0.71
L-Phenylalanine 6.61 X 10" 3 M 1.91 X 10" 2 M 2.89
L-Proline 1.51 X 10~2 M 3.72 X 10- 2 M 2.46
L-Serine 2.09 X 10- 2 M 2.63 X 10- 2 M 1.26
L-Threonine 2.57 X 10- 2 M 2.00 X 10- 2 M 0.78
L-Tryptophan 2.29 X 10" 3 M 2.88 X 10- 3 M 1.26
L-Valine 4.16 X 10" 3 M 1.15 X 10" 2 M 2.76

III. CAUSES OF TASTE AND SMELL
LOSSES
A brief description of the anatomy and phys-
iology of the taste and smell systems is useful
for an understanding of the causes of taste and
smell loss'.1"3 A taste bud is a pear-shaped organ
composed of approximately 50 cells. Taste buds
develop at particular sites in the oral cavity in
stratified squamous epithelium and pseudostra-
tified ciliated epithelium. These sites are fungi-
form, foliate, and vallate papillae of the tongue;

20
 TABLE 6
Mean Detection Thresholds for Glutamate Compounds
(with and without lnosine-5'-Monophosphate—IMP)

Stimulus Young (Y) Elderly (E) E/Y

Sodium 9.02 x 10-" M 2.83 x 10"3/W 3.14

glutamate
Sodium glutamate 1.13 x 1 0 " 4 M 8.88 x 10-/W 7.86
with 0.1 m/W IMP
Sodium glutamate 4.80 x 10-= M 1.45 x 10"4/W 3.02
with 1 m/W IMP
Potassium 9.02 x 10-" M 7.69 x 10"3/W 8.53
glutamate
Potassium glutamate 1.06 x 10-"/W 5.49 x 1O~4M 5.18
with 0.1 m/W IMP
Potassium glutamate 1.08 x 10"5/W 9.28 x 10"5/W 8.59
with 1 rrVW IMP
Ammonium 1.08 x 1 0 " 3 M 4.26 x 10"3/W 3.94
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glutamate
Ammonium 1.39 x 10-" M 4.58 x 10"4/W 3.29
glutamate
with 0.1 mM IMP
Ammonium 3.43 x 10-5/W 1.29 x 10~4/W 3.76
glutamate
with 1 mM IMP
Calcium 2.92 x 10-4/W 1.09 x 10"3/W 3.73
diglutamate
Calcium diglutamate 6.06 x 10" 5 M 3.27 x 1 0 - " M 5.40
with 0.1 m/W IMP
Calcium diglutamate 1.90 x 10"5/W 6.92 x io-=/W 3.64
with 1 m/W IMP
Magnesium 2.53 x 10~AM 1.86 x 10"3/W 7.35
diglutamate
Magnesium 4.21 x 10~5/W 2.89 x 1O~4M 6.86
diglutamate
with 0.1 m/W IMP
Magnesium 2.57 x 10~5/W 4.52 x 1O"5/W 1.76
diglutamate
with 1 m/W IMP
IMP (inosine 5'- 4.30 x 10-" M 1.99 x 10~3/W 4.63
monophosphate)

tongue cheek margin; base of the tongue near the
ducts of the sublingual glands; soft palate; larynx;
pharynx; epiglottis; uvula; and upper third of the
esophagus. The lips and cheeks may also contain
taste buds, especially in the newborn. The normal
rate of renewal for the cells of buds is 10.5 d.
Losses in taste perception in the elderly are some-
times related to alterations in this process of turn-
over and renewal of buds. For instance, radiation
treatment may destroy gustatory epithelium so
completely that taste buds are prevented from
reforming; mitosis can be interrupted by some
medications, including antiproliferative agents.
The number of buds may also be affected by
testosterone or estrogen levels just as reduced
mitosis in gastrointestinal epithelium may be
caused by low hormone levels.
Another cause of loss of taste perception is
disease or damage to the relevant nerves. Three
cranial nerves (the seventh, ninth, and tenth) in-
nervate taste buds. The taste buds of the anterior
two thirds of the tongue are innervated by the
seventh nerve. The circumvallate papillae, ar-
ranged in a V shape on the back one third of the

21
 tongue, are innervated by the ninth cranial nerve, TABLE 7
which also innervates most of the foliate papillae Medical Conditions That Cause Taste Disorders
located in folds or clefts on the sides of the tongue
just anterior to the circumvallate papillae. The Nervous
Bell's palsy
throat area is innervated by the tenth cranial nerve.
Damage to chorda tympani
Axonal transport in these gustatory nerves9 is Familial dysautonomia
required to maintain viable taste buds. Taste loss Head trauma
may result from diseases that interfere with ax- Multiple sclerosis
onal transport. Information from the seventh, Raeder's paratrigeminal syndrome
ninth, and tenth nerves is transmitted to the me-
dulla (nucleus of the solitary tract), thalamus, and Nutritional
Cancer
cortical taste area. Free nerve endings of the tri- Chronic renal failure
geminal nerve are also found in the oral cavity Liver disease (including cirrhosis)
and tongue. Disease states and medications can Niacin (vitamin B3) deficiency
affect all of these nerves. Thermal burn
Zinc deficiency
Approximately 6 to 10 million neurons found
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in the upper portion of the nasal cavity constitute Endocrine

the receptor cells for olfaction. These cells, like Adrenal cortical insufficiency
taste buds, are constantly being replaced on the Congenital adrenal hyperplasia
average of every 30 d. They, too, are vulnerable Panhypopituitarism
to a variety of conditions, including nutritional Cushing's syndrome
Cretinism
status. The physiological mechanism for the de-
Hypothyroidism
tection of odors is not completely understood as Diabetes mellitus
there does not seem to be a definable relationship Gonadal dysgenesis (Turner's syndrome)
between the quality of an odor and its chemical Pseudohypopara- thyroidism
structure comparable with frequency of vibration
to sound or wavelength to color. Volatile com- Local
Facial hypoplasia
pounds with relatively similar olfactory qualities
Glossitis and other oral disorders
may, in fact, have quite different chemical struc- Leprosy
tures. This issue is further complicated by the Oral Crohn's disease
fact that differing concentrations of odorants re- Radiation therapy
sult in differing odor qualities. The mechanism Sjogren's syndrome
of transduction resulting in depolarization of ol-
Other
factory cells is also unclear; however, most of
Hypertension
the studies indicate the possibility of multiple Influenza-like infections
second-messenger systems and transport pro- Laryngectomy
cesses. Chemically altering one of these systems
can effect dysosmia.
Tables 7 and 8 contain summaries of disease colchicine would be expected to interfere with
conditions and drugs that affect responses to taste cell division and replacement, as it does in many
and smell stimuli. It is not certain whether drugs tissues, local application of colchicine to the glos-
affect perception of taste and smell by the same sopharyngeal nerve inhibits taste response for a
or different mechanisms as those that affect other different reason: interference with axonal
tissues. It is possible that in the chemical senses, transport.9
drugs may block channels and receptors, disrupt
second-messenger systems, interfere with cell re-
IV. ALZHEIMER'S DISEASE
placement, or hinder neural signal propagation
just as they do in other systems. There is evidence Failure of the ability to smell is particularly
to suggest, however, that drugs affect the chem- acute in Alzheimer's disease (AD), a form of
ical senses differently. For instance, although presenile dementia that primarily occurs in older

22
 TABLE 8
Drugs That Alter the Sense of Taste
Classification
Amebicides and anthelmintics
Anesthetics (local)
Anticholesteremic
Anticoagulants
Antihistamines
Antimicrobial agents
Antiproliferative, including
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immunosuppressive agents
Antirheumatic, analgesic-
antipyretic, antiinflammatory
Antiseptics
Antithyroid agents
Agents for dental hygiene
Diuretics and antihypertensive
agents
Hypoglycemic drugs
Muscle relaxants and drugs for
treatment of Parkinson's disease
Psychopharmacologic, including
antiepileptic drugs
Sympathomimetic drugs
Vasodilators
Others
people. One in ten individuals aged 65 have AD,
a proportion that increases to one in three by age
85. l0 Its effects are severe; not only is it the fourth
leading cause of death11 but, in those over the
age of 60, it causes 50% of long-term
institutionalizations.12
Patients with AD have neurofibrillary tangles
and senile plaques in numerous brain structures,
including olfactory epithelium, olfactory bulb,
anterior olfactory nucleus, olfactory tubercle,
Drug
Metronidazole, niridazole
Benzocaine, procaine
hydrochloride (Novocain), and
others
Clofibrate
Phenindione
Chlorpheniramine maleate
Amphotericin B, ampicillin,
bleomycin, cefamandole,
griseofulvin, ethambutol
hydrochloride, lincomycin,
sulfasalazine, tetracyclines
Doxorubicin and methotrexate,
azathioprine, carmustine,
vincristine sulfate
Allopurinol, colchicine, gold,
levamisole, D-penicillamine,
phenylbutazone, 5-thiopyridoxine
Hexatidine
Carbimazole, methimazole,
methylthiouracil, propylthiouracil,
thiouracil
Sodium lauryl sulfate
Acetazolamide, amiloride, captopril,
diazoxide, enalapril, ethacrynic
acid, nifedipine
Glipizide, phenformin and
derivatives
Baclofen, chlormezanone,
levodopa
Carbamazepine, lithium carbonate,
phenytoin, psilocybin,
trifluoperazine
Amphetamines
Bamifylline hydrochloride,
diltiazem, dipyridamole,
oxyfedrine
Germine monoacetate, idoxuridine,
insecticides, iron sorbitex, metal
ions, vitamin D
amygdala, prepiriform cortex, hippocampus, and
entorhinal cortex.13 Impairment of recognition and
recollection of odorants is a result of insult to the
olfactory and limbic structures in the temporal
lobe, whereas difficulties with detecting odors,
determining intensity, and adaption are caused
by damage nearer the periphery (e.g., olfactory
epithelium).14
Such extensive impairment of the olfactory
systems may be more than coincident; one current
23
 theory about the origin of AD itself suggests that
it is caused by a virus or environmental toxin that
enters the brain via the nasal passages.15'11 The
causative agent is presumably transported by the
olfactory receptor cells along the multisynaptic
olfactory pathways to the central brain struc-
tures. 1819 The nasal route may also provide ac-
cess to gold, dyes, and zeolites. It is important
to remember that lower structures may not be
damaged when molecules that damage higher ol-
factory centers enter through the nasal route. For
instance, Nir et al.20 showed that exposure to a
viral aerosol allowed viruses to gain access to
the brain by a nasal route. Immunofluorescence
staining, however, showed pathology at the level
of the olfactory bulbs and not in the olfactory
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mucosa.
The fact that aluminum accumulates in neu-
rofibrillary tangles21 and senile plaques22 has led
to extensive research on the possibility that zeo-
lites are the causative agent in AD. If aluminum
is found to be an etiological factor in AD, its
path of entry may well be through the nose be-
cause it can gain access to the brain by olfactory
transport.23 Aluminum by oral administration is
unlikely to accumulate in toxic amounts in the
brain of humans.24
V. TREATMENT OF CHEMOSENSORY
LOSSES IN THE ELDERLY
In the future, chemosensory losses may be
treatable in two ways. First, drugs may prove
effective in improving the functioning or repro-
duction of chemosensory cells. For instance, tes-
tosterone treatment results in taste bud formation
on vallate papillae.25 Unfortunately, little is cur-
rently understood about using drugs for ampli-
fication of taste or smell signals. A second ap-
proach seems more likely in the near future: the
sensory qualities of food may be improved by
the addition of chemicals.
A. Taste Enhancement
Current research on chemical enhancement
properties may prove useful in treating taste losses
in the elderly.26 Investigations of the mechanism
24
of taste transduction and modulation have re-
vealed four pharmacological agents that enhance
taste perception: caffeine (and other methyl xan-
thines), 5'-ribonucleotides, inosine, and bretyl-
ium tosylate. These agents can provide insight
into the process of amplification of taste sensa-
tions even though other practical considerations
would prevent their use in some or all foods.
1. Methyl Xanthines
Found in coffee, tea, and chocolate, methyl
xanthines include caffeine, theophylline, and
theobromine. By binding to adenosine receptors,
methyl xanthines counteract the effects of ade-
nosine, which helps control and regulate many
biological processes. Among adenosine's effects
are slowing of sinus rate, vasodilation, and
hypotension.
Taste studies have shown that the taste en-
hancement ability of methyl xanthines, including
caffeine, is caused by the blocking of adenosine
receptors. For example, the taste of those arti-
ficial sweeteners with bitter components (e.g.,
sodium saccharin) is enhanced by the treatment
of the anterior tongue with mild concentrations
of caffeine (10 \x.M to 10 mM) for 4 min. On the
other hand, those sweeteners that do not have
bitter components (e.g., sucrose, aspartame) are
not enhanced by methyl xanthines. The tastes of
table salt (NaCl) and salt substitute (KC1) are
potentiated slightly by caffeine. It is theorized
that the taste enhancement effect of methyl xan-
thines is due to their increasing of the mediator
cAMP (cyclic adenosine monophosphate) inside
of cells.
2. 5'-Ribonucleotides
It has been definitely established that the taste
of monosodium glutamate is potentiated by 5'-
ribonucleotides, including inosine-5'-monophos-
phate (IMP) and guanosine-5 '-monophosphate
(GMP). More recent research has shown that the
sweet qualities of aspartame and sucrose can be
enhanced by adaptation of the tongue to 1 mAf
IMP.However, it is also known that adaption to
IMP does not affect many tastes, including sweet-
 eners with bitter components (e.g., calcium cy-
clamate, sodium saccharin) and salty, sour, or
bitter tastes.
3. Inosine
A breakdown derivative of IMP and adeno-
sine, inosine has been shown to enhance sucrose,
aspartame, and sodium saccharin sensations on
the tongue, but it does potentiate other tastes
enhanced by caffeine.
4. Bretylium Tosylate
The compound, bretylium tosylate, contains
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a nitrogen atom with a positive charge that, on
application to the human or rodent tongue for 4
min, enhances salt flavor. Although the mecha-
nism of this effect is unclear, it is possible that
it may open channels in the taste cell membrane,
thus allowing Na + to flow into the taste cell.
B. Practical Limitations of Taste
Enhancers
The majority of these taste enhancers, how-
ever, have practical drawbacks. A 4-min adap-
tation period is required for caffeine, inosine, and
bretylium tosylate to take effect. Furthermore,
caffeine and other methyl xanthines have signif-
icant pharmacological effects, and although IMP
has been used to potentiate the glutamate taste,
it does not enhance most other taste qualities.
Moreover, inosine has never been used as an
enhancer, and bretylium tosylate is an antifibril-
lary drug not to be used in food. Despite these
drawbacks, the use of these pharmacological
probes offers further understanding of the req-
uisite biochemical properties for practical taste
enhancers.
C. Odor Enhancement
Flavors are mixtures of odorous molecules
that can be extracted from natural products or
synthesized after chemical analysis of the natural
products. Commercial flavors have been added
to foods for the elderly to improve intake and
subsequent nutritional status1 with good results.
For example, simulated green bean flavor added
to fresh or frozen beans or bacon flavor added
to soups, vegetables, and meats increases aroma
and, therefore, enjoyment or appreciation. Such
flavor enhancement has been used extensively in
both hospital and nursing home environments to
improve intake of nutrient-dense foods in older
people.
D. Texture Enhancement
Chemosensory losses in the elderly can be
compensated for in part by adding texture sen-
sations of crunchiness or chewiness. Such added
texture is inappropriate for older people with tooth
loss, dental caries, and periodontal disease. For
the elderly with dentition problems, the addition
of functional fiber and flavors to soften textured
foods is more advisable.
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