I've wondered about sense of smell for a long time.

CTenaLouise discussed zinc. And that has a lot to do with it, but not everything. But a lot . . . so if there is any chance you're zinc-deficient, try taking some. However, Nature loves a zinc:copper ratio of about 10:1 (10 mgs zinc, 1 mg copper) so don't go overboard on the zinc and forget the copper.

This discussion reminded me of a brief comment I saw. Here it is:

E-MOVE reports from the 57th Annual Meeting of the American Academy of Neurology, 9-16 April 2005, Miami.
Poster, session and page numbers are from Neurology 2005;64(suppl 1).

Olfaction is normal in essential tremor and can be used to distinguish it from Parkinson’s disease
M Shah, L Findley, N Muhammed, C Hawkes
S27.001, A261

Two forms of smell tests were administered to 59 ET patients, 65 PD patients, and 74 controls. Tests used were the 40-odorant UPSIT and olfactory evoked potential in response to hydrogen sulfide.

Mean UPSIT scores were 33 for controls, 32 for ET patients, and 18 for PD patients.

OEP values were normal in all but 4 ET patients (which included at least one patient who didn’t receive testing). Forty percent of PD patients had no recordable OEP, and the remainder had significantly prolonged latency with normal amplitude.

“A normosmic patient with tremor is more likely to have ET than PD,” the authors conclude.

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Also, here's an abstract from a review article.

Adv Otorhinolaryngol. 2006;63:133-51.
Olfaction in neurodegenerative disorder.
Hawkes C.
Essex Centre for Neuroscience, Oldchurch Hospital, Romford, UK.

There has been gradual increase of interest in olfactory dysfunction since it was realised that anosmia was a common feature of idiopathic Parkinson's disease (IPD) and Alzheimer-type dementia.

It is an intriguing observation that a premonitory sign of a disorder hitherto regarded as one of movement or cognition may be that of disturbed sense of smell.

In this review of aging, IPD, parkinsonian syndromes, tremor, Alzheimer's disease (AD), motor neuron disease (MND), Huntington's chorea (HC) and inherited ataxia, the following observations are made:

(1) olfactory senescence starts at about the age of 36 years in both [genders] and accelerates with advancing years, involving pleasant odours preferentially;

(2) olfactory dysfunction is near-universal, early and often severe in IPD and AD developing before any movement or cognitive disorder;

(3) normal smell identification in IPD is rare and should prompt review of diagnosis unless the patient is female with tremor-dominant disease;

(4) anosmia in suspected progressive supranuclear palsy and corticobasal degeneration is atypical and should likewise provoke diagnostic review;

(5) subjects with hyposmia and one ApoE4 allele have an approximate 5-fold increased risk of later AD;

(6) impaired sense of smell may be seen in some patients at 50% risk of parkinsonism, and possibly in patients with unexplained hyposmia;

(7) smell testing in HC and MND where abnormality may be found is not likely to be of clinical value, and

(8) biopsy of olfactory nasal neurons reveals non-specific changes in IPD and AD and at present will not aid diagnosis.

PMID: 16733338 [PubMed - in process]

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And Harvard's "Massachussetts Eye and Ear Infirmary" says:

Our sense of smell begins when an odor enters the nose and reaches the special smell (olfactory) nerves in the roof of the nasal cavity.

The nerves then send signals to the brain where we recognize a smell. These nerves can be damaged, but luckily as in all animals, these nerves can be replaced with new ones.

When there is an interruption in the ability of an odorant to travel from the outside to inside the nose and from the inside of the nose to the smell nerves of the nasal cavity and from the smell nerves to the brain, a smell disorder occurs.

We call a decreased sense of smell hyposmia, and a total loss of smell anosmia.

Phantosmia is the term given when someone thinks they can smell something when no one else in the room smells the same thing. This can occasionally indicate an infection.

http://www.meei.harvard.edu/patient/tasteandsmell.php

(Quote):
(3) normal smell identification in IPD is rare and should prompt review of diagnosis unless the patient is female with tremor-dominant disease;

This point is very interesting. I would like to see some further explanation of why tremor-dominant females with IPD retain their (our) sense of smell.

The material below is from the NIDCD, which is part of the National Institutes of Health. It's the National Institute on Deafness and Other Communication Disorders.

Smoking cigarettes and loss of smell have been famously linked for many years. Cigarette smoke contains very tiny - ultratrace - amounts of cadmium. You'll note 'cadmium' in the material below.

Drinking alcohol affects smell, also. At least a part of the reason is that metabolizing alcohol requires zinc. And zinc has a connection to an ability to smell; it's not the whole answer, but a significant part.

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Statistics on Smell [NIDCD Health Information]

Statistics 1-2% of the North American population below the age of 65 years experience smell loss to a significant degree.

According to estimates based on reported research, 1-2% of the North American population below the age of 65 years experience smell loss to a significant degree.

Smell loss is much greater in older populations, with nearly half of individuals between the ages of 65 to 80 years seemingly experiencing some loss of the ability to smell, and nearly three-quarters of those over the age of 80 years experiencing such loss.

Note: These are the best estimates available from studies using actual smell tests. Surveys asking about smell ability without the administration of tests are likely to underestimate smell loss,since many individuals are note aware of their dysfunction unless it is marked. This phenomenon has been noted not only in "normal" populations, but in individuals diagnosed with disorders associated with smell disorders such as Alzheimer's disease and idiopathic Parkinson's disease.

Summary Report
The vast majority of patients presenting to physicians with chemosensory (smell and taste) disturbances, including "taste disturbances," exhibit olfactory dysfunction. As with the case of the taste system, the olfactory system plays a significant role in eating, as most food and beverage flavors are, in fact, dependent upon this system.

Such common "tastes" as chocolate, coffee, strawberry, apple, peach, pizza, steak sauce, and chicken actually reflect olfactory-mediated sensations that require the integrity of CN I. Molecules are released and propelled upwards towards the olfactory receptors via the nasal pharynx during mastication and deglutition (Burdach & Doty, 1987).

The olfactory receptors, unlike the receptors of most sensory systems, are directly exposed to the outside environment, save their protection by a thin layer of mucus, making them relatively susceptible to damage from such exogenous agents as viruses, bacteria, pollutants, and airborne toxins.

Moreover, since the axons of the olfactory receptor cells extend through the foramina of the cribriform plate to synapse within the olfactory bulb of the central nervous system (CNS), they are extremely vulnerable to shearing and tearing from movement of the brain relative to the cranium.

This occurs, for example, in accelerative/decelerative head trauma injuries, even in the absence of fractures, contusions or other objective evidence of trauma (Doty et al., 1997b).

The direct route of the olfactory receptor cells from the nasal cavity to the brain makes the olfactory receptors a major conduit for the movement of environmental agents into the brain, in effect bypassing elements of the blood brain barrier. Among agents known to use this route as a means of entrance into the CNS are such viruses as polio virus (e.g., Bodian & Howe, 1940), rabies virus (e.g., Dean et al., 1963), Herpes simplex virus (e.g., Dinn, 1980), and human immunodeficiency virus (e.g., Brody et al., 1991).

In light of the olfactory anatomy, it is perhaps not surprising the most common causes of permanent smell loss are (a) upper respiratory infections, such as the common cold, (b) head trauma or rapid head acceleration or deceleration, and (c) rhinosinusitis.

Although the data are limited, these three causes do account for the majority of patients who present to physicians with chemosensory disturbance (Duncan & Seiden, 1995). The percent of patients presenting to specialized centers with these etiologies vary slightly from institution to institution, depending upon their referral bases or referral criteria.

In general, about a quarter of patients in such populations have smell loss secondary to URI's, about 20% secondary to head trauma, and 15% secondary to rhinosinusitis (Deems et al., 1991).

Other less common causes of smell loss include chronic alcoholism (Shear et al., 1992), epilepsy Kohler et al., 2001), Kallmann's syndrome (Hudson et al., 1994), Korsakoff's psychosis (Mair et al., pseudohypoparathyroidism (Doty et al., 1997a) and a number of common neurological disorders, including multiple sclerosis (Doty et al., 1997b, 1999), schizophrenia (Moberg et al., 1999), Huntington's disease (Blysma et al., 1998; Moberg & Doty, 1997), Alzheimer's disease (Doty et al., 1987; Murphy et al., 1999), and idiopathic Parkinsonism (Doty et al., 1988).

In the case of multiple sclerosis, the smell dysfunction is directly related to the number of plaques within the subtemporal and orbitofrontal cortices, waxing and waning in relation to plaque activity (Doty et al., 1997, 1999).

In the case of AD and PD, smell loss appears to be the first clinical sign of the disorder, occurring long before the cardinal signs of the syndromes.

In the case of PD, smell loss is unrelated to anti-parkinson medication use and is more common (~ 90%) than tremor (~85%) (Doty et al., 1992).

Smell testing can aid in differential diagnosis, since some neurological diseases, often misdiagnosed as Alzheimer's disease or idiopathic Parkinson's disease, are unaccompanied by meaningful olfactory loss (e.g., major affective disorder (McCaffrey et al., 2000), progressive supranuclear palsy (Doty et al., 1993), essential tremor (Busenbark et al., 1992) and MPTP-induced parkinsonism (Doty et al., 1992).

It is important to note that smell testing of patients at risk for AD may be the best predictor of who later will be clinically diagnosed with AD (Murphy et al., 1988). For example, in an epidemiological study of 1,604 non-demented community-dwelling senior citizens 65 years of age or older, scores on a 12-item odor identification test were a better predictor than scores on a global neuropsychological test of cognitive decline over a subsequent 2-year time period (Graves et al., 1999).

Persons who were anosmic and possessed at least one APOE-4 allele had 4.9 times the risk of having cognitive decline than normosmic persons not possessing this allele (i.e., an odds ratio of 4.9). This is in contrast to the 1.23 times greater risk for cognitive decline in normosmic individuals possessing at least one such APOE allele.

When the data were stratified by sex, women who were anosmic and possessed at least one APOE-4 allele had an odds ratio of 9.71, compared to an odds ratio of 1.90 for women who were normosmic and possessed at least one allele. The corresponding odds ratios for men were 3.18 and 0.67, respectively.

Exposure to a number of toxic agents can induce smell loss. Olfactory loss can occur as a result of exposure to toxins in general air pollution and in workplace settings. In addition to directly damaging the olfactory neuroepithelium, some toxins may produce damage indirectly by inducing upper-respiratory inflammatory responses or infections that, in turn, induce such damage.

The best scientific documentation of toxic exposure in humans is for acrylates, methacrylates, and cadmium, with the former being typically being reversible after removal from the workplace and the latter inducing, in unregulated settings, longer-lasting or permanent effects.

Schwartz et al. (1989) tested the olfactory function of 731 workers at a chemical plant that manufactured acrylates and methacrylates. A nested case-control study designed to assess the cummulative effects of exposure on olfactory function found crude exposure odds ratios (95% confidence intervals) of 2.0 (1.1, 3.8) for all workers and 6.0 (1.7, 21.5) for workers who had never smoked cigarettes. Logistic regression analysis, adjusting for multiple confounders, found exposure odds ratos of 2.8 (1.1, 7.0) and 13.5 (2.1, 87.6) in these same respectives groups and a dose-response relationship between the olfactory and cumulative exposure scores.

Decreased odds ratios were associated with increasing duration since last exposure to the chemicals, implying some degree of reversibility. This seems less likely for cadmium, although similarly sophisticated studies have not been performed.

Yin-Zeng et al. (1985) reported that 28% of individuals who had worked five years or more in a cadmium-refining plant claimed having anosmia, although quantitative testing was not performed. The average concentration of airborne cadmium was said to be relatively low (between 0.004 and 0.187 mg/m3), but still slightly above the current OSHA permissible exposure limit of 0.005 mg/m3).

Rose et al. (1992) found moderate to severe hyposmia, but not anosmia, to n-butanol in 55 workers exposed for an average of 12 years to cadmium fumes, a phenomenon correlated with body burden of cadmium, as measured by urinalysis. Rydzewski et al. (1998) compared the olfactory thresholds of 73 workers involved in the production of cadmium-nickel batteries to that of 43 nonexposed, age- and smoking-matched controls.