There is a connection between how well you can smell, brain damage from autoimmune inflammation, and psychiatric disease. Consider this fascinating paper published in the journal Clinical Immunology in which the authors discuss the “inter-relationship between olfactory impairment, autoimmunity and neurological/psychiatric symptoms in several diseases affecting the central nervous system (CNS) such as Parkinson, Alzheimer’s disease, autism, schizophrenia, multiple sclerosis and neuropsychiatric lupus erythematosus. We suggest that common manifestations are not mere coincidences. Current data from animal models show that neuropsychiatric manifestations are intimately associated with smell impairment, and autoimmune dysregulation, via autoantibodies…”

In another paper published in the journal Autoimmunity Reviews the authors note that “Research in the field of immunology as well as in various brain illnesses is beginning to indicate the increasing relevance of smell in pathophysiology.” They further state “…evidence exists that there may be something unique about the olfactory system that is inextricably related to immunological function. In addition, accumulating evidence confirms the existence of olfactory dysfunction in brain disease, much of which appears at early stages including multiple sclerosis, Alzheimer’s Disease, Parkinson’s Disease, schizophrenia and depression…under certain circumstances, olfactory abnormalities may be associated with autoimmune conditions. Since the organization of the olfactory system is so sensitive, impairment may be noted at an early stage. This may become important in the prediction of certain brain illnesses.”

This paper recently published in the International Journal of Neuroscience focuses specifically on the link between olfaction, autoimmunity and Parkinson’s Disease. They first describe “the immune alterations observed in PD patients…the increase in the innate immune components including complement and cytokines within their substantia nigra and cerebrospinal fluid (CSF). These alterations extended to the adaptive immune response with the elevation of T cells and autoantibodies…in the peripheral blood and CSF of PD patients.” (Just the kinds of things we test for in the functional medicine approach.) They then describe the link between PD, autoimmunity and olfaction: “Smell deficit is one of the earliest signs of PD and a unique observation suggesting olfactory declines to be a consequence of autoimmune mechanisms.”

And the authors of this study published recently in the journal Autoimmunity observe that “Psychiatric diseases are often associated with mild alterations in immune functions (e.g., schizophrenia) as well as autoimmune features. Recent evidence suggests that autoimmune diseases (AD) demonstrate a higher prevalence of psychiatric disorders, such as depression and psychosis, than in the normal population. Patients with AD often have an olfactory impairment as well, based on smell studies… ” They report that olfactory gene receptors have brain functions in addition to smell, and go on to describe the genetic polymorphisms (variations) that link autoimmunity, psychiatric disorders and smell impairment.

The paper that concludes this post is tantalizingly entitled Olfaction—A Window to the Mind. Published not long ago in The Israel Medical Association Journal, it is available here in its entirety. The authors comment that “The sense of smell can provide a natural window to the brain. This window provides an opportunity to examine neural mechanisms and brain function in a non-invasive way.” They then undertake a fascinating review of the field of olfactory studies encompassing aspects ranging from autoimmunity and neuropsychiatric disease to sexual function, addiction, social behavior and the discrimination of self from non-self. Their conclusion is worth bearing in mind: “…assessment of the sense of smell and olfactory impairments is usually overlooked by patients and their clinicians. Given the clinical data reviewed here, clinicians should be encouraged to screen for olfactory impairments, which can help in the early diagnosis of CNS diseases such as Parkinson, dementia and schizophrenia, as well as CNS-autoimmune diseases such as neuropsychiatric lupus.”

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If you have a parent who has suffered from Alzheimer’s disease, this paper just published in the Archives on General Psychiatry identifies two vascular factors that you can use for screening and prevention: hypertension (high blood pressure) and pro-inflammatory cytokines (signaling molecules that promote inflammation). The authors conclude: “Hypertension and the expression of an innate pro-inflammatory cytokine profile in middle age are early risk factors of AD in old age. For the offspring of affected families, it provides clues for screening and preventive strategies…” Blood tests that measure cytokines are available at a discount due to our co-op association with Labcorp.

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Factors that place fat around the waist (insulin resistance) and the activity of that fat tissue (production of signaling molecules that promote inflammation) are both at play behind the connection documented recently in this paper published in the journal Neurology. The authors found that “…a midlife WHR [waist hip ratio] greater than 0.80 increased risk for dementia approximately twofold…,” and conclude: “There are midlife and late-life implications for dementia prevention, and analytical considerations related to identifying risk factors for dementia.” Here are a few more papers related to the same finding:

1. Research on diabetes, hyperinsulinemia and dementia in Dementia and Geriatric Disorders
2. A paper on abdominal obesity and Alzheimer Disease published in the same journal
3. A study in Archives of Neurology that concludes: “A larger WHR may be related to neurodegenerative, vascular, or metabolic processes that affect brain structures underlying cognitive decline and dementia.”

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We’re paying careful attention to inflammatory damage to the brain associated with chronic infections in the digestive tract and elsewhere, including periodontal disease. Many studies are documenting the major role this plays in neurodegeneration and dementia:

1. Alzheimer’s disease and peripheral infections
2. Infection and Alzheimer’s disease
3. Eradication of Helicobacter pylori and Alzheimer’s disease
4. H. pylori antibody increased in Alzheimer’s cerebrospinal fluid
5. Herpes simplex and Alzheimer’s disease

This is one of the reasons we place so much value on the Gastrointestinal Function Profile for detecting chronic gut infections.

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You may remember that we use Medium Chain Triglycerides (MCT) in their pure form to make medical foods such as Clearvite® and Ultrameal® more complete. This form of fat is especially easy for the body to burn for energy, supports metabolism and stabilizes blood sugar. Two very interesting papers in the journals Diabetes and Neurobiology of Aging document that MCT oils also oppose neurodegeneration related to glucose dysregulation and improve cognition:

1. Cognitive function improves in Type 1 Diabetes
2. Memory improves with Alzheimer’s

MCT’s are abundant in coconut butter, and easily added to shakes in the form of MCT Oil which is liquid at room temperature.

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Dementia begins in the hippocampus, the part of the brain that converts short to long-term memory. It is also responsible for regulating the daily rhythm of cortisol secretion by the adrenal glands. This paper is one of a number that recognize abnormalities in the cortisol curve (the graph in your adrenal report) as an early screen for dementia. This is important to address as early as possible. When the neurons are gone, they’re gone forever!

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