Potential Cause(s) of Memory Loss-Dementia
The actual "cause" of most forms of chronic memory loss, cognitive dysfunction and dementia syndromes is essentially unknown. There are scientific "theories", but they are just that... theories. No expert really knows what is causing the clinical problem in a majority of cases. There are, however, various categories of "causative" mechanisms that can be investigated in order to identify potentially treatable and, hopefully, reversible mechanisms of memory loss, cognitive dysfunction and/or dementia. Included among these categories are:
|| Neuro-Transmitter deficiency
Included under the broad heading of "toxic"
causes would be the possibility of toxic metals (lead, mercury, aluminum, etc.) effects on neurological function.18-31
factors involved in memory loss include various B vitamins (B12, Folic Acid) deficiencies1
, sugar and carbohydrates toxicity in diabetes and/or metabolic syndrome32-37
, excess cholesterol, animal and/or trans
, The association between memory loss-cognitive dysfunction and vascular disease
has both epidemiologic (statistical-based population studies) and laboratory evidence demonstrating an association.32,38-39
A number of know cardiovascular risk factors (high cholesterol, high homocysteine, high blood pressure, high C-reactive protein, diabetes, etc.) are also found in SDAT and other forms of dementia.32,38-39
In addition, there is increasing evidence that vascular problems leading to tiny, pim-point silent strokes (brain lacunar infarcts) are a much more common and insidious cause of clinically apparent memory and cognitive problems than Alzheimer Disease. In fact, it has been postulated that AD itself may ultimately be determined to be due to Microcirculation
problems. Interestingly, the microscopic changes seen in Alzheimer Disease and SDAT that are thought by evidence-based scientists to be "specific" for the disease have now been documented in patients with cardio vascular disease and
no clinical evidence of dementia
The current clinical evidence for Micro-Vascular
disease as a potential cause for has grown convincingly strong.41
The association of cognitive decline and dementia with diabetes, metabolic syndrome, inflammation and abnormal protein glycation
(Advanced Glycosylation End-Products or AGE products42,43
) appears to be very strong statistically. These conditions are also all known to be clinically associated with the toxic biological effects of sugar on the structural and regulatory function of the neuro-endocrine-immune system and/or brain Micro-Circulation
agents had pretty much been discredited as a cause of Alzheimer Disease, SDAT and other chronic dementia syndromes until the clinical emergence of infectious
prion diseases of the central nervous system (Mad Cow Disease, Creutzfeltd Jakob Disease, "variant" Creutzfeltd Jakob Disease, "Wasting Disease" in Deer and Elk, Scrappy in Sheep, etc.). In the wake of the new clinical realization that infectious agents can cause dementia the "infectious theory" of dementia has been partially revised. Included among possible infectious candidates, as causes for dementia are chronic Lyme disease ("spirochetes"), cell wall deficient organisms, Chlamydia, chronic viral infections (Herpes viruses) and fungal/yeast causes. The last group may be actual fungal or yeast "infection" or possibly due to toxic fungal by-products ("mycotoxins").
Among the possible hormonal
causes of memory loss, cognitive decline and/or dementia are Estrogen deficiency44,45
, Testosterone deficiency8
, and possibly DHEA46
and/or Growth Hormone deficiency44,48,49
. A possible relationship between immune system dysfunction and memory loss-cognitive dysfunction has also been postulated.43,50-52
The most commonly cited scientific, "evidence-based" causes of Alzheimer/SDAT are neuro-transmitter deficiency
and/or genetics. Genetics
is thought to be involved with only about 20% of AD patients, leaving the cause(s) for the other 80% of clinical cases unaccounted for1
. Currently, the only FDA approved treatments for Alzheimer disease are pharmaceuticals that either increase the amount of the neuro-transmitter Acetyl-Choline or antagonize the NMDA receptor in the brain. These drugs only sometimes help symptoms and their clinical effects may be only be temporary. There are also side effects from these medications. Why this neuro-transmitter deficiency actually occurs is not clear from laboratory or clinical research. The problem with citing genetics
or inheritance of affected genes as a cause of Alzheimer/SDAT syndrome is that any and all genetically determined traits, whether disease or not, require an environmental signal to manifest
. For example, all human fetal development manifests a genetically determined gill stage, exactly like fish. This gill phase of human embryonic fetal development is genetically programmed, but we don't see any adult humans walking around with gills! The simple reason is there is no environmental trigger causing the "gene" to manifest. So, if someone has a gene or chromosome that might lead to AD/SDAT, there still must be an environmental trigger(s)
to set the genetic pattern into motion. Hence, to simply say that it runs in one's family is genetic and its fate is to not understand
how "genetic" inheritance actually works. In addition to the preceding list of possible causes, there will undoubtedly be additional mechanistic causes of brain and mind dysfunction proposed in the future
Finally, the primary problem with researching the actual "cause(s)" of memory loss, cognitive dysfunction or dementia is the very real possibility that most of the clinical problems actually encountered result for the interaction of a number of these possible causes... scientifically referred to as "Multi-Factorial causation"
. Given all the current theories related to possible cause(s) of memory loss, cognitive dysfunction and dementia, it would appear logical that any plan of prevention and/or treatment should involve methods that would also treat multiple possible causes, whether they be biochemical neuro-transmitter deficiency (Acetyl choline), Micro-Circulatory
vascular dysfunction, neural dysregulation, toxin accumulation, etc.
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