By the time a cognitive impairment (memory, attention, etc) manifests itself, a certain amount of damage has been done… otherwise no overt symptoms would be observable or experienced. Inflammation is the cause of virtually everything that ails us, and certain hormones like insulin or cortisol, influencing and modifying inflammation, are big players.
What you put in is what you get out. Diagnosis.
It should be clear by now, that a good look at the inflammatory state of the body, stress as well as nutritional building blocks supplied plus environmental influences such as toxins, relate to a communication failure of some sort. Depending on the type of failure and the system affected, the breakdown will take its toll. This article has but vaguely touched on the actual processes within digestion and the usage and essentiality of certain building blocks. Cholesterol, high blood pressure and cardiovascular disease arise out of the same thematic pool and are just as problematic within the scope of neurodegenerative diseases affecting memory – so are gene expressions and DNA mutations, but will have to be included in another discussion.
The ‘take-out’ so far is: Imbalances are the precursors to the signs and symptoms detected by diagnosing.
Next to Neuropsychological assessment, concerned with the individual’s attention and concentration, visuo-motor and visuo-spatial, construction abilities, language abilities, executive functioning and intellectual abilities, assessment in relation to memory (according to currently practiced medicine) focuses specifically on testing the individuals capacity to retain information and the use thereof for adaptive purposes. Neuropsychological memory assessments are commonly started by obtaining information about the patient’s attention and concentration abilities, including the use of a Digit Span Test or the Serial Sevens/ Threes test (Lezak, Howieson&Loring, 2004).
A comprehensive memory assessment usually includes the orientation of time, place and person, assessing the learning and retention of meaningful information resembling a conversation (verbal recall tests, e.g. Wechsler’s Logical Memory Stories), the rote learning ability (free and recognition trials rendering a learning curve as in the Auditory Verbal Learning Test or the Californian Verbal Learning Test), the Complex Figure Test assessing Visuo-spatial memory (followed by a recognition trial on availability) and remote as well as personal & autobiographical memory (Lezak et al, 2004).
In order to scope a patients strengths and weaknesses in their totality, three aspects are commonly considered according to current assessment methods:
- A delay trial is necessary to examine learning and possible slowed integration ability of new info,
- Continuous Rehearsal Prevention is achieved by interference during delay, manifesting whether recall following delay was of studied material, or of info held in continually rehearsed temporary storage,
- Test learning by recognition cued tasks to determine whether reduced retrieval is due to a retrieval problem or a learning dysfunction. (Lezak et al, 2004)
The inclusion of a rather vague but poignant glimpse of the important influences such as nutrition in the disease progress is but one factor to be considered as part of an interconnected web impeding on optimal functioning. Despite the crumbling health systems around us, we are adhering to a system of differential diagnosis, biochemical homogeneity and pharmaceutical therapy as the answer to most chronic lifestyle and long-latency deficiency diseases (Hyman, Baker&Jones, 2010). The current paradigm of diagnosis and classification of diseases into organ system pathologies (in correspondence to medical specialities) becomes less useful considering the basic mechanisms of dysfunction in the human body.
‘One disease can have multiple causes, and one initiating factor may cause multiple diseases’ (Hyman et al 2010 p.59)
As we have seen in the formation of plaques, the development can be triggered by multiple factors including insulin resistance, folate deficiency, occult infections, heavy metal toxicity, stress and other factors increasing inflammation. Having barely touched on nutrition-genomics, proteomics, as well as metabolomics must not be forgotten. For a detailed elaboration on the topics of an integrated, functional medicine approach to disease and health please consult the referenced ‘Textbook of Functional Medicine’ (2010).
In many cases, a single nutrient catalyses hundreds of chemical reactions, where suboptimal levels lead to molecular and cellular dysfunction.
Contrary to stipulated RDA’s, higher dose administration of vitamins and minerals might not be at all wrong, especially considering the evidence of sub-optimal nutrient status contributions to long-latency deficiency diseases, which have reached epidemic proportions: cardiovascular, cancer, osteoporosis, neurodegenerative disease and immune dysfunctions. A protocol of having homocysteine levels checked in conjunction with performance on function tests (elevated homocysteine has been directly linked to dementia, causing direct damage to the hippocampus) in the knowledge of high homocysteine co-occurring with high levels of inflammation, could be extremely useful as well as being a reliable function predictor (Colman&Perlmutter, 2005).
High inflammatory markers as well as the assessment of toxin exposure can only add to any diagnosis in order to optimise treatment: e.g. usage of ‘good’ fats versus trans saturated fats (lipids are essential for any brain) and vitamin supplementation to decrease the free radical attack – are both proven methods of slowing down the progression of neurodegenerative disease/ dysfunction (Colman&Perlmutter, 2005). All degenerative diseases of the brain benefit from reducing the free radical attack and cooling down inflammation. Not only is this possible by correctly administering supplementation, but by keeping the insulin levels (generally assessing chemical system imbalance) in check and advising on optimal nutrition in light of the respective individual’s concurrent disease deficiencies.
If the patient takes all supplements and drugs (if so prescribed) necessary, but continues to pass his mealtimes at McDonalds (or even adheres to std. government heart healthy fat free diets) and rather watches Rugby than plays it, the Healthcarer’s efforts will be in vain.
The Nobel laureate Albert Szent-Györgyi stated in his later years: ‘Whenever we seperate two things, we lose something, something which may have been the essential feature’ (Szent-Györgyi, 1988, p.193). Transition is needed from an acute care, reductionist model to a systems model based on networks of biological function and biochemical individuality. The core clinical imbalances needing to be addressed and considered in relation to any disease or mood/ cognitive dysfunction are: Hormonal and neurotransmitter imbalances, oxidation-reduction imbalances and mitochondriopathy, detoxification and biotransformational imbalances, immune and inflammatory balances, digestive, absorptive, and microbiological imbalances plus structural imbalances from the cellular membrane function to the muscoskeletal system. Functional tests will serve to support the results of imbalance testing, aiding to assist in determining the extent or progression level of the damage – and making a final decision on what treatment the patient can benefit from most.
I have always found it difficult to look at any diagnosis from a viewpoint of absolute determinism based on one causal domain, knowing that a brain is just as individual as the body – both manipulated by the environment, various inputs and stressors, psychosocial factors etc.
All technical advances the human race has made within our organic systems biology seem to lead us back full circle: that the human body is better equipped and far more capable of self-repair than any patented drug ever put on the market – if only we would let it.
It does not simply self-destruct or happen to be schizophrenic, be born with autism or loose its memory. What we put in is what we get out.
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