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Nutrition and Behaviour Psychology - Part 5 and 6 Lecture Notes
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Nutrition and Behaviour Psychology - Part 5 and 6 Lecture Notes
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Nutrition and Behaviour20th February 2017
Lecture 5-6: Diet and Ageing
Ageing Background
When there is any form of data being reported, it must be put within a context and given an importance.
Memory:
Memory can be divided into two types, there is a basic distinction:
Declarative Explicit, can be stated verbally, can reflect on it consciously. Can be further divided into:
Episodic memory Personally experienced events, based in a time and place, e.g. when, where and who you
married.
Semantic memory General knowledge, unlikely to recall when learnt (in Alzheimer’s?, likely to recall in general
population?), e.g. a young dog is called a puppy.
Non-Declarative Implicit, cannot be verbalised, automatic, memories for behaviours, e.g. riding a bike. You can
remember how to do it and remember doing it but you cannot describe the process of completing the task verbally.
Cognitive changes with age: Benton et al. (2005)
Primary Memory Ability to hold information for short periods.
Can be tested using digit span.
Only limited changes with age.
Episodic Memory
Short-term recall changes little with age.
Retrieval from long-term stores can be a problem. More so with free rather than cued recall.
Tends to be episodic memory that is associated with problems that arise throughout ageing, e.g. AD.
Prospective Memory Ability to remember to do something in future.
Poorer in elderly
Semantic Memory
Tends to be relatively spared with age
,Methodological Issues:
Over what time-scale should we be looking? What is the appropriate time scale: across a life-time, during the stages
of MCI, mild or moderate Alzheimer’s symptoms present, acute/chronic impact?
What population?
Biomarkers?
One disease?
Over what time-scale?
Incidence of Dementia: Figures from developed countries, Europe, USA, Australasia and Japan. The incidence of
disease means that long-term studies with large samples will be needed? Do we need high-risk groups?
Ferri et al. (2005): Although not very recent...Used the Delphi consensus method to determine the dementia
prevalence for each world region. Evidence from well-planned, representative epidemiological surveys is scarce in
many regions. Estimated that 24·3 million people have dementia today, with 4·6 million new cases of dementia every
year (one new case every 7 seconds). The number of people affected will double every 20 years to 81·1 million by
2040. Most people with dementia live in developing countries (60% in 2001, rising to 71% by 2040). Rates of increase
are not uniform; numbers in developed countries are forecast to increase by 100% between 2001 and 2040, but by
more than 300% in India, China, and their south Asian and western Pacific neighbours.
Not everyone gets dementia, not even the majority of people so what sets those who do, apart from the rest.
On average, brain weight declines 5-10% between 20 and 90 years of age.
With severe cases of Alzheimer’s disease there is 20% or more reduction of the weight compared to the normal
brain.
Reversal of such changes is unrealistic, slowing the process or reducing the impact should be the aim therefore
focusing on lifestyle (diet) prior to the development would be the most beneficial.
Can we identify the groups who will be more likely to benefit from some form of intervention and if so, when will the
intervention need to take place?
Katzman et al. (1988):
Understandably thought that there would be a relationship between degeneration of the brain and cognitive
function.
Group with an average age of 85.5 years.
Discovered inconsistency between biological measures of Alzheimer’s disease and clinical symptoms.
At post-mortem, some individuals with extensive pathology had displayed few or no symptoms before death.
This pattern was associated with heavier brains and more neurones compared to controls.
Cognitive Reserve
Cognitive Reserve The capacity of the brain to sustain the effects of disease without manifesting clinical
symptoms.
Pre-morbid IQ is a useful measure of cognitive reserve.
,Premorbidity refers to the state of functionality prior to the onset of a disease or illness.
Richards and Sacker (2003):
British 1946 birth cohort study.
Cognitive reserve was indicated by difference in National Adult Reading Test (NART) scores at 53 years and various
cognitive outcomes.
Cognitive ability in childhood, education and adult occupation all prevented intellectual decline.
Cognitive ability when 15 years old had the strongest influence.
NART: Widely accepted and commonly used method in clinical settings for estimating pre-morbid intelligence levels
of English-speaking patients with dementia in neuropsychological research and practice.
Carroll (1987): 12 consecutive out-patients had their performance on the NART audiotaped. This tape was then
'scored' for accuracy of pronunciation by 10 experienced clinical psychologists who use the NART in their routine
clinical practice. The results indicate that the NART has a relatively high degree of inter-rater reliability.
Starr et al. (2000):
1921 Scottish birth cohort study.
Intelligence at 11 years related to health at 77 years.
Pre-morbid mental ability was an independent predictor of later-life functional independence.
Whalley et al. (2000):
Late-onset dementia is associated with lower mental ability in childhood.
Early-onset dementia is not associated with lower childhood mental ability.
Mechanisms differ
Early-onset Happens to people younger than age 65. It is less common than late-onset dementia. Often related to
genetics...familial AD.
Janssen et al. (2002): Three causative genes have been identified for autosomal dominant AD: Amyloid precursor
protein (APP), Presenilin 1 (PSEN1) and Presenilin 2 (PSEN2). Objective was to determine the proportion of patients
with early onset AD with a positive family history accounted for by mutations in these genes. Sequence variants
in APP and PSEN1 accounted for the majority of neuropathologically confirmed autosomal dominant early onset AD;
no mutations in PSEN2 were detected. There may be a further genetic factor involved in the etiology of autosomal
dominant early onset AD.
If we are thinking about protecting against ageing, perhaps we should be, in the first instance, is improving the
functioning of children.
Snowdon (1997) – The nun study
A longitudinal study of ageing and Alzheimer’s disease that began in 1986.
Following 678 School Sisters of Notre Dame aged over 75 years.
They had agreed to donate their brain after death.
, Correlations for head circumference and intra-cranial volume was 0.5 to 0.8.
Low education may be associated with events that increase risk of dementia.
Education increases neuronal conductivity.
Education leads to a more stimulating life style and neuronal growth/activity.
Similar lifestyle, social support, diet
Increased neuronal conductivity providing a buffer against neuronal death is the most likely explanation.
Case histories presented included a: Centenarian who was a model of healthy aging, a 92-year-old with dementia
and clinically significant Alzheimer disease neuropathology and vascular lesions, a cognitively and physically intact
centenarian with almost no neuropathology, and an 85-year-old with well-preserved cognitive and physical function
despite a genetic predisposition to Alzheimer disease and an abundance of Alzheimer disease lesions. These case
histories provide examples of how healthy aging and dementia relate to the degree of pathology present in the brain
and the level of resistance to the clinical expression of the neuropathology.
As intellectual functioning in childhood influences the chances of dementia, need to consider the dietary influences
at these early stages,
Rather than slowing decline, should we aim to create a brain with as much surplus capacity as possible?
However:
A series of studies of patients with AD have suggested that once AD emerges, those with higher reserve have poorer
outcomes.
Stern et al. (1999): High education, a factor associated with increased cognitive reserve, was associated with more
rapid cognitive decline in patients with prevalent AD.
Because people with higher CR can tolerate more AD pathology, memory function will begin to be affected later in
time, after more pathology has accumulated. Thus, the “point of inflection” where memory begins to decline will
occur later in patients with higher CR. Another assumption is that at some point AD pathology must become too
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