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Eef Hogervorst* and Angela Clifford
SSEHS, Loughborough University, Brockington building Loughborough LE11 3TU, UK
Received date: January 02, 2013; Accepted date: January 06, 2013; Published date: January 20, 2013
Citation: Hogervorst E, Clifford A (2013) What is the Relationship between Higher Levels of Education Delaying Age at Onset of Dementia? J Alzheimers Dis Parkinsonism 3:e128. doi:10.4172/2161-0460.1000e128
Copyright: © 2013 Hogervorst E. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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The importance of a socioeconomic deprived childhood status for risk of later life morbidity has received increasingly more attention over the last decades. For instance, childhood IQ in several studies was linked to age at onset of dementia [1]. IQ is associated with education, which is often used as a proxy for socioeconomic status. We believe that there are fundamentally five theoretical models to explain this association, which is important when deciding at which age-group to target health-promoting activities to prevent dementia. Currently there is no treatment for dementia and prevention seems the only option. With increasing pressure on economic resources worldwide, scientific evidence for these models to guide policy is thus important. In this editorial we discuss which of these models is more salient and when interventions should be introduced for maximum and cost-effective results.
The first two models discuss how a higher childhood IQ reflects a better education, and suggest that better education promotes access to more adult socioeconomic resources leading to better health, including a lower dementia risk.
In model 1, high IQ assessed in childhood reflects a good education, and/or, alternatively and reversely, being able to attend good education. Data from the United States of America [2] also show that a high IQ is strongly linked to better adult Socioeconomic Status (SES). Having a high IQ as a child thus increases the chance of obtaining a better education (or having had good education) as a child and obtaining more financial and social resources as an adult.
Health and morbidity are strongly linked to adult SES and education. For instance, in the UK, more low classed or manual (‘blue collar’) workers were twice as likely to die prematurely of all causes as ‘white collar’ (higher classed office and non-manual) workers between 2001 and 2003 [3]. Model 1 suggests that having a higher IQ as a child leads to having more social and financial resources as an adult, and thus leading to a lower risk for morbidity and later onset of dementia specifically.
According to this model, interventions should mainly focus on adulthood and indeed some data suggest that midlife is the most important time to promote healthy lifestyle behaviours to prevent later life dementia, such as cessation of smoking, reducing obesity, and treating high blood pressure and cholesterol [4].
However, midlife adult social status attainment is also linked to father’s social class independent of childhood obtained education and/ or IQ [5]. The second model focuses on parental SES. Having parents with high SES perhaps increases the likelihood of childhood exposure to healthier environments with better access to health care, more varied diets with fruits and vegetables, less physical and environmental stress caused by overcrowding, smoking and other pollutants, more frequent winter-sun holidays (e.g. skiing in winter) to boost vitamin D levels etc. This model places interventions much earlier, in childhood or even before that.
As discussed earlier [4], midlife obesity is an important risk factor for dementia. A review of 135 studies showed that early childhood markers for adult obesity included maternal obesity and smoking and childhood obesity and growth patterns (often an indicator for nutritional deficiency), as well as father’s employment status as a proxy for SES [6]. Poverty in childhood (low father’s employment status) is thus at least partly responsible for a higher risk of obesity in adulthood and later life cardiovascular disease and dementia. This may be because poor nutrition characterised by high fat and processed carbohydrates is relatively cheap and filling as compared to nutritious more expensive foods, such as lean meats, fish, fruit and vegetables [7]. Data also suggest that genetics, adverse dietary patterns and/or inactivity copied from mothers further predispose to obesity [8,9]. Losing weight in adulthood is often difficult and hence promoting a healthy weight in expecting mothers would perhaps help promote a healthy lifetime weight in their offspring.
Other data also indicate a ‘preaching to the converted effect’ where healthy, well-educated, white, middle-class parents engage in clusters of health related behaviours which are not necessarily taken up by those who have received less education and live in deprived areas, possibly because of a lack of time, money and/or knowledge. This cluster of health related behaviours includes better prenatal care, parental health promoting behaviour (exercise, diet, not smoking) and more stimulation including access to better schools resulting in better brain development and subsequently higher IQ and higher adult SES [10].
As such, in the UK, much effort has been put into improving schooling for children from deprived areas, but top universities (which attendance increases the chances of obtaining high SES [11]) still only have a minority of children from deprived backgrounds, with the majority of students coming from middle to high SES [12].
Partly the association between childhood IQ and later life dementia then perhaps just reflects the consequences of poor social mobility and clustering of much beneficial preventative behaviour only in those who can afford this and paradoxically would need it least.
From model 2 it would follow that a focus on promoting prenatal care in deprived mothers may be crucial to promote better cognition in childhood to be able to benefit from good schooling to prevent later life morbidity and poor health. Prenatal care is indeed an important World Health organisation focus. Giving combination nutritional supplements of zinc, iron, folic acid and vitamin A to deprived prenatal Nepalese mothers (as compared to vitamin A alone) produced children who had better cognitive function at age 7 [13]. In contrast, studies with single supplements showed worse cognition in childhood after mothers had been given zinc or iron supplements only [14]. A large European study showed that fish oil and folate given prenatally did not change cognition in childhood, although maternal DHA (from the fish oil) was associated with better cognition in their offspring [15]. There has thus been limited success of prenatal supplements to improve cognition in offspring, but this may be modified by the level of deprivation and the fact that supplements may not necessarily have linear positive effects, but rather show optimum levels to promote better health. Also perhaps prenatal nutrition is insufficient to sustain optimal brain development and other factors (childhood nutrition and exercise, healthy environments) need to be included too to predict this.
More worryingly, this relative failure of prenatal nutritional supplements to make a huge impact on child cognition (and subsequent adult health) may also be caused by intergenerational transfer of risk and a potential role of epigenetics. Data could reflect the complexity of planning health-promoting interventions, because these issues are multi-factorial.
For instance, low vitamin B12 status in rural pregnant women from a developing country (India) led to a higher risk of adiposity and insulin resistance (a risk factor for diabetes) in their children at 6 years, both which are risk factors for later life morbidity including dementia [16]. Mothers exposed to environmental pollutants promoting DNA methylation were also found to be more likely to have obese offspring [17,18], which in turn is linked to obesity in adulthood, early mortality and dementia.
If epigenetics play a role and foetal environmental factors affect child brain development and later life obesity, this could explain why high blood pressure and obesity in midlife are related to childhood IQ according to Scottish data [19]. As we discussed earlier, these type of midlife risk factors also individually double the risk for dementia in later life [4]. However, high blood pressure was only predicted by childhood IQ up to age 65. After this, variation increases. Interestingly, data showed that high blood pressure is only predictive for age at onset of dementia 15 years before onset of dementia (in midlife), but starts to decrease in prospective cases 1-2 years before clinical onset of symptoms [20]. This would explain why several studies found lower blood pressure in dementia cases compared to controls. Similarly weight-while higher in midlife-is often lower or similar in dementia cases as controls and Mielke found that a decline in total cholesterol levels is a better predictor for age at onset of dementia than midlife cholesterol levels [21].
This indicates a change in risk factors, so for these cardiovascular risk factors (obesity, high blood pressure and high cholesterol) an early intervention (possibly prenatally) is crucial as once dementia is apparent, these risk factors are no longer treatable and/or no longer pose risk. Whether inter-generational risk transfer and potential epigenetic effects can be overruled by combinations of maternal and childhood exercise and nutritional interventions, as well as promotion of better schooling and early stimulating but stress and pollutant free environments remains to be investigated.
Importantly, however, in most risk predicting models, education remains independently (from cardiovascular risk factors) protective against development of dementia. In addition, in models predicting dementia, when education and adult SES were entered in regression analyses, only education remained significant [22]. This might indicate that better SES is not necessarily the main driver for protection against dementia by promoting better health by allowing access to health promoting resources, such as medical help, less (environmental stress) and better nutrition (models 1 and 2). These data favour three other models where a higher obtained childhood education may lead to better SES but by itself drives an independent effect in maintaining health and reducing risk for dementia.
This association could be explained in model 3 where education promotes knowledge of healthier lifestyles and actively pursuing health promotion (e.g. by visiting primary care for treatments for high blood pressure and high cholesterol and eating better diets, etc.). However, having knowledge does not necessarily transmit to engaging in healthier lifestyles. In a large multi country European cohort, men with highest education had a 43% reduced risk for total mortality compared to men with lowest education (for women this was 29%). However, this was only partly explained by smoking, body weight, alcohol consumption, leisure physical activity and fruit/vegetable intake [23]. So effects of education are not only due to engaging in better health related behaviour. Possibly these data suggest success of public health promoting activities to the general public.
However, as education showed independent effects in these models for largely unknown reason, it could play another role in a fourth model. Education could promote cognitive resources by giving access to alternative coping and a wider vocabulary. In dementia once word finding problems and executive functions start to decline, these cognitive reserves could buffer severity of symptom display. Indeed studies have shown that high education is associated with later age at onset of dementia, but a steeper and faster decline [24]. This rapid decline probably occurs when pathological neuronal damage has overruled cognitive reserve capacity which is expected to be later in those with higher education. A combination of different dementia pathologies (vascular, AD and often LBD pathology is often found to co-occur at post-mortem) leading to a pathology load combined with better education (reflecting a positive cognitive reserve balance) could predict a later age at onset of dementia symptoms [25].
The last model is often referred to as the ‘use it or lose it model’. Here education would stimulate the active use of mental facilities, and the brain then acts as a muscle which needs to be stimulated to be maintained. To date whether mental activity can treat dementia is controversial. Staying mentally active was found to be protective in studies [26,27] but whether this is causal is questionable. Rather older people who can still read and write may continue to do so, but having dementia symptoms with word finding problems etc. might impede these activities already at an early stage of the dementia syndrome. On the other hand limited data from the US and Japan did show that engaging in reading and arithmetic exercises improved dementia symptoms after 6 months [28]. Data also indicate that older rats still express neurogenesis when exposed to novel environments [29]. However, rats exposed to novel environments are also more physically active which is an important confound in these studies. In dementia we did see some cognitive improvement after moderate exercise in some studies but this seemed mainly confined to women [4].
In sum, in all likelihood the association between childhood IQ and age at dementia onset is complicated, but our models may give some pointers as to when interventions are best applied. Cardiovascular risk associated with dementia needs to be reduced at the latest in midlife, but early acquired healthy lifestyles and good education are crucial to prevent these cardiovascular risk markers (obesity, high blood pressure, high cholesterol) and subsequent dementia. Once people have developed dementia, nutritional interventions in all likelihood play a less important role, but more research needs to investigate whether physical and perhaps mental activity could sustain cognitive function at this stage.
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