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The Elephant in the Room

Let’s talk about the elephant in the room, cognitive decline.

We are so fortunate to live in a time where longevity is the norm, rather than the exception, particularly in developed countries. However, there is a price to pay for being alive much longer than our ancestors. Our minds are subject to genetic, environmental, and lifestyle challenges that not one of us can escape.

Image credit: Wilma Kirsten

Favreault and Johnson (2021) project that one in three of today’s working class adults who survive to age 65 will become significantly cognitively impaired before the end of their lives; 40% of those individuals will need care for five or more years. The cost of care and associated medical expenses can leave many families out of pocket, even in countries with social health care.

Unlike early onset dementia, sporadic Alzheimer’s disease (AD) is not a genetic disorder despite the correlation with the presence of the apolipoprotein E (APOE*ε4) gene – classified as a risk factor, not a definitive cause. Hugo and Canguli (2014) state that age is the most definitive factor that predisposes some individuals to cognitive decline and is partly due to the buildup of beta-amyloid protein (Aβ) and subsequent formation of amyloid plaques that leads to neuronal death over time. Limited education, physical inactivity, co-morbidities, lifestyle and diet furthermore appear to increase risk of disease progression. This emphasises the fact that the majority of dementia cases cannot be classified as a genetic disorder.

Unfortunately a diagnosis of dementia or AD only occurs once disease progression is irreversible, hence why we called it progressive cognitive decline. We do however know that there are many years preceding such a diagnosis that play a vital part in disease formation. Crucially, midlife (age of 40 years and onwards) is the pivotal period during which our choices lay down the foundation for long-term health outcome.

There are clearly big differences between genetic predisposition to early onset dementia, brain trauma, and accelerated cognitive decline. If your parents passed on the relevant genes pertaining to early onset dementia there is unfortunately, as of yet, little that can protect you from your eventual premature destination. Similarly, if you experience a traumatic brain injury then your fate is also predestined.

In all other circumstances we can ameliorate the path of natural cognitive decline via our diet and lifestyle choices. What protects your heart is as functional when it comes to protecting your brain. Tobacco use and exposure, illicit drugs, alcohol, and bad dietary choices are all within your control. 

De la Monte (2017) note that there are many other major abnormalities associated with AD other than Aβ and phosphorylated tau protein. The primary risk factor for AD remains age and as Caselli et al. (2020) state, an ageing brain is subject to an increase in neuroinflammation, cellular senescence, oxidative stress, reduced DNA repair with resulting genomic instability, and altered protein homeostasis with reduced clearance of misfolded proteins – all of which are thought to contribute to neurodegeneration. In fact Ritchie et al. (2010) posited that focus on diabetes, diet, and depression as population-wide intervention strategies would have the biggest impact in dementia prevention. Caselli et al. (2020) additionally include physical and social activity effects over a lifetime as adjunct risk factors for AD.

Sleep deprivation is an additional component that play a significant role in cognitive decline. As much as repeated stress exposure leaves scars on even the most resilient amongst us, impaired sleep disallows our brains from repairing damage, mopping up unwanted substances, and maintaining necessary neuronal connections.

What can you do?

The gut is referred to as the second brain. If we have a healthy gut then we stand a much better chance of improved brain function. 

Step 1: assess your current gut status to determine what is amiss and how best to address those anomalies. 

Step 2: measure your stress response as that directly affects your natural sleep and eating patterns.

Step 3: focus on daily optimal nutrition if you want to ensure a better long-term health outcome. 

There remains conflicting information regarding what constitutes healthy eating. Every season brings forth the next wonder diet or supplemental product, often at considerable cost. 

As a decades long leader in the field of nutrition, gut, and hormonal health, I am here to help you with your journey through this maze.

Your brain is your biggest asset. Act today to protect yourself.


Caselli, R.J., Knopman, D.S. and Bu, G. (2020) ‘An agnostic reevaluation of the amyloid cascade hypothesis of Alzheimer’s disease pathogenesis: The role of APP homeostasis’, Alzheimer’s & Dementia, vol. 16, pp. 1582-1590.

de la Monte, S.M. (2017) ‘Insulin resistance and neurodegeneration: progress towards the development of new therapeutics for Alzheimer’s disease’, Drugs, vol. 77, no. 1, pp. 47-65.

Favreault, M.M. and Johnson, R.W. (2021) ‘The Risks and Costs of Severe Cognitive Impairment at Older Ages: Literature Review and Projection Analyses’, Office of the Assistant Secretary for Planning and Evaluation, 31 January 2021.

Hugo, J. and Ganguli, M. (2014) ‘Dementia and cognitive impairment: epidemiology, diagnosis, and treatment’, Clinics in Geriatric Medicine, vol. 30, no. 3, pp. 421-442.

Ritchie, K., Carrière, I., Ritchie, C.W., Berr, C., Artero, S. and Ancelin, M. L. (2010) ‘Designing prevention programmes to reduce incidence of dementia: prospective cohort study of modifiable risk factors’, British Medical Journal, vol. 341, article c3885.