Support Your Brain Health

Why should you care about the health of your brain?

Of the four biggest threats to your health (cardiovascular disease, neurodegenerative disease, cancer and metabolic disease), neurodegenerative is perhaps the one that people find the most frightening. This is because neurodegenerative disease has the potential to, ultimately, eradicate your sense of self, your identity, your very personality itself. Even those conditions that don’t attack your memory and personality can destroy language, motor skills, concentration, planning and a range of other cognitive functions.

Currently, one in three older adults dies with Alzheimer’s or another form of dementia [1]. Given the high prevalence and horrific impact of neurodegenerative disease, it’s really important to understand exactly what we mean by this term (as there are several conditions grouped under this category) and then to think about what you can do to protect yourself as much as possible from such conditions.

What are the most common conditions?

The term Neurodegenerative Disease is an umbrella classification for a range of conditions that primarily affect your neurons. Neurons are the building blocks of your nervous system, consisting of the brain and spinal cord. Crucially, unlike skin or muscle cells, neurons normally cannot reproduce or replace themselves. When they become damaged or die, the body cannot easily regenerate them

• Alzheimer’s Disease: This is the most common form of neurodegenerative disease, accounting for 60% to 80% of all dementia cases. It progresses systematically, typically starting in the brain’s memory centre before spreading to those areas responsible for language, reasoning, and social behaviour. Alzheimer’s disease manifests with progressive short-term memory loss, confusion, disorientation regarding time and place, language difficulties, and profound personality alteration. Alzheimer’s is characterised by the abnormal accumulation of two proteins: amyloid-beta (which forms sticky plaques outside the neurons) and tau (which forms neurofibrillary tangles inside the neurons). Together, they block cell-to-cell communication and trigger massive, localised chronic inflammation, causing the brain to physically shrink (atrophy).

• Vascular Dementia: Strictly speaking, this is caused by cardiovascular events. It occurs when the brain’s intricate network of micro-vessels becomes blocked, narrowed, or damaged, starving brain cells of oxygen and vital nutrients. Vascular dementia can happen suddenly after a major stroke, or insidiously over time via small vessel disease — a slow, silent accumulation of microscopic damage (mini-strokes) often driven by chronically high blood pressure and poor insulin management. Vascular dementia manifests with slowness of thought, difficulty planning or organising, problems with concentration, and step-like cognitive decline (where a patient stays stable, suddenly drops after a small vascular event, and levels out again).

• Parkinson’s Disease: This condition is primarily a motor system disorder, though it frequently progresses to include cognitive decline in its later stages. It manifests with resting tremors (typically starting in one hand), muscle rigidity, extreme slowness of voluntary movement, and a shuffling, unstable gait. It is characterised by damage to neurons in the region of the brain responsible for producing dopamine, the chemical messenger that coordinates smooth, fluid muscle movement. In Parkinson’s, these cells die due to the misfolding and clustering of a protein called alpha-synuclein, which forms toxic clumps known as Lewy bodies.

• Lewy Body Dementia: This condition is similar to Parkinson’s disease but attacks different areas of the brain first. Instead of starting in the motor control centres, the toxic protein deposits spread widely throughout the cerebral cortex right from the beginning. It manifests with vivid, detailed visual hallucinations, severe fluctuations in alertness and attention, and Parkinson’s-like motor stiffness. Like Parkinson’s it is characterised by alpha-synuclein proteins forming Lewy bodies, but its aggressive spread across the cortex rapidly breaks down the brain’s cognitive and visual processing networks.

• Frontotemporal Dementia: This condition is the most common form of dementia for individuals under the age of 60. It selectively targets the frontal lobes (the seat of judgment, impulse control, and personality) and the temporal lobes (the seat of language). It manifests with changes in social behaviour and personality (loss of empathy, inappropriate behaviour, impulsivity), accompanied by a progressive loss of the ability to speak or understand language, while short-term memory often remains surprisingly intact early on. It is characterised by rapid cellular death exclusively in the front and sides of the brain caused by a variety of abnormal protein mutations.

Alzheimer’s and Vascular Dementia are increasingly viewed as metabolic disorders of the brain. Scientists frequently refer to Alzheimer’s by the nickname “Type 3 Diabetes” because insulin resistance in the body directly mirrors insulin resistance in the brain, preventing neurons from absorbing the glucose they need to survive. So, let’s move on and take a look at lifestyle and environmental factors related to these conditions.

What factors contribute to Neurodegenerative Disease?

Although neurodegenerative disease is a terrifying prospect, the landmark Lancet report [2] confirms that up to 45% of dementia cases are entirely preventable or delayable through specific, modifiable lifestyle and environmental factors. Thus, in this section, we map the primary lifestyle and environmental causes onto the exact neurodegenerative conditions they trigger:

Cardiovascular & Metabolic Factors

• High Blood Pressure & High LDL Cholesterol: Directly affects Vascular Dementia (Primary) and Alzheimer’s Disease (Secondary) as chronic high blood pressure and elevated LDL cholesterol tear the microscopic linings of the brain’s blood vessels. This leads to Small Vessel Disease — a slow, silent accumulation of micro-strokes that starves brain tissue. Furthermore, blood-vessel damage breaks down the blood-brain Barrier, allowing systemic toxins to leak into the brain, which speeds up the formation of Alzheimer’s amyloid plaques.
• Type 2 Diabetes & Insulin Resistance: Directly affects Alzheimer’s Disease since when your body is insulin-resistant, your brain cells become insulin resistant too. Neurons rely heavily on insulin to absorb glucose; without it, they literally starve. Chronically high blood sugar also blocks the body’s Insulin-Degrading Enzyme (IDE). Because IDE is the exact same enzyme responsible for chewing up and destroying Alzheimer’s amyloid-beta plaques, keeping your insulin high means amyloid plaques are left to pile up freely in your brain.

Neurological Cleaning Factors

• Poor Sleep Quality & Sleep Apnoea: Directly affects Alzheimer’s Disease and Lewy Body Dementia since the brain has a dedicated nightly waste-clearance system called the glymphatic system. During deep, slow-wave sleep, your brain cells literally shrink, allowing cerebrospinal fluid to rush through like a dishwasher, flushing out toxic metabolic waste. Missing out on deep sleep means amyloid-beta, tau, and alpha-synuclein proteins are never washed away. They stick around, crystallise, and form the plaques and Lewy bodies that drive Alzheimer’s and Parkinson’s related dementias
• Mid-Life Hearing Loss & Uncorrected Vision Loss: Directly affects Alzheimer’s Disease and Frontotemporal Dementia. The Lancet Commission ranks midlife hearing loss as the single largest modifiable risk factor, accounting for 7% of all global dementia cases. When you suffer from untreated hearing or vision loss, the volume of sensory input entering your brain drops drastically. The brain behaves like a muscle: if you don’t use it, you lose it. Deprived of sensory data, the auditory and visual cortices experience rapid atrophy, destroying your brain’s “cognitive reserve” and speeding up the onset of Alzheimer’s and Frontotemporal decline.

Structural & Chemical Factors

• Traumatic Brain Injury (TBI) / Head Impacts: Directly affects Frontotemporal Dementia and Parkinson’s Disease because severe concussions or repetitive sub-concussive head impacts (from rugby, boxing, mixed martial arts, or ‘heading’ in football) create severe physical shearing forces inside the brain. This structural trauma snaps axons and triggers an immediate, massive release of a specific protein called TDP-43 and tau. This localised mechanical damage often begins in the frontal and temporal lobes, causing Frontotemporal Dementia or Parkinsonian motor decay later in life
• Smoking & Air Pollution: Directly Affects: Vascular Dementia and Alzheimer’s Disease since inhaling cigarette smoke or ultrafine environmental air pollution allows microscopic toxins to pass directly from your lungs into your bloodstream, and even up through your nasal passages directly into the brain’s olfactory bulb. These toxins cause severe oxidative stress and localised systemic inflammation, stiffening the carotid arteries (fuelling Vascular Dementia) and directly mutating neural proteins into Alzheimer’s plaques.

Genetic Factors

• Deterministic Genes: There are three genes (APP, PSEN1 and PSEN2) which are rare, inherited mutations. If you inherit one of these genes from a parent, you have a 50/50 chance of passing it on to your children. Carrying it means you are virtually guaranteed to develop the disease, usually at a young age. However, these account for less than 1% of all cases.
• Susceptibility Genes: Unlike the deterministic genes, these adjust the likelihood of you developing Neurodegenerative Disease — but require environmental or metabolic triggers to actually manifest as a disease. The absolute most studied and powerful risk gene is APOE (Apolipoprotein E). Its primary job is producing a protein that moves cholesterol and fats through the brain. APOE comes in 3 variants, but it is APOE E4 that is the primary genetic risk factor for late-onset Alzheimer’s Disease, Vascular Dementia, and Lewy Body Dementia. As you get a copy from both your parents, there are 6 possibilities in total from the three variants. The most worrying would be E4/E4 (i.e. inheriting the risky version from both parents) which means a person has up to a 70% lifetime probability of developing Alzheimer’s, often showing symptoms years earlier than non-carriers.

How can you protect your brain from these risks?

The great news here is that if you are already actively working on your heart health (Big10 #4 Monitor Your Heart Health), your blood sugar (Big10 #1 Avoid Ultra-Processed Foods and Control Your Insulin Levels) and your sleep (Big10 #3 Get Enough Good Quality Sleep) you are already well on your way to driving down your risk of Neurodegenerative disease.

Exercise is arguably the most powerful non-pharmaceutical lever we have for defending the brain across a number of areas [3]:

• Zone 2 Aerobic Exercise (e.g. running, cycling, steady swimming): This low-intensity, long-duration exercise is great for optimising the brain’s nightly waste disposal unit (the glymphatic system), metabolic stability, and triggering angiogenesis — the creation of brand-new, healthy networks of microscopic capillaries inside the brain.

• High-Intensity Intervals or Heavy Resistance Training: The high physical stress of hitting a high heart rate or lifting heavy loads triggers the release of Irisin, which crosses the blood-brain barrier and, in turn, triggers the systemic release of Brain-Derived Neurotrophic Factor (BDNF), which stimulates neurogenesis (the birth of new neurons) and repairs the synaptic connections between existing cells.

However, we can still add a few more interventions to our defences:

• Visit an optician and get an eye test: As seen above, loss of sensory input is a high risk factor. Any irritation or embarrassment of wearing glasses pales into insignificance when compared to the consequences of dementia.
• Get a hearing test: Often your optician can do a hearing assessment as well. No one wants to wear a hearing aid as we get older, but if you are starting to drop out of conversation or no longer be as subtle and clever in conversation due to difficulty hearing, it’s just not worth the risk.
• Stop any contact sports that involve head impacts or, at least, make sure you are as well protected as possible: As seen above, these impacts can cause damage to the brain which can cause Frontotemporal Dementia or Parkinsonian motor decay later in life.

Should you get tested for genetic factors if you have no symptoms?

Major medical bodies (like the Alzheimer’s Society) generally do not recommend consumer testing for risk variants outside research or clinical screening because genetics is not destiny and knowing that you do carry such factors can cause great psychological distress. It may be better simply (until such time as there are gene therapies available) to live a healthy, low-inflammatory lifestyle whilst sleeping well and exercising regularly. These in themselves will be preventing the factors that may combine with a genetic risk to manifest as dementia.

Further sources of information

The Examine web site for independent, unsponsored meta-analyses of health research

Outlive: The Science and Art of Longevity by Pete Attia MD

References

[1] Alzheimer’s Association. (2026). 2026 Alzheimer’s Disease Facts and Figures. Alzheimer’s & Dementia.

[2] Livingston, G., et al. (2024). Dementia prevention, intervention, and care: 2024 report of the Standing Lancet Commission. The Lancet,

[3] Framingham Heart Study Group. (2025). Physical Activity Over the Adult Life Course and Risk of Dementia in the Framingham Heart Study. Nature Medicine / NIH Cohort Analysis