Australia has one of the most effective health systems in the world. For more than four decades, Medicare has ensured that every Australian can access healthcare, helping lift our life expectancy to the highest among English-speaking nations. Yet recent experiences have highlighted the gaps that remain - particularly between the thresholds that trigger intervention and the evidence that could prevent those triggers from ever arising.
A couple of months before my 49th birthday, I experienced my first real age-related health issue. I went to the doctor with a headache and found my blood pressure was dangerously high - readings reached 230/160, and medications initially struggled to bring them down. A series of scans followed, and thankfully they showed no damage. My calcium score was zero, my arteries were clear, and my kidneys were functioning perfectly.
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With no clear culprit, I was referred from one specialist to another - renal, cardiac, endocrine - each ruling out their respective domains. When all came back normal, I was left with the standard advice: eat well, exercise, and manage stress. I’d already given up drinking, cut sodium, and trained daily. Nothing changed - until I tried a keto diet. My blood pressure fell noticeably. When the pattern repeated months later, I began to suspect I wasn’t dealing with simple “hypertension” but something further upstream - a metabolic imbalance quietly shaping my physiology for years.
Insulin resistance: the hidden upstream driver
Over time, insulin became the obvious suspect. It’s easy to think of insulin purely as a glucose regulator, but it’s also a vascular and neural signalling hormone - governing how flexible our blood vessels are, how efficiently we use oxygen, and even how our brain processes information. When tissues begin to resist insulin’s signals - insulin resistance (IR) - the effects extend far beyond blood sugar. The same pathways that trigger vasodilation and nutrient delivery start to falter. Endothelial cells (see diagram above) lining the arteries lose responsiveness; circulation becomes more rigid, especially in the small vessels that feed the brain and muscles. That mechanical stiffness translates directly into higher blood pressure - but also, more ominously, into reduced perfusion where it matters most.
What stands out in current research is the growing evidence linking insulin resistance to cognitive decline. Even in non-diabetics, IR disrupts neuronal metabolism, energy use, and memory formation. Some researchers call it “type 3 diabetes” - the same metabolic dysfunction affecting body cells can occur in the brain. Large population studies reinforce the link: people with higher IR scores are significantly more likely to develop dementia, regardless of blood sugar status.
I recognised this pattern in my mother’s alcohol-related dementia. While alcohol was the obvious driver, I suspect long-term metabolic stress - insulin resistance, inflammation, oxidative damage - amplified the decline. It wasn’t a single cause, but a systemic failure playing out over decades.
The nitric oxide axis: the missing link
At the centre of this process is nitric oxide (NO) — the tiny, short-lived molecule that links metabolism, vascular health, and cognition. In a healthy body, when insulin binds to its receptors on blood-vessel walls, it triggers a relay known as the PI3K–Akt–eNOS pathway. This is a sequence of enzymes inside the endothelial cells that line our arteries: PI3K (phosphoinositide-3-kinase) and Akt (a protein kinase) act like electrical switches, turning on eNOS — endothelial nitric oxide synthase — the enzyme that produces nitric oxide. NO then diffuses into the surrounding muscle, causing blood vessels to relax and improving oxygen and nutrient delivery.
When insulin resistance develops, NO production plummets. Blood vessels stiffen, micro-circulation weakens, and the very mechanism that lets arteries “breathe” is lost. In the brain, that means neurons receive less oxygen and glucose at the precise moments they need it, mimicking early dementia patterns. Add alcohol’s role in depleting NO and increasing oxidative stress, and the overlap between metabolic and neurological decline becomes hard to ignore.
A practical prevention map
Since then, my focus has shifted toward restoring insulin sensitivity and supporting NO production - through high-intensity exercise, low-glycaemic whole foods, leafy greens and nitrate-rich vegetables, sunlight exposure, and inflammation control. The research on dietary nitrates, L-citrulline, arginine and NO pathways is promising - not as quick fixes, but as tools to repair the body’s communication systems. It’s about addressing the signalling, not just the symptoms.
Integrating the metabolic view into care
What makes this difficult is how fragmented modern medicine can be. Cardiologists manage pressure, renal specialists track filtration, and endocrinologists monitor blood sugar - yet few consider how these systems interact. My experience, and my mother’s decline, both underscored how chronic conditions rarely appear suddenly; they unfold molecule by molecule, year by year. Recognising the metabolic and nitric oxide links between hypertension, insulin resistance, and dementia turns what feels like an inevitable decline into something actionable. The challenge now is ensuring our health system catches these patterns earlier - before they become disease.