Below the Neck, Above the Neck: How Cardiometabolic Health Shapes the Brain

For years I’ve suspected a tight, clinically meaningful link between insulin resistance and neurodegenerative disease, especially Parkinson’s. Many of the patients I worried about didn’t show overt diabetes or runaway glucose. Instead, they carried the quieter fingerprints of metabolic dysfunction—a pro-inflammatory state, low HDL, central adiposity, elevated blood pressure—and heavy coronary calcium on scans. Their arteries told a story their fasting glucose did not. Recent large-scale data now support this clinical hunch: metabolic syndrome raises the future risk of Parkinson’s, and the risk is highest when poor metabolism meets higher genetic vulnerability. In other words: what happens below the neck profoundly affects what happens above the neck.

Think of your body as a solar system. At the center is your metabolic sun—insulin signaling, mitochondrial efficiency, vascular tone, and inflammatory balance. Around that sun orbit the “planets”: heart, brain, liver, muscle, adipose tissue, gut microbiome, and endocrine organs. When the metabolic sun burns clean—stable insulin dynamics, healthy lipids, responsive endothelium—each planet keeps a steady orbit. But insulin resistance dims the sun and distorts the gravitational pull. Orbits wobble:

• The heart develops endothelial dysfunction and plaque; coronary calcium accumulates.

• The brain sees microvascular stress, impaired insulin signaling at neurons and glia, and a drift toward neuroinflammation—conditions that can set the table for cognitive decline and Parkinsonian vulnerability.

• The liver stores excess fat (NAFLD), spiking triglyceride-rich lipoproteins that further aggravate vessels.

• Skeletal muscle loses insulin sensitivity and mitochondrial flexibility; energy gets shunted from oxidation to storage.

• Adipose tissue expands viscerally, secreting cytokines that amplify systemic inflammation and erode vascular and neural resilience.

• The gut microbiome shifts toward dysbiosis, feeding back into inflammation and insulin resistance.

Crucially, this can all unfold before hyperglycemia. Glucose is a late marker. Insulin resistance, dyslipidemia (especially low HDL and small dense particles), hypertension, and central adiposity create a cardiometabolic weather system that bathes the brain. The result isn’t merely “risk factors” on paper but real, structural change: stiffer arteries, noisier immune signaling, leakier blood-brain barriers, and neurons trying to function in a low-grade storm.

Recent population data are clarifying, not surprising. They show that metabolic syndrome—defined by a cluster of waist circumference, blood pressure, HDL, triglycerides, and glycemic markers—tracks with higher Parkinson’s incidence, and that the relationship strengthens when genetic predisposition is high. That’s a wake-up call for prevention: genes load the gun; metabolism pulls the trigger. (Metabolic Syndrome and Incidence of Parkinson Disease.https://doi.org/10.1212/WNL.0000000000214033 )

What You Can Do Now (Action Steps)

1) Get insulin-centric, not just glucose-centric.
Normal fasting glucose doesn’t clear you. Ask for fasting insulin and, when appropriate, a post-load insulin/glucose response. Early hyperinsulinemia signals risk while there’s still time to reverse course.

2) Map the vascular terrain.
A CT coronary calcium (CAC) score is an objective snapshot of hidden atherosclerosis—powerful, inexpensive, and actionable. If your CAC is non-zero, you’ve moved from theoretical risk to visible disease; prevention now looks a lot like secondary prevention.

3) Rebuild the metabolic sun.

• Resistance training 2–3×/week preserves/increases lean mass and improves insulin sensitivity—critical for both heart and brain.

• Whole-food nutrition that prioritizes protein adequacy, fiber, and minimized ultra-processed foods reduces insulin volatility and inflammatory burden.

• Sleep & circadian alignment stabilize appetite hormones, insulin action, and vascular tone.

• Targeted therapeutics, when appropriate (e.g., insulin sensitizers, triglyceride-lowering strategies, omega-3 EPA), should serve the strategy—not replace it.

4) Track the right signals.
Beyond A1c, follow waist circumference, blood pressure, HDL, triglycerides, and, where helpful, hs-CRP or other inflammation markers. Improvement across these levers predicts better vascular—and cerebral—resilience.

5) Think systems, not silos.
The brain isn’t a free-floating moon. It orbits the same metabolic sun as your heart. Improving cardiometabolic health is neurologic care. Protecting the endothelium protects synapses. Reducing visceral fat reduces neuroinflammatory noise. Your cardiometabolic plan is a cognitive and movement-disorder plan.

At CardioCore Metabolic Wellness Center, we align care with these realities. Our approach starts with insulin-centric assessment, adds objective vascular imaging when indicated, and deploys a personalized plan that integrates nutrition, resistance training, sleep/circadian hygiene, and appropriate therapeutics. The goal is not simply to lower a number—it’s to brighten the metabolic sun so every organ-planet holds a stable, healthy orbit.

If you’ve ever been told “your labs look fine” while your gut says something isn’t, or your scan shows calcium that doesn’t square with a “normal” glucose, you’re not imagining things.

The brain hears the whispers of the body long before glucose shouts.

Your next step:

• 📞 Book a free call to review your insulin, lipid, and vascular profile.

• 🌐 Learn how we personalize this strategy at CCMWC.com.

• 🤖 Prefer chat? Speak to our Virtual Assistant for quick answers and more information.

Below the neck shapes above the neck. Protect the heart–brain axis by fixing the sun at the center.