Cardiometabolic Risk Hub

Navigator for the cardiovascular-risk cluster — estimating a person’s baseline risk, the exposures and drugs that move hard CV events, and the behavioural big rocks. Nucleus of the exposure side: Sodium Intake and Blood Pressure.

Estimating baseline cardiovascular risk

• SCORE2 Baseline Risk and the ESC Treatment Thresholds — turns a relative effect into an absolute one: what a person’s 10-year CVD risk is, and what that number licenses treating
• Lifetime Benefit - The Frame for Younger Adults — when a 10-year horizon under-states the case for acting, and what frame replaces it
• Risk Modifiers - When Extra Information Changes a Risk Estimate — when an extra test moves a risk estimate enough to change the decision, and why very few modifiers clear the bar

Blood pressure levers

• Blood Pressure Lowering and Cardiovascular Events — the one cardiometabolic lever whose hard-outcome benefit is proven to reach primary prevention; does benefit depend on baseline BP?
• Sodium Intake and Blood Pressure — how much sodium, and what reducing it actually buys
• Potassium Intake and Blood Pressure — how much potassium, what raising intake buys, and for whom
• DASH Diet and Blood Pressure — the DASH pattern lowers BP/lipids (surrogates); a sodium-independent, whole-pattern lever, not double-counted with sodium reduction; DASH->events unproven, rides BP transmission
• Dietary Nitrate and Blood Pressure — inorganic nitrate/beetroot lowers resting SBP ~4.4 mmHg (surrogate, short-term, ambulatory-disconfirmed); a modest peripheral supplement-class lever
• Dietary Magnesium and Cardiometabolic Outcomes — dietary Mg per +100 mg/day tracks lower T2D/stroke/HF/ mortality (observational); likely a marker of the whole-food pattern, not a separately-actionable lever
• Stress Management and Cardiometabolic Health — whether a structured stress-management program lowers BP enough to matter, weighed against established BP levers (primary home: Psychosocial and Environmental Exposures Hub)

The wider psychosocial / HPA-channel exposures that reach cardiometabolic risk through cortisol — social connection, sense of purpose, allostatic load, depression — plus sun/UV live in Psychosocial and Environmental Exposures Hub; most are observational mortality markers, not proven BP levers.

Lipids, drugs, and dietary patterns for CV events

• LDL Lowering and Cardiovascular Events — how much does lowering LDL/apoB buy per unit (CTT: RR 0.78 events + RR 0.90 mortality per mmol, no threshold), and which lipid number to target (Marston: apoB)?

• LDL ApoB and Cumulative Exposure — the causal model beneath the lipid axis (why LDL/apoB causes disease, why the dose is cumulative, why measure apoB)

• Statins for Primary Prevention and the Power of Zero CAC — for a primary-prevention adult, does a statin help, and does a zero coronary-calcium score change that decision?

• Aspirin for Primary Prevention of Cardiovascular Disease — does daily aspirin prevent enough CV events to outweigh its bleeding harm? (net wash-to-harm; benefit ARR 0.41% offset by bleeding ARI 0.47%, in every risk stratum — the de-adoption anchor)

• Eggs Dietary Cholesterol and Cardiovascular Risk — whether dietary cholesterol from eggs raises CV risk (near-null in general cohorts; the signal, where any, is in diabetics), and why the headline swings

• Levothyroxine for Subclinical Hypothyroidism — the standing-drug de-escalation anchor: for the modal SCH adult (mildly elevated TSH), levothyroxine normalizes the defining lab but moves no patient-important outcome (QoL/symptoms SMD ~0, GRADE high) — a lever not worth starting, bounded away from TSH >10, age >80, and high symptom burden

• Mediterranean Diet and Cardiovascular Events — whether a whole dietary pattern (not a single nutrient) reduces hard CV events, in whom and on which outcomes

• Does Weight Loss Reduce Cardiovascular Events — whether intentional lifestyle weight loss prevents hard CV events, and what the Look AHEAD null bounds

• Inflammation as a Modifiable Lever — inflammation as a second causal axis beside lipids: two RCTs (CANTOS canakinumab, LoDoCo2 colchicine) cut CV events with lipids unchanged, but CRP is a marker not a cause (MR), the benefit is on events not all-cause mortality, and the anti-inflammatory diet is an observational proxy for MedDiet, not a shown independent lever

Behavioural big rocks

• Smoking and Mortality — the size of smoking’s mortality effect and how much cessation recovers as a function of age at quitting
• Electronic Cigarettes and Cardiovascular Risk — a distinct, much thinner exposure: acute surrogate harm (HR/BP rise) shown, hard CV endpoints insufficient; valence flips by stratum (smoker switching = harm reduction vs continued smoking; never-smoker starting = new harm)
• Alcohol and Mortality and Vascular Disease — whether moderate intake is protective, harmful, or neutral, and whether the J-curve survives scrutiny; now also the drinking-PATTERN axis (binge at fixed volume, Roerecke), the red-wine/resveratrol null (Semba), and the population “no safe level” burden (GBD, Rumgay)

Neurodegeneration (dementia · Parkinson’s)

Most modifiable dementia levers ARE the cardiometabolic big rocks (hypertension, diabetes, obesity, LDL, smoking, inactivity, alcohol) — pulling them buys cognition as a second patient-important outcome. Parkinson’s, by contrast, has few credible levers and mostly critically-low evidence. Home of the dementia and parkinsons clusters until they warrant their own hub.

• Dementia Prevention and Modifiable Risk Factors — the 14-factor life-course framework and the ~45% population-attributable-fraction headline, with the modelled-attribution caveats (nucleus)
• Multidomain Lifestyle Intervention and Cognitive Decline — the FINGER RCT: does intervening on the levers as a bundle actually move cognition? Yes, but small (d=0.13), on a surrogate, non-decomposable
• Hearing Loss and Dementia — a dementia-specific, correctable lever: does treating hearing loss with hearing aids lower dementia risk, and for whom is the effect largest?
• Parkinsons Disease Modifiable Risk Factors — Chen 2021 umbrella review (46 SRs, 39 critically-low AMSTAR-2); the parkinsons cluster nucleus. The thin-field finding: physical activity is the one credible protective lever (already a big rock), most other signals are reverse-causation-suspect (the long prodrome) or confounded-by-indication. Smoking’s inverse-PD association is an artifact, never a lever