Preventive care program tracks modest metabolic gains without a blood pressure or SCORE2 shift
A prospective observational study from a single preventive health center in Paris followed 279 men who completed two standardized evaluations within a multidimensional prevention program. The cohort was middle-aged, with a median age of 51.2 years, a median body mass index of 24.5 kg/m2, and a median SCORE2 of 2.9% at baseline. Over a median interval of 13.3 months, the program was associated with small but measurable shifts in body composition, lipids, and muscular strength. Blood pressure, LDL cholesterol, glycemic markers, and estimated cardiovascular risk stayed flat.
The pattern is clinically familiar. Lifestyle counseling, targeted supplementation, and medication changes can improve the markers that are most responsive to behavior and adherence, while leaving harder endpoints and more inertia-prone risk estimates largely unchanged over a single year.
Visceral adiposity fell as muscle strength rose
The most biologically coherent changes appeared in body composition and function. Visceral adipose tissue mass decreased by a median of 49 g, with a 95% confidence interval from -80.5 to -18.5, and the adjusted q value was 0.006. Body mass and fat mass also declined slightly. In parallel, handgrip strength improved on both sides, rising by 2.35 kg in the right hand and 1.70 kg in the left, both with q values below 0.001.
A one-sentence signal stands out: muscle strength improved while visceral fat declined.
That combination matters physiologically. Visceral fat is metabolically active, tied to insulin resistance, inflammatory signaling, and adverse lipid handling, while grip strength functions as a practical surrogate for global musculoskeletal fitness and aging resilience. Even small changes in these markers can reflect a program that is not merely chasing a lab result but addressing the underlying cardiometabolic substrate through exercise, diet, and other behavior-linked interventions.
Transitions across threshold values reinforced the same direction of travel. The proportion of men below the grip strength reference value fell from 60.1% to 47.6%, with a paired odds ratio of 0.34 and a 95% confidence interval of 0.19 to 0.61. For a preventive setting, that shift is important because a movement from below-reference into a higher functional range suggests the body is not just lighter; it is stronger.
HDL moved upward while atherogenic ratios improved
Lipid changes were selective rather than broad. HDL cholesterol increased by 3.5 mg/dL, with a 95% confidence interval of 2.5 to 4.5 and q below 0.001. The triglyceride-to-HDL and total cholesterol-to-HDL ratios also fell. Yet LDL cholesterol did not change meaningfully, and blood pressure remained stable.
These results fit the biology of a multidimensional prevention program. HDL often responds to physical activity, weight change, diet quality, and improved insulin sensitivity, while LDL typically requires a more direct pharmacologic strategy if substantial lowering is the goal. A more favorable triglyceride-to-HDL ratio can also point to improved metabolic handling of lipids, even when LDL does not budge. In preventive cardiology, those ratios may carry practical meaning because they summarize the balance between atherogenic load and metabolic risk more compactly than a single lipid number.
The threshold analysis, however, cuts in an unexpected direction for HDL. The proportion of men with HDL above 46 mg/dL fell from 26.7% to 16.5%, with a paired odds ratio of 0.25 and a 95% confidence interval of 0.12 to 0.54. The summary statistics indicate a rise in HDL overall, yet fewer men crossed the preset threshold at the second assessment. That apparent tension suggests the distribution may have shifted in a way that does not map cleanly onto a single cut point, or that the threshold selected may not have captured the whole pattern of change.
Blood pressure, insulin resistance markers and SCORE2 stayed unchanged
Despite the favorable movement in select markers, several core cardiovascular variables were essentially stable. Blood pressure did not change. Fasting glucose did not change after adjustment, and insulin, HOMA-IR, SCORE2, salivary cortisol, and DHEA also remained unchanged.
This stability is not a failure of the intervention; it is a useful constraint on interpretation. In a health-engaged population with a relatively low baseline cardiovascular risk profile, there may be limited room for dramatic movement in clinic blood pressure, risk scores, or glycemic indices over a 13-month interval. SCORE2, in particular, is designed to translate a cluster of baseline risk factors into projected event risk, so short-term behavioral gains may not register strongly unless they are large enough to shift the underlying inputs substantially.
The endocrine markers were similarly quiet. Salivary cortisol and DHEA did not change, which leaves open whether the program influenced stress biology in a measurable way or whether the assays were simply too blunt, too variable, or too distal from the behavioral changes being encouraged. At the bedside, that means the visible improvement in strength and body composition should not be over-read as proof of systemic hormonal reprogramming.
What this preprint can and cannot claim
This is a prospective observational cohort, not a randomized trial. The comparison is within individuals, which is useful for detecting paired change, but the design cannot separate program effects from regression to the mean, repeat testing, seasonal drift, or other secular influences. Only 279 of 865 eligible men completed both evaluations, representing 32.3% of the eligible pool, so the analyzed group likely reflects a selected subset of men who remained engaged enough to return for follow-up. That makes the findings more representative of adherent participants than of all men entering the program.
The cohort was drawn from a single preventive health center in Paris, and the assessments were standardized, but generalizability remains limited. Men who seek repeated preventive evaluation tend to differ from the broader population in motivation, health literacy, baseline concern about risk, and willingness to act on recommendations. Those factors can amplify apparent success in a prevention program without proving that the same effects would appear in less engaged patients.
Still, the direction of change is coherent enough to merit attention. Visceral adiposity fell, handgrip strength improved, and HDL-related measures moved in a favorable direction, while blood pressure, LDL cholesterol, glycemia, and SCORE2 stayed static over roughly one year. For clinicians, the practical message is narrow: multidimensional prevention may shift functional and metabolic markers before it produces obvious changes in conventional cardiovascular risk estimates. The unanswered question is whether those intermediate gains persist, widen, or translate into fewer events once a comparison group and longer follow-up enter the picture.