Electrocardiogram (ECG) biometric provides an authentication to identify an individual on the basis of specific cardiac potential measured from a living body. Convolutional neural networks (CNN) outperform traditional ECG biometrics because convolutions can produce discernible features from ECG through machine learning. Phase space reconstruction (PSR), using a time delay technique, is one of the transformations from ECG to a feature map, without the need of exact R-peak alignment. However, the effects of time delay and grid partition on identification performance have not been investigated. In this study, we developed a PSR-based CNN for ECG biometric authentication and examined the aforementioned effects. Based on a population of 115 subjects selected from the PTB Diagnostic ECG Database, a higher identification accuracy was achieved when the time delay was set from 20 to 28 ms, since it produced a well phase-space expansion of P, QRS, and T waves. A higher accuracy was also achieved when a high-density grid partition was used, since it produced a fine-detail phase-space trajectory. The use of a scaled-down network for PSR over a low-density grid with 32 × 32 partitions achieved a comparable accuracy with using a large-scale network for PSR over 256 × 256 partitions, but it had the benefit of reductions in network size and training time by 10 and 5 folds, respectively.

Background: Population aging is driving a convergent rise in three disorders historically managed in isolation: cardiovascular disease, neurocognitive decline, and osteoporotic bone loss. Accumulating mechanistic data indicate that these systems are coupled through shared regulators of calcium trafficking, inflammation resolution, vascular integrity, and inflammaging, supporting the concept of an integrated "Heart-Brain-Bone" axis. Three lipid-soluble nutrients-long-chain omega-3 polyunsaturated fatty acids (EPA/DHA), vitamin D3 (cholecalciferol), and vitamin K2 (menaquinone-7 [MK-7])-act on overlapping nodes of this network. Methods: We conducted a structured narrative review of mechanistic, observational, and randomized controlled trial (RCT) evidence, grading the strength of support for each claim. Results: Vitamin K2-dependent gamma-carboxylation of matrix Gla protein (MGP) and osteocalcin is proposed to reciprocally direct calcium away from the arterial wall and toward the bone matrix, offering a candidate mechanistic resolution of the "calcium paradox" associated with isolated vitamin D3 supplementation; EPA/DHA-derived specialized pro-resolving mediators may support resolution of endothelial and neuronal inflammation; and bone-, vascular-, and brain-derived signals (osteocalcin, FGF23, the neurovascular unit) interconnect the three organs. Human clinical evidence, however, is heterogeneous and formulation- and population-dependent: cardiovascular omega-3 RCTs are discordant (REDUCE-IT, which used icosapent ethyl [an EPA ethyl ester], positive; VITAL/STRENGTH/ASCEND null, predominantly in lower-risk or replete cohorts), cognitive trials are largely null or subgroup-dependent (MAPT, DO-HEALTH), and MK-7 improves surrogate bone and calcification biomarkers, with only a single recent hard-endpoint coronary calcification RCT (VitaK-CAC). Conclusions: The combined use of long-chain omega-3, vitamin D3, and MK-7 is mechanistically rational and hypothesis-generating rather than clinically established; benefit appears most plausible in individuals with elevated risk or demonstrable nutritional insufficiency, and least in replete, low-risk populations. Findings should be interpreted within a broader healthy-aging context that includes lifestyle and psychosocial factors. Adequately powered factorial RCTs stratified by baseline Omega-3 Index, 25(OH)D, and vitamin K status, with prespecified mechanistic biomarkers and hard endpoints, are required.

Background: Population aging is driving a convergent rise in three disorders historically managed in isolation: cardiovascular disease, neurocognitive decline, and osteoporotic bone loss. Mechanistic data indicate that these systems are coupled through shared regulators of calcium trafficking, inflammation resolution, vascular integrity, and inflammaging. On this basis, a “Heart–Brain–Bone” axis has been proposed; it should be understood as an integrative conceptual framework that organizes evidence drawn from three separate studies, not as a validated physiological entity with agreed diagnostic criteria or demonstrated modifiability. Three lipid-soluble nutrients—long-chain omega-3 polyunsaturated fatty acids (EPA/DHA), vitamin D3 (cholecalciferol), and vitamin K2 (menaquinone-7 [MK-7])—act on overlapping nodes of this network. Methods: We performed a structured narrative review. PubMed/MEDLINE, Embase, the Cochrane Library, and Web of Science were searched from database inception to 25 June 2026 using predefined term blocks for each nutrient, each organ domain, and each candidate mechanism, and the search was updated on 7 August 2026. Records were screened against prespecified inclusion and exclusion criteria by two authors independently, with disagreements resolved by a third. The strength of evidence for each nutrient–organ relationship was graded with an explicitly defined four-level scheme ((−) to (+++)) applied separately to preclinical, observational, randomized and meta-analytic evidence. Results: Vitamin K2-dependent gamma-carboxylation of matrix Gla protein (MGP) and osteocalcin has been proposed to influence whether calcium is incorporated into the bone matrix or deposited in the arterial wall, offering a candidate mechanistic account of the “calcium paradox” associated with isolated vitamin D3 supplementation; EPA/DHA-derived specialized pro-resolving mediators may support resolution of endothelial and neuronal inflammation; and bone-, vascular- and brain-derived signals (osteocalcin, FGF23, the neurovascular unit) interconnect the three organs. These mechanisms are biologically plausible but remain insufficiently confirmed in humans. The clinical evidence is heterogeneous, formulation- and population-dependent, and comprises positive, neutral and null results: cardiovascular omega-3 trials are discordant (REDUCE-IT, which used icosapent ethyl [an EPA ethyl ester], positive; VITAL/STRENGTH/ASCEND null, predominantly in lower-risk or replete cohorts); cognitive trials are largely null or subgroup-dependent (MAPT, DO-HEALTH, VITAL); and MK-7 improves surrogate bone and calcification biomarkers and slowed coronary artery calcification in one recent randomized imaging trial (VitaK-CAC), whereas combined MK-7 plus vitamin D3 did not slow aortic valve or coronary calcification in AVADEC and MK-7 did not reduce bone loss in early menopausal women. Recognized safety signals include a dose-dependent increase in atrial fibrillation with high-dose omega-3, adverse skeletal effects of high-dose or bolus vitamin D, and clinically relevant interference of even low-dose MK-7 with vitamin K antagonist therapy. Conclusions: No adequately powered randomized trial has demonstrated that the combination of long-chain omega-3, vitamin D3 and MK-7 is superior to its individual components or to placebo for any clinical endpoint. The combined regimen is therefore mechanistically rational and hypothesis-generating rather than clinically established; benefit appears most plausible in individuals with elevated risk or demonstrable nutritional insufficiency, and least in replete, low-risk populations. Findings should be interpreted within a broader healthy-aging context that includes lifestyle and psychosocial factors. Adequately powered factorial randomized controlled trials stratified by baseline Omega-3 index, 25(OH)D and vitamin K status, with prespecified mechanistic biomarkers and hard endpoints, are required.