Navigate peer-reviewed breakthroughs by pharmacological class, genetic target, circulating biomarker, or diagnostic modality. Select any clinical entity to inspect all linked studies.
While stopping statins after 70 might initially seem safe for those without prior heart events, the long-term risks suggest a careful discussion with your doctor is essential. For years, the medical community has debated the optimal duration of statin therapy, especially as patients enter advanced age.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
Fructose metabolism, particularly post-chemotherapy, may represent a novel and actionable therapeutic target to impede ovarian cancer metastasis. Ovarian cancer often presents at an advanced stage, and despite initial responses to chemotherapy, recurrence and metastasis remain the primary causes of morbidity and risk of death.
2/5 Preclinical
Evidence Meter · 2/5
Animal & Preclinical Data
Demonstrated in living animal models before large-scale human safety and dosing trials begin.
Coronary Artery Calcium (CAC) guided statin initiation resulted in similar major cardiovascular event rates with fewer prescriptions and significantly improved patient adherence compared to traditional risk assessments. Current standard of care for primary prevention statin initiation heavily relies on calculated risk scores (e.g., ASCVD risk in the US), which estimate the 10-year risk of atherosclerotic cardiovascular disease events based on factors like age, sex, race, cholesterol levels, blood pressure, and diabetes status.
5/5 Gold Standard
Evidence Meter · 5/5
Gold-Standard Human Evidence
Backed by randomized controlled human trials or a formal meta-analysis pooling multiple clinical studies.
Full-fat dairy may not be the metabolic villain once thought, prompting a review of dietary advice. These findings suggest current dietary guidelines regarding dairy consumption may need re-evaluation, potentially impacting patient counseling.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
While gene editing offers the potential for lifelong disease prevention, its permanent effects demand rigorous, extended safety validation before widespread clinical use. If successful, this could significantly improve patient adherence and outcomes for chronic conditions by eliminating the need for daily medication.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
Rejuvenating the liver with novel therapies could unexpectedly offer protection against both Alzheimer's disease and heart disease. This surprising discovery suggests that targeting liver health could offer a novel therapeutic strategy for preventing or treating both Alzheimer's disease and cardiovascular disease.
2/5 Preclinical
Evidence Meter · 2/5
Animal & Preclinical Data
Demonstrated in living animal models before large-scale human safety and dosing trials begin.
A newly identified cholesterol regulation pathway and a drug in early development targeting it hold promise for future high LDL-C treatments. This discovery offers a novel therapeutic target for managing high cholesterol, potentially benefiting patients whose LDL levels are not adequately controlled by current treatments.
2/5 Preclinical
Evidence Meter · 2/5
Animal & Preclinical Data
Demonstrated in living animal models before large-scale human safety and dosing trials begin.
Targeting a novel pathway that disrupts natural cholesterol regulation could soon provide a powerful new strategy for managing high LDL cholesterol. This breakthrough offers a potential new therapeutic avenue for individuals with high cholesterol, especially those who may not respond optimally to current treatments.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
Inflammation contributes to SA burden, as assessed by direct plaque quantification, beyond the effects of LDLc and SBP. These findings indicate that inflammation, captured through the use of systemic inflammatory markers, is a risk factor relevant across the entire continuum of atherosclerosis, exerting a deleterious impact comparable to that of LDLc and SBP.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
Results of this study show that after using a state-of-the art LLM, nearly 9 in 10 ASCVD encounters with above-goal LDL-C level did not have patient LLT escalated, most often because of adverse effects, patient preference, preference for lifestyle changes, therapeutic inertia (eg, repeat laboratory tests), and near-goal LDL-C level. These findings highlight an avenue for personalizing system-level digital health interventions to help discover and minimize guideline-discordant care gaps in secondary prevention of ASCVD.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
Within a target-directed LDL-C-lowering strategy, cardiovascular efficacy (real-world effectiveness in the trial) and safety did not differ significantly, whether initiated as statin-ezetimibe combination therapy or as statin monotherapy, but combination therapy facilitated achievement of a lower LDL-C target. In a target-directed low-density lipoprotein cholesterol (LDL-C)-lowering strategy, the impact of the initial treatment regimen has not been investigated in patients with atherosclerotic cardiovascular disease.
5/5 Gold Standard
Evidence Meter · 5/5
Gold-Standard Human Evidence
Backed by randomized controlled human trials or a formal meta-analysis pooling multiple clinical studies.
This secondary analysis of the FLOWPROMOTE randomized clinical trial demonstrated that in statin-naive patients with CAD, more intensive lipid-lowering therapy was associated with significantly greater regression of total and noncalcified coronary plaque burden compared with intensive therapy. The extent of plaque regression was related to achieved LDL-C levels, supporting the potential for partial reversal of coronary atherosclerosis with intensive lipid reduction.
5/5 Gold Standard
Evidence Meter · 5/5
Gold-Standard Human Evidence
Backed by randomized controlled human trials or a formal meta-analysis pooling multiple clinical studies.
Our results indicate that individuals with combined autoimmunity and lower insulin sensitivity present with clinical diabetes earlier than classic type 1 diabetes along the β-cell decline trajectory, identifying a potential timeframe for disease-modifying interventions in specific type 1 diabetes subtypes. Adult-onset type 1 diabetes exhibits substantial heterogeneity.
4/5 Strong Trial
Evidence Meter · 4/5
Strong Clinical Evidence
Tested directly in patients through a prospective clinical trial or large multicenter human cohort.
A better understanding of the differences between metabolically divergent groups and the physiological responses to weight loss can help identify the factors responsible for the link between excess adiposity and metabolic dysfunction and disease. In this Review, we discuss metabolic differences at the cellular, organ-system and systemic levels between people with metabolically healthy and metabolically unhealthy obesity; we also discuss heterogeneity in the therapeutic effects of weight reduction.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
In particular, the substantial contribution of non-ischaemic conditions and maternal hypertensive disorders to the burden in women, alongside distinct patterns of risk exposure and wider geographic disparities, underscore the importance of adopting a life-course and sex- and gender-informed approach to cardiovascular prevention and policy. Major differences were also apparent in risk profiles, particularly for behavioural risk factors-with summary exposure values of tobacco and alcohol being 10%-20% points higher in men than women; contrasting with cardiometabolic factors, such as high body mass index and low physical activity, that were often 5%-15% points higher in women than men, and more modest differences in environmental and biological risks, including air pollution, fasting glucose, or cholesterol.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
Acquired gemcitabine resistance drives metabolic reprogramming that suppresses pyrimidine salvage while creating a therapeutically exploitable dependence on the mevalonate pathway. These findings identify pharmacologic inhibition of HMGCR as a metabolic vulnerability in gemcitabine resistance and support HMGCR expression as a candidate biomarker (measurable biological signal) for treatment stratification in PDAC patients.
2/5 Preclinical
Evidence Meter · 2/5
Animal & Preclinical Data
Demonstrated in living animal models before large-scale human safety and dosing trials begin.
Hypercholesterolaemia was associated with reduced thymic output, while statin-treated patients showed partially preserved circulating CD4+ RTE levels, supporting integrated metabolic and immunologic strategies for FH management. Lifelong exposure to elevated low-density lipoprotein cholesterol in familial hypercholesterolaemia (FH) patients not only increases the risk of atherosclerotic cardiovascular disease, but also affects other organs beyond the cardiovascular system.
3/5 Observational
Evidence Meter · 3/5
Real-World Observation
Finds meaningful patterns in human health records or cohorts, though observational data cannot prove direct cause.
Ours study found chronic hepatic metabolic stress induced by PD. Healthy mice and mice with chronic kidney disease (5/6 nephrectomy C57BL/6 aged 12-14 weeks) underwent seven weeks of PD.
2/5 Preclinical
Evidence Meter · 2/5
Animal & Preclinical Data
Demonstrated in living animal models before large-scale human safety and dosing trials begin.
Interpretation is limited by the observational design, absence of a comparator group, self-pay population and 6-month follow-up. These findings support the feasibility of delivering structured, digitally enabled obesity pharmacotherapy at scale and provide prospective real-world implementation evidence for this care model.
5/5 Gold Standard
Evidence Meter · 5/5
Gold-Standard Human Evidence
Backed by randomized controlled human trials or a formal meta-analysis pooling multiple clinical studies.
1 min read·Nature Medicine·
Patient & Student Companion
Everyday Lab & Drug Translator
Instant plain-English guides for common blood tests and prescriptions—what normal ranges mean, what high/low values signal, and what to ask your clinician.
Lab Marker3-Month Blood Sugar
HbA1c
Measures the percentage of red blood cell hemoglobin coated with glucose over roughly 90 days.
Normal: below 5.7% · Prediabetes: 5.7%–6.4%
6.5% or higher on two tests diagnoses diabetes; very low values can occur alongside hypoglycemia or hemolytic anemia.
Ask your doctor: “Does my HbA1c match my daily fasting/post-meal glucose trends?”
Estimated glomerular filtration rate—how many milliliters of blood your kidneys filter every minute.
Healthy adult filter rate: 90+ mL/min/1.73m²
Values persistently below 60 for 3+ months (or elevated urine albumin) mark chronic kidney disease; single dips can simply reflect dehydration or NSAID use.
Ask your doctor: “Should we pair eGFR with a urine albumin-to-creatinine test (uACR)?”