BACKGROUND:Understanding the total burden of human papillomavirus (HPV)-related cancers is crucial for improving prevention strategies. While organized cervical cancer (CC) screening has been implemented for many years, other HPV-related cancers lacked screening programs. Primary prevention through HPV vaccination has been implemented through national programs, initially for girls and later for boys. To analyze changes in HPV-attributable cancer incidence for both men and women, we used data from the Cancer Registry of Norway (CRN). METHODS:This was an observational population-based study using high-quality data from the CRN. The proportion of cancers at each site attributed to HPV was calculated based on existing literature. We estimated HPV cancer incidence rates from 1990 to 2023 and forecasted incidences until 2038 for cervical squamous cell carcinoma (SCC) and adenocarcinoma, along with other HPV-related SCCs. RESULTS:Among men, HPV-attributable cancer incidence was rising, with male oropharyngeal SCC showing the fastest increase (annual percentage change [APC], 4.5; P < .01). Overall, the incidence of HPV-attributable cancers not prevented by screening steadily increased (APC, 2.8; P < .01), surpassing CC incidence and projected to continue rising until 2038. In women, CC remains the most common HPV cancer. However, after an increasing trend since 2004, cervical SCC incidence rates decreased 6% annually from 2018 to 2023 (95% confidence interval [CI], -9.9 to -1.9; P < .01). CONCLUSIONS:The burden of HPV-related cancers beyond CC is increasing in Norway, whereas CC incidence is declining. Addressing the rising total burden of HPV-attributable cancers requires additional preventive measures.

In Scandinavia, human papillomavirus (HPV) vaccination programs started in 2007-2008 in Sweden and Denmark with HPV vaccination offered to multiple cohorts of young girls, while in Norway this was offered to a single cohort only. Interestingly, in Sweden and Denmark, cervical cancer incidence in young women decreased markedly from 2017 to 2018, while in Norway a steady increase was seen until 2020. As the 3 countries are very similar in other factors important for cervical cancer incidence rates, like cervical cancer screening, the observed difference is most likely due to differences in the multicohort vaccination.

Neuroblastoma (NBL), one of the main death-causing cancers in children, is known for its remarkable genetic heterogeneity and varied patient outcome spanning from spontaneous regression to widespread disease. Specific copy number variations and single gene rearrangements have been proven to be associated with biological behavior and prognosis; however, there is still an unmet need to enlarge the existing armamentarium of prognostic and therapeutic targets. We performed whole exome sequencing (WES) of samples from 18 primary tumors and six relapse samples originating from 18 NBL patients. Our cohort consists of 16 high-risk, one intermediate, and one very low risk patient. The obtained results confirmed known mutational hotspots in ALK and revealed other non-synonymous variants of NBL-related genes (TP53, DMD, ROS, LMO3, PRUNE2, ERBB3, and PHOX2B) and of genes cardinal for other cancers (KRAS, PIK3CA, and FLT3). Beyond, GOSeq analysis determined genes involved in biological adhesion, neurological cell-cell adhesion, JNK cascade, and immune response of cell surface signaling pathways. We were able to identify novel coding variants present in more than one patient in nine biologically relevant genes for NBL, including TMEM14B, TTN, FLG, RHBG, SHROOM3, UTRN, HLA-DRB1, OR6C68, and XIRP2. Our results may provide novel information about genes and signaling pathways relevant for the pathogenesis and clinical course in high-risk NBL.

In Norway, single-cohort vaccination with quadrivalent human papillomavirus (qHPV) vaccine targeting 12-year-old girls took place in 2009-2016. In 2020, the oldest vaccinated cohort was 23 years old and had approached the age where risk of being diagnosed with cervical intraepithelial neoplasia grade 2 or worse (CIN2+) increases rapidly. The aim of this cohort study was to assess direct qHPV vaccine effectiveness (VE) against CIN2+ among Norwegian women aged 16-30 years in 2007-2020. By using population-based health registries and individual-level data on vaccination status and potential subsequent CIN2+ incidence, we found 82% qHPV VE among women vaccinated before age 17 years. Using individual-level data from Norwegian population-based health registries, this study found 82% vaccine effectiveness against CIN2+ among women vaccinated before 17 years of age.

BACKGROUND:Individual variation in the need for healthcare constitutes knowledge gaps for young atrial fibrillation (AF) patients. We aimed to estimate the prevalence and primary care burden of early-onset AF in Norway, emphasising sex differences, in a nationwide healthcare database. METHODS:We used data from the Norwegian Control and Payment of Health Reimbursement database to identify all Norwegian residents ≥18 years of age registered with a primary care physician (PCP) in 2019, with onset of AF at ≤50 years of age (early-onset AF) in the period 2006-2019. From the accumulated number of early-onset AF cases among current residents, we calculated the prevalence in 2019. The group-level primary care burden was calculated as the total number of annual AF consultations divided by the annual number of AF patients (2014-2018), and individual burden as the mean number of consultations per AF patient per year within the study period. We analysed the distribution of AF consultations between PCP and primary care emergency room (ER) services in total and by sex. RESULTS:We identified 10 925 Norwegian residents with early-onset AF in 2019 (26.3% women, mean age 48.4 years). The prevalence of early-onset AF was 0.34% (women: 0.19%, men: 0.50%). The early-onset AF population had on average one annual primary care consultation for AF. The individual burden of annual AF consultations varied widely; <1: 66% of women and 54% of men, (1-5]: 25% of women and 36% of men, (5-10]: 6% of women and 8% of men, ≥10: 2% of women and 2% of men. A higher proportion of men (71%) than women (38%) attended both PCP and ER services due to AF. CONCLUSIONS:The study confirmed a low prevalence of early-onset AF, with substantial sex differences and individual variation in primary healthcare needs. Our results signal a need for a higher resolution with regard to age groups in future research on burden and sex differences in early-onset AF.

Mechanical load is a potent regulator of cardiac structure and function. Although high workload during heart failure is associated with disruption of cardiomyocyte t-tubules and Ca2+ homeostasis, it remains unclear whether changes in preload and afterload may promote adaptive t-tubule remodelling. We examined this issue by first investigating isolated effects of stepwise increases in load in cultured rat papillary muscles. Both preload and afterload increases produced a biphasic response, with the highest t-tubule densities observed at moderate loads, whereas excessively low and high loads resulted in low t-tubule levels. To determine the baseline position of the heart on this bell-shaped curve, mice were subjected to mildly elevated preload or afterload (1 week of aortic shunt or banding). Both interventions resulted in compensated cardiac function linked to increased t-tubule density, consistent with ascension up the rising limb of the curve. Similar t-tubule proliferation was observed in human patients with moderately increased preload or afterload (mitral valve regurgitation, aortic stenosis). T-tubule growth was associated with larger Ca2+ transients, linked to upregulation of L-type Ca2+ channels, Na+-Ca2+ exchanger, mechanosensors and regulators of t-tubule structure. By contrast, marked elevation of cardiac load in rodents and patients advanced the heart down the declining limb of the t-tubule-load relationship. This bell-shaped relationship was lost in the absence of electrical stimulation, indicating a key role of systolic stress in controlling t-tubule plasticity. In conclusion, modest augmentation of workload promotes compensatory increases in t-tubule density and Ca2+ cycling, whereas this adaptation is reversed in overloaded hearts during heart failure progression. KEY POINTS: Excised papillary muscle experiments demonstrated a bell-shaped relationship between cardiomyocyte t-tubule density and workload (preload or afterload), which was only present when muscles were electrically stimulated. The in vivo heart at baseline is positioned on the rising phase of this curve because moderate increases in preload (mice with brief aortic shunt surgery, patients with mitral valve regurgitation) resulted in t-tubule growth. Moderate increases in afterload (mice and patients with mild aortic banding/stenosis) similarly increased t-tubule density. T-tubule proliferation was associated with larger Ca2+ transients, with upregulation of the L-type Ca2+ channel, Na+-Ca2+ exchanger, mechanosensors and regulators of t-tubule structure. By contrast, marked elevation of cardiac load in rodents and patients placed the heart on the declining phase of the t-tubule-load relationship, promoting heart failure progression. The dependence of t-tubule structure on preload and afterload thus enables both compensatory and maladaptive remodelling, in rodents and humans.

Cervical cancer screening represents an excellent model system for the development of personalized cancer-prevention strategies [...]

Ultrasound diagnosis of adenomyosis involves many diagnostic signs that vary in their diagnostic significance. Our objective was to validate a previously developed multivariate prediction model for diagnosing adenomyosis that weights predictors based on their diagnostic performance and evaluate the model's performance between less experienced examiners and experts. Prospective, observational, multicentre study including premenopausal women scheduled for hysterectomy for benign indications. All patients underwent preoperative 2D and 3D-transvaginal ultrasound. Nine diagnostic predictors as previously defined (hyperechoic islets, fan-shaped shadowing, myometrial cysts, globular or normal uterine shape, uterine wall thickest/thinnest ratio, maximum width of the junctional zone (JZ) in sagittal plane, regular JZ, grade of dysmenorrhea) were documented. Images, videos and 3D-volumes were stored and re-assessed by a blinded expert. Histopathological examination of the hysterectomy specimen followed a dedicated protocol. The weight of each sign (β) was predefined earlier; the diagnostic performance [area under the curve (AUC), sensitivity, specificity] of the model was evaluated. Of 528 women, 465 were included in the final analysis. Adenomyosis was present in 255/465 (54.8%). The diagnostic performance of the model in the hand of non-experts showed a poor test quality [AUC= 0.61 (95%CI 0.55-0.66), sensitivity 65%, specificity 58%]. When asked to subjectively assess the presence of adenomyosis, the overall performance was comparably low [sensitivity 72% (95%CI 0.66-0.77), specificity 54% (95%CI 0.47-0.61), PPV 65%, NPV 61%, accuracy 64%]. The results for the test quality for the expert reader are pending and will be presented during the congress. The use of hormonal medication did not influence the model's performance. The preliminary results of the validated model show a poor test quality for non-expert readers. Adjustment of the predictors might improve diagnostic quality.

Excessive iron accumulation or deficiency leads to a variety of pathologies in humans and developmental arrest in the nematode Caenorhabditis elegans. Instead, sub-lethal iron depletion extends C. elegans lifespan. Hypoxia preconditioning protects against severe hypoxia-induced neuromuscular damage across species but it has low feasible application. In this study, we assessed the potential beneficial effects of genetic and chemical interventions acting via mild iron instead of oxygen depletion. We show that limiting iron availability in C. elegans through frataxin silencing or the iron chelator bipyridine, similar to hypoxia preconditioning, protects against hypoxia-, age-, and proteotoxicity-induced neuromuscular deficits. Mechanistically, our data suggest that the beneficial effects elicited by frataxin silencing are in part mediated by counteracting ferroptosis, a form of non-apoptotic cell death mediated by iron-induced lipid peroxidation. This is achieved by impacting on different key ferroptosis players and likely via gpx-independent redox systems. We thus point to ferroptosis inhibition as a novel potential strategy to promote healthy aging.

Background: In 2009, Norway initiated routine quadrivalent HPV (qHPV) vaccination for girls at 12-13 years of age to protect against virus types causing cervical cancer, HPV16/18, and HPV6/11 which cause anogenital warts (AGW). We wanted to investigate qHPV vaccine effectiveness (VE) against AGW in females before and after first AGW episode and to assess the impact of female vaccination in males.Materials and methods: QHPV vaccination and AGW episodes were collected for the time period 2006-2016 for birth cohorts 1975-2003. Cox models were applied to age at first, as well as at second AGW episode. Finally, we estimated the impact of the female vaccination program on unvaccinated males.Results: The VE against the first episode of AGW was strongly dependent on vaccination age, with hazard ratios (HRs) compared to unvaccinated individuals of 0.2, 0.2, 0.3, 0.5, 1.0, 1.3, and 2.7, for age groups of & LE;13, 14-15, 16-17, 18-19, 20-24, 25-29, and 30+ years at first vaccination, respectively. Among women who had suffered a first episode of AGW, subsequent qHPV vaccination did not protect against a second episode, with HRs of 0.8, 1.0, and 1.4, for age groups of & LE;17, 18-24, and 25+ years at first vaccination. A gradually decreasing AGW risk was seen in unvaccinated male cohorts neighboring the first routinely vaccinated female 1997 cohort.Conclusions: When administered before 14 years of age, qHPV vaccination reduced the probability of AGW about fivefold. The effect decreased sharply with vaccination age, and was not significant among women vaccinated after age 20 years. QHPV administered after the first AGW episode did not protect against a second AGW episode. Herd effects were indicated in unvaccinated males, as we observed a gradual decrease in AGW rates from the 1993 male birth cohort and onwards.

BACKGROUND:Ion mobility spectrometry (IMS) allows for online quantification of exhaled propofol concentrations. We aimed to validate a bedside online IMS device, the Edmon® , for predicting plasma concentrations of propofol in normal-weight and obese patients.METHODS:Patients with body mass index (BMI) >20 kg/m2 scheduled for laparoscopic cholecystectomy or bariatric surgery were recruited. Exhaled propofol concentrations (CA ), arterial plasma propofol concentrations (CP ) and bispectral index (BIS) values were collected during target-controlled infusion (TCI) anaesthesia. Generalised estimation equation (GEE) was applied to all samples and stable-phase samples at different delays for best fit between CP and CA . BMI was evaluated as covariate. BIS and exhaled propofol correlations were also assessed with GEE.RESULTS:A total of 29 patients (BMI 20.3-53.7) were included. A maximal R2 of 0.58 was found during stable concentrations with 5 min delay of CA to CP ; the intercept a = -0.69 (95% CI -1.7, 0.3) and slope b = 0.87 (95% CI 0.7, 1.1). BMI was found to be a non-significant covariate. The median absolute performance error predicting plasma propofol concentrations was 13.4%. At a CA of 5 ppb, the model predicts a CP of 3.6 μg/ml (95% CI ±1.4). There was a maximal negative correlation of R2  = 0.44 at 2-min delay from CA to BIS.CONCLUSIONS:Online monitoring of exhaled propofol concentrations is clinically feasible in normal-weight and obese patients. With a 5-min delay, our model outperforms the Marsh plasma TCI model in a post hoc analysis. Modest correlation with plasma concentrations makes the clinical usefulness questionable.

The literature on treatment patterns for paediatric atopic dermatitis (AD) is scarce and is rarely based on real-world data. Using national registers, we sought to establish up-to-date, population-based prevalence estimates, predictors of risk and disease burden and a comprehensive overview of treatment patterns and course for paediatric patients with AD. Dispensed prescriptions for the entire Norwegian child population aged 0–10 years from 2014 to 2020 were analysed. There were 176,458 paediatric patients with AD. Of these, 99.2% received topical corticosteroids, 5.1% received topical calcineurin inhibitors, 37.1% received potent topical corticosteroids and 2.1% received systemic corticosteroids. Of the 59,335 live births in Norway (2014), 14,385 [24.8%; 95% confidence interval (CI) 24.5–25.1] paediatric patients were treated for AD before the age of 6 years, and of these, only 934 (6.5%; 95% CI 6.1–6.9) received medication annually for 5 years or more. Compared with girls, 17.9% (95% CI 6.5–27.9) more boys were treated for at least 5 years, receiving 6.4% (95% CI 1.2–11.3) more potent topical corticosteroids and 12.4% (95% CI 6.5–18.0) more were treated for skin infections. Compared with patients with late-onset treatment, 18.9% (95% CI 7.5–29.0) more paediatric patients with early-onset treatment were still receiving treatment at 5 years of age, 15.7% (95% CI 7.1–23.4) more paediatric patients received potent topical corticosteroids and 44.4% (95% CI 36.5–51.2) more paediatric patients were treated for skin infections. Most paediatric patients were treated for a mild disease for a limited period. Although the prevalence of AD is higher at a younger age, these paediatric patients were the least likely to receive potent topical corticosteroids. Male sex and early-onset AD are associated with and are potential predictors of long-term treatment and treatment of potent topical corticosteroids, antihistamines and skin infections, which may have clinical utility for personalised prognosis, healthcare planning and future AD prevention trials.

Abstract Background: Identification of screening tests for the detection of head and neck cancer (HNC) at an early stage is an important strategy to improving prognosis. Our objective was to identify plasma circulating miRNAs for the diagnosis of HNC (oral and laryngeal subsites), within a multicenter International Head and Neck Cancer Epidemiology consortium. Methods: A high-throughput screening phase with 754 miRNAs was performed in plasma samples of 88 cases and 88 controls, followed by a validation phase of the differentially expressed miRNAs, identified in the screening, in samples of 396 cases and 396 controls. Comparison of the fold changes (FC) was carried out using the Wilcoxon rank-sum test and the Dunn multiple comparison test. Results: We identified miR-151-3p (FC = 1.73, P = 0.007) as differentially expressed miRNAs in the screening and validation phase. The miR-151-3p was the only overexpressed miRNA in validation sample of patients with HNC with early stage at diagnosis (FC = 1.81, P = 0.008) and it was confirmed upregulated both in smoker early-stage cases (FC = 3.52, P = 0.024) and in nonsmoker early-stage cases (FC = 1.60, P = 0.025) compared with controls. Conclusions: We identified miR-151-3p as an early marker of HNC. This miRNA was the only upregulated in patients at early stages of the disease, independently of the smoking status. Impact: The prognosis for HNC is still poor. The discovery of a new diagnostic biomarker could lead to an earlier tumor discovery and therefore to an improvement in patient prognosis.

Severe oxygen and iron deficiency have evolutionarily conserved detrimental effects, leading to pathologies in mammals and developmental arrest as well as neuromuscular degeneration in the nematode C. elegans. Yet, similar to the beneficial effects of mild hypoxia, non-toxic levels of iron depletion, achieved with the iron chelator bipyridine or through frataxin silencing, extend C. elegans lifespan through hypoxia like-induction of mitophagy. The positive health outcomes of applying hypoxia preconditioning are obvious but have low feasible application. Here, we thus tested the potential beneficial effects of non-toxic, preconditioning interventions acting on iron instead of oxygen availability. We show that, similar to hypoxia preconditioning, limiting iron availability through frataxin silencing, iron chelating or iron competing agents, has evolutionarily conserved beneficial effects protecting against severe hypoxia-induced cellular and neuromuscular alterations. Moreover, we identify inhibition of ferroptosis - a form of non-apoptotic cell death specifically mediated by iron-induced lipid peroxidation - as a mediator of the beneficial effects elicited by frataxin silencing, most likely through gpx-independent suppression. We find that limitation of iron availability also protects against age-associated neuromuscular deficits, pointing to ferroptosis inhibition as a novel strategy to promote healthy aging.

Small-molecule tankyrase 1 and tankyrase 2 (TNKS1/2) inhibitors are effective antitumor agents in selected tumor cell lines and mouse models. Here, we characterized the response signatures and the in-depth mechanisms for the antiproliferative effect of tankyrase inhibition (TNKSi). The TNKS1/2-specific inhibitor G007-LK was used to screen 537 human tumor cell lines and a panel of particularly TNKSi-sensitive tumor cell lines was identified. Transcriptome, proteome, and bioinformatic analyses revealed the overall TNKSi-induced response signatures in the selected panel. TNKSi-mediated inhibition of wingless-type mammary tumor virus integration site/β-catenin, yes-associated protein 1 (YAP), and phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT signaling was validated and correlated with lost expression of the key oncogene MYC and impaired cell growth. Moreover, we show that TNKSi induces accumulation of TNKS1/2-containing β-catenin degradasomes functioning as core complexes interacting with YAP and angiomotin proteins during attenuation of YAP signaling. These findings provide a contextual and mechanistic framework for using TNKSi in anticancer treatment that warrants further comprehensive preclinical and clinical evaluations.

Background and aims: Atherogenesis involves a complex interaction between immune cells and lipids, processes greatly influenced by the vascular smooth muscle cell (VSMC) phenotype. The DNA glycosylase NEIL3 has previously been shown to have a role in atherogenesis, though whether this is due to its ability to repair DNA damage or to other non-canonical functions is not yet clear. Hereby, we investigate the role of NEIL3 in atherogenesis, specifically in VSMC phenotypic modulation, which is critical in plaque formation and stability. Methods: Chow diet-fed atherosclerosis-prone Apoe(-/-) mice deficient in Neil3, and NEIL3-abrogated human primary aortic VSMCs were characterized by qPCR, and immunohistochemical and enzymatic-based assays; moreover, single-cell RNA sequencing, mRNA sequencing, and proteomics were used to map the molecular effects of Neil3/NEIL3 deficiency in the aortic VSMC phenotype. Furthermore, BrdU-based proliferation assays and Western blot were performed to elucidate the involvement of the Akt signaling pathway in the transdifferentiation of aortic VSMCs lacking Neil3/NEIL3. Results: We show that Neil3 deficiency increases atherosclerotic plaque development without affecting systemic lipids. This observation was associated with a shift in VSMC phenotype towards a proliferating, lipid-accumulating and secretory macrophage-like cell phenotype, without changes in DNA damage. VSMC transdifferentiation in Neil3-deficient mice encompassed increased activity of the Akt signaling pathway, supported by cell experiments showing Akt-dependent proliferation in NEIL3-abrogated human primary aortic VSMCs. Conclusions: Our findings show that Neil3 deficiency promotes atherosclerosis development through non-canonical mechanisms affecting VSMC phenotype involving activation of the Akt signaling pathway.

The demographic shift toward an older population will increase the number of prostate cancer cases. A challenge in the treatment of prostate cancer is to avoid undertreatment of patients at high risk of progression following curative treatment. These men can benefit from early salvage treatment. An explorative cohort consisting of tissue from 16 patients who underwent radical prostatectomy, and were either alive or had died from prostate cancer within 10 years postsurgery, was analyzed by mass spectrometry analysis. Following proteomic and bioinformatic analyses, major vault protein (MVP) was identified as a putative prognostic biomarker. A publicly available tissue proteomics dataset and a retrospective cohort of 368 prostate cancer patients were used for validation. The prognostic value of the MVP was verified by scoring immunohistochemical staining of a tissue microarray. High level of MVP was associated with more than 4-fold higher risk for death from prostate cancer (hazard ratio = 4.41, 95% confidence interval: 1.45-13.38; P = 0.009) in a Cox proportional hazard models, adjusted for Cancer of the Prostate Risk Assessments Post-surgical (CAPRA-S) score and perineural invasion. Decision curve analyses suggested an improved standardized net benefit, ranging from 0.06 to 0.18, of adding MVP onto CAPRA-S score. This observation was confirmed by receiver operator characteristics curve analyses for the CAPRA-S score versus CAPRA-S and MVP score (area under the curve: 0.58 versus 0.73). From these analyses, one can infer that MVP levels in combination with CAPRA-S score might add onto established risk parameters to identify patients with lethal prostate cancer.

Background There is a need for validated clinical risk scores to identify patients at risk of severe disease and to guide decision-making during the covid-19 pandemic. The National Early Warning Score 2 (NEWS2) is widely used in emergency medicine, but so far, no studies have evaluated its use in patients with covid-19. We aimed to study the performance of NEWS2 and compare commonly used clinical risk stratification tools at admission to predict risk of severe disease and in-hospital mortality in patients with covid-19. Methods This was a prospective cohort study in a public non-university general hospital in the Oslo area, Norway, including a cohort of all 66 patients hospitalised with confirmed SARS-CoV-2 infection from the start of the pandemic; 13 who died during hospital stay and 53 who were discharged alive. Data were collected consecutively from March 9th to April 27th 2020. The main outcome was the ability of the NEWS2 score and other clinical risk scores at emergency department admission to predict severe disease and in-hospital mortality in covid-19 patients. We calculated sensitivity and specificity with 95% confidence intervals (CIs) for NEWS2 scores ≥5 and ≥ 6, quick Sequential Organ Failure Assessment (qSOFA) score ≥ 2, ≥2 Systemic Inflammatory Response Syndrome (SIRS) criteria, and CRB-65 score ≥ 2. Areas under the curve (AUCs) for the clinical risk scores were compared using DeLong’s test. Results In total, 66 patients (mean age 67.9 years) were included. Of these, 23% developed severe disease. In-hospital mortality was 20%. Tachypnoea, hypoxemia and confusion at admission were more common in patients developing severe disease. A NEWS2 score ≥ 6 at admission predicted severe disease with 80.0% sensitivity and 84.3% specificity (Area Under the Curve (AUC) 0.822, 95% CI 0.690–0.953). NEWS2 was superior to qSOFA score ≥ 2 (AUC 0.624, 95% CI 0.446–0.810, p < 0.05) and other clinical risk scores for this purpose. Conclusion NEWS2 score at hospital admission predicted severe disease and in-hospital mortality, and was superior to other widely used clinical risk scores in patients with covid-19.

A high intake of linoleic acid (LA), the major dietary polyunsaturated fatty acid (PUFA), has previously been associated with reduced cardiovascular (CV) morbidity and mortality in observational studies. However, recent secondary analyses from clinical trials of LA-rich diet suggest harmful effects of LA on CV health. A total of 3706 participants, all born in 1950, were included in this cross-sectional study. We investigated associations between plasma phospholipid levels of LA and CV risk factors in a Norwegian general population, characterized by a relative low LA and high marine n-3 PUFA intake. The main statistical approach was multivariable linear regression. Plasma phospholipid LA levels ranged from 11.4 to 32.0 wt%, with a median level of 20.8 wt% (interquartile range 16.8–24.8 wt%). High plasma LA levels were associated with lower serum low-density lipoprotein cholesterol levels (standardized regression coefficient [Std. β-coeff.] −0.04, p = 0.02), serum triglycerides (Std. β-coeff. −0.10, p < 0.001), fasting plasma glucose (Std. β-coeff. −0.10, p < 0.001), body mass index (Std. β-coeff. −0.13, p < 0.001), systolic and diastolic blood pressure (Std. β-coeff. −0.04, p = 0.03 and Std. β-coeff. −0.02, p = 0.02, respectively) and estimated glomerular filtration rate (Std. β-coeff. −0.09, p < 0.001). We found no association between plasma LA levels and high-density lipoprotein cholesterol levels, glycated hemoglobin, carotid intima-media thickness, or C-reactive protein. High plasma LA levels were favorably associated with several CV risk factors in this study of a Norwegian general population.