BEVITAL AS

Nutrition & Lifestyle

41 biomarkers of 5 different classes from 300μl sample volume on GC- and LC-MS/MS platforms. Contact our experts for any questions or inquiries.

Why did we design this panel?

We developed this targeted metabolomics panel for investigating nutritional status and lifestyle to accurately measure specific nutrients and metabolites, assess status and dietary intake, and understand metabolic responses to intervention. This supports nutrition focused research, and can be used for developing personalized dietary recommendations and lifestyle interventions, improving individual health outcomes and informing public health strategies. The panel supports:

Assessment of Nutritional Status: The panel measures specific vitamins and other nutrients, giving a picture of a person’s current nutritional state. This helps identify deficiencies or excesses that may not be apparent through diet assessment alone.
Personalized Dietary Recommendations: Based on the results, dietary and supplementation recommendations can be tailored to meet the individual’s unique needs, improving overall health and wellbeing.
Early Detection of Deficiencies: The panel can detect deficiencies before symptoms arise, allowing for timely interventions to prevent related health issues.
Monitoring and Managing Chronic Conditions: Many chronic diseases, such as diabetes, cardiovascular disease, and gastrointestinal disorders, are affected by nutrition. Longitudinal monitoring can guide dietary adjustments to better manage these conditions.
Supporting Immune Function: Nutrients like vitamins A, D, and E play a crucial role in immune health. The panel can identify imbalances that may impact immunity, helping prevent infections and improve resilience.

Applications: Aging and frailty, autoimmune diseases, bone health and osteoporosis, cancer prevention, cardiovascular diseases, digestive disorders, exercise and athletic performance, kidney disease, liver disease, mental health, nutrient deficiencies, obesity, pregnancy and prenatal health, type 2 diabetes and metabolic syndrome.

B-vitamins, functional markers, and methyl donors

17 markers by GC- and LC-MS/MS

Measuring B-vitamins, functional markers, and methyl donors is vital for assessing nutritional status and understanding their impact on health and disease. B-vitamins are essential for various metabolic functions, and their levels indicate potential deficiencies or excesses that can lead to adverse health outcomes. Functional markers like homocysteine reflect methylation status, crucial for regulating gene expression and metabolic processes. Dysregulation of methylation is linked to diseases such as cardiovascular conditions and neurological disorders. Methyl donors, including folate and choline, influence epigenetic regulation, affecting gene expression without altering DNA sequences. Imbalances in methyl donor levels can disrupt epigenetic signaling, contributing to disease development. Suboptimal levels of these biomarkers are associated with increased disease risk, making their measurement important for assessing overall health. Additionally, monitoring these biomarkers helps evaluate the effectiveness of treatments and nutritional interventions aimed at improving health outcomes. In short, measuring these biomarkers provides valuable insights into nutritional status, methylation processes, disease risk, and treatment effectiveness, facilitating proactive management of patient health.

Betaine, Choline, Cobalamin, Flavin mononucleotide, Folate, Methylmalonic acid, N1-methylnicotinamide, Nicotinamide, Nicotinic acid, Pyridoxal, 4-Pyridoxic acid, Pyridoxal 5-phosphate, Pyridoxine, Riboflavin, Thiamine, Thiamine monophosphate, Total homocysteine

Fat-soluble vitamins

4 markers by LC-MS/MS

Measuring fat-soluble vitamins (A, D, E, and K) is essential for assessing nutritional status, preventing diseases, and supporting immune function. These vitamins play crucial roles in various physiological functions, including vision, bone health, antioxidant defense, and blood clotting. Deficiencies in fat-soluble vitamins are linked to increased risks of conditions like vision impairment, osteoporosis, oxidative stress-related diseases, and bleeding disorders. Monitoring vitamin levels aids in disease prevention and management and informs therapeutic development. Additionally, fat-soluble vitamins modulate immune function and inflammation, with vitamin D and A being particularly important in immune regulation. Research on fat-soluble vitamins guides interventions to improve health outcomes and informs public health strategies such as food fortification programs. Overall, measuring fat-soluble vitamins is crucial for promoting optimal health and well-being and reducing the burden of deficiency-related diseases.

25-Hydroxy vitamin D2, 25-Hydroxy vitamin D3, α-Tocopherol (Vit. E), All-trans retinol (Vit. A), Phylloquinone (Vit. K1), y-Tocopherol (Vit. E)

Essential amino acids metabolites

9 markers by GC-MS/MS

Measuring essential amino acids (EAAs) is crucial for understanding protein synthesis, assessing nutritional status, and evaluating metabolic functions crucial for overall health. EAAs serve as building blocks for protein synthesis, impacting muscle health and tissue repair. Imbalances in EAAs can disrupt metabolic pathways, contributing to disease development, and monitoring the metabolites can help in assessment of disease risk and progression, and can guide dietary interventions to promote health. Additionally, EAAs play a role in sports nutrition, influencing muscle recovery and performance. Research on EAAs informs therapeutic development for conditions related to amino acid metabolism. In summary, measuring EAAs provides insights into nutritional adequacy, metabolic function, disease risk, and sports performance, aiding in proactive health management and intervention strategies.

Histidine, Isoleucine, Leucine, Lysine, Methionine, Phenylalanine, Threonine, Tryptophan, Valine

Meat & fish intake

4 markers by GC- and LC-MS/MS

3-Methylhistidine (3-MH) is formed by methylation of histidine as a posttranslational modification of actin and myosin. 3-MH is liberated during degradation of myofibrillar proteins, is not metabolized or used in proteosynthesis, but is excreted unchanged into the urine. 3-MH in plasma or urine may serve as a marker of muscle degradation, but also reflects dietary meat intake. Endogenous versus dietary 3-MH can be distinguished by simultaneous measurement of 1-Methylhistidine (1-MH), which is not formed in humans but occurs in skeletal muscle of several other species.
Choline, phosphatidylcholine and L-carnitine are cleaved by the gut microbiota to trimethylamine (TMA), which is oxidized to trimethylamine-N-oxide (TMAO) in the liver. TMAO seems to be proatherogenic in animal models and plasma levels are associated with risk of cardiovascular and other diseases in humans. Circulating TMAO increases during renal failure, and has been regarded as an uremic toxin. Many species of fish and seafood naturally contain high levels of TMAO, which serves as an osmolyte to protect against pressure and cold in aquatic environments. Consuming fish or seafood can lead to a significant but transient increase in circulating TMAO levels in humans.
β-Alanine is a naturally occurring beta-amino acid that is formed during degradation of carnosine and anserine, but also serves as a precursor for the synthesis of these histidine-containing dipeptides. This explains why beta-alanine may reflect the amount of carnosine/anserine in the body, and serves as a biomarker for the consumption of meat, especially red meat. β-Alanine is used as a supplement. High levels, as encountered in some inborn errors of metabolism causing hyper-beta-alaninemia, may act as a neurotoxin and as a mitochondrial toxin. Circulating levels is inversely associated with dementia.

Methylhistidine, 3-Methylhistidine, β-Alanine, Creatine, Creatinine, TMAO

Tobacco use & coffee intake

3 markers by LC-MS/MS

Cotinine is a stable metabolite of nicotine, and is the most widely used biomarker to measure tobacco use and exposure, i.e. both active and passive smoking. Serum cotinine has a half-life of 15 to 40 h and reflects tobacco exposure during the prior 3 to 5 days. The half-life of cotinine is longer than that of nicotine. Thus, the cotinine concentration is therefore rather stable throughout the day.
Trans-3′-hydroxycotinine (OHCot) is the main metabolite of cotinine with a half-life of 6.6 h. The metabolism of cotinine to OHCot is mediated by the enzyme cytochrome p450 2A6 (CYP2A6), encoded by the highly polymorphic CYP2A6 gene, with genotypes strongly associated with nicotine clearance and the nicotine metabolite ratio (NMR), defined as OHCot:cotinine. Other factors, including ethnicity, sex, hormones, smoking intensity, mentholated cigarettes, alcohol use, BMI, are weak predictors of NMR, and account for less than 8 % of NMR variation. Thus, NMR, OHCot/cotinine ratio, is a marker of CYP2A6 activity, and individuals can be categorized into “slow” versus “normal/fast metabolizers” based on their NMR value. The status of “slow metabolizer” has been associated with less nicotine dependence, lower smoking intensity, higher rates of smoking cessation and lower risk of lung cancer.
Trigonelline is a phytohormone particularly abundant in coffee beans, and is a marker of coffee consumption. Roasting of coffee beans partially converts trigonelline to nicotinic acid.

Cotinine, Trans-3-hydroxycotinine, Trigonelline

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Per Christian Eriksen

Øivind

Per Magne Ueland has been Professor at the University of Bergen 1987-2018. He is one of the founders of Bevital AS and the scientific advisor in Bevital since 2023. His interests includes biomarkers related to nutrition, inflammation, ageing and life-style related chronic diseases. Per is committed to the development of precise, high-throughput mass spectrometry methods, tailored for metabolic profiling of biobank specimens from large cohorts.

Marit holds a degree in chemical engineering from Bergen Ingeniørhøyskole, which is now part of the Western Norway University of Applied Sciences. She works with quantitative analysis and method development on LC-MS/MS at the laboratory of Bevital AS.

Ove completed a bachelor’s degree in Biomedical Laboratory Sciences at the Western Norway University of Applied Sciences in Bergen. With extensive experience in method development and expertise in GC-MS/MS, he specializes in optimizing analytical techniques for research-focused studies. At Bevital, Ove is dedicated to advancing laboratory methods and workflows, contributing to innovative research through precise and reliable analytical solutions.

Lene holds a bachelor’s degree in Biomedical Laboratory Science from the Western Norway University of Applied Sciences, where she is also completing her master’s degree in Medical Laboratory Technology. At Bevital, she works with GC-MS/MS analyses, focusing on accurate and reliable testing of biological samples. With her strong laboratory background, Lene is committed to delivering high-quality results that support medical research.

Klaus holds a PhD in physics from the University of Münster in Germany. He has over three decades of experience in Time-of-Flight mass spectrometry. He leverages his extensive expertise to provide customers with cutting-edge MALDI-MS analysis and the newest Olink Proteomics services.

Adrian holds a PhD in diabetes research, along with bachelor’s and master’s degrees in biomedical science and public health, respectively. With over 20 years of experience in laboratory science, he leads high-precision metabolite analyses and method development at Bevital. His expertise centers on quantifying biomarkers, metabolite classes, and metabolic pathways related to nutrition, cardiovascular and neurodegenerative diseases, and cancer. Adrian is committed to advancing research quality and actively collaborates nationally and internationally, leveraging targeted metabolomics to support innovative, multidisciplinary research.

Statistical power is the probability that a statistical test will correctly reject a false null hypothesis (H0​) when a specific alternative hypothesis (H1​) is true. H0​ is the null hypothesis, which states there is no effect or no difference. H1​ is the alternative hypothesis, which states there is a real effect or difference. Alpha (α) is the probability of a Type I error (a false positive), which is the risk of incorrectly rejecting the H0​ when it is actually true. You set this value before the experiment, commonly at 0.05. Beta (β) is the probability of a Type II error (a false negative), which is the risk of failing to reject the H0​ when it is actually false.

Power is calculated as 1−β. Increasing power means you are decreasing the probability of making a Type II error.

Several factors can be adjusted to increase the power of a statistical test:

  • Effect Size: This is the magnitude of the difference you are trying to detect. A larger effect size is easier to detect, thus increasing power. 

  • Sample Size: The number of observations in a study. A larger sample size provides more information about the population, reducing the margin of error and increasing the power to detect a true effect.

  • Variation: Refers to the spread or standard deviation of the data within the population. Less variation makes it easier to distinguish a real effect from random noise, thereby increasing power.

  • Alpha (): Increasing the alpha level (e.g., from 0.05 to 0.10) also increases power, but at the cost of a higher risk of a Type I error. This trade-off is often undesirable.

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541.

Refsum, H; Yajnik, C S; Gadkari, M; Schneede, J; Vollset, S E; Orning, L; Guttormsen, A B; Joglekar, A; Sayyad, M G; Ulvik, A; Ueland, P M

Hyperhomocysteinemia and elevated methylmalonic acid indicate a high prevalence of cobalamin deficiency in Asian Indians Journal Article

In: Am J Clin Nutr, vol. 74, no. 2, pp. 233–241, 2001, ISSN: 0002-9165.

Abstract | Links | BibTeX

542.

Vollset, S E; Refsum, H; Tverdal, A; Nygård, O; Nordrehaug, J E; Tell, G S; Ueland, P M

Plasma total homocysteine and cardiovascular and noncardiovascular mortality: the Hordaland Homocysteine Study Journal Article

In: Am J Clin Nutr, vol. 74, no. 1, pp. 130–136, 2001, ISSN: 0002-9165.

Abstract | Links | BibTeX

543.

Ulvik, A; Evensen, E T; Lien, E A; Hoff, G; Vollset, S E; Majak, B M; Ueland, P M

Smoking, folate and methylenetetrahydrofolate reductase status as interactive determinants of adenomatous and hyperplastic polyps of colorectum Journal Article

In: Am J Med Genet, vol. 101, no. 3, pp. 246–254, 2001, ISSN: 0148-7299.

Abstract | Links | BibTeX

544.

Chambers, J C; Ueland, P M; Wright, M; Doré, C J; Refsum, H; Kooner, J S

Investigation of relationship between reduced, oxidized, and protein-bound homocysteine and vascular endothelial function in healthy human subjects Journal Article

In: Circ Res, vol. 89, no. 2, pp. 187–192, 2001, ISSN: 1524-4571.

Abstract | Links | BibTeX

545.

Guttormsen, A B; Ueland, P M; Kruger, W D; Kim, C E; Ose, L; Følling, I; Refsum, H

Disposition of homocysteine in subjects heterozygous for homocystinuria due to cystathionine beta-synthase deficiency: relationship between genotype and phenotype Journal Article

In: Am J Med Genet, vol. 100, no. 3, pp. 204–213, 2001, ISSN: 0148-7299.

Abstract | Links | BibTeX

546.

El-Khairy, L; Ueland, P M; Refsum, H; Graham, I M; and, S E Vollset

Plasma total cysteine as a risk factor for vascular disease: The European Concerted Action Project Journal Article

In: Circulation, vol. 103, no. 21, pp. 2544–2549, 2001, ISSN: 1524-4539.

Abstract | Links | BibTeX

547.

Ueland, P M; Hustad, S; Schneede, J; Refsum, H; Vollset, S E

Biological and clinical implications of the MTHFR C677T polymorphism Journal Article

In: Trends Pharmacol Sci, vol. 22, no. 4, pp. 195–201, 2001, ISSN: 0165-6147.

Abstract | Links | BibTeX

548.

Nurk, E; Tell, G S; Nygård, O; Refsum, H; Ueland, P M; Vollset, S E

Plasma total homocysteine is influenced by prandial status in humans: the Hordaland Hhomocysteine Sstudy Journal Article

In: J Nutr, vol. 131, no. 4, pp. 1214–1216, 2001, ISSN: 0022-3166.

Abstract | Links | BibTeX

549.

Vollset, S E; Refsum, H; Ueland, P M

Population determinants of homocysteine Miscellaneous

2001, ISSN: 0002-9165.

Links | BibTeX

550.

Dekou, V; Whincup, P; Papacosta, O; Ebrahim, S; Lennon, L; Ueland, P M; Refsum, H; Humphries, S E; Gudnason, V

The effect of the C677T and A1298C polymorphisms in the methylenetetrahydrofolate reductase gene on homocysteine levels in elderly men and women from the British regional heart study Journal Article

In: Atherosclerosis, vol. 154, no. 3, pp. 659–666, 2001, ISSN: 0021-9150.

Abstract | Links | BibTeX

551.

Ueland, P M; Nygård, O; Vollset, S E; Refsum, H

The Hordaland Homocysteine Studies Journal Article

In: Lipids, vol. 36 Suppl, pp. S33–S39, 2001, ISSN: 0024-4201.

Abstract | Links | BibTeX

552.

Bolann, B J; Solli, J D; Schneede, J; Grøttum, K A; Loraas, A; Stokkeland, M; Stallemo, A; Schjøth, A; Bie, R B; Refsum, H; Ueland, P M

Evaluation of indicators of cobalamin deficiency defined as cobalamin-induced reduction in increased serum methylmalonic acid Journal Article

In: Clin Chem, vol. 46, no. 11, pp. 1744–1750, 2000, ISSN: 0009-9147.

Abstract | BibTeX

553.

Chambers, J C; Ueland, P M; Obeid, O A; Wrigley, J; Refsum, H; Kooner, J S

Improved vascular endothelial function after oral B vitamins: An effect mediated through reduced concentrations of free plasma homocysteine Journal Article

In: Circulation, vol. 102, no. 20, pp. 2479–2483, 2000, ISSN: 1524-4539.

Abstract | Links | BibTeX

554.

Louwman, M W; van Dusseldorp, M; van de Vijver, F J; Thomas, C M; Schneede, J; Ueland, P M; Refsum, H; van Staveren, W A

Signs of impaired cognitive function in adolescents with marginal cobalamin status Journal Article

In: Am J Clin Nutr, vol. 72, no. 3, pp. 762–769, 2000, ISSN: 0002-9165.

Abstract | Links | BibTeX

555.

Hustad, S; Ueland, P M; Vollset, S E; Zhang, Y; Bjørke-Monsen, A L; Schneede, J

Riboflavin as a determinant of plasma total homocysteine: effect modification by the methylenetetrahydrofolate reductase C677T polymorphism Journal Article

In: Clin Chem, vol. 46, no. 8 Pt 1, pp. 1065–1071, 2000, ISSN: 0009-9147.

Abstract | BibTeX

556.

Ueland, P M; Refsum, H; Beresford, S A; Vollset, S E

The controversy over homocysteine and cardiovascular risk Journal Article

In: Am J Clin Nutr, vol. 72, no. 2, pp. 324–332, 2000, ISSN: 0002-9165.

Abstract | Links | BibTeX

557.

Nexo, E; Engbaek, F; Ueland, P M; Westby, C; O'Gorman, P; Johnston, C; Kase, B F; Guttormsen, A B; Alfheim, I; McPartlin, J; Smith, D; Møller, J; Rasmussen, K; Clarke, R; Scott, J M; Refsum, H

Evaluation of novel assays in clinical chemistry: quantification of plasma total homocysteine Journal Article

In: Clin Chem, vol. 46, no. 8 Pt 1, pp. 1150–1156, 2000, ISSN: 0009-9147.

Abstract | BibTeX

558.

Mudd, S H; Finkelstein, J D; Refsum, H; Ueland, P M; Malinow, M R; Lentz, S R; Jacobsen, D W; Brattström, L; Wilcken, B; Wilcken, D E; Blom, H J; Stabler, S P; Allen, R H; Selhub, J; Rosenberg, I H

Homocysteine and its disulfide derivatives: a suggested consensus terminology Journal Article

In: Arterioscler Thromb Vasc Biol, vol. 20, no. 7, pp. 1704–1706, 2000, ISSN: 1079-5642.

Links | BibTeX

559.

Vollset, S E; Refsum, H; Irgens, L M; Emblem, B M; Tverdal, A; Gjessing, H K; Monsen, A L; Ueland, P M

Plasma total homocysteine, pregnancy complications, and adverse pregnancy outcomes: the Hordaland Homocysteine study Journal Article

In: Am J Clin Nutr, vol. 71, no. 4, pp. 962–968, 2000, ISSN: 0002-9165.

Abstract | Links | BibTeX

560.

Lien, E A; Nedrebø, B G; Varhaug, J E; Nygård, O; Aakvaag, A; Ueland, P M

Plasma total homocysteine levels during short-term iatrogenic hypothyroidism Journal Article

In: J Clin Endocrinol Metab, vol. 85, no. 3, pp. 1049–1053, 2000, ISSN: 0021-972X.

Abstract | Links | BibTeX

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