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BETA
Jernerén, Fredrik
Alternative names
Publications (10 of 18) Show all publications
Elshorbagy, A., Jernerén, F., Basta, M., Basta, C., Turner, C., Khaled, M. & Refsum, H. (2017). Amino acid changes during transition to a vegan diet supplemented with fish in healthy humans.. European Journal of Nutrition, 56(5), 1953-1962
Open this publication in new window or tab >>Amino acid changes during transition to a vegan diet supplemented with fish in healthy humans.
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2017 (English)In: European Journal of Nutrition, ISSN 1436-6207, E-ISSN 1436-6215, Vol. 56, no 5, p. 1953-1962Article in journal (Refereed) Published
Abstract [en]

PURPOSE: To explore whether changes in dietary protein sources can lower plasma branched-chain amino acids (BCAAs), aromatic amino acids and sulfur amino acids (SAAs) that are often elevated in the obese, insulin-resistant state and in type 2 diabetes.

METHODS: Thirty-six subjects (mean age 31 ± 2 years) underwent a voluntary abstinence from meat, poultry, eggs, and dairy products for 6 weeks, while enriching the diet with fish, in fulfillment of a religious fast. Subjects were assessed 1 week before the fast (V1), 1 week after initiation of the fast (V2) and in the last week of the fast (V3). Thirty-four subjects completed all three visits.

RESULTS: Fasting plasma BCAAs decreased at V2 and remained low at V3 (P < 0.001 for all). Valine showed the greatest decline, by 20 and 19 % at V2 and V3, respectively. Phenylalanine and tryptophan, but not tyrosine, also decreased at V2 and V3. The two proteinogenic SAAs, methionine and cysteine, remained stable, but the cysteine product, taurine, decreased from 92 ± 7 μmol/L to 66 ± 6 (V2; P = 0.003) and 65 ± 6 μmol/L (V3; P = 0.003). A progressive decline in plasma glutamic acid, coupled with an increase in glutamine, was observed. Plasma total and LDL cholesterol decreased at V2 and V3 (P < 0.001 for all).

CONCLUSION: Changing dietary protein sources to plant- and fish-based sources in an ad libitum setting lowers the plasma BCAAs that have been linked to diabetes risk. These findings point to habitual diet as a potentially modifiable determinant of fasting plasma BCAA concentrations.

Keyword
Body mass index, Branched-chain amino acids, Egyptian Orthodox Christians, Lean mass, Mass spectrometry, Sulfur amino acids
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-343226 (URN)10.1007/s00394-016-1237-6 (DOI)27289540 (PubMedID)
Available from: 2018-02-26 Created: 2018-02-26 Last updated: 2018-02-26
Haj-Yasein, N. N., Berg, O., Jernerén, F., Refsum, H., Nebb, H. I. & Dalen, K. T. (2017). Cysteine deprivation prevents induction of peroxisome proliferator-activated receptor gamma-2 and adipose differentiation of 3T3-L1 cells.. Biochimica et Biophysica Acta, 1862(6), 623-635, Article ID S1388-1981(17)30033-1.
Open this publication in new window or tab >>Cysteine deprivation prevents induction of peroxisome proliferator-activated receptor gamma-2 and adipose differentiation of 3T3-L1 cells.
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2017 (English)In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1862, no 6, p. 623-635, article id S1388-1981(17)30033-1Article in journal (Refereed) Published
Abstract [en]

Plasma cysteine is strongly associated with body fat mass in human cohorts and diets low in cysteine prevents fat accumulation in mice. It is unclear if plasma cysteine affects fat development or if fat accumulation raises plasma cysteine. To determine if cysteine affects adipogenesis, we differentiated 3T3-L1 preadipocytes in medium with reduced cysteine. Cells incubated in media with 10-20μM cysteine exhibited reduced capacity to differentiate into triacylglycerol-storing mature adipocytes compared with cells incubated with 50μM cysteine. Low cysteine severely reduced expression of peroxisome proliferator-activated receptor gamma2 (Pparγ2) and its target genes perlipin1 (Plin1) and fatty acid binding protein-4 (Fabp4). Expression of stearoyl-CoA desaturase-1 (Scd1), known to be repressed with cysteine depletion, was also reduced with low cysteine. Medium depletion of the essential amino acids leucine, valine, and isoleucine had only a modest effect on adipocyte specific gene expression and differentiation. Stimulation with the PPARγ agonist BRL-49653 or addition of a hydrogen sulfide donor enhanced differentiation of 3T3-L1 cells cultured in low cysteine. This demonstrates that the ability to induce PPARγ expression is preserved when cells are cultured in low cysteine. It therefore appears that cysteine depletion inhibits adipogenesis by specifically affecting molecular pathways required for induction of PPARγ expression, rather than through a general reduction of global protein synthesis. In conclusion, we show that low extracellular cysteine reduces adipocyte differentiation by interfering with PPARγ2 and PPARγ target gene expression. Our results provide further evidence for the hypothesis that plasma cysteine is a casual determinant for body fat mass.

Keyword
3T3-L1 cells, Adipocytes, Cysteine, Differentiation, Obesity, Peroxisome proliferator-activated receptor gamma
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-343217 (URN)10.1016/j.bbalip.2017.02.009 (DOI)28219719 (PubMedID)
Available from: 2018-02-26 Created: 2018-02-26 Last updated: 2018-02-26
Farina, N., Jernerén, F., Turner, C., Hart, K. & Tabet, N. (2017). Homocysteine concentrations in the cognitive progression of Alzheimer's disease. Experimental Gerontology, 99, 146-150
Open this publication in new window or tab >>Homocysteine concentrations in the cognitive progression of Alzheimer's disease
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2017 (English)In: Experimental Gerontology, ISSN 0531-5565, E-ISSN 1873-6815, Vol. 99, p. 146-150Article in journal (Refereed) Published
Abstract [en]

Objectives: Hyperhomocysteinemia in Alzheimer's disease (AD) is widely reported and appears to worsen as the disease progresses. While active dietary intervention with vitamins B12 and folate decreases homocysteine blood levels, with promising clinical outcomes in Mild Cognitive Impairment (MCI), this so far has not been replicated in established AD populations. The aim of the study is to explore the relationship between hyperhomocystenemia and relevant vitamins as the disease progresses. Methods: In this longitudinal cohort study, 38 participants with mild to moderate AD were followed for an average period of 13 months. Plasma folate, vitamin B12 and homocysteine concentrations were measured at baseline and at follow-up. Dietary intake of B vitamins was also measured. Spearman's correlations were conducted by homocysteine and B vitamin status. Results: As expected, cognitive status significantly declined over the follow-up period and this was paralleled by a significant increase in homocysteine concentrations (p = 0.006). However, during this follow-up period there was no significant decline in neither dietary intake, nor the corresponding blood concentrations of vitamin B12/folate, with both remaining within normal values. Changes in blood concentrations of B vitamins were not associated with changes in homocysteine levels (p > 0.05). Conclusion: In this study, the increase in homocysteine observed in AD patients as the disease progresses cannot be solely explained by dietary and blood levels of folate and vitamin B12. Other dietary and non-dietary factors may contribute to hyperhomocysteinemia and its toxic effect in AD, which needs to be explored to optimise timely intervention strategies.

Place, publisher, year, edition, pages
PERGAMON-ELSEVIER SCIENCE LTD, 2017
Keyword
Homocysteine, B vitamins, Alzheimer's disease, Cognition
National Category
Geriatrics
Identifiers
urn:nbn:se:uu:diva-343562 (URN)10.1016/j.exger.2017.10.008 (DOI)000415591300019 ()29024723 (PubMedID)
Available from: 2018-03-02 Created: 2018-03-02 Last updated: 2018-03-02Bibliographically approved
Chen, Y., Jernerén, F. & Oliw, E. (2017). Purification and site-directed mutagenesis of linoleate 9S-dioxygenase-allene oxide synthase of Fusarium oxysporum confirms the oxygenation mechanism. Archives of Biochemistry and Biophysics, 625-626, 24-29
Open this publication in new window or tab >>Purification and site-directed mutagenesis of linoleate 9S-dioxygenase-allene oxide synthase of Fusarium oxysporum confirms the oxygenation mechanism
2017 (English)In: Archives of Biochemistry and Biophysics, ISSN 0003-9861, E-ISSN 1096-0384, Vol. 625-626, p. 24-29Article in journal (Refereed) Published
Abstract [en]

Plants and fungi form jasmonic acid from a-linolenic acid. The first two steps of biosynthesis in plants occur by sequential transformation by 13S-Iipoxygenase and allene oxide synthase (AOS). The biosynthesis in fungi may follow this classical scheme, but the only fungal AOS discovered so far are cytochromes P450 (CYP) fused to 8- and 9-dioxygenases (DOX). In the present report, we purified recombinant 9S-DOX-AOS of Fusarium oxysporum from cell lysate by cobalt affinity chromatography to near homogeneity and studied key residues by site-directed mutagenesis. Sequence homology with 8R-DOX-linoleate diol synthases (8R-DOX-LDS) suggested that Tyr414 catalyzes hydrogen abstraction and that Cys1051 forms the heme thiolate ligand. Site-directed mutagenesis (Tyr414Phe; Cys1051Ser) led to loss of 9S-DOX and 9S-AOS activities, respectively, but other important residues in the CYP parts of 5,8 and 7,8-LDS or 9R-AOS were not conserved. The UV-visible spectrum of 9S-DOX-AOS showed a Soret band at 409 nm, which shifted to 413 nm in the Cys1051Ser mutant. The 9S-AOS of the Tyr414Phe mutant transformed 9S-hydroperoxides of alpha-linolenic and linoleic acids to allene oxides/alpha-ketols, but it did not transform 13-hydroperoxides. We conclude that 9S- and 8R-DOX catalyze hydrogen abstraction at C-11 and C-8, respectively, by homologous Tyr residues.

Place, publisher, year, edition, pages
ELSEVIER SCIENCE INC, 2017
Keyword
Cobalt affinity chromatography, Cyclooxygenase, Fusion enzymes, Jasmonic acid, Site-directed mutagenesis, Liquid chromatography-mass spectrometry
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-328970 (URN)10.1016/j.abb.2017.05.007 (DOI)000404318700004 ()28502466 (PubMedID)
Funder
Swedish Research Council, 03X-06523Knut and Alice Wallenberg Foundation, KAW 2004.123
Available from: 2017-09-12 Created: 2017-09-12 Last updated: 2017-09-12Bibliographically approved
Pierozan, P., Jernerén, F., Ransome, Y. & Karlsson, O. (2017). The Choice of Euthanasia Method Affects Metabolic Serum Biomarkers. Basic & Clinical Pharmacology & Toxicology, 21, 113-118
Open this publication in new window or tab >>The Choice of Euthanasia Method Affects Metabolic Serum Biomarkers
2017 (English)In: Basic & Clinical Pharmacology & Toxicology, ISSN 1742-7835, E-ISSN 1742-7843, Vol. 21, p. 113-118Article in journal (Refereed) Published
Abstract [en]

The impact of euthanasia methods on endocrine and metabolic parameters in rodent tissues and biological fluids is highly relevant for the accuracy and reliability of the data collected. However, few studies concerning this issue are found in the literature. We compared the effects of three euthanasia methods currently used in animal experimentation (i.e. decapitation, CO2 inhalation and pentobarbital injection) on the serum levels of corticosterone, insulin, glucose, triglycerides, cholesterol and a range of free fatty acids in rats. The corticosterone and insulin levels were not significantly affected by the euthanasia protocol used. However, euthanasia by an overdose of pentobarbital (120 mg/kg intraperitoneal injection) increased the serum levels of glucose, and decreased cholesterol, stearic and arachidonic acids levels compared with euthanasia by CO2 inhalation and decapitation. CO2 inhalation appears to increase the serum levels of triglycerides, while euthanasia by decapitation induced no individual discrepant biomarker level. We conclude that choice of the euthanasia methods is critical for the reliability of serum biomarkers and indicate the importance of selecting adequate euthanasia methods for metabolic analysis in rodents. Decapitation without anaesthesia may be the most adequate method of euthanasia when taking both animal welfare and data quality in consideration.

National Category
Pharmacology and Toxicology Other Basic Medicine
Identifiers
urn:nbn:se:uu:diva-321814 (URN)10.1111/bcpt.12774 (DOI)000404863600005 ()28244216 (PubMedID)
Funder
Carl Tryggers foundation
Available from: 2017-05-11 Created: 2017-05-11 Last updated: 2018-01-13Bibliographically approved
Elshorbagy, A. K., Jernerén, F., Scudamore, C. L., McMurray, F., Cater, H., Hough, T., . . . Refsum, H. (2016). Exploring the Lean Phenotype of Glutathione-Depleted Mice: Thiol, Amino Acid and Fatty Acid Profiles.. PLoS ONE, 11(10), Article ID e0163214.
Open this publication in new window or tab >>Exploring the Lean Phenotype of Glutathione-Depleted Mice: Thiol, Amino Acid and Fatty Acid Profiles.
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2016 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 11, no 10, article id e0163214Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Although reduced glutathione (rGSH) is decreased in obese mice and humans, block of GSH synthesis by buthionine sulfoximine (BSO) results in a lean, insulin-sensitive phenotype. Data is lacking about the effect of BSO on GSH precursors, cysteine and glutamate. Plasma total cysteine (tCys) is positively associated with stearoyl-coenzyme A desaturase (SCD) activity and adiposity in humans and animal models.

OBJECTIVE: To explore the phenotype, amino acid and fatty acid profiles in BSO-treated mice.

DESIGN: Male C3H/HeH mice aged 11 weeks were fed a high-fat diet with or without BSO in drinking water (30 mmol/L) for 8 weeks. Amino acid and fatty acid changes were assessed, as well as food consumption, energy expenditure, locomotor activity, body composition and liver vacuolation (steatosis).

RESULTS: Despite higher food intake, BSO decreased particularly fat mass but also lean mass (both P<0.001), and prevented fatty liver vacuolation. Physical activity increased during the dark phase. BSO decreased plasma free fatty acids and enhanced insulin sensitivity. BSO did not alter liver rGSH, but decreased plasma total GSH (tGSH) and rGSH (by ~70%), and liver tGSH (by 82%). Glutamate accumulated in plasma and liver. Urine excretion of cysteine and its precursors was increased by BSO. tCys, rCys and cystine decreased in plasma (by 23-45%, P<0.001 for all), but were maintained in liver, at the expense of decreased taurine. Free and total plasma concentrations of the SCD products, oleic and palmitoleic acids were decreased (by 27-38%, P <0.001 for all).

CONCLUSION: Counterintuitively, block of GSH synthesis decreases circulating tCys, raising the question of whether the BSO-induced obesity-resistance is linked to cysteine depletion. Cysteine-supplementation of BSO-treated mice is warranted to dissect the effects of cysteine and GSH depletion on energy metabolism.

National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-343224 (URN)10.1371/journal.pone.0163214 (DOI)27788147 (PubMedID)
Available from: 2018-02-26 Created: 2018-02-26 Last updated: 2018-02-26
Zhang, W., Jernerén, F., Lehne, B. C., Chen, M.-H., Luben, R. N., Johnston, C., . . . Kooner, J. S. (2016). Genome-wide association reveals that common genetic variation in the kallikrein-kinin system is associated with serum L-arginine levels.. Thrombosis and haemostasis, 116(6), 1041-1049
Open this publication in new window or tab >>Genome-wide association reveals that common genetic variation in the kallikrein-kinin system is associated with serum L-arginine levels.
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2016 (English)In: Thrombosis and haemostasis, ISSN 2567-689X, Vol. 116, no 6, p. 1041-1049Article in journal (Refereed) Published
Abstract [en]

). Together these two loci explain 7 % of the total variance in serum L-arginine concentrations. The associations at both loci were replicated in independent cohorts with plasma L-arginine measurements (p<0.004). The two sentinel SNPs are in nearly complete LD with the nonsynonymous SNP rs3733402 at KLKB1 and the 5'-UTR SNP rs1801020 at F12, respectively. SNPs at both loci are associated with blood pressure. Our findings provide new insight into the genetic regulation of L-arginine and its potential relationship with cardiovascular risk.

Keyword
Serum L-arginine concentration, coagulation, genome-wide association, kallikrein-kinin system
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-343225 (URN)10.1160/TH16-02-0151 (DOI)27656708 (PubMedID)
Available from: 2018-02-26 Created: 2018-02-26 Last updated: 2018-02-26
Oulhaj, A., Jernerén, F., Refsum, H., Smith, A. D. & de Jager, C. A. (2016). Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment.. Journal of Alzheimer's Disease, 50(2), 547-57
Open this publication in new window or tab >>Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment.
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2016 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 50, no 2, p. 547-57Article in journal (Refereed) Published
Abstract [en]

A randomized trial (VITACOG) in people with mild cognitive impairment (MCI) found that B vitamin treatment to lower homocysteine slowed the rate of cognitive and clinical decline. We have used data from this trial to see whether baseline omega-3 fatty acid status interacts with the effects of B vitamin treatment. 266 participants with MCI aged ≥70 years were randomized to B vitamins (folic acid, vitamins B6 and B12) or placebo for 2 years. Baseline cognitive test performance, clinical dementia rating (CDR) scale, and plasma concentrations of total homocysteine, total docosahexaenoic and eicosapentaenoic acids (omega-3 fatty acids) were measured. Final scores for verbal delayed recall, global cognition, and CDR sum-of-boxes were better in the B vitamin-treated group according to increasing baseline concentrations of omega-3 fatty acids, whereas scores in the placebo group were similar across these concentrations. Among those with good omega-3 status, 33% of those on B vitamin treatment had global CDR scores >0 compared with 59% among those on placebo. For all three outcome measures, higher concentrations of docosahexaenoic acid alone significantly enhanced the cognitive effects of B vitamins, while eicosapentaenoic acid appeared less effective. When omega-3 fatty acid concentrations are low, B vitamin treatment has no effect on cognitive decline in MCI, but when omega-3 levels are in the upper normal range, B vitamins interact to slow cognitive decline. A clinical trial of B vitamins combined with omega-3 fatty acids is needed to see whether it is possible to slow the conversion from MCI to AD.

Keyword
Alzheimer’s disease, B vitamins, clinical dementia rating scale, cognition, omega–3 fatty acids
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-343228 (URN)10.3233/JAD-150777 (DOI)26757190 (PubMedID)
Available from: 2018-02-26 Created: 2018-02-26 Last updated: 2018-02-26
Elshorbagy, A. K., Jernerén, F., Samocha-Bonet, D., Refsum, H. & Heilbronn, L. K. (2016). Serum S-adenosylmethionine, but not methionine, increases in response to overfeeding in humans.. Nutrition & Diabetes, 6, Article ID e192.
Open this publication in new window or tab >>Serum S-adenosylmethionine, but not methionine, increases in response to overfeeding in humans.
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2016 (English)In: Nutrition & Diabetes, ISSN 2044-4052, E-ISSN 2044-4052, Vol. 6, article id e192Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Plasma concentration of the methyl donor S-adenosylmethionine (SAM) is linearly associated with body mass index (BMI) and fat mass. As SAM is a high-energy compound and a sensor of cellular nutrient status, we hypothesized that SAM would increase with overfeeding.

METHODS: Forty normal to overweight men and women were overfed by 1250 kcal per day for 28 days.

RESULTS: Serum SAM increased from 106 to 130 nmol/l (P=0.006). In stratified analysis, only those with weight gain above the median (high-weight gainers; average weight gain 3.9±0.3 kg) had increased SAM (+42%, P=0.001), whereas low-weight gainers (weight gain 1.5±0.2 kg) did not (Pinteraction=0.018). Overfeeding did not alter serum concentrations of the SAM precursor, methionine or the products, S-adenosyl-homocysteine and homocysteine. The SAM/SAH (S-adenosylhomocysteine) ratio was unchanged in the total population, but increased in high-weight gainers (+52%, P=0.006, Pinteraction =0.005). Change in SAM correlated positively with change in weight (r=0.33, P=0.041) and fat mass (r=0.44, P=0.009), but not with change in protein intake or plasma methionine, glucose, insulin or low-density lipoprotein (LDL)-cholesterol.

CONCLUSION: Overfeeding raised serum SAM in proportion to the fat mass gained. The increase in SAM may help stabilize methionine levels, and denotes a responsiveness of SAM to nutrient state in humans. The role of SAM in human energy metabolism deserves further attention.

National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-343227 (URN)10.1038/nutd.2015.44 (DOI)26807510 (PubMedID)
Available from: 2018-02-26 Created: 2018-02-26 Last updated: 2018-02-26
Jernerén, F., Elshorbagy, A. K., Oulhaj, A., Smith, S. M., Refsum, H. & Smith, A. D. (2015). Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial.. American Journal of Clinical Nutrition, 102(1), 215-21
Open this publication in new window or tab >>Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial.
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2015 (English)In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 102, no 1, p. 215-21Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Increased brain atrophy rates are common in older people with cognitive impairment, particularly in those who eventually convert to Alzheimer disease. Plasma concentrations of omega-3 (ω-3) fatty acids and homocysteine are associated with the development of brain atrophy and dementia.

OBJECTIVE: We investigated whether plasma ω-3 fatty acid concentrations (eicosapentaenoic acid and docosahexaenoic acid) modify the treatment effect of homocysteine-lowering B vitamins on brain atrophy rates in a placebo-controlled trial (VITACOG).

DESIGN: This retrospective analysis included 168 elderly people (≥70 y) with mild cognitive impairment, randomly assigned either to placebo (n = 83) or to daily high-dose B vitamin supplementation (folic acid, 0.8 mg; vitamin B-6, 20 mg; vitamin B-12, 0.5 mg) (n = 85). The subjects underwent cranial magnetic resonance imaging scans at baseline and 2 y later. The effect of the intervention was analyzed according to tertiles of baseline ω-3 fatty acid concentrations.

RESULTS: There was a significant interaction (P = 0.024) between B vitamin treatment and plasma combined ω-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid) on brain atrophy rates. In subjects with high baseline ω-3 fatty acids (>590 μmol/L), B vitamin treatment slowed the mean atrophy rate by 40.0% compared with placebo (P = 0.023). B vitamin treatment had no significant effect on the rate of atrophy among subjects with low baseline ω-3 fatty acids (<390 μmol/L). High baseline ω-3 fatty acids were associated with a slower rate of brain atrophy in the B vitamin group but not in the placebo group.

CONCLUSIONS: The beneficial effect of B vitamin treatment on brain atrophy was observed only in subjects with high plasma ω-3 fatty acids. It is also suggested that the beneficial effect of ω-3 fatty acids on brain atrophy may be confined to subjects with good B vitamin status. The results highlight the importance of identifying subgroups likely to benefit in clinical trials. This trial was registered at www.controlled-trials.com as ISRCTN94410159.

Keyword
B vitamin, brain atrophy, homocysteine, mild cognitive impairment, ω-3
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-343229 (URN)10.3945/ajcn.114.103283 (DOI)25877495 (PubMedID)
Available from: 2018-02-26 Created: 2018-02-26 Last updated: 2018-02-26
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