Co-Administration of Iron and a Bioavailable Curcumin Supplement Increases Serum BDNF Levels in Healthy Adults

Brain-derived neurotrophic factor (BDNF) is key for the maintenance of normal neuronal function and energy homeostasis and has been suggested to improve cognitive function, including learning and memory. Iron and the antioxidant curcumin have been shown to influence BDNF homeostasis. This 6-week, double blind, randomized, placebo-controlled study examined the effects of oral iron supplementation at low (18 mg) and high (65 mg) ferrous (FS) iron dosages, compared to a combination of these iron doses with a bioavailable formulated form of curcumin (HydroCurcTM; 500 mg) on BDNF levels in a healthy adult cohort of 155 male (26.42 years ± 0.55) and female (25.82 years ± 0.54) participants. Participants were randomly allocated to five different treatment groups: both iron and curcumin placebo (FS0+Plac), low dose iron and curcumin placebo (FS18+Plac), low dose iron and curcumin (FS18+Curc), high dose iron and curcumin placebo (FS65+Plac) and high dose iron and curcumin (FS65+Curc). Results showed a significant increase in BDNF over time (26%) in the FS18+Curc group (p = 0.024), and at end-point between FS18+Curc and FS18+Plac groups (35%, p = 0.042), demonstrating for the first time that the combination with curcumin, rather than iron supplementation alone, results in increased serum BDNF. The addition of curcumin to iron supplementation may therefore provide a novel approach to further enhance the benefits associated with increased BDNF levels

Co-Administration of Iron and Bioavailable Curcumin Reduces Levels of Systemic Markers of Inflammation and Oxidative Stress in a Placebo-Controlled Randomised Study

Ferrous sulphate (FS) is widely used as an iron supplement to treat iron deficiency (ID), but is known to induce inflammation causing gastric side-effects resulting in poor adherence to supplement regimens. Curcumin, a potent antioxidant, has been reported to suppress inflammation via down regulation of NF-κB. The aim of the present double blind, placebo-controlled randomised trial was to assess whether co-administration of FS with a formulated, bioavailable form of curcumin (HydroCurc™) could reduce systemic inflammation and/or gastrointestinal side-effects. This study recruited 155 healthy participants (79 males; 26.42 years ± 0.55 and 76 females; 25.82 years ± 0.54), randomly allocated to one of five different treatment groups: iron and curcumin placebo (FS0_Plac), low dose (18 mg) iron and curcumin placebo (FS18_Plac), low dose iron and curcumin (FS18_Curc), high dose (65 mg) iron and curcumin placebo (FS65_Plac), and high dose iron and curcumin (FS65_Curc). Completed questionnaires and blood samples were collected from all participants at baseline (day 1), mid-point (day 21), and at end-point (day 42). Results showed a significant reduction in IL-6 in the FS65_Curc group (0.06 pg/mL ± 0.02, p = 0.0073) between the mid-point and end-point. There was also a significant reduction in mean plasma TNF levels in the FS65_Curc (0.65 pg/mL ± 0.17, p = 0.0018), FS65_Plac (0.39 pg/mL ± 0.15, p = 0.0363), and FS18_Curc (0.35 pg/mL ± 0.13, p = 0.0288) groups from mid-point to end-point. A significant increase was observed in mean plasma TBARS levels (0.10 µM ± 0.04, p = 0.0283) in the F18_Plac group from baseline to end-point. There was a significant association with darker stools between FS0_Plac vs. FS65_Plac (p = 0.002, Fisher’s exact test) suggesting that high iron dose in the absence of curcumin leads to darker stools. A reduction in inflammation-related markers in response to co-administering supplemental iron alongside formulated curcumin suggests a reduction in systemic inflammation. This supplementation approach may therefore be a more cost effective and convenient alternative to current oral iron-related treatments, with further research to be conducted

Rational Management of Iron-Deficiency Anaemia in Inflammatory Bowel Disease

Anaemia is the most frequent, though often neglected, comorbidity of inflammatory bowel disease (IBD). Here we want to briefly present (1) the burden of anaemia in IBD, (2) its pathophysiology, which mostly arises from bleeding-associated iron deficiency, followed by (3) diagnostic evaluation of anaemia, (4) a balanced overview of the different modes of iron replacement therapy, (5) evidence for their therapeutic efficacy and subsequently, (6) an updated recommendation for the practical management of anaemia in IBD. Following the introduction of various intravenous iron preparations over the last decade, questions persist about when to use these preparations as opposed to traditional and other novel oral iron therapeutic agents. At present, oral iron therapy is generally preferred for patients with quiescent IBD and mild iron-deficiency anaemia. However, in patients with flaring IBD that hampers intestinal iron absorption and in those with inadequate responses to or side effects with oral preparations, intravenous iron supplementation is the therapy of choice, although information on the efficacy of intravenous iron in patients with active IBD and anaemia is scare. Importantly, anaemia in IBD is often multifactorial and a careful diagnostic workup is mandatory for optimized treatment. Nevertheless, limited information is available on optimal therapeutic start and end points for treatment of anaemia. Of note, neither oral nor intravenous therapies seem to exacerbate the clinical course of IBD. However, additional prospective studies are still warranted to determine the optimal therapy in complex conditions such as IBD

Toksiske og essensielle metaller, status hos gatenarkomane

Bakgrunn og mål: Gatenarkomane har en komplisert livssituasjon, blant annet med mange utfordringer tilknyttet helse og ernæring. Høy risiko for infeksjoner og et mangelfullt og ensidig kosthold gjør dem svært utsatt for sykdom. I hvilken grad status av toksiske og essensielle metaller kan bidra til en forverret helsetilstand hos gatenarkomane har hittil vært uklart. Hensikten med denne oppgaven var derfor å beskrive forekomst av toksiske og essensielle metaller hos gatenarkomane, sammenligne denne med en referansegruppe som representerer normalpopulasjonen i Norge, i tillegg til referanse – og grenseverdier der det finnes. Utvalg og metode: Materialet til denne oppgaven ble samlet inn i forbindelse med en studie gjort på gatenarkomane i Oslo i tidsrommet november 2001 til april 2003. Datainnsamlingen besto i antropometriske målinger, intervju, 24 timers kostholdsundersøkelse, samt blod- og hårprøver. Hos 85 gatenarkomane ble det foretatt komplette blodanalyser av toksiske og essensielle metaller. I tillegg ble det utført håranalyser på 19 respondenter for de metallene der også hår er en god biomarkør. Det ble deretter utført statistiske beregninger på tallmaterialet. Resultater: Blodkonsentrasjonen av de toksiske metallene bly, kvikksølv og arsen og de essensielle metallene sink, selen og jern viste seg å være signifikant lavere hos gatenarkomane sammenlignet med referansegruppen, mens mangan var signifikant høyere. Konklusjon : Ved å sammenligne matinntak hos gatenarkomane med referansegruppen og NORKOST 3, ses det et lavere inntak hos gatenarkomane for de fleste matvaregrupper. Det er sannsynlig at dette ligger til grunn for de tilfellene der gatenarkomane har lavere status av toksiske og essensielle metaller enn referansegruppen. Det er også rimelig å anta at høyere mangankonsentrasjonen skyldes de lave nivåene av serum ferritin. Den største trusselen mot gatenarkomanes helse som ble funnet i disse resultatene er sannsynligvis lave konsentrasjoner av de essensielle metallene sink, selen og jern. Mangel på disse metallene gjør en allerede sårbar gruppe, med høy infeksjonsrisiko, ytterligere utsatt for sykdom. Det er mye usikkerhet rundt helserisikoen forbundet med funnene av toksiske metaller hos gatenarkomane, og selv med lavere konsentrasjoner enn referansegruppen kan ikke skadelige helseeffekter utelukkes. Likevel forteller dette sannsynligvis mest om et generelt dårlig kosthold og en dårlig ernæringsstatus blant de gatenarkomaneMaster i samfunnsernærin

Serum carbohydrate deficient transferrin as a marker for alcohol abuse

Aim: To examine serum carbohydrate-deficient transferrin (CDT) as a marker of alcohol abuse and to determine possible reasons for false positive and false negative results. Background: Alcohol misuse constitutes a major problem for medical and social agencies world-wide. Early detection and meticulous monitoring of drinking behaviour in individuals, once identified, remain the mainstays of effective management. Objective markers are required to facilitate this process. Serum CDT has been proposed for this purpose but the performance of the available commercial kits appears to fall short of the more sophisticated HPLC techniques used for research purposes. Methods: Two commercial assays, CDTect (Pharmacia & Upjohn, Sweden) and AXIS %CDT (AXIS Biochemicals ASA, Norway), were used. Results: In a study population of 590 individuals with well-documented and widely divergent drinking behaviour the sensitivity/specificity of serum CDT was 47.9% and 78.4% (CDTect) and 47.9% and 90.3% (AXIS %CDT). The false positive rates in patients with non-alcoholic liver disease, 26.4% (CDTect) and 7.7% (AXIS %CDT), and the false positive and false negative rates in alcohol misusers, 33.6 / 52.1% (CDTect) and 25.5 / 52.1% (AXIS %CDT) were unacceptably high. An additional 363 individuals were studied with similar results. Monitoring performance was assessed in 40 alcohol misusers followed serially from detoxification over 6 months. Poor assay performance could not be attributed to chronic inflammation or iron status. There was evidence that some false positive results reflected changes in the transferrin isoform profile on HPLC which differed from changes associated with alcohol misuse. Conclusion: CDT was unsatisfactory using commercial kits and when used alone. In combination with other laboratory markers of alcohol misuse improved overall performance for both screening and monitoring. Further developments are needed in order to maximise the performance of the commercial techniques for assaying serum CDT