Effect of anti-inflammatory diets on inflammation markers in adult human populations: a systematic review of randomized controlled trials.

CONTEXT: Chronic inflammation, characterized by prolonged elevated inflammation markers, is linked to several chronic conditions. Diet can influence the levels of inflammation markers in the body. OBJECTIVE: The aim of this systematic review was to assess the effects of anti-inflammatory diets on 14 different inflammation markers in adults. DATA SOURCES: This systematic review conducted searches using Medline, PubMed, EMCare, Cochrane, and CINAHL, to locate randomized controlled trials (RCTs). DATA EXTRACTION: Two researchers independently screened 1537 RCTs that measured changes in inflammation markers after prescription of an intervention diet. DATA ANALYSIS: In total, 20 RCTs were included and assessed qualitatively. The results demonstrated that a Mediterranean diet can bring about statistically significant and clinically meaningful between-group differences in interleukins -1α, -1ß, -4, -5, -6, -7, -8, -10, and -18, interferon γ, tumor necrosis factor α, C-reactive protein, and high-sensitivity C-reactive protein, as compared with a control diet. CONCLUSIONS: There may be a link between diet, inflammation markers, and disease outcomes in various adult populations. However, further research using consistent RCT protocols is required to determine correlations between diet, specific inflammation markers, and clinically relevant outcomes.

Validation of a Short Food Frequency Questionnaire to Measure Dietary Intake of a Selection of Micronutrients in Oncology Patients Undergoing Systemic Therapy.

Dietary intake, specifically consumption of anti-inflammatory micronutrients, can play a role in both cancer initiation as well as the treatment-related outcomes experienced by patients receiving systemic cancer therapy. Increasing research is being conducted to determine whether micronutrient supplementation can aid in altering the tumor microenvironment (TME), reducing inflammatory side effects and immune-related adverse events (irAEs). However, further research pertaining to the adequacy of dietary micronutrient intake is indicated in the oncology cohort. Currently, no tool measuring dietary intakes of various micronutrients exists in the oncology population. In this study, a 21-item food frequency questionnaire (FFQ) measuring intakes of 14 different micronutrients was validated using diet history as the reference method in 112 oncology patients. Bland Altman plot and Passing Bablok regression analysis were conducted to determine agreement between the two methods. The results showed adequate agreement between FFQ and diet history for 12 nutrients including copper, iron, vitamins A, E, and D, alpha linolenic acid (ALA), long-chain omega 3 fatty acids (LC n3-FA), arginine, glutamic acid, isoleucine, leucine, and valine. This 21-item FFQ, which takes an average of 10 min to complete, can be utilized as a quick screening tool to determine adequacy for 12 different micronutrients in place of a diet history.

Effect of Dietary or Supplemental Vitamin C Intake on Vitamin C Levels in Patients with and without Cardiovascular Disease: A Systematic Review.

Atherosclerosis is a pro-oxidative and pro-inflammatory disease state, which is the underlying cause of most cardiovascular events, estimated to affect 5.2% of the Australian population. Diet, and specifically vitamin C, through its antioxidant properties can play a role in impeding the development and progression of atherosclerosis. This systematic review conducted comprehensive searches in Medline, Emcare, Scopus, PubMed, and Cochrane using key search terms for vitamin C, plasma vitamin C, supplementation, and cardiovascular disease (CVD). The results demonstrated that vitamin C supplementation resulted in a significant increase in vitamin C levels in populations with or without CVD, except for one study on the CVD population. It was also seen that the healthy population baseline and post-intervention vitamin C levels were high compared to the CVD population. However, further research is indicated for CVD population groups with varying baseline vitamin C levels, such as low baseline vitamin C, within a more representative elderly cohort in order to formulate and update vitamin C repletion guidelines.

Spinocerebellar ataxias types 1, 2 and 3: age adjusted clinical severity of disease at presentation correlates with size of CAG repeat lengths.

OBJECTIVE: The objective of this study was to determine the correlation, if any, between the clinical rate of disease progression at presentation with the CAG repeat size in patients with spinocerebellar ataxias 1, 2 and 3 (SCA1, SCA2 and SCA3). METHODS: The severity of ataxia was measured using the International Cooperative Ataxia Rating Scale (IARS) in 31 patients of SCA1 (mean+/-SD age: 35.1+/-12.6 years; age at onset (AAO): 29.9+/-10.7 years), 25 patients of SCA2 (age: 34.9+/-14.9 years; AAO: 29.7+/-14.0 years) and 15 patients of SCA3 (age: 40.9+/-8.6 years; AAO: 36.9+/-10.1). The rate of disease progression at presentation was measured by the age adjusted IARS (IARS/Age). For each SCA, correlations of AAO, raw scores of IARS, age adjusted IARS and duration adjusted IARS (IARS/Duration) with the CAG repeat size were determined. RESULTS: The number of CAG repeats of the abnormal allele ranged from 42 to 67 in SCA1, 38 to 66 in SCA2, and 69 to 79 in SCA3. In all the three types of SCAs, there were significant inverse correlations of AAO with CAG repeat size (SCA1: r=-0.9, p<0.0001; SCA2: r=-0.7, p<0.0001; SCA3:-0.8, p=0.0003) and significant positive correlations of IARS/Age with CAG repeat size (SCA1: r=0.6, p=0.0015; SCA2: r=0.9, p<0.0001; SCA3:0.7, p=0.0057). However, the raw IARS scores and the duration adjusted IARS scores did not correlate significantly with the CAG repeat sizes. CONCLUSIONS: These data suggest that the rate of clinical disease progression at presentation, especially in SCA2, is dependent on the CAG repeat size, and may commence linearly from birth.

Synthesis, biological evaluation, and molecular modeling of 3,5-substituted-N1-phenyl-N4,N4-di-n-butylsulfanilamides as antikinetoplastid antimicrotubule agents.

Dinitroanilines are of interest as antiprotozoal lead compounds because of their selective activity against the tubulin of these organisms, but concern has been raised due to the potentially mutagenic nitro groups. Analogues of N(1)-phenyl-3,5-dinitro-N(4),N(4)-di-n-butylsulfanilamide (GB-II-150, compound 2b), a selective antimitotic agent against African trypanosomes and Leishmania, have been prepared where the nitro groups are replaced with amino, chloro, cyano, carboxylate, methyl ester, amide, and methyl ketone moieties. Dicyano compound 5 displays IC(50) values that are comparable to 2b against purified leishmanial tubulin assembly (6.6 vs 7.4 microM), Trypanosoma brucei brucei growth in vitro (0.26 vs 0.18 microM), Leishmania donovani axenic amastigote growth in vitro (4.4 vs 2.3 microM), and in vitro toxicity against Vero cells (16 vs 9.7 microM). Computational studies provide a rationale for the antiparasitic order of activity of these analogues and further insight into the role of the substituents at the 3 and 5 positions of the sulfanilamide ring.

Antikinetoplastid antimitotic activity and metabolic stability of dinitroaniline sulfonamides and benzamides.

N(1)-Phenyl-3,5-dinitro-N(4),N(4)-di-n-propylsulfanilamide (1) and N(1)-phenyl-3,5-dinitro-N(4),N(4)-di-n-butylsulfanilamide (2) show potent in vitro antimitotic activity against kinetoplastid parasites but display poor in vivo activity. Seventeen new dinitroaniline sulfonamide and eleven new benzamide analogs of these leads are reported here. Nine of the sulfonamides display in vitro IC(50) values under 500 nM against African trypanosomes, and the most active antikinetoplastid compounds also inhibit the in vitro assembly of purified leishmanial tubulin with potencies similar to that of 2. While several of the potent compounds are rapidly degraded by rat liver S9 fractions in vitro, N(1)-(3-hydroxy)phenyl-3,5-dinitro-N(4),N(4)-di-n-butylsulfanilamide (21) displays an IC(50) value of 260 nM against African trypanosomes in vitro and is more stable than 2 in the in vitro metabolism assay.