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Trial of the MIND Diet for Prevention of Cognitive Decline in Older Persons.
Barnes, LL, Dhana, K, Liu, X, Carey, VJ, Ventrelle, J, Johnson, K, Hollings, CS, Bishop, L, Laranjo, N, Stubbs, BJ, et al
The New England journal of medicine. 2023;389(7):602-611
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Lifestyle interventions targeting diet are a possible approach that could affect public health. Most clinical trials have investigated comprehensive diets, in contrast to dietary manipulation of single foods or nutrients. The aim of this study was to evaluate the effects of a 3-year dietary intervention on cognitive decline and brain-imaging markers of dementia and Alzheimer’s disease in older, cognitively unimpaired adults at risk for dementia because of family history. This study was a 3-year, two-site, randomised, controlled trial. The participants were randomly assigned to follow the MIND diet with mild caloric restriction for weight loss or their usual diet with the same mild caloric restriction for weight loss (control diet). Participants were randomly assigned in a 1:1 ratio. Results showed that the participants who followed the MIND diet had small improvements in a global measure of cognition that were similar to those who followed a control diet with mild caloric restriction. Authors concluded that brain health, cognitive function and brain imaging outcomes (after 3 years) did not differ significantly between participants who followed the MIND diet and those who followed a control diet with a mild caloric restriction.
Abstract
BACKGROUND Findings from observational studies suggest that dietary patterns may offer protective benefits against cognitive decline, but data from clinical trials are limited. The Mediterranean-DASH Intervention for Neurodegenerative Delay, known as the MIND diet, is a hybrid of the Mediterranean diet and the DASH (Dietary Approaches to Stop Hypertension) diet, with modifications to include foods that have been putatively associated with a decreased risk of dementia. METHODS We performed a two-site, randomized, controlled trial involving older adults without cognitive impairment but with a family history of dementia, a body-mass index (the weight in kilograms divided by the square of the height in meters) greater than 25, and a suboptimal diet, as determined by means of a 14-item questionnaire, to test the cognitive effects of the MIND diet with mild caloric restriction as compared with a control diet with mild caloric restriction. We assigned the participants in a 1:1 ratio to follow the intervention or the control diet for 3 years. All the participants received counseling regarding adherence to their assigned diet plus support to promote weight loss. The primary end point was the change from baseline in a global cognition score and four cognitive domain scores, all of which were derived from a 12-test battery. The raw scores from each test were converted to z scores, which were averaged across all tests to create the global cognition score and across component tests to create the four domain scores; higher scores indicate better cognitive performance. The secondary outcome was the change from baseline in magnetic resonance imaging (MRI)-derived measures of brain characteristics in a nonrandom sample of participants. RESULTS A total of 1929 persons underwent screening, and 604 were enrolled; 301 were assigned to the MIND-diet group and 303 to the control-diet group. The trial was completed by 93.4% of the participants. From baseline to year 3, improvements in global cognition scores were observed in both groups, with increases of 0.205 standardized units in the MIND-diet group and 0.170 standardized units in the control-diet group (mean difference, 0.035 standardized units; 95% confidence interval, -0.022 to 0.092; P = 0.23). Changes in white-matter hyperintensities, hippocampal volumes, and total gray- and white-matter volumes on MRI were similar in the two groups. CONCLUSIONS Among cognitively unimpaired participants with a family history of dementia, changes in cognition and brain MRI outcomes from baseline to year 3 did not differ significantly between those who followed the MIND diet and those who followed the control diet with mild caloric restriction. (Funded by the National Institute on Aging; ClinicalTrials.gov number, NCT02817074.).
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Dietary Inflammatory Index, Dietary Non-Enzymatic Antioxidant Capacity, and Colorectal and Breast Cancer Risk (MCC-Spain Study).
Obón-Santacana, M, Romaguera, D, Gracia-Lavedan, E, Molinuevo, A, Molina-Montes, E, Shivappa, N, Hebert, JR, Tardón, A, Castaño-Vinyals, G, Moratalla, F, et al
Nutrients. 2019;11(6)
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This study aims to correlate the risk factors of inflammation and antioxidant capacity in cases of colon and breast cancer, using data from a large Spanish case-controlled study (1852 colon cancer subjects, 1567 breast cancer subjects and a total 4933 controls). The role of diet in colon cancer is widely accepted, however it is more controversial with breast cancer where genetic mutations and other lifestyle factors are cited as primary risk factors. What unites these cancers is the inter-related presence of both inflammation and oxidative stress. The dietary inflammatory index (DII®) and non-enzymatic antioxidant capacity (NEAC) were used to evaluate inflammation and oxidative stress using 30 nutrient parameters and 6 inflammatory blood markers. The results showed that colon cancer subjects typically ate a more pro-inflammatory diet compared to controls, with a higher odds ratio of men to women, and tended to be older, heavier and less physically active. The breast cancer subjects also had higher inflammatory scores versus controls but demographically were younger, premenopausal, frequently with a first-degree family link to breast cancer, and including a higher percentage of smokers. For both cancers, inflammation significantly and statistically increased risk factors. Adding in oxidative stress results showed a statistically higher risk of developing colon cancer whilst in breast cancer subjects the risk was increased but non-statistically valid. They did report that meat-eaters had a relative 9% increased risk of Breast cancer. Overall the study concluded that dietary components of inflammation and oxidative stress increased risk of colon cancer but were not statistically valid for breast cancer.
Abstract
Inflammation and antioxidant capacity have been associated with colorectal and breast cancer. We computed the dietary inflammatory index (DII®), and the total dietary non-enzymatic antioxidant capacity (NEAC) and associated them with colorectal and breast cancer risk in the population-based multi case-control study in Spain (MCC-Spain). We included 1852 colorectal cancer and 1567 breast cancer cases, and 3447 and 1486 population controls, respectively. DII score and NEAC were derived using data from a semi-quantitative validated food frequency questionnaire. Unconditional logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95%CI) for energy-adjusted DII (E-DII), and a score combining E-DII and NEAC. E-DII was associated with colorectal cancer risk (OR = 1.93, highest quartile versus lowest, 95%CI:1.60-2.32; p-trend: <0.001); this increase was observed for both colon and rectal cancer. Less pronounced increased risks were observed for breast cancer (OR = 1.22, highest quartile versus lowest, 95%CI:0.99-1.52, p-trend: >0.10). The combined score of high E-DII scores and low antioxidant values were associated with colorectal cancer risk (OR = 1.48, highest quartile versus lowest, 95%CI: 1.26-1.74; p-trend: <0.001), but not breast cancer. This study provides evidence that a pro-inflammatory diet is associated with increased colorectal cancer risk while findings for breast cancer were less consistent.
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The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial.
Mortensen, SA, Rosenfeldt, F, Kumar, A, Dolliner, P, Filipiak, KJ, Pella, D, Alehagen, U, Steurer, G, Littarru, GP
JACC. Heart failure. 2014;2(6):641-9
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Optimal therapy of heart failure (HF) is a considerable challenge. Standard treatments are administered to block rather than to enhance cellular processes. Coenzyme Q10 (CoQ10) is a powerful lipid-soluble antioxidant. This study is a prospective, randomized, double-blind, placebo-controlled, multi-centre trial of CoQ10 as adjunctive treatment of chronic HF focusing on changes in symptoms, biomarker status, and long-term outcome. A total of 420 patients were randomly assigned to active treatment with CoQ10 (n = 202) or placebo (n = 218). Results show that supplementation with CoQ10 significantly reduced major adverse cardiovascular events and cardiovascular death by 43% and all-cause mortality by 42%. Furthermore, CoQ10 supplementation improved the patients’ symptoms according to the New York Heart Association functional classification after 2 years. Authors conclude that treatment with CoQ10 in addition to standard therapy for patients with moderate to severe HF is safe, well tolerated, and associated with a reduction in symptoms and major adverse cardiovascular events.
Abstract
OBJECTIVES This randomized controlled multicenter trial evaluated coenzyme Q10 (CoQ10) as adjunctive treatment in chronic heart failure (HF). BACKGROUND CoQ10 is an essential cofactor for energy production and is also a powerful antioxidant. A low level of myocardial CoQ10 is related to the severity of HF. Previous randomized controlled trials of CoQ10 in HF were underpowered to address major clinical endpoints. METHODS Patients with moderate to severe HF were randomly assigned in a 2-year prospective trial to either CoQ10 100 mg 3 times daily or placebo, in addition to standard therapy. The primary short-term endpoints at 16 weeks were changes in New York Heart Association (NYHA) functional classification, 6-min walk test, and levels of N-terminal pro-B type natriuretic peptide. The primary long-term endpoint at 2 years was composite major adverse cardiovascular events as determined by a time to first event analysis. RESULTS A total of 420 patients were enrolled. There were no significant changes in short-term endpoints. The primary long-term endpoint was reached by 15% of the patients in the CoQ10 group versus 26% in the placebo group (hazard ratio: 0.50; 95% confidence interval: 0.32 to 0.80; p = 0.003) by intention-to-treat analysis. The following secondary endpoints were significantly lower in the CoQ10 group compared with the placebo group: cardiovascular mortality (9% vs. 16%, p = 0.026), all-cause mortality (10% vs. 18%, p = 0.018), and incidence of hospital stays for HF (p = 0.033). In addition, a significant improvement of NYHA class was found in the CoQ10 group after 2 years (p = 0.028). CONCLUSIONS Long-term CoQ10 treatment of patients with chronic HF is safe, improves symptoms, and reduces major adverse cardiovascular events. (Coenzyme Q10 as adjunctive treatment of chronic heart failure: a randomised, double-blind, multicentre trial with focus on SYMptoms, BIomarker status [Brain-Natriuretic Peptide (BNP)], and long-term Outcome [hospitalisations/mortality]; ISRCTN94506234).