Nutritional advice

Objectives:
Is there a relationship between the levels of vitamin C, vitamin E and β-carotene in the plasma and Alzheimer's disease risk?

Study design:
This review article included studies with data of levels of vitamin C, vitamin E and β-carotene in the plasma of Alzheimer's disease patients.

Results and conclusions:
The investigators found meta-analysis showed that, compared with the control group, the level of vitamin E in the plasma of Alzheimer's disease patients declined significantly [SMD = -1.49 μmol/L, 95% CI = -2.08 to -0.89 μmol/L, p 0.001].

However, no differences were determined in the levels of the plasma vitamin C and β-carotene between the two groups [vitamin C: SMD = -1.43 μmol/L, 95% CI = -3.05 to 0.19 μmol/L, p = 0.083 and β-carotene: SMD = -0.61 μmol/L, 95% CI = -1.40 to 0.18 μmol/L, p = 0.131].

The investigators concluded increasing vitamin E level in the plasma through vitamin E riched diet is useful to prevent Alzheimer's disease. However, it is not yet believed the beneficial role on Alzheimer's disease to increase vitamin C and β-carotene.

Original title:
Meta-analysis of vitamin C, vitamin E and β-carotene levels in the plasma of Alzheimer's disease patients by Dong R, Yang Q, […], Zhao H.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/30081996  

Additional information of El Mondo:
Find more information/studies on vitamin E, C, β-carotene and dementia right here.
 

Objectives:
Although several studies have been conducted on the association of vitamins with glaucoma, it is often noticed that the results are conflicting leaving physicians and patients in doubt about the effect of vitamins on glaucoma. Therefore, this review article has been conducted.

Does dietary vitamin intake reduce risk of the eye disease glaucoma? 

Study design:
This review article included 5 cohort studies with a total of 940 open-angle glaucoma (OAG) cases and 123,697 controls (persons without open-angle glaucoma).

Results and conclusions:
The investigators found a significantly reduced risk of 55% [pooled OR = 0.45, 95% CI = 0.30-0.68, I2 = 0%] for open-angle glaucoma for dietary intake of vitamin A.

The investigators found a significantly reduced risk of 61% [pooled OR = 0.39, 95% CI = 0.23-0.67, I2 = 0%] for open-angle glaucoma for dietary intake of vitamin C.

The investigators found a significantly reduced risk of 61% [pooled OR = 0.39, 95% CI = 0.22-0.70, I2 = 0%] for open-angle glaucoma for dietary intake of green leafy vegetables (a source for vitamin A, C and nitrate).

The investigators concluded dietary intake of vitamin A, C and green leafy vegetables show a beneficial association with the eye disease open-angle glaucoma.

Original title:
The Effect of Vitamins on Glaucoma: A Systematic Review and Meta-Analysis by Ramdas WD, Schouten JSAG and Webers CAB.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5872777/

Additional information of El Mondo:
Find more information/studies on vitamin A and C, vegetables and elderly right here.
 

Objectives:
The associations of various dietary or circulating antioxidants with the risk of all-cause mortality in the general population have not been established yet. Therefore, this review article has been conducted.

Do dietary or circulating antioxidants reduced risk of all-cause mortality in the general population?

Study design:
This review article included 41 prospective observational studies with a total of 507,251 participants and 73,965 cases of all-cause mortality.

Results and conclusions:
The investigators found for the highest compared with the lowest category of circulating total carotenes concentrations a significantly reduced risk of 40% [RR = 0.60, 95% CI = 0.46 to 0.74] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of circulating vitamin C concentrations a significantly reduced risk of 39% [RR = 0.61, 95% CI = 0.53 to 0.69] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of circulating selenium concentrations a significantly reduced risk of 38% [RR = 0.62, 95% CI = 0.45 to 0.79] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of circulating β-carotene concentrations a significantly reduced risk of 37% [RR = 0.63, 95% CI = 0.57 to 0.70] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of circulating α-carotene concentrations a significantly reduced risk of 32% [RR = 0.68, 95% CI = 0.58 to 0.78] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of circulating total carotenoids concentrations a significantly reduced risk of 32% [RR = 0.68, 95% CI = 0.56 to 0.80] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of circulating lycopene concentrations a significantly reduced risk of 25% [RR = 0.75, 95% CI = 0.54 to 0.97] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of circulating α-tocopherol concentrations a significantly reduced risk of 16% [RR = 0.84, 95% CI = 0.77 to 0.91] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of dietary intakes of total carotenoids a significantly reduced risk of 24% [RR = 0.76, 95% CI = 0.66 to 0.85] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of dietary intakes of total antioxidants a significantly reduced risk of 23% [RR = 0.77, 95% CI = 0.73 to 0.81] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of dietary intakes of selenium a significantly reduced risk of 21% [RR = 0.79, 95% CI = 0.73 to 0.85] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of dietary intakes of α-carotene a significantly reduced risk of 21% [RR = 0.79, 95% CI = 0.63 to 0.94] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of dietary intakes of β-carotene a significantly reduced risk of 18% [RR = 0.82, 95% CI = 0.77 to 0.86] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of dietary intakes of vitamin C a significantly reduced risk of 12% [RR = 0.88, 95% CI = 0.83 to 0.94] for all-cause mortality.  

The investigators found for the highest compared with the lowest category of dietary intakes of total carotenes a significantly reduced risk of 11% [RR = 0.89, 95% CI = 0.81 to 0.97] for all-cause mortality.  

The investigators found for the highest compared with the lowest category a nonsignificant inverse association between dietary zinc, zeaxanthin, lutein and vitamin E and all-cause mortality risk.

The investigators found in nonlinear dose-response meta-analyses a linear inverse association in the analyses of dietary β-carotene and total antioxidant capacity, as well as in the analyses of circulating α-carotene, β-carotene, selenium, vitamin C and total carotenoids.

The investigators found the association appeared to be U-shaped in the analyses of serum lycopene and dietary vitamin C.

The investigators concluded that a diet with high antioxidant properties reduces the risk of all-cause mortality. These findings confirm current recommendations that promote higher intake of antioxidant-rich foods such as fruit and vegetables.

Original title:
Dietary Antioxidants, Circulating Antioxidant Concentrations, Total Antioxidant Capacity, and Risk of All-Cause Mortality: A Systematic Review and Dose-Response Meta-Analysis of Prospective Observational Studies by Jayedi A, Rashidy-Pour A, […], Shab-Bidar S.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/30239557

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Objectives:
Low carbohydrate diets, which restrict carbohydrate in favour of increased protein or fat intake, or both, are a popular weight-loss strategy. However, the long-term effect of carbohydrate restriction on mortality is controversial and could depend on whether dietary carbohydrate is replaced by plant-based or animal-based fat and protein. Therefore, this review article has been conducted.

Is there a relationship between carbohydrate diet and all-cause mortality?

Study design:
This review article included 8 cohort studies with a total of 432,179 participants, of which 40,181 deaths.

Results and conclusions:
The investigators found in the meta-analysis of 8 cohort studies, low carbohydrate consumption (40 En%) significantly increased all-cause mortality risk with 20% [pooled HR = 1.20, 95% CI = 1.09-1.32].

The investigators found in the meta-analysis of 8 cohort studies, high carbohydrate consumption (>70 En%) significantly increased all-cause mortality risk with 23% [pooled HR = 1.23, 95% CI = 1.11-1.36].

The investigators found, however, results varied by the source of macronutrients: all-cause mortality increased when carbohydrates were exchanged for animal-derived fat or protein [HR = 1.18, 95% CI = 1.08-1.29] and all-cause mortality decreased when the substitutions were plant-based [HR = 0.82, 95% CI = 0.78-0.87].

The investigators found a U-shaped relationship between carbohydrate intake and all-cause mortality, with minimum risk observed with 50-55% of energy from carbohydrate.

The investigators concluded that both high (>70 En%) and low percentages of carbohydrate diets (40 En%) are associated with increased all-cause mortality, with minimal risk observed at 50-55 En% carbohydrate intake. Low carbohydrate dietary patterns favouring animal-derived protein and fat sources, from sources such as lamb, beef, pork and chicken, are associated with higher all-cause mortality, whereas those that favoured plant-derived protein and fat intake, from sources such as vegetables, nuts, peanut butter and whole-grain breads, are associated with lower all-cause mortality, suggesting that the source of food notably modifies the association between carbohydrate intake and all-cause mortality.

Original title:
Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis by Seidelmann SB, Claggett B, […], Solomon SD.

Link:
https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(18)30135-X/fulltext

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The most easy way to follow a diet with 50-55 En% carbohydrates is to choose only meals/products with 50-55 En% carbohydrates.
However, the most practical way to follow a diet with 50-55 En% carbohydrates is all meals/products that you eat on a daily basis should contain on average 50-55 En% carbohydrates. Check here which products contain 50-55 En% carbohydrates.
 

Objectives:
Oxidative stress has been found to be implicated in the development of Alzheimer's disease (AD). Therefore, this review article has been conducted.

Is there an association between selenium level in the brain and Alzheimer’s disease? 

Study design:
This review article included 14 studies with 40 observations on selenium concentrations in Alzheimer’s disease and control brains (persons without Alzheimer’s disease).

The effect size as standardized mean difference (SMD) was generated using review manager 5.3.

The funnel plot with Egger's [p = 0.88] and Begg's tests [p = 0.24] detected no significant publication bias.

Results and conclusions:
The investigators found random-effects meta-analysis indicated a decrease [SMD = - 0.42] in brain tissue selenium levels in patients with Alzheimer’s disease as compared to non-Alzheimer’s disease controls.
The results of sensitivity analysis indicated that no single study/observation had significantly influenced the overall outcome.

The investigators found the subgroup meta-analysis demonstrated that the selenium levels were decreased in the temporal, hippocampal and cortex regions of the brains in patients with Alzheimer’s disease.
The results of sensitivity analysis indicated that no single study/observation had significantly influenced the overall outcome.

The investigators concluded there is consolidated evidence for a significant decrease of selenium status in Alzheimer’s disease brains compared to controls (persons without Alzheimer’s disease). In line with the evidence supporting selenium's antioxidant role and the involvement of oxidative stress in Alzheimer’s disease development, these findings support new therapeutic strategies aimed at brain tissue selenium homeostasis in Alzheimer’s disease.

Original title:
Brain Selenium in Alzheimer's Disease (BRAIN SEAD Study): a Systematic Review and Meta-Analysis by Varikasuvu SR, Prasad VS, [...], Manne M.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/30171594

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Objectives:
Total dietary fat intake might influence the risk of fracture; however, conflicting findings have been reported to date. Therefore, this review article has been conducted.

Is there an association between dietary fat intake and risk of fracture?

Study design:
This review article included 6 observational studies.

Results and conclusions:
The investigators found no significant association between total dietary fat intake and risk of fracture [pooled effect size = 1.31, 95% CI = 0.95-1.79, p = 0.09].

The investigators found dietary saturated fat intake significantly increased risk of fracture with 79% [pooled effect size = 1.79, 95% CI = 1.05-3.03, p = 0.03].

The investigators found dietary monounsaturated fatty acids (MUFAs) intake derived from animal sources significantly increased risk of fracture with 129% [pooled effect size = 2.29, 95% CI = 1.50-3.50, p 0.0001].

The investigators concluded that both dietary saturated fat and monounsaturated fatty acids (MUFAs) intake derived from animal sources increase risk of fracture.

Original title:
Dietary fat, saturated fatty acid, and monounsaturated fatty acid intakes and risk of bone fracture: a systematic review and meta-analysis of observational studies by Mozaffari H, Djafarian K, […], Shab-Bidar S.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29947872

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Find more information/studies on fat consumption and elderly.

A diet high in saturated fat is a diet that is largely made up of meals/products with more than 10 En% saturated fat. Practically, this means that all meals/products that you eat on a daily basis should on average contain more than 10 En% saturated fat. Check here which products contains more than 10 En% saturated fat.
More than 10 En% saturated fat means that the total amounts of saturated fat make up for more than 10% of the total kcal of the diet.
 

Objectives:
Is there an association between consumption of food groups and the occurrence of age-related macular degeneration (AMD)?

Study design:
This review article included 26 prospective cohort studies with a total of 211,676 subjects and 7,154 cases of age-related macular degeneration.

Results and conclusions:
The investigators found no significant association between age-related macular degeneration and vegetables, fruit, nuts, grains, dairy products or dietary fats such as oils, butter and margarine when comparing the highest vs. the lowest consumption.

The investigators found a significantly reduced risk of 18% for total age-related macular degeneration [RR = 0.82, 95% CI = 0.75-0.90, p  0.05] when comparing the highest vs. the lowest fish consumption.

The investigators found a significantly reduced risk of 16% for early age-related macular degeneration [RR = 0.84, 95% CI = 0.73-0.97, p  0.05] when comparing the highest vs. the lowest fish consumption.

The investigators found a significantly reduced risk of 21% for late age-related macular degeneration [RR = 0.79, 95% CI = 0.70-0.90, p  0.05], when comparing the highest vs. the lowest fish consumption. 

The investigators found a significantly increased risk of 17% for early age-related macular degeneration [RR = 1.17, 95% CI = 1.02-1.34] when comparing the highest vs. the lowest meat consumption. However, no association was found for late age-related macular degeneration.

The investigators found a significantly increased risk of 20% for early age-related macular degeneration [RR = 1.20, 95% CI = 1.04-1.39] when comparing the highest vs. the lowest alcohol consumption.

The investigators concluded that high fish consumption decreases risk of age-related macular degeneration, while high intake of meat and alcohol increases risk of age-related macular degeneration.

Original title:
Food groups and risk of age-related macular degeneration: a systematic review with meta-analysis by Dinu M, Pagliai G, […], Sofi F.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29978377

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Find more information/studies on fish, meat and alcohol consumption and elderly.
 

Objectives:
Cardiovascular risk factors are closely linked with dementia risk, but whether heart disease predisposes to dementia is uncertain. Therefore, this review article has been conducted.

Does heart disease increase risk of dementia?

Study design:
This review article included 16 studies (1,309,483 individuals) regarding coronary heart disease and 7 studies (1,958,702 individuals) about heart failure.

Results and conclusions:
The investigators found that a history of coronary heart disease was associated with a 27% increased risk of dementia [pooled relative risk = 1.27, 95% CI = 1.07-1.50, I2 = 80%].

The investigators found that a history of heart failure was associated with a 60% increased dementia risk [pooled relative risk = 1.60, 95% CI = 1.19-2.13, I2 = 59%].

The investigators found among 9 prospective population-based cohort studies, a significantly increased risk of 26% for dementia among patients with coronary heart disease [pooled relative risk = 1.26, 95% CI = 1.06-1.49, I2 = 0%].
Significantly means that there is an association with a 95% confidence.

The investigators found among 4 prospective population-based cohort studies, a significantly increased risk of 80% for dementia among patients with heart failure [pooled relative risk = 1.80, 95% CI = 1.41-2.31, I2 = 0%].
Significantly means it can be said with a 95% confidence that heart failure really increased the risk of getting dementia with 80%. 

The investigators concluded that both coronary heart disease and heart failure are associated with an increased risk of dementia.

Original title:
Coronary heart disease, heart failure, and the risk of dementia: A systematic review and meta-analysis by Wolters FJ, Segufa RA, […], Sedaghat S.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29494808

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Objectives:
Inflammatory markers are often elevated in patients with dementia, including Alzheimer's disease (AD). However, it remains unclear whether inflammatory markers are associated with the risk of developing dementia. Therefore, this review article has been conducted.

Do inflammatory markers increase risk of dementia and Alzheimer's disease (AD)?

Study design:
This review article included 13 studies in 6 countries.

Results and conclusions:
The investigators found a significantly increased risk of 37% [HR = 1.37, 95% CI = 1.05-1.78] for all-cause dementia for the highest vs. lowest quantile of C-reactive protein. However, this increased risk was not significant for Alzheimer's disease.

The investigators found a significantly increased risk of 40% [HR = 1.40, 95% CI = 1.13-1.73] for all-cause dementia for the highest vs. lowest quantile of interleukin-6. However, this increased risk was not significant for Alzheimer's disease.

The investigators found a significantly increased risk of 54% [HR = 1.54, 95% CI = 1.14-2.80] for all-cause dementia for the highest vs. lowest quantile of α1-antichymotrypsin. However, this increased risk was not significant for Alzheimer's disease.

The investigators found a significantly increased risk of 40% [HR = 1.40, 95% CI = 1.03-1.90] for all-cause dementia for the highest vs. lowest quantile of lipoprotein-associated phospholipase A2 activity. However, this increased risk was not significant for Alzheimer's disease.

The investigators concluded that several inflammatory markers are associated with an increased risk of all-cause dementia; however, these markers are not specific for Alzheimer's disease. Whether inflammatory markers closely involved in Alzheimer's disease pathology are associated with the risk of Alzheimer's disease remains to be elucidated.

Original title:
Inflammatory markers and the risk of dementia and Alzheimer's disease: A meta-analysis by Darweesh SKL, Wolters FJ, […], Hofman A.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29605221

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Objectives:
β-amyloid (Aβ) accumulates abnormally to senile plaque which is the initiator of Alzheimer's disease (AD). As one of the Aβ-degrading enzymes, insulin-degrading enzyme (IDE) remains controversial for its protein level and activity in Alzheimer's brain. Therefore, this review article has been conducted.

Is there an association between insulin-degrading enzyme protein level and risk of Alzheimer's disease (AD)?

Study design:
This review article included 7 studies for IDE protein level (Alzheimer's disease cases = 293 and controls (persons without Alzheimer's disease)  = 126), 3 for mRNA level (Alzheimer's disease cases = 138 and controls = 81) and 3 for enzyme activity (Alzheimer's disease cases = 123 and controls = 75).

Results and conclusions:
The investigators found the insulin-degrading enzyme protein level was significantly lower in Alzheimer's disease patients than in controls [SMD = -0.47, 95% CI = -0.69 to -0.24, p 0.001].
But insulin-degrading enzyme mRNA and enzyme activity had no significant difference [SMD = 0.02, 95% CI = -0.40 to 0.43 and SMD = 0.06, 95% CI = -0.41 to 0.53, respectively].

The investigators found in subgroup analyses (to get more information) that insulin-degrading enzyme protein level was decreased in both cortex and hippocampus of Alzheimer's disease patients [SMD = -0.43, 95% CI = -0.71 to -0.16, p = 0.002 and SMD = -0.53, 95% CI = -0.91 to -0.15, p = 0.006 respectively].
However, insulin-degrading enzyme mRNA was higher in cortex of Alzheimer's disease patients [SMD = 0.71, 95% CI = 0.14 to 1.29, p = 0.01] but not in hippocampus [SMD = -0.26, 95% CI [= -0.58 to 0.06].

The investigators concluded that Alzheimer's disease patients have lower insulin-degrading enzyme protein level. Further relevant studies are still needed to verify whether insulin-degrading enzyme is one of the factors affecting Aβ abnormal accumulation and throw new insights for Alzheimer's disease detection or therapy.

Original title:
Characteristics of Insulin-degrading Enzyme in Alzheimer's Disease: A Meta-analysis by Zhang H, Liu D, […], Zhou H.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29357797

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Objectives:
Is there a dose-response association between serum 25(OH)D (vitamin D level in blood) and risk of dementia and Alzheimer's disease (AD)?

Study design:
This review article included 7 prospective cohort studies and 1 retrospective cohort study involving 1,953 cases of dementia and 1,607 cases of Alzheimer's disease among a total of 28,354 participants.

Results and conclusions:
The investigators found no association between vitamin D insufficiency (10-20 ng/mL) and risk of dementia [pooled HR = 1.09, 95% CI = 0.95 to 1.24].
No association because RR of 1 was found in the 95% CI of 0.95 to 1.24. RR of 1 means no risk/association.

The investigators found no association between vitamin D insufficiency (10-20 ng/mL) and risk of Alzheimer's disease [pooled HR = 1.19, 95% CI = 0.96 to 1.41].

The investigators found vitamin D deficiency (10 ng/mL) significantly increased risk of dementia with 33% [pooled HR = 1.33, 95% CI = 1.08 to 1.58].
Significantly means it can be said with a 95% confidence that vitamin D deficiency really increased the risk of getting dementia with 33%. 

The investigators found vitamin D deficiency (10 ng/mL) non-significantly increased risk of Alzheimer's disease with 31% [pooled HR = 1.31, 95% CI = 0.98 to 1.65].

The investigators found lower risk of dementia was observed at serum 25(OH)D of 25 ng/mL, whereas the risk of Alzheimer's disease decreased continuously along with the increase of serum 25(OH)D up to 35 ng/mL.

The investigators concluded that vitamin D (serum 25(OH)D) levels of 25 to 35 ng/mL decrease risk of dementia and Alzheimer's disease. However, there is no conclusive evidence regarding serum 25(OH)D levels of >35 ng/mL.

Original title:
Vitamin D status and risk of dementia and Alzheimer's disease: A meta-analysis of dose-response by Jayedi A, Rashidy-Pour A and Shab-Bidar S.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29447107

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Objectives:
Dairy product consumption may affect the risk of hip fracture, but previous studies have reported inconsistent findings. Therefore, this review article has been conducted.

Does consumption of dairy products reduce risk of hip fracture?

Study design:
This review article included 10 cohort studies (with a total of 8,613 hip fracture events and 363,557 participants. The length of follow-up ranged from 3 to 22 years) and 8 case-control studies (3,815 hip fracture cases and 6,415 controls/subjects without hip fracture).

Results and conclusions:
The investigators found in cohort studies no association between a high milk consumption and hip fracture risk [pooled RR = 0.91, 95% CI = 0.74-1.12, I2 = 75.0%, p  0.01].
There were no significant changes to the results after using the trim-and-fill method when including 4 missing articles [adjusted random effects summary RR = 1.06, 95% CI = 0.91-1.23].

The investigators found, however, case-control studies indicated that participants in the highest categories of milk consumption had a 29% reduction in the risk of hip fracture [OR = 0.71, 95% CI = 0.55-0.91, I2 = 54%, p = 0.04].
There were no significant changes to the results after using the trim-and-fill method when including 1 missing article [adjusted random effects summary OR = 0.74, 95% CI = 0.57-0.97].

The investigators found in cohort studies no association between a high total dairy consumption and hip fracture risk [pooled RR = 1.02, 95% CI = 0.93-1.12]. No association because RR of 1 was found in the 95% CI of 0.93 to 1.12. RR of 1 means no risk/association.

The investigators found cohort studies indicated that participants in the highest categories of yoghurt consumption had a 25% reduction in the risk of hip fracture [RR = 0.75, 95% CI = 0.66-0.86].
 

The investigators found cohort studies indicated that participants in the highest categories of cheese consumption had a 32% reduction in the risk of hip fracture [RR = 0.68, 95% CI = 0.61-0.77].

The investigators found the summary RR for an increased milk consumption of 200 g/day was 1.00 [95% CI = 0.94-1.07, I2 = 87%, p heterogeneity  0.01] among cohort studies.

The investigators found in cohort studies there was a nonlinear positive association between milk consumption and hip fracture risk [p nonlinearity  0.01], with a rapid increase in risk when milk consumption increased from 0 to 600 g/d. However, there was no further increase in risk with milk consumption between 600 and 1200 g/d.

The investigators found in case-control studies there was a nonlinear association between milk consumption and hip fracture risk [p nonlinearity = 0.28], with a reduction in risk with milk consumption of 200-600 g/d. However, the confidence intervals were wide for all outcomes.

The investigators concluded that a high consumption of yogurt and cheese is associated with a lower risk of hip fracture in cohort studies.

Original title:
Dairy product consumption and risk of hip fracture: a systematic review and meta-analysis by Bian S, Hu J, [...], Ma J.

Link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5778815/

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Objectives:
Does exercise training delay the decline in cognitive function among individuals who are at risk of/or have Alzheimer's disease?  

Study design:
This review article included 19 controlled studies with 23 interventions including 1,145 subjects with a mean age of 77.0 ± 7.5.
The studies included an exercise-only intervention and a nondiet, nonexercise control group and reported pre- and post-intervention cognitive function measurements.

Most subjects were at risk of Alzheimer's disease because they had mild cognitive impairment (64%) or a parent diagnosed with Alzheimer's disease (1%) and 35% presented with Alzheimer's disease.

Exercise interventions were performed 3.4 ± 1.4 days per week at moderate intensity (3.7 ± 0.6 metabolic equivalents) for 45.2 ± 17.0 minutes per session for 18.6 ± 10.0 weeks and consisted primarily of aerobic exercise (65%).

Results and conclusions:
The investigators found overall, there was a modest favourable effect of exercise on cognitive function [d+ = 0.47, 95% CI = 0.26 to 0.68].

The investigators found within-group analyses revealed that exercise improved cognitive function [d+w = 0.20, 95% CI = 0.11 to 0.28], whereas cognitive function declined in the control group [d+w = -0.18, 95% CI = -0.36 to 0.00].

The investigators found within-group analyses revealed that aerobic exercise had a moderate favourable effect on cognitive function [d+w = 0.65, 95% CI = 0.35 to 0.95), but other exercise types did not [d+w = 0.19, 95% CI = -0.06 to 0.43].

The investigators concluded that exercise training (3.4 days per week at moderate intensity for 45.2 minutes per session during 18.6 weeks) delays the decline in cognitive function that occurs in individuals who are at risk of/or have Alzheimer's disease, with aerobic exercise having the most favourable effect. Additional randomized controlled clinical trials that include objective measurements of cognitive function are needed to confirm these findings.

Original title:
Can Exercise Improve Cognitive Symptoms of Alzheimer's Disease? A Meta-Analysis by Panza GA, Taylor BA, […], Pescatello LS.

Link:
https://www.ncbi.nlm.nih.gov/pubmed/29363108

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Metabolic Equivalents (METs) are commonly used to express the intensity of physical activities.
MET is the ratio of a person's working metabolic rate relative to their resting metabolic rate.
One MET is defined as the energy cost of sitting quietly and is equivalent to a caloric consumption of 1 kcal/kg/hour.