Dark chocolate cuts hypertension risk: Sweet news from latest study

 Which of these three is your doctor recommending? Or does your incompetent doctor not even know about them?

Then are you are using Guinness for blood thinning?

Guinness could really be good for you

Or maybe red wine for men red wine, which reduced the risk for AD only in men. Women could be more susceptible to detrimental effects of alcohol.(This won't go over well in my wine groups.)

Dark chocolate cuts hypertension risk: Sweet news from latest study

A study published in the journal Scientific Reports shows that dark chocolate intake can significantly reduce the risk of essential hypertension. Essential hypertension refers to high blood pressure that is multi-factorial and does not have a distinct cause. 

Study: Dark chocolate intake and cardiovascular diseases: a Mendelian randomization study

Background

Cardiovascular diseases are the leading cause of disability and mortality worldwide and are major contributors to the global disease burden. The estimated total number of cardiovascular disease cases was 523 million in 2019, with the Middle East and North Africa having the highest prevalence and Central Asia and Eastern Europe having the highest mortality.

Given the high morbidity and mortality associated with cardiovascular diseases, several studies have been conducted to identify both risk factors and preventive measures. Some small-scale randomized controlled trials have shown that dark chocolates benefit cardiovascular health. The main three flavanols found in dark chocolate, including procyanidin, catechin, and epicatechin are known to have beneficial effects on the cardiovascular system.  

In this study, scientists have explored the causal relationship between dark chocolate intake and cardiovascular disease risk using the Mendelian randomization method.  Mendelian randomization uses measured variation in genes of known function to examine the causal effect of a modifiable exposure on disease in observational studies.

Study design

The scientists obtained genome-wide association study summary-level data for dark chocolate intake from the MRC Integrative Epidemiology Unit (University of Bristol) website. The data included 64,945 European ancestry participants. They identified 21 independent single nucleotide polymorphisms as genetic instrumental variables for predicting dark chocolate intake. An instrumental variable is a kind of variable that is not supposed to have any direct effect on the outcome.

Furthermore, the scientists obtained summary-level data for cardiovascular diseases from various publicly available genome-wide association studies. They synchronized the datasets for dark chocolate intake and cardiovascular diseases to align the direction of alleles of the single nucleotide polymorphisms for both.      

Then, they analyzed the data to determine the causal relationship between genetically predicted dark chocolate intake and risks of 12 cardiovascular diseases, including heart failure, coronary heart disease, myocardial infarction, atrial fibrillation, non-rheumatic valve disease, non-ischemic cardiopathy, essential hypertension, venous thromboembolism, deep vein thrombosis, stroke, ischemic stroke, and transient ischemic attack. They also conducted sensitive analyses to assess the robustness of the Mendelian randomization analysis results.

Important observations

The study findings revealed that dark chocolate intake significantly reduces the risk of essential hypertension. A suggestive negative association between dark chocolate intake and the risk of venous thromboembolism was observed in the study. No significant association with dark chocolate intake was observed for other tested cardiovascular diseases.

Study significance

This study reveals that genetically predicted dark chocolate intake is significantly associated with a lower risk of essential hypertension and suggestively associated with a lower risk of venous thromboembolism.

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Available evidence indicates that flavanols present in dark chocolates can improve endothelial function, promote vasodilation, and prevent platelet aggregation by increasing nitric oxide release. Flavanols are also known to have potent antioxidant and anti-inflammatory activities. All these activities of flavanols are believed to be the main contributing factors towards a healthy cardiovascular system.

The hypertension data used in this study includes cases of secondary hypertension, which is essentially the manifestation of kidney disease, renal vascular disease, and some endocrine diseases in the cardiovascular system. However, the study does not investigate any causal relationship of these diseases with dark chocolate intake. Thus, the scientists advise that people should not rely only on dark chocolate to prevent essential hypertension. Rather, people at high risk for essential hypertension can replace unhealthy snacks with dark chocolate to improve their cardiovascular health.

As mentioned by the scientists, a small sample size of the exposure data was used in this study. The identified single nucleotide polymorphisms also failed to reach the conventional genome-wide significance threshold. However, these single nucleotide polymorphisms can be considered as effective instrumental variables as their Fisher-statistic (a measure of the ratio of variances) values are greater than 10. A Fisher-statistic value of more than 2.5 is needed to reject the null hypothesis. Moreover, the findings of sensitive analyses showed the robustness of the estimated causal effects for almost all outcomes.    

Summer-level data of European ancestry populations was used in this study. This restricts the generalizability of study findings to other populations.

Overall, the study provides valuable information for the prevention of essential hypertension in the general population. More clinical research is needed to firmly establish the causal relationship between dark chocolate intake and the risk of cardiovascular diseases.

Journal reference:

• Yang, Juntao, et al. "Dark Chocolate Intake and Cardiovascular Diseases: A Mendelian Randomization Study." Scientific Reports, vol. 14, no. 1, 2024, pp. 1-9, https://doi.org/10.1038/s41598-023-50351-6, https://www.nature.com/articles/s41598-023-50351-6

The association of arterial stiffness index with cerebrovascular and cardiometabolic disease: A Mendelian randomization study

 

So if you have arterial stiffness what the fuck is your doctor's protocol to address the problem? Maybe something in one of these?

• stiff arteries (11 posts to May 2013)

• Arterial stiffness (25 posts to April 2016) 

The association of arterial stiffness index with cerebrovascular and cardiometabolic disease: A Mendelian randomization study

Show all authors

Weishi Liu, Luyang Zhang, Yuan Gao, ...

First Published January 4, 2022 Brief Report 

https://doi.org/10.1177/17474930211066432

Article information

Abstract

Background:

Arterial stiffness index (ASI) is a potential risk factor for cerebrovascular and cardiometabolic diseases, but the causal links between them are inconclusive. The aim is to evaluate the causal effects of ASI on cerebrovascular and cardiometabolic diseases by Mendelian randomization (MR).

Methods:

Two-sample MR analysis was performed to infer causal links. Genetic variants significantly associated with ASI were extracted. The inverse variance weighted method was used for estimating the effects. Sensitivity analysis was performed to test heterogeneity or pleiotropy.

Results:

MR analysis indicated an effect of genetically predicted ASI on the risk of ischemic stroke (IS) of all causes (OR = 1.894, 95% CI 1.210–2.965, p = 0.005). No links were identified between genetically predicted ASI and other cerebrovascular or cardiometabolic diseases (all p > 0.05). Subgroup analysis of IS etiologies found a suggestive association between genetically predicted ASI and large artery atherosclerosis stroke (LAS) (OR = 3.726, 95% CI 1.230–11.286, p = 0.020). There were no effects of ASI on IS due to cardioembolism or small vessel occlusion.

Conclusion:

The current MR analysis suggested that genetically predicted ASI was associated with higher risk of IS of all causes. The results and the underlying pathways or mechanisms between ASI and IS needs further investigation.

Keywords

Arterial stiffness index, cerebrovascular disease, cardiometabolic disease, ischemic stroke, large artery atherosclerosis

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Cardiac Risk Factors for Stroke: A Comprehensive Mendelian Randomization Study

 I'm sure there is something in here useful but I don't know what it is.

Cardiac Risk Factors for Stroke: A Comprehensive Mendelian Randomization Study

Simon Frerich

,

Rainer Malik

,

Marios K. Georgakis

,

Moritz F. Sinner

,

Steven J. Kittner

,

Braxton D. Mitchell

,

Martin Dichgans

Originally published16 Dec 2021https://doi.org/10.1161/STROKEAHA.121.036306Stroke. 2021;0:STROKEAHA.121.036306

Abstract

Background and Purpose:

Observational studies suggest an association of stroke with cardiac traits beyond atrial fibrillation, the leading source of cardioembolism. However, controversy remains regarding a causal role of these traits in stroke pathogenesis. Here, we leveraged genetic data to systematically assess associations between cardiac traits and stroke risk using a Mendelian Randomization framework.

Methods:

We studied 66 cardiac traits including cardiovascular diseases, magnetic resonance imaging–derived cardiac imaging, echocardiographic imaging, and electrocardiographic measures, as well as blood biomarkers in a 2-sample Mendelian Randomization approach. Genetic predisposition to each trait was explored for associations with risk of stroke and stroke subtypes in data from the MEGASTROKE consortium (40 585 cases/406 111 controls). Using multivariable Mendelian Randomization, we adjusted for potential pleiotropic or mediating effects relating to atrial fibrillation, coronary artery disease, and systolic blood pressure.

Results:

As expected, we observed strong independent associations between genetic predisposition to atrial fibrillation and cardioembolic stroke and between genetic predisposition to coronary artery disease as a proxy for atherosclerosis and large-artery stroke. Our data-driven analyses further indicated associations of genetic predisposition to both heart failure and lower resting heart rate with stroke. However, these associations were explained by atrial fibrillation, coronary artery disease, and systolic blood pressure in multivariable analyses. Genetically predicted P-wave terminal force in V1, an electrocardiographic marker for atrial cardiopathy, was inversely associated with large-artery stroke.

Conclusions:

Available genetic data do not support substantial effects of cardiac traits on the risk of stroke beyond known clinical risk factors. Our findings highlight the need to carefully control for confounding and other potential biases in studies examining candidate cardiac risk factors for stroke.

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Physical activity and risk of Alzheimer disease: A 2-sample Mendelian randomization study

 

Not understandable to me, maybe you'd rather try this article?

This one suggests 8900 steps a day.

Can Exercise Protect Against Alzheimer's?

The latest here:

Physical activity and risk of Alzheimer disease: A 2-sample Mendelian randomization study

Baumeister SE, Karch A, Bahls M, et al.

Neurology|September 29, 2020

Researchers assessed if physical activity can protect against Alzheimer disease (AD) via a 2-sample Mendelian randomization analysis. They used summary data on genome-wide association studies regarding physical activity and AD. The sample consisted of 21,982 patients with AD and 41,944 controls who were cognitively normal. Eight single nucleotide polymorphisms (SNPs) known at p < 5 × 10⁻⁸ to be linked to average accelerations and 8 SNPs correlated at  p < 5 × 10⁻⁷ linked with vigorous(definition?) physical activity (fraction of accelerations > 425 milligravities) acted as instrumental variables. Genetic liability for fraction of accelerations >425 milligravities was irrelevant to the risk of AD. A causal link between physical activity and AD risk is not confirmed by the current research.

Read the full article on Neurology.

 

Circulating lipoprotein lipids, apolipoproteins and ischemic stroke

 No clue.

Circulating lipoprotein lipids, apolipoproteins and ischemic stroke

Yuan S, Tang B, Zheng J, et al.

Annals of Neurology |October 12, 2020

Researchers assessed the comparative effects of lipids and apolipoproteins on ischemic stroke in this Mendelian randomization (MR) study. Instrumental variables were single‐nucleotide polymorphisms correlated with low‐ and high‐density lipoprotein (LDL and HDL) cholesterol, triglycerides, and apolipoprotein A‐I and B (apoA‐I and apoB) at the level of genomewide significance in the UK Biobank. In the main and sensitivity univariable MR analyses, an association of increased levels of apoB, LDL cholesterol, and triglycerides with a higher risk of any ischemic stroke, large artery stroke, and small vessel stroke was seen. This MR study shows that apoB is the predominant trait that accounts for the etiological basis of apoB, LDL cholesterol, and triglycerides in relation to ischemic stroke, especially large artery and small vessel stroke. Whether HDL cholesterol has a protective effect on ischemic stroke independent of apoA‐I requires further study.

Read the full article on Annals of Neurology .

 

 

High blood pressure linked to reduced Alzheimer's risk, meds may be reason

You probably need your complete neurologist/cardiac team at the hospital to analyze this. Or just maybe the fact that this is pushing more oxygenated blood through the brain might be the reason. Why even suggest that meds may be the reason except for continuing to prop up the pharma industry.
The readable article here: 
High blood pressure linked to reduced Alzheimer's risk, meds may be reason

The research/abstract here: 
Associations between Potentially Modifiable Risk Factors and Alzheimer Disease: A Mendelian Randomization Study

• Søren D. Østergaard,
• Shubhabrata Mukherjee,
• Stephen J. Sharp,
• Petroula Proitsi,
• Luca A. Lotta,
• Felix Day,
• John R. B. Perry,
• Kevin L. Boehme,
• Stefan Walter,
• John S. Kauwe,
• Laura E. Gibbons,
• Alzheimer’s Disease Genetics Consortium ,
• The GERAD1 Consortium ,
•  [ ... ],
• Robert A. Scott
• [ view all ]

• 
  
• 
  
• 
  
• 
  
• 
  
• 
  
• 
  
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• 
  
• 
  

• Published: June 16, 2015
• DOI: 10.1371/journal.pmed.1001841 

Abstract

Background

Potentially modifiable risk factors including obesity, diabetes, hypertension, and smoking are associated with Alzheimer disease (AD) and represent promising targets for intervention. However, the causality of these associations is unclear. We sought to assess the causal nature of these associations using Mendelian randomization (MR).

Methods and Findings

We used SNPs associated with each risk factor as instrumental variables in MR analyses. We considered type 2 diabetes (T2D, N_SNPs = 49), fasting glucose (N_SNPs = 36), insulin resistance (N_SNPs = 10), body mass index (BMI, N_SNPs = 32), total cholesterol (N_SNPs = 73), HDL-cholesterol (N_SNPs = 71), LDL-cholesterol (N_SNPs = 57), triglycerides (N_SNPs = 39), systolic blood pressure (SBP, N_SNPs = 24), smoking initiation (N_SNPs = 1), smoking quantity (N_SNPs = 3), university completion (N_SNPs = 2), and years of education (N_SNPs = 1). We calculated MR estimates of associations between each exposure and AD risk using an inverse-variance weighted approach, with summary statistics of SNP–AD associations from the International Genomics of Alzheimer’s Project, comprising a total of 17,008 individuals with AD and 37,154 cognitively normal elderly controls. We found that genetically predicted higher SBP was associated with lower AD risk (odds ratio [OR] per standard deviation [15.4 mm Hg] of SBP [95% CI]: 0.75 [0.62–0.91]; p = 3.4 × 10⁻³). Genetically predicted higher SBP was also associated with a higher probability of taking antihypertensive medication (p = 6.7 × 10⁻⁸). Genetically predicted smoking quantity was associated with lower AD risk (OR per ten cigarettes per day [95% CI]: 0.67 [0.51–0.89]; p = 6.5 × 10⁻³), although we were unable to stratify by smoking history; genetically predicted smoking initiation was not associated with AD risk (OR = 0.70 [0.37, 1.33]; p = 0.28). We saw no evidence of causal associations between glycemic traits, T2D, BMI, or educational attainment and risk of AD (all p > 0.1). Potential limitations of this study include the small proportion of intermediate trait variance explained by genetic variants and other implicit limitations of MR analyses.

Conclusions

Inherited lifetime exposure to higher SBP is associated with lower AD risk. These findings suggest that higher blood pressure—or some environmental exposure associated with higher blood pressure, such as use of antihypertensive medications—may reduce AD risk.