Exercise during middle age may prevent age-related chronic diseases

 Well it didn't prevent my stroke.  I had the cardiovascular fitness of an athlete at the time of my stroke. My fitness caused my stroke. The ability to carry canoe and gear over a 1.5 mile portage and the skills to run 21 miles of wilderness whitewater meant I take chances. Something on that trip caused my right carotid plaque to tear, maybe throwing the 60 lb. canoe on my shoulders, or maybe swimming a fully loaded canoe thru several rapids after capsizing, or maybe just sleeping wrong in the tent.

Exercise during middle age may prevent age-related chronic diseases

Middle-aged endurance athletes have better control of blood pressure and higher arterial elasticity (a noninvasive measure of cardiovascular risk) than sedentary adults in the same age group. They also displayed comparable levels of these factors compared to young adults, thanks to regular aerobic exercise, according to new results from a joint study by physiologists in Texas and Japan. The findings offer strong indications that improvements in blood pressure control and vascular elasticity may contribute to better cerebral blood flow regulation in middle-aged people. The study is published ahead of print in the Journal of Applied Physiology and has been chosen as an APSselect article for December.

Midlife arterial stiffness is linked to a higher risk of stroke and dementia later in life, along with a greater risk of age-related chronic conditions such as high blood pressure, chronic kidney disease and diabetes. The scientists conducting this study set out to investigate how regular aerobic exercise during midlife could mitigate the aforementioned maladies by improving age-related deteriorations of cerebral blood flow regulation, short-term blood pressure control and arterial elasticity.

The study was conducted in 20 middle-aged athletes (ages 45 to 64) with at least 10 years of aerobic training and in 20 adults younger than 45 and 20 middle-aged sedentary adults. Researchers defined regular aerobic exercise in this study as running, cycling, swimming or multimodal training with moderate-to-vigorous intensity.

The long-term benefits of this study potentially mean significant improvements to human health. “Our findings have an important clinical implication,” said co-researcher Takashi Tarumi, PhD, of the National Institute of Advanced Industrial Science and Technology in Tsukuba, Japan. “Regular aerobic exercise during midlife may prevent these age-related chronic diseases and extend a healthy lifespan.”

Read the full article, “Midlife aerobic exercise and dynamic cerebral autoregulation: associations with baroreflex sensitivity and central arterial stiffness.” It is highlighted as one of this month’s “best of the best” as part of the American Physiological Society’s APSselectprogram. Read all of this month’s selected research articles.

To read more, click here

 

 

The Role of Caffeine in Artery Function

You can decide for yourself what you want to do about coffee and caffeine. For me there are way too many benefits, written about in these 102 posts on coffee and 47 posts on caffeine. Your doctor will know nothing concrete.

The Role of Caffeine in Artery Function

Flavanol-rich chocolate acutely improves arterial function and working memory performance counteracting the effects of sleep deprivation in healthy individuals

Fairly useless since it gives no amounts. And our fucking failures of stroke associations and doctors will not followup this with translational research. We are all screwed until a leader steps up to the plate.Bet you don't have a sleep protocol?
http://www.ncbi.nlm.nih.gov/pubmed/27088635

Grassi D¹, Socci V, Tempesta D, Ferri C, De Gennaro L, Desideri G, Ferrara M.

Author information

Abstract

BACKGROUND:

Sleep deprivation is a risk factor for cardiovascular disease. Cocoa flavonoids exert cardiovascular benefits and neuroprotection. Whether chocolate consumption may mitigate detrimental effects of sleep loss on cognitive performance and cardiovascular parameters has never been studied.

AIM:

We investigated the effects of flavanol-rich chocolate consumption on cognitive skills and cardiovascular parameters after sleep deprivation.

METHODS:

Thirty-two healthy participants underwent two baseline sessions after one night of undisturbed sleep and two experimental sessions after one night of total sleep deprivation. Two hours before each testing session, participants were randomly assigned to consume high or poor flavanol chocolate bars. During the tests were evaluated, the Psychomotor Vigilance Task and a working memory task, office SBP and DBP, flow-mediated dilation and pulse-wave velocity.

RESULTS:

Sleep deprivation increased SBP/DBP. SBP/DBP and pulse pressure were lower after flavanol-rich treatment respect to flavanol-poor treatment (SBP: 116.9 ± 1.6 vs. 120.8 ± 1.9 mmHg, respectively, P = 0.00005; DBP: 70.5 ± 1.2 vs. 72.3 ± 1.2 mmHg, respectively, P = 0.01; pulse pressure: 46.4 ± 1.3 vs. 48.4 ± 1.5 mmHg, P = 0.004). Sleep deprivation impaired flow-mediated dilation (5.5 ± 0.5 vs. 6.5 ± 0.6%, P = 0.02), flavanol-rich, but not flavanol-poor chocolate counteracted this alteration (flavanol-rich/flavanol-poor chocolate: 7.0 ± 0.6 vs. 5.0 ± 0.4%, P = 0.000001). Flavanol-rich chocolate mitigated the pulse-wave velocity increase (P = 0.001). Flavanol-rich chocolate preserved working memory accuracy in women after sleep deprivation. Flow-mediated dilation correlated with working memory performance accuracy in the sleep condition (P = 0.04).

CONCLUSION:

Flavanol-rich chocolate counteracted vascular impairment after sleep deprivation and restored working memory performance. Improvement in cognitive performance could be because of the effects of cocoa flavonoids on blood pressure and peripheral and central blood flow.

PMID:

27088635

[PubMed - in process]

 

Systems Biology and Noninvasive Imaging of Atherosclerosis

I couldn't tell at all from this limited part of the article what to ask my doctor to do to image my arteries to see what risks I have. 

Systems Biology and Noninvasive Imaging of Atherosclerosis

1. Claudia Calcagno,
2. Willem J.M. Mulder,
3. Matthias Nahrendorf,
4. Zahi A. Fayad

+ Author Affiliations

1. From the Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY (C.C., W.J.M.M., Z.A.F.); Department of Medical Biochemistry, Academic Medical Center, Amsterdam, The Netherlands (W.J.M.M.); and Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA (M.N.).

1. Correspondence to Claudia Calcagno, MD, PhD, Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029. E-mail claudia.calcagno@mssm.edu

Key Words:

• atherosclerosis
• cardiovascular diseases
• inflammation
• lipids
• risk factors

Atherosclerosis is a systemic disease of the arterial vessel wall. Although the mortality due to cardiovascular events is decreasing, the prevalence of atherosclerosis and its comorbidities, and the consequent heath care costs are expected to rise sharply in the near future.¹

Because the precise cause and pathogenesis of this complex, multifactorial disease are still not fully understood, the clinical assessment of cardiovascular risk has been traditionally based on population risk factors (RFs).² However, this approach still largely fails to capture the individual’s cardiovascular risk: most cardiovascular events occur in patients with 1 or few traditional RFs, whereas individuals classified as high risk may never experience clinical events.³

The past 10 years have seen a significant paradigm shift in our understanding of the mechanisms of atherogenesis. From being considered the mere result of passive lipid accumulation in the vessel wall, atherosclerosis is now classified as an active inflammatory condition.^4,5 The presence of abundant, active inflammatory cells is a known hallmark of high risk, vulnerable atherosclerotic plaques.^4,5 Many studies have identified several systemic proinflammatory conditions (such as lupus,⁶ rheumatoid arthritis,^7–9 and primary cardiovascular events themselves¹⁰) as emerging, independent RFs for atherosclerosis. New evidence suggests that atherosclerosis arises from the complex influence of genetic, environmental, and behavioral variables on systemic and local inflammation through a complex network of molecules, cells, and organs. 

Thanks to the recent technological advancements of high-throughput ‘-omics’, a plethora of the genes, proteins, and cells …

[Full Text of this Article]

New model of arterial thrombus formation is similar to popular video game

This is cool. With some innovative thinking we should be able to come up with a way to disrupt that wave aggregation process. It would have to be much better than going down the stupid route of reducing cholesterol.
Your doctor should be able to explain this version vs. this earlier video of plaque formation.
Inflammation In Atherosclerotic Plaque Formation  
 

New model of arterial thrombus formation is similar to popular video game
A group of biophysicists, including representatives from MIPT, has developed a mathematical model of arterial thrombus formation, which is the main cause of heart attacks and strokes. The scientists described the process of platelet aggregation as being similar to the popular video game Tetris and derived equations that allowed them to reproduce the wave process of platelet aggregate formation in a blood vessel.

Activated thrombocyte on a slide with immobilized fibrinogen, one of the proteins found in the blood. Scanning electron microscopy. Photograph courtesy of Sergey Obydenny / Wikimedia

Researchers from the Dmitry Rogachev Federal Research and Clinical Center of Pediatric Hematology, Oncology and Immunology (FRCC PHOI), the Center for Theoretical Problems of Physico-Chemical Pharmacology, MIPT, Moscow State University, the Institute for Problems of Mechanical Engineering (St Petersburg), and the Free University of Berlin described the new model in the journal PLOS ONE. When discussing the development of the model and the members of the research team, Mikhail Panteleev, one of the authors of the publication, said:
“Fazly Ataullakhanov and I formulated the problem and derived the equation, and Evgenia Babushkina (now a graduate student in Berlin), under the guidance of her mentor Nikolay Bessonov, developed solution methods for the two-dimensional case taking into account the changing hydrodynamics of the flow in which the thrombus is formed. She also performed all the simulations and analyses. Fazly and I are professors of the Department of Translational and Regenerative Medicine of MIPT’s Faculty of Biological and Medical Physics, which is based at FRCC PHOI”.
Develpoment of a continuous adsorption equation under assumption that thrombus formation occurs in the same way as the tiles become stacked up in the classic video game Tetris is a key aspect of the new model. In Tetris, the tiles either drop down onto a flat surface, or become attached to parts sticking out from the rest of the block. The only difference between thrombus formation and the game is that when a layer is complete, it does not disappear, therefore as time passes a thrombus is capable of obstructing the space it is in. In addition, the falling shapes are always the same: the model describes the aggregation of platelets, specialized blood cells.
Having described the mathematical process of how vacant areas on the surface of a growing thrombus are filled, the scientists were able to build first a one-dimensional model (as in Tetris), and then a two-dimensional model (platelets are deposited in a dimensional plane). And at one point, the scientists began to consider certain platelets as being infinitely small, and the thrombus itself as being continuous; in other words, the scientists went from a discrete model to a continuous model.

• Discrete model: the system under study consists of individual particles, and the behaviour of each particle can be tracked individually. This makes it possible to simulate, for example, gas molecules in the problem of Brownian motion – representing each molecule as a particle colliding with a larger particle.
• Continuous model: the system under study consists of solid objects that can freely change their size or any other characteristic. This can be used to model temperature increase in a functioning boiler for example – the output will be the temperature field in the volume under study.

The sequential solution of the equations obtained enabled the researchers to reproduce the dynamics of the growth of a real thrombus and study its behaviour under various conditions – in the case of damage to the vascular wall for example.
Active media and autowaves
In their paper, the researchers emphasize that the process of thrombus formation resembles a travelling wave, and this similarity is by no means accidental. It was previously demonstrated that the thrombus formation process is like an autowave – the blood, which carries blood platelets and a number of special proteins for blood coagulation, is an active medium. At that time the conclusion drawn by the researchers was concerned with blood coagulation as a result of a cascade of biochemical reactions involving proteins, but it is also possible to talk of an active medium in the case of adhered platelets.

NOX2-mediated artery dysfunction in smokers: acute effect of dark chocolate

I assume post-stroke we do want artery dilatation.  So is this in your post-stroke hospital diet? Can your doctor use enough brains to see if this would work even in non-smokers? Do not do this without your doctors prescription. You know how damned dangerous dark chocolate is.

NOX2-mediated artery dysfunction in smokers: acute effect of dark chocolate

1. Lorenzo Loffredo,
2. Roberto Carnevale,
3. Ludovica Perri,
4. Elisa Catasca,
5. Teresa Augelletti,
6. Roberto Cangemi,
7. Fabiana Albanese,
8. Cristina Piccheri,
9. Cristina Nocella,
10. Pasquale Pignatelli,
11. Francesco Violi

+ Author Affiliations

1. I Clinica Medica, Sapienza University, Rome, Italy

1. Correspondence to Professor Francesco Violi, I Clinica Medica, Viale del Policlinico 155, Roma 00161, Italy; francesco.violi@uniroma1.it

1. Contributors Conception and design: FV, LL. Analysis and interpretation of data: FV, LL, RC, PP. Flow-mediated dilation analysis: LL. Patient enrolment: LP, EC, TA, RC, FA. Laboratory analysis: RC, CN, CP. Drafting the article: FV, LL.

• Accepted 30 June 2011
• Published Online First 31 July 2011

Abstract

Background Cocoa seems to exert artery dilatation via oxidative stress inhibition but the mechanism is still unclear.

Objectives To investigate whether in smokers, dark chocolate elicits artery dilatation(noun: dilatation

1. the action of dilating a vessel or opening or the process of becoming dilated.

) via down-regulation of NOX2, the catalytic core of NADPH oxidase.

Methods Flow-mediated dilatation (FMD), oxidative stress (as assessed by urinary isoprostanes excretion), nitric oxide generation (as assessed by serum levels of nitrite/nitrate (NOx)), NOX2 activity (as assessed by blood levels of soluble NOX2 derived peptide (sNOX2-dp)) and serum epicatechin were studied in 20 smokers and 20 healthy subjects (HS) in a crossover, single-blind study. Patients were randomly allocated to 40 g dark chocolate (>85% cocoa) or 40 g of milk chocolate (≤35% cocoa). FMD, urinary isoprostanes, NOx and sNOX2-dp were assessed at baseline and 2 h after chocolate ingestion.

Results Smokers had lower FMD and NOx and higher sNOX2-dp compared to HS. After dark chocolate intake, urinary isoprostanes and sNOX2-dp significantly decreased and FMD and NOx significantly increased in smokers but not in HS. No changes of the above variables were observed after milk chocolate intake. Multiple linear regression analysis showed that in smokers the only independent predictive variable associated with a change in FMD was a change in sNOX2-dp. Serum epicatechin increased in either group only after dark chocolate intake, reaching values higher than 0.1 μM. Platelets from smokers (n=5), but not from HS (n=5), showed lower p47^phox translocation to platelet membrane and higher NOx when incubated with 0.1–10 μM epicatechin.

Conclusion Results suggest that in smokers, cocoa enhances artery dilatation by lowering of NOX2 activation.