Mitochondrial dysfunction is a major cause of cardiovascular disease (CVD)

[haidut]

At a first glance, mitochondrial dysfunction (a "functional" problem) has little in common with the build-up of plaque on arterial walls (a "structural" problem). However, as my readers know quite well, structure and function cannot be separated and a functional pathology is perfectly capable (in fact, guaranteed) to ultimately cause a structural pathology. Case in point - as the study below demonstrates, mitochondrial dys-function is a major causal factor in development of CVD, through the mechanism of "oxidative" stress downstream of the mitochondrial dysfunction. Since mitochondrial dysfunction is not addressed by any of the existing CVD treatments currently in clinical use, the authors argue it is not at all surprising that medicine has made zero progress in both preventing and treating this pathology.

Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?
Mitochondrial dysfunction and endothelial impairment linked to many cardiovascular diseases

"...The paper, "Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?" appears in the International Journal of Molecular Sciences. The authors propose a closer examination is necessary of this relationship between mitochondrial dysfunction, endothelial impairment, and atherosclerosis, to identify new precision medicine targets to better regulate mitochondrial functioning in patients with these conditions. Malfunctioning mitochondria causes endothelial dysfunction due to a molecule called a reactive oxygen species (ROS), or 'free radicals,' which are produced by the dysfunctional mitochondria. The increase in ROS then leads to oxidative stress, inflammation, and a buildup of cholesterol and lipids, forming atherosclerotic plaque in the blood vessels. The modulation of mitochondrial function through precision medicine could delay the development of this endothelial dysfunction. Although mitochondria have been recognized as a new therapeutic target in different pathological contexts, no clinical or preclinical studies have been designed on atherosclerosis."

 

[BRMarshall]

Thanks Haidut!

 

[Regina]

At a first glance, mitochondrial dysfunction (a "functional" problem) has little in common with the build-up of plaque on arterial walls (a "structural" problem). However, as my readers know quite well, structure and function cannot be separated and a functional pathology is perfectly capable (in fact, guaranteed) to ultimately cause a structural pathology. Case in point - as the study below demonstrates, mitochondrial dys-function is a major causal factor in development of CVD, through the mechanism of "oxidative" stress downstream of the mitochondrial dysfunction. Since mitochondrial dysfunction is not addressed by any of the existing CVD treatments currently in clinical use, the authors argue it is not at all surprising that medicine has made zero progress in both preventing and treating this pathology.

Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?
Mitochondrial dysfunction and endothelial impairment linked to many cardiovascular diseases

"...The paper, "Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?" appears in the International Journal of Molecular Sciences. The authors propose a closer examination is necessary of this relationship between mitochondrial dysfunction, endothelial impairment, and atherosclerosis, to identify new precision medicine targets to better regulate mitochondrial functioning in patients with these conditions. Malfunctioning mitochondria causes endothelial dysfunction due to a molecule called a reactive oxygen species (ROS), or 'free radicals,' which are produced by the dysfunctional mitochondria. The increase in ROS then leads to oxidative stress, inflammation, and a buildup of cholesterol and lipids, forming atherosclerotic plaque in the blood vessels. The modulation of mitochondrial function through precision medicine could delay the development of this endothelial dysfunction. Although mitochondria have been recognized as a new therapeutic target in different pathological contexts, no clinical or preclinical studies have been designed on atherosclerosis."

Thx!
And if they do mention diet, it will be to go low carb and no sugar or saturated fats.

 

[yerrag]

Thx!
And if they do mention diet, it will be to go low carb and no sugar or saturated fats.

I can appreciate the sarcasm. I'm glad I'm not the only one.

I read the first article, and it is a melange of terms I have come across, some I understand but more I don't. It used to be when I don't understand, I would say just leave it to these experts as surely they know what they're talking about. It was about trusting the science. But more and more, I have become very cynical and my attitude is that they're just opening up another rabbit hole for me to waste my time on trying to understand (if I have that capacity) or for me to go on a wild goose chase, by a subtle form of misdirection. Instead of me trying to look at the wider scope of general cause and effects relationships, I get mired in the quagmire of something none of us, will ever truly understand due to the complex web they weave.

Sure, there is mitochondrial dysfunction, but is it the first step that leads to downstream problems of atherosclerosis? Is mitochondrial dysfunction a consequence of other more understandable causes, and the dysfunction merely a symptom of these causes? And while they talk of the function of ROS as signalling molecules, which is of good use, they are focusing on ROS as bad because too much of it is produced due to a wayward mitochondria, called mitochondrial dysfunction. Or could it be that the mitochondria is just doing what it is supposed to do, and not being dysfunctional? After all, ROS is also used by our by neutrophils and macrophages and platelets to destroy bacteria and fungi, and by eosinophils as well. Neutrophils and macrophages carry out phagocytosis for the smaller forms, while eosinophils carry spew ROS to kill larger microbes.

In the process of doing so, a lot of spillover ROS is neutralized by the body's primary antioxidant system. Albumin is a primary extracellular antioxidant used heavily by the body, for example.

What is wayward about producing a lot of ROS when the body truly needs it? Wouldn't it be wayward when the mitochondria doesn't produce ROS? What more damage would we incur if the mitochondria fails to produce ROS when it's needed?

The approach they have is same old, same old: Wrap it in gobbledygook, ascribe it to genetics, and then tell us there will be a magic bullet to fix this soon. Meanwhile, focus on this thing you can't possibly understand, and stay away from the simple-minded approaches that are merely anecdotal and where fools and amateurs tread.

 

[AlaskaJono]

Ubiquinol - It's what cells need. Mitochondria specifically.

CoQ10 may be what's needed to boost mitochondrial activity. Apparently we produce less of it when we get older. It was a minor fad back in the 90's for supplementation extras when clients had major issues/Cardio Vascular/ Cancer, etc. . Liver/Lamb/Sardines - herring mackeral oysters tuna. Also extra virgin olive oil. I do my best. Cheers.

 

[cs3000]

"Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?"

so loop of excess oxidative stress from toxins (or lack of protection) -> malfunctioning mitochondria -> more oxidative stress -> more cellular dna enzyme dysfunction -> more malfunctioning mitochondria -> disease

Orange juice consumption induced changes in expression of, 3,422 genes, while hesperidin intake modulated the expression of 1,819 genes. Between the orange juice and hesperidin consumption groups, 1,582 regulated genes were in common. Many of these genes are implicated in chemotaxis, adhesion, infiltration and lipid transport, which is suggestive of lower recruitment and infiltration of circulating cells to vascular wall and lower lipid accumulation. Hesperidin displays relevant role in the nutrigenomic effect of orange juice on blood leukocytes in human volunteers: a randomized controlled cross-over study - PubMed

hesperidin is known to protect mitochondria from a bunch of different oxidative stressors. and also to increase endothelial function
also something as simple as vitamin C , decreases risk of mortality by 20% (and specifically CVD mortality) ,
probably for the same reason

in the present study, the consumption of orange juice induced a +40-μmol/L increase in fasted plasma vitamin C concentration after 4 wk. This result could be particularly relevant considering that a 20-μmol/L rise in plasma vitamin C concentration has been associated with an approximate 20% reduction in risk of total mortality and CVD mortality in the general population (45). Relation between plasma ascorbic acid and mortality in men and women in EPIC-Norfolk prospective study: a prospective population study. European Prospective Investigation into Cancer and Nutrition - PubMed

 

[BRMarshall]

@cs3000
Thanks for your interesting finds concerning research on hesperidin!

 

[cs3000]

@cs3000
Thanks for your interesting finds concerning research on hesperidin!

looks good

@haidut a study you will likely find interesting / useful relevant to mitochondria function if havent seen before

High throughput screening of mitochondrial bioenergetics in human differentiated myotubes identifies novel enhancers of muscle performance in aged mice

Hesperetin increases mitochondrial ATP content 33% - the most potent compound out of 7949 tested for cellular respiration

High throughput screening of mitochondrial bioenergetics in human differentiated myotubes identifies novel enhancers of muscle performance in aged mice Hesperetin (derivative of Hesperidin in orange juice) improves cellular respiration for more ATP which is a key to overall health. increased...

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