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  #1   ^
Old Fri, May-20-16, 06:13
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
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Default elastic fiber fragmentation and plaque

https://www.sciencedaily.com/releas...60518141257.htm


Quote:
Research suggests new contributor to heart disease
Findings could change the scope of heart disease detection, treatment for millions

Medical professionals have long known that the buildup of plaque in arteries can cause them to narrow and harden, potentially leading to a whole host of health problems -- including heart attack, heart disease and stroke. While high blood pressure and artery stiffness are often associated with plaque buildup, new research from engineers at Washington University in St. Louis shows they are not the direct causes.

The team suggests a new culprit: fragmentation of elastic fibers within the arterial wall. The findings, recently published online in the journal Atherosclerosis, could change the scope of heart disease detection and treatment for millions of Americans.

"Our surprising results suggest that treating patients for hypertension and arterial stiffness may have no effect on plaque buildup because we are not treating the underlying defect of elastic fiber fragmentation," said Jessica Wagenseil, associate professor of Mechanical Engineering & Materials Science in the School of Engineering & Applied Science.

Wagenseil's lab used two different groups of mice in the study. Some were genetically predisposed to hypertension and reduced aortic compliance, or increased artery stiffness. The other mice were not genetically predisposed to the heart conditions. All of the mice were fed a Western (high-fat) diet for 16 weeks.

Wagenseil's team hypothesized the mice with the genetic heart issues would have more plaque buildup than the group without. However, their findings proved that hypothesis wrong.

After extensive testing, the team could detect no significant differences in plaque buildup between the two groups of mice. That led them to explore a third factor not typically associated with plaque accumulation: the structure of elastic fibers within the arterial wall.

In aging humans and in previous animal studies, hypertension and increased arterial stiffness are accompanied by fragmentation of the elastic fibers. In Wagenseil's study, the mice had reduced amounts of elastic fibers, which causes hypertension and increased arterial stiffness, but no elastic fiber fragmentation, which may be the critical difference in plaque accumulation.

"We were able to separate the effects of elastic fiber fragmentation from hypertension and arterial stiffness in plaque accumulation," Wagenseil said. "We found that hypertension and arterial stiffness alone, without elastic fiber fragmentation, have no effect on plaque buildup."

In editorial remarks in Atherosclerosis about the research, field experts Laura Hansen and W. Robert Taylor said Wagenseil's findings "suggest a paradigm shift" in the way researchers think about risk factors for plaque buildup, and the strategies for better treatment options.

The idea that increased artery stiffness is a consequence of plaque buildup, as opposed to a cause of it, as suggested by Wagenseil's findings, offers a different approach in the study of heart disease. It also could lead to a re-examination of the relationship between increased plaque and diet, exercise and other lifestyle choices commonly associated with artery health.

"Elastic fiber fragmentation is likely a key player in plaque buildup," Wagenseil said. "The next step is to determine how fragmentation affects the movement and activation of molecules and cells that are involved in plaque formation."


Maybe animals that are lacking in elastic fiber wind up with stiffer blood vessels--but fragmented elastic fibers not only cause a stiffening of arteries, but also a weaker structure, more prone to damage?
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  #2   ^
Old Fri, May-20-16, 06:29
Zuleikaa Zuleikaa is offline
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As Linus Pauling discovered eons ago, thus his Vitamin C therapy for treating heart disease.
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  #3   ^
Old Fri, May-20-16, 07:03
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
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Default

Does seem relevant. Makes sense to look at any other possible causes of fragmentation as well.

I've seen suggestions that plaque tends to form where there's likely to be the greatest levels of hydraulic stress... that might just be where there's the highest level of elastin in the first place.


This might be a jump, but a high fructose diet causes collagen abnormalities in rats--excess collagen in the tail and in the skin, with excessive cross-linking from glycation.

Quote:
Fructose diet-induced skin collagen abnormalities are prevented by lipoic acid.
Thirunavukkarasu V1, Nandhini AT, Anuradha CV.
Author information
Abstract
Nonenzymatic glycation of proteins, leading to chemical modification and cross-linking are of importance in the pathology of diabetic complications. We studied the effect alpha-lipoic acid (LA) on the content and characteristics of the protein collagen from skin of high-fructose fed rats. The rats were divided into 4 groups of 6 each. Two groups of rats were fed with a high fructose diet (60 g/100 g diet) and administered either LA (35 mg/kg b.w., i.p) (FRU+LA) or 0.2 ml vehicle (saline) (FRU) for 45 days. The other 2 groups were fed with control diet containing starch (60 g/100 g diet) and administered either saline (CON) or lipoic acid (CON+LA). The rats were maintained for 45 days and then sacrificed. Plasma glucose, insulin, fructosamine, protein glycation, and blood glycated hemoglobin (HbA1C) were measured. Collagen was isolated from skin and the physicochemical properties of collagen were studied. Fructose administration caused accumulation of collagen in skin. Extensive cross-linking was evidenced by enhanced glycation and AGE-linked fluorescence. Increased peroxidation and changes in physicochemical properties such as shrinkage temperature, aldehyde content, solubililty pattern, susceptibility to denaturing agents were observed in fructose-fed rats. SDS gel pattern of collagen from these rats showed elevated beta component of type I collagen. These changes were alleviated by the simultaneous administration of LA. Administration of LA to fructose-fed rats had a positive influence on both quantitative and qualitative properties of collagen. The results suggest a mechanism for the ability of LA to delay diabetic complications.


http://www.ncbi.nlm.nih.gov/pubmed/15763937

But of course rats can make their own vitamin c.
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  #4   ^
Old Fri, May-20-16, 07:34
Zuleikaa Zuleikaa is offline
Finding the Pieces
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Plan: Mishmash
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Quote:
This might be a jump, but a high fructose diet causes collagen abnormalities in rats--excess collagen in the tail and in the skin, with excessive cross-linking from glycation.
I wonder if that's why another reason Pauling used to rant about HFCS before it was even thought of that it had might have harmful effects. He would constantly mention it was causing structural and liver damage.

Quote:
I've seen suggestions that plaque tends to form where there's likely to be the greatest levels of hydraulic stress... that might just be where there's the highest level of elastin in the first place.
Like near the heart?

Quote:
But of course rats can make their own vitamin c.

But guinea pigs can't. Which is what Pauling used to test/prove his theory/treatment of heart disease.

Last edited by Zuleikaa : Fri, May-20-16 at 07:43.
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