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  #1   ^
Old Fri, Oct-06-17, 07:39
teaser's Avatar
teaser teaser is offline
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Thumbs down potassium and arterial calcification

https://www.sciencedaily.com/releas...71005102712.htm

Quote:
Bananas and avocados -- foods that are rich in potassium -- may help protect against pathogenic vascular calcification, also known as hardening of the arteries.

University of Alabama at Birmingham researchers have shown, for the first time, that reduced dietary potassium promotes elevated aortic stiffness in a mouse model, as compared with normal-potassium-fed mice. Such arterial stiffness in humans is predictive of heart disease and death from heart disease, and it represents an important health problem for the nation as a whole.

The UAB researchers also found that increased dietary potassium levels lessened vascular calcification and aortic stiffness. Furthermore, they unraveled the molecular mechanism underlying the effects of low or high dietary potassium.

Such knowledge of how vascular smooth muscle cells in the arteries regulate vascular calcification emphasizes the need to consider dietary intake of potassium in the prevention of vascular complications of atherosclerosis. It also provides new targets for potential therapies to prevent or treat atherosclerotic vascular calcification and arterial stiffness.

A UAB team led by Yabing Chen, Ph.D., UAB professor of pathology and a Research Career Scientist at the Birmingham VA Medical Center, explored this mechanism of vascular disease three ways: living mice fed diets that varied in potassium, mouse artery cross-sections studied in culture medium with varying concentrations of potassium, and mouse vascular smooth muscle cells grown in culture medium.

Working from living mice down to molecular events in cells in culture, the UAB researchers determined a causative link between reduced dietary potassium and vascular calcification in atherosclerosis, as well as uncovered the underlying pathogenic mechanisms.

The animal work was carried out in the atherosclerosis-prone mouse model, the apoliprotein E-deficient mice, a standard model that are prone to cardiovascular disease when fed a high-fat diet. Using low, normal or high levels of dietary potassium -- 0.3 percent, 0.7 percent and 2.1 percent weight/weight, respectively, the UAB team found that the mice fed a low-potassium diet had a significant increase in vascular calcification. In contrast, the mice fed a high-potassium diet had markedly inhibited vascular calcification. Also, the low-potassium mice had increased stiffness of their aortas, and high-potassium mice had decreased stiffness, as indicated by the arterial stiffness indicator called pulse wave velocity, which is measured by echocardiography in live animals.

The different levels of dietary potassium were mirrored by different blood levels of potassium in the three groups of mice.

When researchers looked at arterial cross-sections in cultures that were exposed to three different concentrations of potassium, based on normal physiological levels of potassium in the blood, they found a direct effect for the potassium on arterial calcification within arterial rings. Arterial rings in low-potassium had markedly enhanced calcification, while high-potassium inhibited aortic calcification.

"The findings have important translational potential," said Paul Sanders, M.D., professor of nephrology in the UAB Department of Medicine and a co-author, "since they demonstrate the benefit of adequate potassium supplementation on prevention of vascular calcification in atherosclerosis-prone mice, and the adverse effect of low potassium intake."

Mechanistic details

In cell culture, low potassium levels in the culture media markedly enhanced calcification of vascular smooth muscle cells. Previous research by several labs including Chen's group has shown that calcification of vascular smooth muscle cells resembles the differentiation of bone cells, which leads to the transformation of smooth muscle cells into bone-like cells.

So the UAB researchers tested the effect of growing vascular smooth muscle cells in low-potassium cell culture. They found that the low-potassium conditions promoted the expression of several gene markers that are hallmarks of bone cells, but decreased the expression of vascular smooth muscle cell markers, suggesting the transformation of the vascular smooth muscle cells into bone-like cells under low-potassium conditions.

Mechanistically, they found that low-potassium elevated intracellular calcium in the vascular smooth muscle cells, via a potassium transport channel called the inward rectifier potassium channel. This was accompanied by activation of several known downstream mediators, including protein kinase C and the calcium-activated cAMP response element-binding protein, or CREB.

In turn, CREB activation increased autophagy -- the intracellular degradation system -- in the low-potassium cells. Using autophagy inhibitors, the researchers showed that blocking autophagy blocked calcification. Thus, autophagy plays an important role in mediating calcification of vascular smooth muscle cells induced by the low-potassium condition.

The roles of the CREB activation and autophagy signals were then tested in the mouse artery cross-section and living-mouse models, with low, normal or high levels of potassium in the media or diet. Results in both of those systems supported the vital role for potassium to regulate vascular calcification through calcium signaling, CREB and autophagy.

Besides Chen and Sanders, co-authors of the paper, "Dietary potassium regulates vascular calcification and arterial stiffness," published in JCI Insight, are Yong Sun, Chang Hyun Byon and Youfeng Yang, UAB Department of Pathology; Wayne E. Bradley, Louis J. Dell'Italia and Anupam Agarwal, UAB Department of Medicine; and Hui Wu, UAB Department of Pediatric Dentistry. Sanders, Agarwal and Chen are also members of the Research Department, Veterans Affairs Birmingham Medical Center.


Always with the bananas and potassium...

This was done in APOE deficient mice, this is a very common mouse model for atherosclerosis, developed with the assumption that dyslipidemia causes heart disease, because, cholesterol bad and stuff.

APOE is a lipoprotein involved in the transport of fat into the lymph and into the brain. One thing usually not brought up--the pattern of transport of fat, large fluffy particles, small dense, high particle count, low particle count--since where goes fat, so go fat soluble vitamins, that changes the pattern of delivery of vitamin a,d,e,k. K and D especially are relevant to calcification of soft tissues. Vitamin D especially relates to cholesterol metabolism. What if the problem with APOE variants had little to do with cholesterol, and lots to do with fat soluble vitamins?

No need to panic from this study that autophagy=atherosclerosis. APOE deficient mice that are calorie restricted have decreased atherosclerosis, also studies in humans who starved to death showed plaque regression, autophagy is a very broad term, this is just a case where autophagic processes were necessary to calcification under very specific conditions.

https://insight.jci.org/articles/view/94920

Full study.

No idea how this applies to humans, but keeping potassium intake from going too low seems low risk. Also sodium gets a bad rap, but most low carbers probably know by now that it has a role to play in preservation of body potassium, so I wonder what effect sodium has on APOE deficient mice?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3568659/

Found this study. Not Apoe deficient, ldl receptor knockout, another model of dyslipidemia.

Quote:
In conclusion, while high dietary sodium intake led to higher systolic blood pressure, low dietary sodium intake augmented atherosclerosis in hypercholesterolemic mice.


Not to jump to any conclusions, especially since all I've read of this study is pretty much the line I posted. But interesting.
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  #2   ^
Old Fri, Oct-06-17, 08:41
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Plan: Ketogenic (LCHFKD)
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Quote:
Originally Posted by teaser
This was done in APOE deficient mice, this is a very common mouse model for atherosclerosis, developed with the assumption that dyslipidemia causes heart disease, because, cholesterol bad and stuff.

APOE is a lipoprotein involved in the transport of fat into the lymph and into the brain. One thing usually not brought up--the pattern of transport of fat, large fluffy particles, small dense, high particle count, low particle count--since where goes fat, so go fat soluble vitamins, that changes the pattern of delivery of vitamin a,d,e,k. K and D especially are relevant to calcification of soft tissues. Vitamin D especially relates to cholesterol metabolism. What if the problem with APOE variants had little to do with cholesterol, and lots to do with fat soluble vitamins?

This is a very reasonable assumption and along with Vitamin D, K2 could also be a complementary mechanism to move calcium to where it really belongs.
Quote:
Originally Posted by teaser
No need to panic from this study that autophagy=atherosclerosis. APOE deficient mice that are calorie restricted have decreased atherosclerosis, also studies in humans who starved to death showed plaque regression, autophagy is a very broad term, this is just a case where autophagic processes were necessary to calcification under very specific conditions.

Right, that was my first reaction as I read the following quote:
Quote:
In turn, CREB activation increased autophagy -- the intracellular degradation system -- in the low-potassium cells. Using autophagy inhibitors, the researchers showed that blocking autophagy blocked calcification. Thus, autophagy plays an important role in mediating calcification of vascular smooth muscle cells induced by the low-potassium condition.

The takeaway for me is that we are dealing with a very complex metabolism where controlled autophagy is a positive thing, and uncontrolled autophagy due to chemical shortfalls or distortions, like anything else, may result in an unhealthy outcome.

Quote:
Originally Posted by teaser
No idea how this applies to humans, but keeping potassium intake from going too low seems low risk. Also sodium gets a bad rap, but most low carbers probably know by now that it has a role to play in preservation of body potassium, so I wonder what effect sodium has on APOE deficient mice?

Here again, the mechanism of sodium resulting in somewhat higher systolic blood pressure may be protective. The following excerpt from the study's Discussion section:
Quote:
In this study, selected dietary sodium intakes displayed differential effects on systolic blood pressure and atherosclerotic lesions. While high dietary sodium increased systolic blood pressure, it decreased both plasma renin concentrations and atherosclerotic lesion area in aortic roots of male LDL receptor −/− mice fed a saturated fat-enriched diet for 12 weeks.

One could posit that since dietary sodium has the effect of decreasing atherosclerotic lesions, the dynamic of higher systolic BP caused by sodium may also be a helpful mechanism. Lots to learn.
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  #3   ^
Old Fri, Oct-06-17, 10:19
locarb4avr locarb4avr is offline
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Default Study reveals link between dietary potassium and vascular calcification

A need for bananas? Dietary potassium regulates calcification of arteries
by Jeff Hansen

Bananas and avocados foods that are rich in potassium may help protect against pathogenic vascular calcification, also known as hardening of the arteries.
University of Alabama at Birmingham researchers have shown, for the first time, that reduced dietary potassium promotes elevated aortic stiffness in a mouse model, as compared with normal-potassium-fed mice. Such arterial stiffness in humans is predictive of heart disease and death from heart disease, and it represents an important health problem for the nation as a whole.

The UAB researchers also found that increased dietary potassium levels lessened vascular calcification and aortic stiffness. Furthermore, they unraveled the molecular mechanism underlying the effects of low or high dietary potassium.

Such knowledge of how vascular smooth muscle cells in the arteries regulate vascular calcification emphasizes the need to consider dietary intake of potassium in the prevention of vascular complications of atherosclerosis. It also provides new targets for potential therapies to prevent or treat atherosclerotic vascular calcification and arterial stiffness.

--snip snip--

Some low carb high K fruits/veggies

Tomato carb=3.89g/100g, Potassium=237mg/100g, Sodium=5mg/100g
Cucumber carb=3.63g/100g, Potassium=147mg/100g, Sodium=2mg/100g


Tomatoes and cardiovascular health.
https://www.ncbi.nlm.nih.gov/pubmed/12587984

Diet is believed to play a complex role in the development of cardiovascular disease, the leading cause of death in the Western world. Tomatoes, the second most produced and consumed vegetable nationwide, are a rich source of lycopene, beta-carotene, folate, potassium, vitamin C, flavonoids, and vitamin E. The processing of tomatoes may significantly affect the bioavailability of these nutrients. Homogenization, heat treatment, and the incorporation of oil in processed tomato products leads to increased lycopene bioavailability, while some of the same processes cause significant loss of other nutrients. Nutrient content is also affected by variety and maturity. Many of these nutrients may function individually, or in concert, to protect lipoproteins and vascular cells from oxidation, the most widely accepted theory for the genesis of atherosclerosis. This hypothesis has been supported by in vitro, limited in vivo, and many epidemiological studies that associate reduced cardiovascular risk with consumption of antioxidant-rich foods. Other cardioprotective functions provided by the nutrients in tomatoes may include the reduction of low-density lipoprotein (LDL) cholesterol, homocysteine, platelet aggregation, and blood pressure. Because tomatoes include several nutrients associated with theoretical or proven effects and are widely consumed year round, they may be considered a valuable component of a cardioprotective diet.


Conclusion: slow cook tomato + oil/fat soup is the perfect food for both low carb and non low carb diets. This one get both K and lycopene bioavailability.
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  #4   ^
Old Fri, Oct-06-17, 11:21
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Edited to confirm the two threads have been joined. Thanks to the Admin.

Last edited by GRB5111 : Sat, Oct-07-17 at 08:16.
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  #5   ^
Old Fri, Oct-06-17, 17:07
TucsonBill's Avatar
TucsonBill TucsonBill is offline
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And 2600mg in one teaspoon of French's NoSalt

https://www.fatsecret.com/calories-...frenchs/no-salt
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  #6   ^
Old Sat, Oct-07-17, 07:12
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WereBear WereBear is offline
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Quote:
Originally Posted by GRB5111
The takeaway for me is that we are dealing with a very complex metabolism where controlled autophagy is a positive thing, and uncontrolled autophagy due to chemical shortfalls or distortions, like anything else, may result in an unhealthy outcome.


Yes, and when I skip a meal, I am doing more than my waistline some good.

I need more guacamole...
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