Peter J Anderson

Published Researcher. Conduct Clinical Trials. Research nitric oxide, ASCVD and endothelium chemistry. BlackBelt Fudoshin Bujutsu. Port Adelaide FC .

[Peter J Anderson @PeterJAnderson_]

My latest publication in the Australian Veterinary Journal.

Researched natural agents can provide efficacy

[Peter J Anderson @PeterJAnderson_]

Interestingly nitric oxide can also stabilise plaque whilst inhibiting artery and valve calcification

‘Nitric oxide donor molsidomine favors features of atherosclerotic plaque stability and reduces myocardial infarction in mice’

https://t.co/QNHIwAnKR8

‘Anti-inflammatory actions of inorganic nitrate stabilize the atherosclerotic plaque’

https://t.co/NjcWd0ISCf

[Peter J Anderson @PeterJAnderson_]

Hi,

Another potential mechanism:

Vitamin K2-MK-7 improves nitric oxide-dependent endothelial function in ApoE/LDLR-/- mice
https://t.co/Vqp3l8g3ZF

Nitric oxide regulates vascular calcification by interfering with TGF-β signalling
https://t.co/w7UIEbJC71

Nitric oxide prevents aortic valve calcification by S-nitrosylation of USP9X to activate NOTCH signalling
https://t.co/7pmhvX9W4U

[Peter J Anderson @PeterJAnderson_]

@slowup_fastdown The thing is to keep an open mind and read a lot
There’s some great knowledgeable people to follow like lipofan for eg

[Peter J Anderson @PeterJAnderson_]

@slowup_fastdown Re coupling eNOS is the ‘Holy Grail’ potentially of atherosclerosis

[Peter J Anderson @PeterJAnderson_]

@NutritionMadeS3 https://t.co/O39PhGEglW

https://t.co/zS2UVbgo5M

https://t.co/GVTSvPsNj9

https://t.co/Zi0KunvXnE

[Peter J Anderson @PeterJAnderson_]

@NutritionMadeS3 Hi Gil
related, nitric oxide can stabilise plaque whilst inhibiting calcification via inhibition of TGF-b

[Peter J Anderson @PeterJAnderson_]

Cheers

Yes I do appreciate the many systemic great and necessary roles of LDL - and I am on record stating it’s not always the causal factor -
I write a lot how it’s mostly the midstream substrate ( and post studies demonstrating hypercholesterolemia but no plaque of any type- including FH)

But I also note it can be causal upstream via the same mechanisms as the other 6/7 major risk factors ( they can all singularly or in sum produce ROS in excess that oxidises BH4 and uncouples eNOS creating endothelial retention chemistry)

Uncoupling not being binary .. I’m more articulating a way of avoiding ASCVD ( maintain/ replenish/ boost eNOS and NO)
In the arteries in particular I can’t see any resistance or repair of the retention mechanisms ( what ever the cause of uncoupling) by LDL

LDL doesn’t resist binding to GAG chains , doesn’t stop their elongation to bind, doesn’t inhibit the superoxude or peroxynitrite production

LDL doesn’t inhibit VSMC proliferation, ICAM and VCAM adhesion factor increases nor TGF -b or PDGF increases

I genuinely can’t find any of the lipoprotein retention mechanisms or chemistry inhibited or repaired by LDL once eNOS is uncoupled

Maybe very high LDL can saturate some trancytosis receptors inhibiting entry

[Peter J Anderson @PeterJAnderson_]

Now it’s ’plenty of people ‘ not me lol
Like I was saying not a good start to your argument just making things up
If something is complicated to you-it doesn’t always mean the author used AI … jeez

How about instead arguing my actual mechanistic points - I keep an open mind to being persuaded

How about

[Peter J Anderson @PeterJAnderson_]

lol not a good start of your argument
- its pretty basic writing that no one would need AI to write ( or understand)

Anyone that bothered to check my post/ tweet history would see it’s my normal subject matter

Isn’t there apps that can check if a text is composed by AI?
Before we or anyone else does check let’s agree who ever is wrong deletes themselves from x … deal?

[Peter J Anderson @PeterJAnderson_]

@isengrimm3 @ApoDudz @lipo_fan Reducing risk factors is consistently shown to be able to slow and even regress ( non calcified) plaque
Reducing risk factors = potentially reducing oxidative stress ,restoring BH4 function, recoupling eNOS

[Peter J Anderson @PeterJAnderson_]

@isengrimm3 @ApoDudz @lipo_fan If HTN is the major contributor of ROS and uncoupling … one would think so

Uncoupling and swapping in superoxide and peroxynitrite instead of nitric oxide is not binary
Even if HTN was only a part of the uncoupling, any reduction woukd trend the right way

[Peter J Anderson @PeterJAnderson_]

@mtm14 @ApoDudz @lipo_fan Pic of the month

[Peter J Anderson @PeterJAnderson_]

@mtm14 @ApoDudz @lipo_fan https://t.co/5KdKnfJRZo

[Peter J Anderson @PeterJAnderson_]

@ZKForTre As a fibrolytic enzyme… is there any adverse effects on stent stability?

[Peter J Anderson @PeterJAnderson_]

Whilst we cannot make plaque without LDL - regardless of risk factors….

LDL is only 1 of 6/7 upstream major causal risk factors that can create the endothelial chemistry to retain the LDL downstream

When we have highly active endothelial retention chemistry…. it doesn’t require much LDL to be retained and make plaque (why sometimes we see atherosclerosis with very low LDL)

Behoves us to also keep working on all risk factors

[Peter J Anderson @PeterJAnderson_]

@DrEricRodgers @BenBikmanPhD I haven’t looked into L-BHB but this paper shows BHB restoring eNOS by reducing ROS in a smoking rat model ( whilst still smoking!)

IMT changes also reversed whilst still smoking

How are you assaying NO improvements @BenBikmanPhD ?

[Peter J Anderson @PeterJAnderson_]

A bit closer look at this paper is warranted.

The administration of BHB to these rats in the P2 dose is similar to levels that can be achieved in ketosis.

Considering loss of eNOS function and nitric oxide may be the preeminent step for the endothelial chemistry changes that initiate lipoprotein retention…..

…..and that all cardio metabolic risk factors directly uncouple/reduce eNOS function (Ageing, HTN, IR, smoking, obesity, dyslipideamia)…..

……this paper shows a level of BHB can totally negate the deleterious affects of smoking on eNOS function and indeed restore its full function in the still smoking cohorts…..

Question:
Can keto diet induced increases of BHB levels then also negate other risk factors affects on eNOS? (including ROS/peroxynitrite uncoupling) ?

Also, the VCAM results were non defining over a 28 day timeline

‘The Effects of Ketone Body β-hydroxybutyrate on eNOS Levels and
VCAM-1 Expression in Wistar Rats Exposed to Cigarette Smoke

β-hydroxybutyrate acts as a stress response
molecule and regulates antioxidant defense mechanisms,
thereby maintaining redox homeostasis
By reducing free radicals through its radical scavenging activity, β-hydroxybutyrate may help preserve eNOS activity and prevent endothelial dysfunction induced by cigarette
smoke2
The decrease in eNOS observed in our study
can be attributed to the free radicals present in cigarette
smoke, which can react with NO and form peroxynitrite,
a highly reactive species with prooxidant properties,
thereby reducing the availability of active NO

Results: The administration of β-hydroxybutyrate led to a significant increase in eNOS levels in the Wistar
rat aorta ….
….and a reduction of aortic IMT compared to control with no intervention or treatment’

https://t.co/cpFTiAyCZl