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Reversing arterial plaque

artery cardiovascular disease lipids matrix gla protein vitamin k2 mk4 vitamin k2 mk7 xanthohumol plaque

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#271 brosci

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Posted 26 August 2017 - 05:44 AM

Most grape seed products in the market are not good  OPC grape seed extract. Currently I'm taking Tom Andre's product. I may add the "Terry Naturally" product in the future. 

 

I wonder how these two OPC products might compare:

I've been taking a resveratrol complex (resveratrol + quercetin + egcg) and have been thinking about tacking on one of those OPC supplements for cardiovascular health (although there is a case that more polyphenols taken via high-dose extracts is not necessarily better.)



#272 Darryl

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Posted 26 August 2017 - 06:39 PM

Given my past literature research on amino acid ratios in cardiometabolic health and lifespan, I thought this was an interesting study:

 

Venkatesh et al, 2017. Effect of arginine: lysine and glycine: methionine intake ratios on dyslipidemia and selected biomarkers implicated in cardiovascular disease: A study with hypercholesterolemic ratsBiomedicine & Pharmacotherapy91, pp.408-414.

The effect of intake ratios of arginine (Arg): lysine (Lys) and glycine (Gly): methionine (Met) on lipid profile and selected cardiovascular disease markers, was studied, in rats maintained on a hypercholesterolemic diet. The rise in blood cholesterol was countered by 32%, 24%, and 49%, respectively, through increased oral supplementation of Arg, Gly, and Arg + Gly; a corresponding increase in plasma phospholipids at the end of the 8-week study was observed. The elevated plasma cholesterol to phospholipids ratio was countered by 27, 40, and 57%, respectively, through oral supplementation of Arg, Gly, and Arg + Gly. The elevation in hepatic cholesterol was lowered by 18, 29, and 51%, respectively, while phospholipids concentration was concomitantly increased by these amino acids. The elevated cholesterol to phospholipids ratio was, thus, significantly countered in the hypercholesterolemic situation by orally supplemented Arg, Gly, and Arg + Gly. Increased plasma asymmetric dimethylarginine (ADMA) levels, under hypercholesterolemic conditions, were lowered by 12, 15 and 34%, respectively, while plasma symmetric dimethylarginine (SDMA) levels were lowered by 14, 10 and 17%, respectively, with orally supplemented Arg, Gly and Arg + Gly. Only Gly and Arg + Gly decreased plasma homocysteine levels. Total nitric oxide (NO) concentration was considerably increased by Gly supplementation in hypercholesterolemic rats. Thus, altered ratios of Arg:Lys or Gly:Met offered beneficial influence on the lipid profile and plasma levels of ADMA, SDMA and homocysteine in hypercholesterolemic rats. Optimal beneficial effects, among ratios tested, was observed when Arg:Lys and Gly:Met ratios were maintained in ratios of 1:1 and 2:1, respectively.

 

 


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#273 Daniel Cooper

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Posted 28 August 2017 - 01:35 AM

I believe we've discussed the anti-atherosclerosis properties of tocotrienols in this thread before.  In case not, here a dump of the articles I've collected on the subject.

 

I'm looking for some rationale on exactly what to take here.  I've seen some advocacy for taking just gamma or just delta tocotrienol, taking a mix of just tocotrienols (alpha, beta, delta, and gamma, and then even some advocacy of taking a taking a mix of tocotrienols and their more well known cousins the tocopherols.. 

 

Right now I'm taking "A.C. Grace - Unique E Tocotrienol Complex Tocopherol Free" which is 125mg 90% delta and 10% gamma tocotrienol.

 

The thing is, tocotrienols have positive effects beyond just reducing atherosclerosis, notably causing apoptosis of many cancer cell types.  And, I've seen some that seem to say that there is some synergy between the tocotrienols and the tocopherols. 

 

It's a lot to sort through.  Anyone that has given this some thought I'd love to hear your conclusions and the reasoning behind them.

 

In any case, the papers I have on tocotrienols:

 

 

Attached File  Multifaceted role of tocotrienols in cardioprotection supports their structure - function relation.pdf   277.06KB   7 downloads

 

Attached File  Novel Tocotrienols of Rice Bran Inhibit Atherosclerotic Lesions in C57BL-6 ApoE-Deficient Mice.pdf   707.33KB   5 downloads

 

Attached File  Oil palm phenolics and vitamin E reduce atherosclerosis in rabbits.pdf   571.81KB   7 downloads

 

Attached File  Tocotrienols Health Benefits (PowerPoint).pdf   24.75KB   8 downloads


Edited by Daniel Cooper, 28 August 2017 - 01:37 AM.

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#274 PWAIN

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Posted 28 August 2017 - 03:45 AM

Wondering what people here think of this:

https://www.theguard...isk-study-finds

Would this be the same mechanism as Rapamycin uses?
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#275 PWAIN

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Posted 28 August 2017 - 03:56 AM

This is a better article:

https://www.cnbc.com...flammation.html

Mechanism is reducing CRP which reduces inflammation. Also talks about Repatha which is a PCSK9 inhibitor but is very expensive. It lowers cholesterol even more that statins when used in combination with statins. I'm hoping a multi prong approach may help to actually reverse rather than just slow of stop plaque build up.
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#276 Daniel Cooper

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Posted 28 August 2017 - 05:59 PM

That's good stuff PWAIN.

 

The only issue is that canakinumab is a monoclonal antibody which I will assume means that it is expensive and currently no insurance is going to pay for it's use to prevent atherosclerosis, at least not until it becomes more established therapy.  And, there are some downsides to monoclonal antibody therapy but it doesn't seem like they'd be too bad for how often they are dosing (every 3 months I think).  Needless to say, we probably can't procure monnoclonal antibodies for experimentation on our pet rats.

 

But it does highlight that the underlying pathology is probably more inflammation rather than cholesterol.  And we can certainly look at other anti-inflammatory treatments that might be available to us.

 

 

Thanks for posting it.

 

 


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#277 aconita

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Posted 28 August 2017 - 06:43 PM

Arterial plaque seems due to inflammation not cholesterol, cholesterol deposit itself on inflamed arterial walls as a patch, low inflammation means low plaque formation.

 

OK, that's a bit simplistic...but gives the idea.  

 

Focusing on cholesterol isn't smart, high inflammation AND high cholesterol is risky, lowering inflammation should be the priority since it is the cause, cholesterol depositing is just the consequence.

 

I would rather perform CPR blood tests relatively often than scans, keeping checked the cause instead of the outcome.


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#278 mikey

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Posted 28 August 2017 - 07:12 PM

I would so much rather take DQ (not really, because of side-effects) and keep eating a healthy, organic fruits  veggies and nuts, grass-fed dairy, wild caught fish omnivore diet to reverse plaque.

 

However, I find data that says it's simpler than that. Not easy, because it requires a significant change in my tastes for foods.

 

A "simple" solution is generally not easy though.

 

But the data is clear ---

 

https://www.youtube....h?v=lXXXygDRyBU

 

https://www.youtube....h?v=cavI_FnIrh4


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#279 zen

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Posted 30 August 2017 - 12:46 PM

I would so much rather take DQ (not really, because of side-effects) and keep eating a healthy, organic fruits  veggies and nuts, grass-fed dairy, wild caught fish omnivore diet to reverse plaque.

 

However, I find data that says it's simpler than that. Not easy, because it requires a significant change in my tastes for foods.

 

A "simple" solution is generally not easy though.

 

But the data is clear ---

 

https://www.youtube....h?v=lXXXygDRyBU

 

https://www.youtube....h?v=cavI_FnIrh4

I agree, it is quite simple.
Unfortunately it seems that the majority of people would rather undergo open heat surgery then change their diets.

To add to you links here are two videos I found quite interesting:





 


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#280 RWhigham

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Posted 04 September 2017 - 01:27 AM

1 capsule per day for 6 months of inexpensive bergamot extract reduces heart risk factors.

Bergamot Reduces Plasma Lipids, Atherogenic Small Dense LDL, and Subclinical Atherosclerosis in Subjects with Moderate Hypercholesterolemia: A 6 Months Prospective Study

 

After 6 months: (80 patients  55 +/- 13 yrs of age)

  • Cholesterol      -12%
  • LDL                  -20%
  • Triglycerides    -17%
  • Carotid IMT      -25%
  • HDL                  +8%

Also see Benefits of Bergamot by Dr. Julian Whitaker

Also see Bergamot: Does It Lower Cholesterol? Review of Research (Updated 2017)  <--  research summary

 


Edited by RWhigham, 04 September 2017 - 01:34 AM.

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#281 zorba990

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Posted 04 September 2017 - 02:26 AM

Ultrasound looks promising
https://www.ncbi.nlm...les/PMC4314792/

"Journal of Therapeutic Ultrasound
BioMed Central
Removing atherosclerotic plaque created using high cholesterol diet in rabbit using ultrasound
Christakis Damianou, Christos Christofi, and Nicos Mylonas

Additional article information

Abstract
Background
The aim of the proposed study was to conduct a feasibility study using a flat rectangular (3 × 10 mm2) transducer operating at 5 MHz for removing atherosclerotic plaque in an in vivo model. The proposed method can be used in the future for treating atherosclerotic plaques in humans.

Methods and results
The plaque in the rabbits was created using high cholesterol diet for 4 months. The amount of plaque removed was studied as a function of intensity, with a fixed pulse repetition frequency (PRF), and duty factor (DF).

Conclusions
The amount of plaque removed is directly related to the acoustic intensity. It was found that the presence of bubbles accelerates the removal of plaque. In order to ensure that pure mechanical mode ultrasound was used, the intensity used does not produce temperatures that exceed 1°C.

Keywords: Ultrasound, Atherosclerotic, Plaque, Pulse
Introduction
Atherosclerosis is a condition in which fatty material collects along the walls of arteries. This fatty material thickens and may eventually block the arteries [1]. The plaque is composed of distinctly morphological features including a fibrous cap comprised of smooth muscle cells, fibrotic tissue, and lipid core containing fat-laden macrophages and extracellular lipids [1]. In the advanced stage, atherosclerotic plaque contains large amounts of calcium salt [2], which significantly increases the mechanical properties of the plaque. Histology studies have also led to the recognition that plaque structure influences the risk of plaque rupture. Specifically, a plaque with a thin fibrous cap and a large lipid core is more prone to rupture [3].

Lifestyle changes, such as eating a healthy diet and exercising, are often the best treatment for atherosclerosis. But sometimes, medication or surgical procedures may be recommended as well [4]. Atherosclerosis treatment may require special surgical procedures such as Balloon Angioplasty [5-7], balloon angioplasty and stenting [8,9], cutting balloon [10-12], atherectomy [13,14], and surgical bypass [15,16], to open an artery and improve blood flow. The main treatment for the carotid artery is endarterectomy [17-19].

Recently therapeutic ultrasound has been employed in the hospitals for many applications. Therapeutic ultrasound was utilized on prostate carcinoma in rats, where it was proven that thermal ultrasound has the potential to treat small localized prostate cancer lesions [20]. Clinical trials utilizing thermal ultrasound and ultrasound imaging were published thereafter [21,22]. The two dominant clinically available systems using transrectal HIFU are Ablatherm HIFU (Technomed International, Lyon, France) and HIFU Sonablate 500 (Focal Surgery, Milpitas, CA now SonaCare Medical, Charlotte, NC, USA). Recent advances of the transrectal device includes a phased-array probe for more efficient treatment of the prostate [23]. Another clinical success that employs therapeutic ultrasound with magnetic imaging guidance (MRI) is the technology introduced by the Israeli company InSightec [24]. This technology resulted in the first commercial system for the treatment of uterine fibroids (using also thermal ultrasound), which received approval by the Food and Drug Administration (FDA) in 2004. This system is incorporated in the table of a General Electric MRI scanner. The system initially was approved for the treatment of various gynecological tumors [25-28]. An endorectal thermal ultrasound system produced by the same company has been utilized recently for the treatment of prostate cancer [29,30]. The same company utilized thermal ultrasound for pain palliation of bone metastases [31-33]. Finally, InSightec developed a transcranial MRI-guided HIFU system for the non-invasive treatment of various brain diseases [34] such as brain cancer, and Parkinson’s disease (thermal ultrasound), and stroke (mechanical ultrasound using microbubbles). Philips Healthcare, Netherland showed interest in this technology recently and, as a result the MRI guide HIFU system, Sonalleve was developed as a commercial product [35] for the treatment of uterine fibroids and bone palliation using thermal ultrasound. This system is incorporated in the table of a Philips MRI scanner. Besides the two systems providing therapy for prostate diseases, there is another technology from China [36-39] that establishes extracorporeal thermal ablation for various organ using focused ultrasound and ultrasonic imaging (liver, breast, kidney, osteosarcoma, and pancreas).

Recently at the University of Minnesota, researchers attempted to treat atherosclerosis with noninvasive method such as HIFU [40]. The University of Minnesota recently developed a new HIFU technology that performs noninvasive, real-time ultrasonic imaging and localized treatment using thermal ultrasound.

In this paper, pulsed ultrasound was utilized for the first time for removing atherosclerotic plaque in an in vivo rabbit model. In order to ensure that pure mechanical mode ultrasound was used, the protocols were designed so that the temperature does not exceed 1°C. However, to our knowledge, no prior studies have been reported on ultrasound ablation of atherosclerotic plaque using pulsed ultrasound.

This paper describes a feasibility study that was carried out, in order to investigate the effectiveness of a therapeutic protocol in removing atherosclerotic plaque through pulsed ultrasound using a planar unfocused transducer operating at 5.3 MHz. An existing good model for developing atherosclerotic plaque [41,42] was used. In this animal model, high cholesterol diet is administered to rabbits. As a result, atherosclerotic plaque is formed in various arteries of the rabbit (aorta, abdominal, and carotid). The efficacy of pulsed ultrasound was monitored with ultrasonic imaging. The growth of the plaque was evaluated with histology of the arteries. Although the aorta is the biggest artery with size comparable to important arteries of humans (for example coronary), we have chosen to use the carotid artery for therapy, mainly to avoid breathing and because access to this artery with ultrasound is easy.

The main ultrasonic parameter evaluated for its effect on the treatment was the intensity. The duty factor (DF) was varied in just one experiment to show that there is limit on the value of DF to be used, since high DF may cause thermal effects. Thus, the main therapy parameter used in this study was the acoustic intensity.

Materials and methods
Experimental setup
Figure 1A shows the schematic diagram of the ultrasound system. The apparatus is divided into two subsystems: (1) ultrasound generation, and (2) passive cavitation detection (a hydrophone was employed to monitor cavitation activity). A 5.3-MHz sinusoidal input was generated by a function generator (Agilent 33120 15 MHz Function/Arbitrary Waveform Generator, Englewood, CO, USA). The electrical signal is amplified by an RF amplifier (75 W, AR, Souderton, PA, USA), and then delivered through an impedance matching network designed exclusively for this particular transducer. Figure 1B shows the coupling of the transducer to the rabbit carotid artery.

Figure 1
Figure 1
System diagram and coupling to animal. Diagram of the pulsed high intensity ultrasound system which includes a generator/amplifier, a temperature reader, and a passive cavitation detector; (A) and coupling of the transducer to the carotid artery (B) ...
The active size of the transducer is 3 × 10 mm2. The transducer material is P762-type PZT piezoceramic (Quartz & Silice, Nemours, France) with air backing, operating at 5.3 MHz. Figure 2A shows the transducer holder manufactured using acrylonitrile butadiene styrene (ABS). The ABS parts of the robot were designed using computer-aided design (CAD) software (Microstation V8, Bentley Systems, Inc., Exton, PA, USA). The files were then exported to computer-aided manufacturing (CAM) software (Insight V. 6.4.1, Stratasys Inc., Eden Prairie, Minnesota, USA). The files were sent to a 3D printer (FDM400, Stratasys, 7665 Commerce Way, Eden Prairie, MN, USA) for production. This structure contains two inlets for transducer cooling and two inlets for transducer wiring. Figure 2B shows the drawing of the transducer holder indicating the water inlets and wiring inlets. Figure 2C shows the final assembly of the transducer inside the plastic holder. Because in future clinical trials the transducer will be incorporated in a catheter that will be guided through arteries (1–3 mm wide), the transducer element must be as compact as possible. Since the catheter will be inserted in the body, after the treatment the catheter will be destroyed (therefore it is considered consumable).

Figure 2
Figure 2
Transducer design. Transducer holder manufactured using ABS. This structure contains two inlets for transducer cooler and two inlets for the transducer wires (A). Drawing of the transducer holder indicating the water inlets and wiring inlets (B). Final ...
Using the acoustic balance technique [43], the electroacoustic efficiency of the applicator was measured (55% at 5.3 MHz). The external face of the transducer was cooled by a continuous flow of degassed water circulating the length of the transducer. The water cooling circuit was maintained at 15°C and was driven by a Masterflex peristaltic pump (Cole Parmer Instrument Co., Chicago, IL, USA) at a flow of 0.15 L/min.

Sonication parameters
The spatial-average pulse-average (SAPA) intensity was estimated, by dividing the power with the surface area of the transducer. The PRF used was 100 Hz. The duty factor varied from 10% to 40%. The sonication duration was 5 min because the ultrasound bubbles injected in the circulation system of the rabbit last for 5 min. Several 5-min sessions were used to effectively remove all the plaque desired.

Cavitation detection
The cavitation activity was monitored using a hydrophone (Specialty Eng. Associates, Irvine, CA, USA). The signal from the hydrophone was fed to a custom-made amplifier (×20 amplification), and was high-pass-filtered using a custom-made filter. Fast Fourier transform (FFT) spectrums of the acoustic emission signals were acquired using a PC-based interface card (Gage, Lockport, NY, USA). The hydrophone was aligned perpendicular to the sample under investigation.

Animals and diet
Totally 17 New Zealand rabbits (3.8–4 kg) were used during the experiments. The rabbits were divided randomly into two groups. The animals of group A (n = 2) were fed with normal chow. In group B (n = 15) the animals were fed with 2% high cholesterol diet (T2030, Harlan laboratories SRL, Udine, Italy). Twelve (12) rabbits in this group B were sacrificed without any treatment. These rabbits were used as a reference for evaluating the reduction of artery at the first month (n = 3), second month (n = 3), third month (n = 3), and fourth month (n = 3). Three (n = 3) rabbits were treated with ultrasound and microbubbles. Animals going through the high cholesterol diet were sacrificed to a maximum of 4 months, because severe side effects appeared (hypercholesteremic side effects such as weight loss, appetite loss, and jaundice).

In vivo experiments
The rabbits were anaesthetized using a mixture of 500 mg of ketamine (100 mg/mL, Aveco, Ford Dodge, IA, USA), 160 mg of xylazine (20 mg/mL, Loyd Laboratories, Shenandoah, IA, USA), and 20 mg of acepromazine (10 mg/mL, Aveco, Ford Dodge, IA) at a dose of 1 mL/kg. The animal experiments protocol was approved by the national body in Cyprus responsible for animal studies (Ministry of Agriculture, Animal Services).

Statistical analysis
Statistical analysis was performed using the software SIMA. Paired t-test analyses were used to compare lumen area reduction with and without high cholesterol. Correlation analyses were performed using linear regression analysis with 95% confidence intervals (p = 0.05). Same analysis was performed when assessing the effect of ultrasonic intensity on the plaque reduction.

Ultrasound bubbles
Prior to the application of ultrasound a bolus of an ultrasound contrast agent (SonoVue; Bracco SpA, Milan, Italy) was injected intravenously through the ear vein at a dose of 0.02 mL/kg.

Hematoxylin and eosin (ΗΕ) staining
By the end of the experiments the rabbits were sacrificed and transcardially perfused with 60 mL phosphate-buffered saline and 120 mL 4% paraformaldehyde. The artery was then soaked in paraformaldehyde for 24 h. Hematoxylin and eosin staining was performed on paraffin-embedded artery with a slice thickness of 10 μm for histologic examinations.

Ultrasonic imaging
An ultrasonic system (Philips HD7 series Ultrasound Systems, Philips and Neusoft Medical Systems Co. Ltd, Shenyang, China) was used to monitor the plaque removal during ultrasound therapy using a 12-MHz probe dedicated for small structures.

Temperature measurement
A data acquisition board (6251 DAQ, National Instruments, TX, USA) was used to measure the temperature in the artery. An analogue input of the board is used to capture the temperature. An Omega (M2813-1205, OMEGA Engineering, Inc. Stamford, CT, USA) voltage-to-temperature converter was used to measure temperature using a software written in MatLab (The Mathworks Inc., Natick, MA, USA). A thermocouple (Omega Engineering) was placed in the carotid artery to measure temperature elevation at the surface of the transducer since at that point maximum temperature is achieved. The size of the thermocouple was chosen to be 50 μm, so that the interaction with the beam of ultrasound is minimized.

Results
Figure 3 shows photos of the rabbit aorta with HE staining indicating the growth of the plaque within the artery: A) 0 months, B) 1 month, C) 2 months, and D) 3 months. In order to acquire histology for a specific rabbit, the animal was sacrificed. Therefore, the photos of Figure 3 are taken from different rabbits. Care was taken that all three rabbits in this study were of the same age and weight (as much as possible).

Figure 3
Figure 3
Photos of the rabbit aorta with HE staining indicating the growth of the plaque within the artery. 0 months (A), 1 month (B), 2 months ©, and 3 months (D).
Table 1 shows the lumen area reduction obtained using histology, expressed as percentage with respect to the original size for the three arteries under examination (aorta, abdominal, and carotid), as a function of months elapsed after the initiation of the diet. The standard deviation of the average reduction in the lumen size is also provided. The reduction of lumen area with cholesterol diet at any month was compared with the lumen area without the diet. It was demonstrated that there is a significant reduction of the lumen area (p < 0.02, paired t-test, n = 3) with high cholesterol diet. A value of p > 0.05 was only observed when comparing months 4 and 3, indicating that after month 3, the lumen area is not reduced further.

Table 1
Table 1
Lumen reduction extracted from histology as percentage with respect to the original size for the three arteries under examination (aorta, abdominal, and carotid) as a function of month elapsed after the initiation of the diet
Figure 4 shows typical plaques in the carotid artery as imaged with ultrasound at 12 MHz. In three of the cases, the reduction occurs in one side of the carotid artery. In one case the plaque appears on both sides of the carotid artery (Figure 4C).

Figure 4
Figure 4
Typical plaques in the rabbit carotid as imaged with ultrasound at 12 MHz. In three of the cases, the reduction occurs in one side of the rabbit carotid artery (A, B, D). In one case, the plaque appears on both sides of the artery ©. Plaques ...
Figure 5 shows the steady state temperature measured with a thermocouple in the carotid with respect to duty factor (DF) with intensity of 30 W/cm2 (SAPA), and PRF = 100 Hz. Note that with DF greater than 10%, the steady state temperature increases above 1°C and therefore some thermal effects are observed.

Figure 5
Figure 5
Steady state temperature measured in the carotid with respect to DF with intensity of 30 W/cm 2 (SAPA), and PRF = 100 Hz. Note that with DF above 10%, the temperature increases above 1°C and therefore some thermal ...
Figure 6A shows the ultrasonic image of plaque in the carotid of the rabbit with a plaque after 3 months of diet. Figure 6B shows the ultrasonic image after the application of ultrasound with I = 30 W/cm2 (SAPA), PRF = 100 Hz, and DF = 10%. The plaque was removed after five sessions of 5-min injection of microbubbles. Note that almost all the plaque is removed. Figure 6C shows the photo of the HE staining of the carotid artery showing small amount of residual plaque. Figure 6D shows the temperature measured during the destruction of plaque, indicating temperature increase of approximately 1°C. Figure 6E shows the frequency spectrum at one instance, during the destruction of plaque, indicating only subharmonic emissions which are indicative of stable cavitation.

Figure 6
Figure 6
Therapy results. Ultrasonic image of the plaque in the carotid of the rabbit, photo of the HE staining of the carotid artery, temperature during plaque destruction, and frequency spectrum during the destruction of plaque. Ultrasonic image of plaque in ...
The effect of the intensity on the removal of plaque was investigated. The carotid of three rabbits was exposed to different spatial average, pulse average (SAPA) intensity varying from 10 to 30 W/cm2, with the D.F. and PRF at 10% and 100 Hz, respectively. Figure 7 shows the size of the plaque removed, as measured from the ultrasound images, versus intensity (SAPA). During these experiments, the temperature did not exceed 1°C. The reduction of lumen size with the application of ultrasonic intensity at different levels was compared to the size of the untreated lumen. It was demonstrated that there is a significant reduction of the lumen size (p < 0.05, paired t-test, n = 3) with ultrasonic intensity.

Figure 7
Figure 7
Effect of intensity. Size of the plaque removed as measured from the ultrasound images versus intensity (SAPA), D.F. = 10%, and PRF = 100 Hz.
Conclusions
This paper includes a feasibility study that investigates the effectiveness of pulsed ultrasound in removing atherosclerotic plaque, created in rabbit with the final intention to remove atherosclerotic plaque from vessels. This feasibility study includes the effect of intensity and DF.

The experiments were conducted in the rabbit carotid with protocols leading to temperatures less than 1°C (safe temperature). It was demonstrated in a set of experiments that if the DF is increased, then the safe temperature is exceeded. Another parameter that increases the temperature is the intensity. In these experiments the intensity used was carefully chosen, and, therefore no temperature elevation above 1°C was produced. The removed plaque, as expected, increases with the intensity.

Very promising results were obtained in carrying out experiments in the carotid of rabbits. With this transducer and protocol we were able to remove atherosclerotic plaque up to a depth of 2 mm in 25 min. This type of technology looks promising for the removal of atherosclerotic plaque in humans, provided that the dissolved material from the plaque is collected. The collected material must not flow through the blood stream to other arteries, thus causing blockage of arteries. Care should be taken to collect all the removed particles. For example, in studies involving atherectomy [44,45], a suction mechanism was used to collect the removed particles. Such suction technology can also be incorporated with this ultrasound technology to remove the residual particles.

Also, it is possible that if the particle size is too small, then there is no need to collect the residual particles and, therefore, the deployment of ultrasound technology would be more feasible. Yet, clinical studies need to be done in order to reveal how small this residual particle must be. This specific device, with this size, can be used probably in peripheral arteries or in the carotid. Special design of the device needs to be done so as not to block the artery. For the application in the heart arteries, the device must be scaled down to possibly 1 mm.

Previously [40], therapeutic ultrasound was utilized using its thermal capabilities to ablate plaque in swine. With thermal ultrasound, plaques are heated and eventually destroyed. Due to the close proximity of the plaque to the artery, crucial thermal damaged tissue could be produced in the artery. With our method, pulse ultrasound is used in combination with microbubbles, and therefore plaque is detached leaving potentially no severe damage to the artery.

We clearly see the destruction of plaque using ultrasonic imaging, but what content of the plaque (lipid, calcium, or microphage) is destroyed first cannot be assessed accurately with ultrasound imaging.

The combination of pulsed ultrasound and microbubbles has been shown to be effective for removing clot [46] which is a much softer tissue than plaque. The use of ultrasound alone was ineffective to remove clot [46] in a rabbit carotid model. Microbubbles are known to cause stable cavitation and therefore assist the removal of clots. We speculated that the same effect (stable cavitation) could accelerate plaque removal. Further experiments need to be conducted to show that pulsed ultrasound alone will not be efficient in removing plaque as compared to pulsed ultrasound in synergy with microbubbles.

This technology can be used in the future for clinical trials primarily to treat plaques in the carotid. Unstable plaques in the carotid are a major source of plaques, which can reach the brain and cause stroke. The device can be attached to a catheter of appropriate size and the catheter can be guided intravenously to the carotid for ultrasonic treatment. Care will be taken to avoid the escape of debris reaching the brain, thus causing stroke.

Acknowledgements
This work was supported by the Research Promotion Foundation (RPF) of Cyprus (program ΕΠΙΧΕΙΡΗΣΕΙΣ/ΠΡΟΪΟΝ/0311/01 and the European regional development structural funds).

Footnotes
Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

CD carried out the ultrasonic experiments and wrote the manuscript. CC was responsible for the histology evaluation and the delivery of the high cholesterol diet. NM designed the transducer setup and performed the ultrasonic imaging. All authors read and approved the final manuscript.

Contributor Information
Christakis Damianou, Email: yc.moc.tenatyc@uonaimadc.

Christos Christofi, Email: yc.moc.tenatyc@amlad.

Nicos Mylonas, Email: yc.ca.tif@nm.sub.

Article information
J Ther Ultrasound. 2015; 3: 3.
Published online 2015 Jan 29. doi: 10.1186/s40349-015-0025-8
PMCID: PMC4314792
Christakis Damianou,corresponding author Christos Christofi, and Nicos Mylonas
Electrical Engineering Department, Cyprus University of Technology, Limassol, Cyprus
R&D Department, MEDSONIC, LTD, Limassol, Cyprus
Computer Science Department, Frederick Research Center, Limassol, Cyprus
Christakis Damianou, Email: yc.moc.tenatyc@uonaimadc.
Contributor Information.
corresponding authorCorresponding author.
Received 2014 Oct 20; Accepted 2015 Jan 13.
Copyright © Damianou et al.; licensee BioMed Central. 2015
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommo...licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Articles from Journal of Therapeutic Ultrasound are provided here courtesy of BioMed Central
References
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2. Romer TJ, Brennan JF, Fitzmaurice M, Feldstein ML, Deinum G, Myles JL, et al. A rotational ablation tool for calcified atherosclerotic plaque removal. Biomed Microdevices. 1998;97:8.
3. Insull W. The pathology of atherosclerosis: plaque development and plaque responses to medical treatment. Am J Med. 2009;122(1):S3–14. doi: 10.1016/j.amjmed.2008.10.013. [PubMed] [Cross Ref]
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7. Dake MD, Ansel GM, Jaff MR, Ohki T, Saxon RR, Smouse HB, et al. Paclitaxel-eluting stents show superiority to balloon angioplasty and bare metal stents in femoropopliteal disease: twelve-month Zilver PTX randomized study results. Circ Cardiovasc Interv. 2011;4(5):495–504. doi: 10.1161/CIRCINTERVENTIONS.111.962324. [PubMed] [Cross Ref]
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10. Takebayashi H, Haruta S, Kohno H, Ichinose H, Taniguchi M, Shimakura T, et al. Immediate and 3-month follow-up outcome after cutting balloon angioplasty for bifurcation lesions. J Interv Cardiol. 2004;17(1):1–7. doi: 10.1111/j.1540-8183.2004.00246.x. [PubMed] [Cross Ref]
11. Bergersen LJ, Perry SB, Lock JE. Effect of cutting balloon angioplasty on resistant pulmonary artery stenosis. Am J Cardiol. 2003;91(2):185–9. doi: 10.1016/S0002-9149(02)03107-7. [PubMed] [Cross Ref]
12. Unterberg C, Buchwald AB, Barath P, Schmidt T, Kreuzer H, Wiegand V. Cutting balloon coronary angioplasty-initial clinical experience. Clin Cardiol. 1993;16(9):660–4. doi: 10.1002/clc.4960160907. [PubMed] [Cross Ref]
13. Safian RD, Grines CL, May MA, Lichtenberg A, Juran N, Schreiber TL, et al. Clinical and angiographic results of transluminal extraction coronary atherectomy in saphenous vein bypass grafts. Circulation. 1994;89(1):302–12. doi: 10.1161/01.CIR.89.1.302. [PubMed] [Cross Ref]
14. Mangiacapra F, Heyndrickx GR, Puymirat E, Peace AJ, Wijns W, De Bruyne B, et al. Comparison of drug-eluting versus bare-metal stents after rotational atherectomy for the treatment of calcified coronary lesions. Int J Cardiol. 2012;154(3):373–6. doi: 10.1016/j.ijcard.2011.11.048. [PubMed] [Cross Ref]
15. Forouzannia SK, Abdollahi MH, Mirhosseini SJ, Hosseini H, Moshtaghion SH, Golzar A, et al. Clinical outcome and cost in patients with off-pump vs. on-pump coronary artery bypass surgery. Acta Med Iran. 2011;49(7):414–9. [PubMed]
16. Lee EJ, Choi KH, Ryu JS, Jeon SB, Lee SW, Park SW, et al. Stroke risk after coronary artery bypass graft surgery and extent of cerebral artery atherosclerosis. J Am Coll Cardiol. 2011;57(18):1811–8. doi: 10.1016/j.jacc.2010.12.026. [PubMed] [Cross Ref]
17. Warren JA, Jordan WD, Jr, Heudebert GR, Whitley D, Wirthlin DJ. Determining patient preference for treatment of extracranial carotid artery stenosis: carotid angioplasty and stenting versus carotid endarterectomy. Ann Vasc Surg. 2003;17(1):15–21. doi: 10.1007/s10016-001-0332-0. [PubMed] [Cross Ref]
18. Hollenbeak CS, Bowman AR, Harbaugh RE, Casale PN, Han D. The impact of surgical specialty on outcomes for carotid endarterectomy. J Surg Res. 2010;159(1):595–602. doi: 10.1016/j.jss.2008.03.049. [PubMed] [Cross Ref]
19. McDonald RJ, Cloft HJ, Kallmes DF. Intracranial hemorrhage is much more common after carotid stenting than after endarterectomy: evidence from the national inpatient sample. Stroke. 2011;42(10):2782–7. doi: 10.1161/STROKEAHA.111.618769. [PubMed] [Cross Ref]
20. Gelet A, Chapelon JY, Margonari J, Theillère Y, Gorry F, Souchon R, et al. High intensity focused ultrasound experimentation on human benign prostatic hypertrophy. Eur Urol. 1993;23(1):44–7. [PubMed]
21. Chaussy C, Thuroff S. The status of high-intensity focused ultrasound in the treatment of localized prostate cancer and the impact of a combined resection. Curr Urol Rep. 2003;4(3):248–52. doi: 10.1007/s11934-003-0077-0. [PubMed] [Cross Ref]
22. Madersbacher S, Marberger M. High-energy shockwaves and extracorporeal high-intensity focused ultrasound. J Endourol. 2003;17(8):667–72. doi: 10.1089/089277903322518680. [PubMed] [Cross Ref]
23. Saleh KY, Smith NB. A 63 element 1.75 dimensional ultrasound phased array for the treatment of benign prostatic hyperplasia. Biomed Eng Online. 2005;4(1):39. doi: 10.1186/1475-925X-4-39. [PMC free article] [PubMed] [Cross Ref]
24. Yehezkeli O, Freundlich D, Magen N, Marantz C, Medan Y, Vitek S, et al. INSIGHTEC-TXSONICSLTD, assignee. Mechanical positioner for MRI guided ultrasound therapy system WO0209812, Inventors Word intellectual property organization 2002.
25. Stewart EA, Gedroyc W, Tempany CM, Quade B, Inbar Y, Ehrenstein T, et al. Focused ultrasound treatment of uterine fibroids: safety and feasibility of a noninvasive thermoablative technique. Am J Obstet Gynecol. 2003;189(1):48–54. doi: 10.1067/mob.2003.345. [PubMed] [Cross Ref]
26. Tempany CM, Stewart EA, McDannold N, Quade B, Jolesz F, Hynynen K. MRI guided focused ultrasound surgery (FUS) of uterine leiomyomas: a feasibility study. Radiology. 2003;227(3):897–905. doi: 10.1148/radiol.2271020395. [PubMed] [Cross Ref]
27. Stewart EA, Rabinovici J, Tempany C, Inbar Y, Regan L, Gostout B, et al. Clinical outcomes of focused ultrasound surgery for the treatment of uterine fibroids. Fertil Steril. 2006;85(1):22–9. doi: 10.1016/j.fertnstert.2005.04.072. [PubMed] [Cross Ref]
28. Kim HS, Baik JH, Pham LD, Jacobs MA. MR-guided high-intensity focused ultrasound treatment for symptomatic uterine leiomyomata long-term outcomes. Acad Radiol. 2011;18(8):970–6. doi: 10.1016/j.acra.2011.03.008. [PMC free article] [PubMed] [Cross Ref]
29. Zini C, Elisabeth H, Stephen T, Alessandro N, Carlo C, Aytekin O. Ultrasound and MR-guided focused ultrasound surgery for prostate cancer. World J Radiol. 2012;4(6):247–52. doi: 10.4329/wjr.v4.i6.247. [PMC free article] [PubMed] [Cross Ref]
30. Napoli A, Anzidei M, De Nunzio C, Cartocci G, Panebianco V, De Dominicis C, et al. Real-time magnetic resonance–guided high-intensity focused ultrasound focal therapy for localised prostate cancer: preliminary experience. Eur Urol. 2013;63(2):395–8. doi: 10.1016/j.eururo.2012.11.002. [PubMed] [Cross Ref]
31. Napoli A, Anzidei M, Marincola BC, Brachetti G, Ciolina F, Cartocci G, et al. Primary pain palliation and local tumor control in bone metastases treated with magnetic resonance-guided focused ultrasound. Invest Radiol. 2013;48(6):351–8. doi: 10.1097/RLI.0b013e318285bbab. [PubMed] [Cross Ref]
32. Lee JE, Yoon SW, Kim KA, Lee JT, Shay L, Lee KS. Successful use of magnetic resonance-guided focused ultrasound surgery for long-term pain palliation in a patient suffering from metastatic bone tumor. J Korean Soc Radiol. 2011;65(2):133–8.
33. Catane R, Beck A, Inbar Y, Rabin T, Shabshin N, Hengst S, et al. MR-guided focused ultrasound surgery (MRgFUS) for the palliation of pain in patients with bone metastases-preliminary clinical experience. Ann Oncol. 2006;18(1):163–7. doi: 10.1093/annonc/mdl335. [PubMed] [Cross Ref]
34. McDannold N, Clement G, Black P, Jolesz F, Hynynen K. Transcranial MRI-guided focused ultrasound surgery of brain tumors: Initial findings in three patients. Neurosurgery. 2010;66(2):323–32. doi: 10.1227/01.NEU.0000360379.95800.2F. [PMC free article] [PubMed] [Cross Ref]
35. Dorenberg EJ, Courivaud F, Ring E, Hald K, Jakobsen JA, Fosse E, et al. Volumetric ablation of uterine fibroids using Sonalleve high-intensity focused ultrasound in a 3 Tesla scanner—first clinical assessment. Minim Invasive Ther. 2013;22(2):73–9. doi: 10.3109/13645706.2012.702672. [PubMed] [Cross Ref]
36. Wu F, Chen WZ, Bai J, Zou JZ, Wang ZL, Zhu H, et al. Pathological changes in malignant carcinoma treated with high-intensity focused ultrasound. Ultrasound Med Biol. 2001;27(8):1099–106. doi: 10.1016/S0301-5629(01)00389-1. [PubMed] [Cross Ref]
37. Wu F, Wang ZB, Chen WZ, Zou JZ, Bai J, Zhu H, et al. Advanced hepatocellular carcinoma: treatment with high-intensity focused ultrasound ablation combined with transcatheter arterial embolization. Radiology. 2005;235(2):659–67. doi: 10.1148/radiol.2352030916. [PubMed] [Cross Ref]
38. Li CX, Xu GL, Jiang ZY, Li JJ, Luo GY, Shan HB, et al. Analysis of clinical effect of high-intensity focused ultrasound on liver cancer. World J Gastroenterol. 2004;10(15):2201–4. [PMC free article] [PubMed]
39. Wu F, Wang ZB, Chen WZ, Zhu H, Bai J, Zou JZ, et al. Extracorporeal high intensity focused ultrasound ablation in the treatment of patients with large hepatocellular carcinoma. Ann Surg Oncol. 2004;11(12):1061–9. doi: 10.1245/ASO.2004.02.026. [PubMed] [Cross Ref]
40. Shehata IA, Ballard JR, Casper AJ, Liu D, Mitchell T, Ebbini ES. Feasibility of targeting atherosclerotic plaques by high-intensity-focused ultrasound: an in vivo study. J Vasc Interv Radiol. 2013;24(12):1880–7. doi: 10.1016/j.jvir.2013.08.013. [PubMed] [Cross Ref]
41. Hur SJ, Min B, Nam KC, Lee EJ, Ahn DU. Effect of dietary cholesterol and cholesterol oxides on blood cholesterol, lipids, and the development of atherosclerosis in rabbits. Int J Mol Sci. 2013;14(6):12593–606. doi: 10.3390/ijms140612593. [PMC free article] [PubMed] [Cross Ref]
42. Hosseini M, Asgary S. Effects of dietary supplementation with ghee, hydrogenated oil, or olive oil on lipid profile and fatty streak formation in rabbits. ARYA Atherosclerosis. 2012;8(3):119–24. [PMC free article] [PubMed]
43. Davidson F. Ultrasonic power balances. In: Preston RC, editor. Output measurements for medical ultrasound. New York: Springer; 1991. pp. 75–90.
44. Kim MH, Kim HJ, Kim NN, Yoon HS, Ahn SH. A rotational ablation tool for calcified atherosclerotic plaque removal. Biomed Microdevices. 2011;13(6):963–71. doi: 10.1007/s10544-011-9566-y. [PubMed] [Cross Ref]
45. Pizzulli L, Köhler U, Manz M, Lüderitz B. Mechanical dilatation rather than plaque removal as major mechanism of transluminal coronary extraction atherectomy. J Interv Cardiol. 1993;6(1):31–9. doi: 10.1111/j.1540-8183.1993.tb00439.x. [PubMed] [Cross Ref]
46. Damianou C, Hadjisavvas V, Ioannides K. In vitro and in vivo evaluation of an MRI-guided focused ultrasound system for dissolving clots in combination with thrombolytic drugs. J Stroke Cerebrovasc Dis. 2014;23(7):1956–64. doi: 10.1016/j.jstrokecerebrovasdis.2014.01.028. [PubMed] [Cross Ref]"
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#282 Daniel Cooper

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Posted 04 September 2017 - 01:28 PM

Assuming that ultrasound technique works, I wonder how many decades it will take for the FDA to approve it.

 

The FDA never seems to include in their risk calculation the number of people that die or have significantly reduced quality of life while effective treatments are kept off the market while they do their navel gazing.

 

 

 

 

 

 

 

 

 

 

 


Edited by Daniel Cooper, 04 September 2017 - 01:36 PM.


#283 pamojja

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Posted 04 September 2017 - 03:50 PM

I agree, it is quite simple.
Unfortunately it seems that the majority of people would rather undergo open heat surgery then change their diets.

 

Zen, I always seem compelled to respond when you paint reducing CAC score as simple as changing the diet. Now for the 3rd time in this thread over the years.

 

I've been vegan since age 10 and added loads of healthy fats, eggs and fish after a diagnosis of a 80% blockage at my abdominal aorta. Yes, I was willing to change my diet, but the opposite you still suggest. And No,I'm not willing to undergo open heart surgery.

 

With my approach, including much more than just changing diet I could reverse a 60% walking-disabilty due to PAD. With the diet change you suggest PAD silently developed over the course of 30 years.


Edited by pamojja, 04 September 2017 - 03:53 PM.

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#284 Benko

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Posted 04 September 2017 - 04:15 PM

Agree.  Even Dr. Gregor (the vegan MD popular currently) has a video in which he points out that vegans can get coronary artery disease, the reason being lack of omega 3 fatty acids.  



#285 mikey

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Posted 04 September 2017 - 05:12 PM

 

I agree, it is quite simple.
Unfortunately it seems that the majority of people would rather undergo open heat surgery then change their diets.

 

Zen, I always seem compelled to respond when you paint reducing CAC score as simple as changing the diet. Now for the 3rd time in this thread over the years.

 

I've been vegan since age 10 and added loads of healthy fats, eggs and fish after a diagnosis of a 80% blockage at my abdominal aorta. Yes, I was willing to change my diet, but the opposite you still suggest. And No,I'm not willing to undergo open heart surgery.

 

With my approach, including much more than just changing diet I could reverse a 60% walking-disabilty due to PAD. With the diet change you suggest PAD silently developed over the course of 30 years.

 

 

 

Good information. Will you please elaborate on what you changed from and to, including the other things besides changing diet?

 

Also, did your vegan diet include oils, such as what is regarded as "heart healthy oils," such as olive oil?

 

Thank you!


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#286 zen

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Posted 04 September 2017 - 06:01 PM

 

I agree, it is quite simple.
Unfortunately it seems that the majority of people would rather undergo open heat surgery then change their diets.

 

Zen, I always seem compelled to respond when you paint reducing CAC score as simple as changing the diet. Now for the 3rd time in this thread over the years.

 

I've been vegan since age 10 and added loads of healthy fats, eggs and fish after a diagnosis of a 80% blockage at my abdominal aorta. Yes, I was willing to change my diet, but the opposite you still suggest. And No,I'm not willing to undergo open heart surgery.

 

With my approach, including much more than just changing diet I could reverse a 60% walking-disabilty due to PAD. With the diet change you suggest PAD silently developed over the course of 30 years.

 

Hi pamojja,

Thank you for replying, I am really happy that whatever you are doing seems to be working for you.

I am not sure if you watched Dr Esselstyn video or read his and Dr Campbell's books, but they do not simply say that *any* vegan diet will work, their recommendations are much more specific. As I have already said in my other reply, everyone is different, and if something works for you it does not mean it is going to work for me, and the opposite is also true.

My personal choice is to follow Dr. Esselstyn (and Dr Campbel, Dr Greger, Dr Barnard and many other great doctors) recommendation and this seems to be working quite well for me.
​I think it also worked quite well for the person the below video


Finally, since I have mentioned Dr Barnard, here is one of his great presentations 


Take care,
​Zen

 

 


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#287 pamojja

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Posted 04 September 2017 - 07:34 PM

My personal choice is to follow Dr. Esselstyn (and Dr Campbel, Dr Greger, Dr Barnard and many other great doctors) recommendation and this seems to be working quite well for me.

 

Thanks for your friendly reply, despite me always correcting your enthusiasm.  ;)  What method you used to assess that it seem to work for you?

 

Good information. Will you please elaborate on what you changed from and to, including the other things besides changing diet?

 

Also, did your vegan diet include oils, such as what is regarded as "heart healthy oils," such as olive oil?

 

Thank you!

 

My vegan diet with 10 started out of ethical and logical reasons. Curious as I was, I watched the industrial killing process in my neighborhood a bit to closely. And I simply didn't want to nourish off meat infused with stress hormones. But soon I lost taste for any animal products, like, eggs and wild caught fish, and added no oils or fats.

 

With my diagnosis it basically changed to 68% of calories from fat, 19% of calories from protein and 13% of carbs. However, that were the results from tracking my food for 3 years starting 9 years ago. And due to still singling out most offending foods with post-prandial blood glucose reading, meanwhile the carb-intake might be even lower.

 

Beside diet I first eliminated any added sugar, gradually introduced Linus Pauling's therapy, then on the TrackYourPlaque forum started to add their strategies. Here in detail:

 

http://www.longecity...nal-remissions/


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#288 zen

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Posted 04 September 2017 - 08:49 PM

 

My personal choice is to follow Dr. Esselstyn (and Dr Campbel, Dr Greger, Dr Barnard and many other great doctors) recommendation and this seems to be working quite well for me.

 

Thanks for your friendly reply, despite me always correcting your enthusiasm.  ;)  What method you used to assess that it seem to work for you?

​No worries, I am only sharing what I found worked for me in hope that it may be helpful for some other person.

​As for the method of assessment, I used to have a problem with the elevated blood pressure and now, after 1.5 year on whole food plant based diet, the problem is gone.
​I am attaching a sample of my 2015 blood pressure readings (taken with Omron HEM-790IT) and also a sample of my 2017 blood pressure readings.

Note, that even if the 2017 results look only a little bit better, the real difference is that in 2015 I was taking a tablet of BenicarHCT 40/12.4 daily and currently I off all meds.

 

Attached Files


Edited by zen, 04 September 2017 - 09:03 PM.

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#289 mikey

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Posted 09 October 2017 - 05:17 PM

@Kevinsan, I could tolerate any stinging without anti-inflammatory agents if CD, etc. are effective in reducing arterial plaque. I guess one would need to be careful and not let some naegleria fowleri work its way to the brain from a contaminate syringe!  :|o

 

mikey states in post #247: "Testosterone is not an anti-inflammatory steroid."

 

Sample study 1

"On the other hand, observational and interventional studies suggest that T supplementation reduces inflammatory markers in both young and old hypogonadal men."

"This study, together with previous observations, suggests that a close relationship exists between the development of a pro-inflammatory state and the decline in T levels, two trends that are often observed in aging men."

 "We advocate the notion that changes in inflammatory markers and T in aging men are causally linked. However, longitudinal and interventional studies are needed to confirm that T can be used therapeutically, based on its anti-inflammatory properties."

 

Sample study 2

"Androgens are known to exert anti-inflammatory effects but their impact on mast cells (MCs) remains to be determined."

Sample study 3

"Decreased testosterone production in men with rheumatoid arthritis is a common finding (Stafford et al 2000), and it is now generally recognized that androgens have the capacity to suppress both the hormonal and cellular immune response and so act as one of the body’s natural anti-inflammatory agents (Cutolo et al 2002)."

"This known anti-inflammatory action of testosterone has led to studying the effect of testosterone therapy in men with rheumatoid disease."

 

Your statement, mikey, and the above studies seem contradictory. Do you have some cites that will substantiate your position?

 

I apologize for providing confusing terms.

 

It's simply the difference between catabolic (cortisol) and anabolic (testosterone) steroids. Although, cortisol is a more of an anti-inflammatory agent and an antioxidant, T has anti-inflammatory properties, as when there is too little, inflammatory conditions, such as RA and Type II diabetes can increase, but T does not cause the catabolism of tissues, as cortisol does. Men with low T tend to have more inflammation, and supplementation with T can reduce RA and Type II diabetes, but a doctor wouldn't inject T into an inflamed joint to reduce inflammation, as they do with cortical steroids. 


Edited by mikey, 09 October 2017 - 05:18 PM.

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#290 rubegoldberg

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Posted 10 October 2017 - 01:47 AM

A number of substances used to treat atherosclerosis are listed here...  http://en.medicine-c...om/pains_30.htm

 

I have used Troxerutin (Troxevasin) - a semi-synthetic active bioflavonoid - analogue of rutin.

 

 


Adroxonum 
Aevitum 
Aekol (Aecolum) 
Anavenol 
Bezafibrate 
Benfothiaminum 
Videcholum 
Vikasol (Vicasolum) 
Vitohepat (Vitohepatum) 
Galascorbinum 
Gemfibrozil (Gemfibrozil) 
Hyposolum (Hiposolum) 
Dragee "Hexavitum" 
Dragee "Hendevitum" (Dragee "Hendevitum") 
Dragee "Revitum" 
Dragee "Undevitum" 
Isotretinoin (Isotretinoine) 
Iodum 
Potassium iodide (Kalii iodidum) 
Calcium glutaminate (Calcii glutaminas) 
Calcium dobesilate (Calcii dobesilas) 
Calcium pangamate 
Calcium pantothenate (Calcii pantothenas) 
Calcium folinas (Calcium-folinate) 
Carotolin (Carotolinum) 
Quercetinum (Quercetinum) 
Acidum ascorbic acid (Acidum ascorbinicum) 
Acidum lipoicum 
Acid nicotinic (Acidum nicotinicum) 
Acid folicum (Acidum folicum) 
Clofibrate 
Cobamamidum 
Cocarboxylase (Cocarboxylasum) 
Complivitum 
Linetol (Linaetholum) 
Lipamidum 
Lipostabil (Lipostabil) 
Lovastatin (Lovastatin) 
Magnesium sulfate (Magnesii sulfas) 
Seabuckthorn oil (Oleum ex fructibus et foliis Hippopheae) 
Rosehip oil (Oleum Rosae) 
Methylmethionine sulfonium chloride (Methylmethioninsulfonii chloridum) 
Methionine (Methioninum) 
Anti-asthma medicine (Mixtura antiasthmatica Trascovi) 
Sodium iodide (Natrii iodidum) 
Nicotinamide (Nicotinamid) 
Oxidevitum 
Oxycobalamin (Oxycobalaminum) 
Olasolum 
Oligovit 
Panthenol (Panthenol) 
Parmidinum (Parmidinum) 
Pyracetamum 
Pyriditol (Pyriditolum) 
Pyridoxalphosphatum (Pyridoxalphosphatum) 
Pyridoxine (Pyridoxinum) 
Films "Oblekol" (Membranula "Oblecolum") 
Fruit of rowan (Fructus Sorbi aucuparitae) 
Fruits of wild rose (Fructus Rosae) 
Polysponinum (Polysponinum) 
Probucol 
A solution of iodine alcohol 5% (Solutio Iodi spirituosa 5%) 
Lugol solution (Solutio Lugoli) 
Reparil 
Retinolum 
Riboflavinum (Riboflavinum) 
Riboflavin mononucleotide (Riboflavinum-mononucleotidum) 
Rutinum 
Fish oil (Oleum jecoris) 
Collections of vitamin () 
Tablets "Amitetravit" (Tabulettae "Amitetravitum" obductae) 
Tablets "Asnithine" (Tabulettae "Asnithinum") 
Tablets "Aerovit" (Tabulettae "Aerovitum" obductae) 
Tablets "Glutamevit" (Tabulettae "Glutamevitum" obductae) 
Tablets "Decamewith" (Tabulettae "Decamevitum" obductae) 
Tablets "Quadevet" (Tabulettae "Quadevitum" obductae) 
Tablets "Microroyod" (Tabulettae "Microiodum" obductae) 
Tablets "Pangexavit" (Tabulettae "Panhexavitum" obductae) 
Tablets "Pentovit" (Tabulettae "Pentovitum" obductae) 
Tablets "Tetravit" (Tabulettae "Tetravitum" obductae) 
Tablets "Tetrafolevit" (Tabulettae "Tetrafolevitum" obductae) 
Thiamin (Thiaminum) 
Tocopherol Acetate (Tocopheroli acetas) 
Tribenozide (Tribenozidum) 
Tribusponinum 
Troxevasin 
Fenofibrate (Phenofibrate) 
Phytomenadionum 
Flavinatum 
Phosphothiaminum 
Cholestyramine (Cholestyraminum) 
Choline Chloride (Cholini chloridum) 
Cyanocobalamin (Cyanocobalaminum) 
Cinnarizine 
Ergocalciferolum (Ergocalciferolum) 
Aescusan 
Essentiale 
Esflazid (Aesflazidum) 
Etamsylate (Etamsylatum) 
Etretinate (Etretinate)

 


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#291 rubegoldberg

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Posted 10 October 2017 - 11:02 AM

James Watson at AntiAgingFirewalls suggests PCSK9 inhibition in their August 2017 post.  PCSK9 protein, which is a circulating protein in blood.

 

They go one to state that barring cost-prohibitive pharmaceuticals one can...

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Reduce Insulin signaling with diet, SIRT6 activation, fasting, and the Salvia extract, Tanshinone IIA

For those who do not have $14,000 per year to “burn”, there is a much simpler way of “shutting off” PCSK9.  As mentioned in the beginning of this section, the “longevity gene” FoxO3a functions as a suppressor of PCSK9 gene expression when the FoxO3a transcription factor can enter the cell nucleus. Unfortunately to do this, you must reduce insulin signaling, since insulin prevents FoxO3a from entering the cell nucleus (due to the Insulin/IGF-1/PI3K/Akt pathway).  Once you reduce insulin signaling, FoxO3a can enter the cell nucleus and be recruited by SIRT6.

Unfortunately, with aging, SIRT6 cannot be activated due to declining levels of NAD+ within the cell.  This can be ameliorated (at least in theory) by restoring NAD+ levels within the cell with NAD+ precursors like NR or NMN, or possibly with NAD+ given IV.  (you can look at our blog postings on the NAD World that describe the mechanisms involved.)   Specifically, however there is a fascinating phytochemical that has been isolated from the Salvia miltiorrhiza Bunge plant called Tanshinone IIA. This compound is the most pharmacologically bioactive compound found in the Salvia plan and has anti-inflammation, anti-cancer, anti-LDL-cholesterol, neuroprotective, and hypolipidemic properties. 

>

 

 


Edited by rubegoldberg, 10 October 2017 - 11:03 AM.

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#292 albedo

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Posted 22 October 2017 - 12:23 PM

The recent article by LEF and the references therein might be a useful read:

Vitamin K Reverses Arterial Stiffness

http://www.lifeexten...-See-It/Page-01


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#293 hav

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Posted 24 October 2017 - 05:15 PM

Wondering what people here think of this:

https://www.theguard...isk-study-finds

Would this be the same mechanism as Rapamycin uses?

 

Looks like the operative mechanism of Canakinumab (trade name Ilaris) is to inhibit the IL-1B protein by stimulating the IL-1B receptor... which may be unique in that it doesn't also inhibit IL-1A. But it's apparently very, very expensive. Here's an interesting discussion of IL-1B inhibitors which seems to include many antioxidants... and makes me wonder where c60 might fit in. 

 

https://selfhacked.c...1betaInhibitors

 

Howard



#294 Rocket

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Posted 25 October 2017 - 01:05 AM

I haven't seen anything I here about one of my heroes, Linus Paling and megadosing of vitamin c.

I have a question: how reversible is arteriosclerosis with addressing hardening of the vascular system and without addressing scensesence?
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#295 pamojja

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Posted 25 October 2017 - 08:41 AM

I haven't seen anything I here about one of my heroes, Linus Paling and megadosing of vitamin c.

 

Admittedly, this has become a long thread to read through. But I did write in it somewhere about my success with Pauling's therapy.

 

 

PS: Recently summed up here again.
 


Edited by pamojja, 25 October 2017 - 08:46 AM.

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#296 Richard McGee

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Posted 03 November 2017 - 12:18 AM

Trodusquemine reverses atherosclerosis

http://www.longecity...is/#entry831857

 

Paper
http://www.clinsci.o...0/2489.full.pdf

 

From the cited paper:

 

We demonstrate here, using the LDLR−/− mouse model of atherosclerosis, that pharmacological PTP1B systemic in- hibition leads to protection against and reversal of atherosclerosis development, suggesting beneficial effects of PTP1B inhibition for the treatment of CVDs and reduction in CVD risk. We present evidence that, in addition to its improve- ment in glucose homeostasis and adiposity, PTP1B inhibition results in activation of aortic Akt and AMPKα1, that is independent of the effects on the IR itself. Most importantly, for the first time, we demonstrate that inhibition of PTP1B results in a decrease in circulating serum cholesterol and triglyceride levels and protection against atheroscle- rotic plaque formation.

 

 

 

 

 

 

There are a number of compounds available to the general public that inhibit PTP1B. One example is Magnolia Officinalis Extract. Assuming PTP1B inhibition is the effective cause, you might have similar success with this compound.

 

https://www.hindawi....ri/2015/139451/

 

Not expensive at all, BTW:

 

https://www.swansonv...-400-mg-60-caps


Edited by Richard McGee, 03 November 2017 - 12:19 AM.

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#297 RWhigham

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Posted 06 November 2017 - 05:36 PM

Pycnogenol® and Centella Asiatica for asymptomatic atherosclerosis progression.  (pine bark and gotu kola supplements)

 

The article is behind a paywall, but here is summary from Dr Paul Rivas  link  (in the comments section of a Josh Mitteldorf blog link)

 

"They took a group aged 45-60 with group( iv ) atherosclerotic plaque lesions. The control group was instructed on diet and exercise only, whereas another group followed those recommendations as well as 100mg of pine bark extract with 100mg of gotu kola extract. Two common and dirt cheap supplements.

 
They looked at the percentage of plaques progressing from class 4 to class 5 over a 30 month period. The control group saw a 21.3% progression over this period, the supplement group had an amazing 1%progression.
 
Plaque progression was an incredible 95% less in the supplement group over the control.
 
Do you think that that study ever saw the light of day? What percent of people with CAD are aware of this? How many doctors had cute little drug reps visit them with this news while offering free trips to the Bahamas? NONE.  PS ( I take both daily and my coronary artery calcium score remains at zero)"
 
The article is also reviewed on LEF magazine website at link
 
"This study showed a standardized extract from the French maritime pine combined with an extract of the Centella asiatica plant stabilized soft plaques, boosting the odds that they will stay put and not suddenly rupture. These two nutrients also demonstrated reversal of the number and size of arterial plaque deposits that progress to atherosclerosis"

Edited by RWhigham, 06 November 2017 - 05:53 PM.

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#298 PWAIN

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Posted 07 November 2017 - 07:34 AM

Trodusquemine reverses atherosclerosis

http://www.longecity...is/#entry831857

 

Paper
http://www.clinsci.o...0/2489.full.pdf

 

From the cited paper:

 

We demonstrate here, using the LDLR−/− mouse model of atherosclerosis, that pharmacological PTP1B systemic in- hibition leads to protection against and reversal of atherosclerosis development, suggesting beneficial effects of PTP1B inhibition for the treatment of CVDs and reduction in CVD risk. We present evidence that, in addition to its improve- ment in glucose homeostasis and adiposity, PTP1B inhibition results in activation of aortic Akt and AMPKα1, that is independent of the effects on the IR itself. Most importantly, for the first time, we demonstrate that inhibition of PTP1B results in a decrease in circulating serum cholesterol and triglyceride levels and protection against atheroscle- rotic plaque formation.

 

 

 

 

 

 

There are a number of compounds available to the general public that inhibit PTP1B. One example is Magnolia Officinalis Extract. Assuming PTP1B inhibition is the effective cause, you might have similar success with this compound.

 

https://www.hindawi....ri/2015/139451/

 

Not expensive at all, BTW:

 

https://www.swansonv...-400-mg-60-caps

 

Interesting, I have ordered 6 bottles, I'll probably ramp up to use 2g (5 caps) per day and see how it goes.

 

What are your thoughts on GW510516? looks like it might also be useful for tackling cholesterol and plaque? Also have you looked at Semaglutide? There seems to be a few things coming up recently which seem to tackle plaque and cholesterol.



#299 William Sterog

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Posted 07 November 2017 - 12:30 PM

 

Pycnogenol® and Centella Asiatica for asymptomatic atherosclerosis progression.  (pine bark and gotu kola supplements)

 

The article is behind a paywall, but here is summary from Dr Paul Rivas  link  (in the comments section of a Josh Mitteldorf blog link)

 

"They took a group aged 45-60 with group( iv ) atherosclerotic plaque lesions. The control group was instructed on diet and exercise only, whereas another group followed those recommendations as well as 100mg of pine bark extract with 100mg of gotu kola extract. Two common and dirt cheap supplements.

 
They looked at the percentage of plaques progressing from class 4 to class 5 over a 30 month period. The control group saw a 21.3% progression over this period, the supplement group had an amazing 1%progression.
 
Plaque progression was an incredible 95% less in the supplement group over the control.
 
Do you think that that study ever saw the light of day? What percent of people with CAD are aware of this? How many doctors had cute little drug reps visit them with this news while offering free trips to the Bahamas? NONE.  PS ( I take both daily and my coronary artery calcium score remains at zero)"
 
The article is also reviewed on LEF magazine website at link
 
"This study showed a standardized extract from the French maritime pine combined with an extract of the Centella asiatica plant stabilized soft plaques, boosting the odds that they will stay put and not suddenly rupture. These two nutrients also demonstrated reversal of the number and size of arterial plaque deposits that progress to atherosclerosis"

 

 

As a man, I don't enjoy the antiandrogenic effects of Centella Asiatica:

 

 

The inductive effects of Centella asiatica on rat spermatogenic cell apoptosis in vivo.

Centella asiatica (L.) Urban has been traditionally used for the treatment of various disease and as a food for thousands of years in various parts of the world including eastern Asia, China and India. The goal of this study was to investigate the effects of Centella asiatica aqueous leaf extract on the induction of spermatogenic cell apoptosis in male rats. After lethal dose (LD(50)) assessment of plant extract, rats were divided in five groups. The experimental groups received orally 10, 50, 80 and 100 mg/kg aqueous leaf extract daily for 60 days and the control group received just water. After 60 days, body and testis weight were measured and blood samples were taken from the heart. To evaluate apoptosis and histological changes, tissue samples obtained from rat testes were stained by TUNEL assay and hematoxylin and eosin stain. Results showed that the sperm count, motility, and viability and the number of spermatogenic cells in the seminiferous tubules were significantly decreased compared with the control group. The number of apoptotic germ cells per seminiferous tubule cross-section was significantly increased in the experimental group (18.11 ± 3.5) compared with the control group (8.7 ± 0.81) (P < 0.05). Serum testosterone, follicle-stimulating hormone, and luteinizing hormone levels also showed significant decreases in the experimental groups (P < 0.05). There was also a significant decrease in testis weight in experimental groups compared with the control group (P < 0.05). It is concluded that Centella asiatica has toxicological effects on the reproductive system in male rats and, therefore, it is suggested that leaf extracts of Centella asiatica possess antifertility effects in the male rat.

 

 


Edited by William Sterog, 07 November 2017 - 12:31 PM.

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#300 mikey

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Posted 07 November 2017 - 06:46 PM

 

Trodusquemine reverses atherosclerosis

http://www.longecity...is/#entry831857

 

Paper
http://www.clinsci.o...0/2489.full.pdf

 

From the cited paper:

 

We demonstrate here, using the LDLR−/− mouse model of atherosclerosis, that pharmacological PTP1B systemic in- hibition leads to protection against and reversal of atherosclerosis development, suggesting beneficial effects of PTP1B inhibition for the treatment of CVDs and reduction in CVD risk. We present evidence that, in addition to its improve- ment in glucose homeostasis and adiposity, PTP1B inhibition results in activation of aortic Akt and AMPKα1, that is independent of the effects on the IR itself. Most importantly, for the first time, we demonstrate that inhibition of PTP1B results in a decrease in circulating serum cholesterol and triglyceride levels and protection against atheroscle- rotic plaque formation.

 

 

 

 

 

 

There are a number of compounds available to the general public that inhibit PTP1B. One example is Magnolia Officinalis Extract. Assuming PTP1B inhibition is the effective cause, you might have similar success with this compound.

 

https://www.hindawi....ri/2015/139451/

 

Not expensive at all, BTW:

 

https://www.swansonv...-400-mg-60-caps

 

Interesting, I have ordered 6 bottles, I'll probably ramp up to use 2g (5 caps) per day and see how it goes.

 

What are your thoughts on GW510516? looks like it might also be useful for tackling cholesterol and plaque? Also have you looked at Semaglutide? There seems to be a few things coming up recently which seem to tackle plaque and cholesterol.

 

 

The Swanson product that you point is is not an extract, just raw herb.

 

The also sell a good extract - https://www.swansonv...mg-120-veg-caps

 

The extract is what the study was conducted with. They do this because extracts can be standardized, so that we know how much of the active ingredient(s) is in them.

 

The product that you bought is raw herb, not an extract, thus, will have somewhat to considerably less activity.

 

When buying herbs, for the most part, only buy extracts, especially standardized extracts, so that you get the parts of the herb that do the job.

 

Thank you for the good information.


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Also tagged with one or more of these keywords: artery, cardiovascular disease, lipids, matrix gla protein, vitamin k2 mk4, vitamin k2 mk7, xanthohumol, plaque

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