“Arterial cancer” (aka CAD) and its amelioration is found to be associated with two areas of therapeutic focus. The first being the understanding of the initiation of the insult to the artery and the second being the understanding and action concerning the rehabilitation of the artery before significant mechanical intervention is taken or death occurs.
Initial insult is found in three basic causal areas. The first being mechanical where the artery cracks due to blood pressure, geometry, etc. - - - in engineering terms - - - if it moves it will eventually break. The second being that the artery is chemically attacked (inflammation related chemicals - - - such as the MMP-2 and MMP-9 chemicals). The third being that the artery is biologically attacked via bacteria and/or virus.
Note: for discussion sake, all three can occur, or any combination can occur, resulting in the initial insult (fancy term for damage).
“Arterial Cancer” or otherwise known as Coronary Artery Disease (CAD) occurs typically in adult males after reaching andropause and in adult females after menopause. This CAD is not typically found in humans older than five years and younger than thirty-five years (with the exception of combat related CAD). So, from this perspective something hormonally is going on.
So how does this start?:
After initial insult (aka damage), the macrophages that jump in (the repair crew) do not experience aptosis (cell death) once the patch is applied (they don’t die), with the result that they are transformed into active foam cells which grow inside the arterial wall. The artery is in reality, a pipe in a pipe in a pipe and the foam cells grow in between the layers. As the foam cells propagate, they leave a calcium trail (aka plaque) that is visible via CT type scanning equipment. This plaque or calcium score is then used as a surrogate for the determination of the degree of arteriole disease and as an indicator of the potential for a major coronary event (a heart attack).
Note: Foam cells exhibit the same behavior as bone cells (the clue here is that vitamins D, K, & Magnesium thus have to play a role in coronary artery disease as they do with bone)
Eventually foam cells break through the epithelial layer of the artery (the pipe closest to the blood) which in turn leads to clot formation which in turn prompts one of the following mechanistic interventions by physicians- - - grafting or stinting. Without prompt intervention, death is inevitable.
One mode of prevention of this wall breakthrough is the strengthening of the artery wall via the use of Citrulline and Arginine which are HGH stimulators. This worked for the author and its measure was the thickness and the diameter of the aorta - - - the internal diameter stayed the same but the wall thickness increased thus the pipe became stronger.
The objective of arterial therapy is as follows:
* Slow the growth of the foam cells
* “Kill” the foam cells (prevent breakthrough)
* “Clean out” the plaque (restoration of arterial range of motion)
* Prevent reoccurrence
Note: In the ideal world all four objectives occur at the same time. But we are not that fortunate. It takes time.
Presently the American Medical Association and American Heart Association both recommend therapy where the blood pressure must be lowered, stress managed, fats managed, sugar levels controlled, HDL increased, LDL decreased, TriGlycerides decreased, diet is controlled, visceral (inside the body cavity fat) and adipose fat is reduced, and exercise is incorporated. The following logic stream shows that they may be misguided, as even when these guidelines are followed, Coronary Artery Disease events still occur. So, it does appear that something is amiss with the guidelines, and perhaps they are incomplete, inaccurate, or both. From the author’s personal experience, the guidelines are well intentioned, but that is all one can say.
From personal experience and experimentation, the recommended therapy should also state that HDL should be higher than 60, LDL be between 120 to 160, and TGs lower than 100. Blood pressure must be low (less than 150), sleep encouraged, sugar and insulin levels minimized, body fat reduced, exercise is incorporated, Lp(a) is reduced via Vitamin C, C-reactive protein (CRP) is reduced via Vitamin C, homocysteine is reduced via B vitamins, HbA1c (Hemoglobin A1c) is lowered via diet, the ratio of O-3 to O-6 is managed, TSH (thyroid stimulating hormone) is minimized, Free T3 is maximized (a thyroid hormone), Vitamin D is optimized, vitamin K1 and vitamin K2 levels are maximized, beta carotene levels are stabilized, and finally, trans fats and partially hydrogenated oils are avoided. Exogenous fat type intake is closely monitored and kept at 60% of diet while protein is kept at nominally 30% of the diet with the remainder being complex carbs. (Do note that this is opposite of the current food pyramid, but nonetheless this is the accurate proportions your diet should include.) Stress (cortisol) is to be minimized. PGE-2 (PGE stands for prostaglandin) to be minimized and PGE-1 optimized. Small LDL particles are minimized and hormonal levels are balanced. ApoA-1 is optimized and ApoB-100 is minimized (Apoliprotein A1 and B belong to the lipoprotein family and play important roles in lipid metabolism). Basic minerals such as Iodine, Copper, Zinc, Sodium, Selenium, Calcium, Magnesium, and Manganese are optimized. Additionally MMP-2 and 9 are minimized via either vitamin K alone or vitamin K with Astaxanthin, or K plus Astaxanthin plus low dose Doxycycline. (MMP-2 and 9 refer to matrix metallopepitase 2 and 9 and is involved in the regulation of vascularization and inflammatory responses. The MMP's chemically irritate the lining of the arteries). This is where and how vitamin K acts as an anti-oxidant.
The author’s program is monitored via blood analysis routinely and CT scans on a bi-annual basis.
Remember: Foam cells are stimulated via insulin, thus sugar and sugar substitute intake has to be managed (read as minimized)
NO WHEAT or CHEAP CARBS
The above has lead to the following postulation:
Coronary artery disease, CAD, is a function of the interaction of endogenous hormones on the bacteria and villi in the small and large intestines. These hormones produced from within are at minimum, vitamin D (a pro-hormone), vitamins K and A (never considered pro-hormones), Thyroid, Estriol, Estradiol, Estrone, Insulin, Progesterone and to a lesser extent, DHEA, and Testosterone. DHEA is the most abundant circulating steroid hormone in people, and has potent biological effects binding to cell surface receptors. As the hormonal levels change, the chemicals produced by intestinal bacteria apparently change. The villi within the intestine change their permeability and thus the chemical balance of the body is negatively impacted. Additionally, the re-population of the intestinal bacterial is of equal importance to the hormone impact and apparently occurs at the same time or is at least induced.
To date, this hormonal/bacterial/villi feedback loop has not been fully explored or identified with regard to its significance to CAD. since CAD is primarily age-related and since vitamin D levels drop with age, this triad must be a significant contributor. Additionally, this triad must be implicated via vaccination and infection outcomes and literature has supported this, where people given vaccinations or high dose antibiotics induce a drop in vitamin K levels.
The following is the clarification of the symbiosis between these hormones and bacteria/villi as it relates to CAD:
In a fully functioning human system the intestinal bacteria, in consort with the digestive process, produce the demanded chemicals in available amounts given the proper levels of precursors into the stomach (read as the right food). As one ages, the drop in hormone levels signal the bacteria to either slow down production of essential chemicals or induce a change in the intestinal flora and fauna and villi to such an extent that the essential chemical(s) is no longer produced in significant amounts or absorbed in physiological demanded quantities.
Some of the “marker tests” for the lack of these chemicals are homocysteine, C-reactive protein (CRP), Lp(a), vitamin K1, ApoB-100, PIVKA-II, uncarboxylated osteocalcin, MMP-9, and Magnesium. PIVKA measures proteins induced by vitamin K deficiency.
As this chemical/hormonal change occurs, it is postulated that the level of small dense LDL particles increase (via ApoB-100) which appears to be a function of available folic acid, Arachidonic Acid and trans-fats/partially hydrogenated oils. The production of Menaquinone–7 and 4 (K2) in the intestine drops off along with the lack of absorption of Phylloquinone (K1). This is demonstrated by the increasing degree of undercarboxylation of osteocalcin and by the increasing PIVKA II levels as one ages. This uncarboxylation is indicative of the fact that the intestinal bacteria are either not liberating the K1 from the diet or the K2 production is suppressed from the K1. Or more importantly, the “K” is not absorbed as required due to changes in the villi.
Vitamins K1 and K2 are fat soluble and are transported via CM (chylomicron) and CMr (chylomicron remnants), as is Vitamin D and A.
What appears to be occurring is that the small LDL (when produced in the liver) preferentially attaches vitamins A and the D first. The result is that there is apparently little to no room to attach the K, or the surface is such that the K that is attached is not released by the small LDL when near a Foam cell. At the same time the large LDL continues to transport the vitamins A, D, and K (its job,) but since there is more small LDL than large LDL, CAD progresses. Both LDLs end up in the liver for re-processing. How vitamin K impacts HDL is that when the HDL is produced there is little to no K to attach to it, as it appears that the D and the A are added first. This leaves the HDL void of significant amounts of K because the small LDL is “coated first” and the large LDL “coated second” but the HDL still has adequate D & A. Now in the absence of D this follows the same path as K. This apparent surface chemistry condition can explain why CAD progresses even when all the “right things” are done.
How the vitamins K, D, and A, and HDL & LDL work is that the K “kills” the foam cell when the large LDL goes in. Without K the LDL has no “ammo”. The logic here is that apparently small amounts of D are required for Foam cell growth - - - thus the bone formation. So, D is not the “magic bullet”. Vitamins D and A are most likely surface-active agents that allow the LDL and HDL to move through the vessel walls. So what occurs is that the LDL targets the foam cells because the foam cells apparently attract LDL and thus, the LDL “moves in for the kill”. A and D provide the “lubricity” for the LDL to move through the arteriole wall and when the LDL comes in contact with the foam cell, it “fires” the K and “boom” the foam cell is dead. Once the Foam cell is dead, the HDL goes in and cleans out the “trash”. The HDL cannot “get near” the foam cell unless, on the outer coat of the HDL is K/D/A (a surface chemistry issue). Put another way, the fat soluble vitamin “wets” the epithelial surface, which in turn allows the HDL to slip into the vicinity of the foam cell and slip out with the dead cell attached to be disposed of in the liver.
Occam’s Razor at its best.
In reality, the large LDL plays no negative role in heart disease if not oxidized.
In fact, large LDL’s role in hormone production is critical via pregnenolone. So, if one drops one’s large LDL and at the same time small LDL, for instance via a statin, the resulting drop in hormone production could have a significant negative impact on the intestinal bacteria and villi and on their subsequent production/transport of essential chemicals such as vitamin K and not to mention the impact on cancer due to the reduction in hormones.
Medical literature has demonstrated that statins do not retard foam cell growth. Statins, basically provide a treatment modality for incremental vitamin K and D absorption onto the HDL via increased HDL supply. Simply put, when a statin is employed, there is less small LDL available, more HDL created and available, and thus incrementally more vitamins K/D for the HDL to absorb, with the assumption that the intestinal bacteria/villi are not negatively impacted by the incremental reduction in hormone levels. This assumption of the response of the bacteria has never been researched or validated so it cannot be assumed to be true. In fact, the opposite must be true, meaning that statins do not directly contribute in a positive manner to the slowing down, killing, cleaning out, or prevention of CAD. From the author’s own experimentation (much like Dr. Ehrlich), this is true.
Literature is replete with case studies and research in mice, rats, and humans with regard to the lack of Vitamin K in the diet and the binding of K via (“warfarin”) and the resultant arteriole calcifications. This is the reason that K is added to primate chow, and the “talk” out there is that vitamin K is being added to the grains given to third world countries. Literature has also demonstrated that in the case of rats, the addition of vitamin K2 (MK-7) to the diet in supra-physiological amounts induces the removal of arterial plaques, most likely due to the saturation of HDL with the K molecule.
Lets now take this to the next level.
First looking at the paleo diet: “Og” and his tribe ate the WHOLE mastodon. Why? The meat and fat was loaded with vitamin K, so is the brain, thyroid, pancreas, and stomach contents. They ate the “whole thing”. Along with their mastodon was the ingestion of veggies and fruits and nuts (complex carbs) and throw in a fish or two, and bird’s eggs and well, you get the idea.
Vitamin K is a scarce nutrient. Thus the body craves it. Evidenced by the fact that the body has no limit to its ingestion and when ingested, the LDL goes up (the transport mechanism) and the HDL goes up. Once the system is saturated with vitamin K, then the LDL and HDL level off.
Since the author has been on vitamin K his LDL has gone up - - - to almost 100% - - - while on a statin!!!!!!!!
So, given the above, the availability of adequate amounts of vitamin K has to work in the following fashion:
The brain drives the production of LDL so that the brain has sufficient K going to it for neural repair via the SXR enzyme. The body has learned that with the brain driving need, the rest of the organs by default get what they need. This is the feedback system and the feed forward system is when the liver “sees” K coming in on the CM and CMr and reacts by producing LDL in spite of statin and in spite of “demand”. Just like “Og”, the body has to “make hay”.
An example of brain driven nutritional needs is the event called the “hang over” - - - here the brain increases blood circulation so as to obtain the required B vitamins and fluid so that function can be maintained. The result is a “headache” and general weakness until the brain is “made whole” via the extraction of the required nutrition and water from the body whole.
What happens to people, is that as they age the K absorption rate drops and thus the CAD cascade results.
Statins prevent the manufacture of LDL and due to the lowering of the LDL, this results in more LDL being completely covered by A/D/K. That is why the discussion is to drive LDL to below 50. When the LDL is lowered, the liver reacts to produce more HDL but if there is not sufficient vitamin K to coat it, it is all for naught. But you get close.
The LDL takes a K remnant to the respective cell where the respective cell converts it to the needed K derivative. So, in the case of mitochondria it is MK-9 through 15. In the case of the brain, it is vitamin K1 transformed into Mk-4. Eack K has their own specific role.
Take too much statin and the mitochondria go “south” resulting in muscle soreness and general tiredness.
REMEMBER = = = your body just does not produce "Stuff" for giggles. There is a reason and generally a very simple one if one understands the reactions going on. So, lets try this on for size:
Your liver is an ACTIVE organ meaning it is taking in chemical signals (feed back) and reacting to them and most likely taking (feed forward) signals via the parasympathetic nervous system. Ok, so what? Your liver is also a very old organ genetically so its been doing this for many generations (read as millions of years).
When we ingest fat it goes into our blood and then to our liver via CM and CMr. We genetically “know” that “fat” is rich in K, D, & A vitamins.
The liver sees the fat and sez to itself - - -if there is fat that means there must be K available - - - so bingo, make LDL and attach K to it. It’s not waiting to see if there is or is not K coming in. Out comes the LDL with supposedly K attached for distribution. If it does not attach any - - - - ooops now you have oxidized LDL floating around as there is no K to attach to it. Oxidized LDL (oxy-LDL) can be best described as a chemical irritant (your car without paint or primer).
So, now we give folks statins to reduce the amount of LDL = = = fine = = = so the body reacts by producing more HDL as a backup. Now we have high HDL (the backup delivery system) and a low amount of LDL and still no K. Fine, but now we have less oxy-LDL to deal with statistically. That makes one incrementally slow down the rate of plaque growth. The author personally knows that to be true.
Ok, now lets take the statin away and introduce a "whole bunch" (supra-physiological dose) of vitamin K into the system. The liver now goes "wow", look at all this K and say… little fat in proportion. The liver starts producing a whole bunch of LDL of the right configuration to grab the K which historically has been in short supply. This is the back up system. The key here is that the Liver needs a great deal of “K” to react.
Historically, LDL has been characterized as bad as it is correlated with CAD - - - but not causal - - only correlated. So, ask one’s self - why is LDL there? Just hormone production? Numerous studies have found LDL in the Foam cell area cuz the body is using the LDL as a K and possibly D carrier to kill the foam cells. Where there is not enough K present to be effective, the LDL still goes there but cannot do its job cuz no K is attached so it then appears as the BAD ACTOR when in reality it is the missing K that is the problem as it relates to CAD with the negative cascade resulting from the oxyLDL.
If one has no chrome on the bumper, the bumper rusts (oxidation)
Also, K is transported by LDL all over the body as needed and cannot be over ingested (hmmmmm) so the body is set up to really "suck it up" when given a chance.
Here is a piece of evidence just gathered from my latest blood work:
Position: Elevated vitamin K concentrations may be associated with increased lipid concentrations was the thought and then proven via testing.
my latest LDL (VAP) total is 124 with a 63 HDL and also a fully pattern A - - -
TGs were 72
total Cholesterol was 202
my ApoB/A1 ratio was 0.52 with A1 at 171
K1 was at 8.7 ng/ml or 4x higher than "normal"
in summary: if one maximizes K then one does not need a statin = = = = the liver will make enough LDL and HDL to transport it. Additionally the liver will also make and attach the vitamin A required along with attaching the required D.
The brain, pancreas, and thyroid are sending out signals to the liver either chemically or using the parasympathetic nervous system which sez "K" me.
The liver is somewhat dumb and only knows that when the signal is made it sends out LDL because it assumes there is some "K" attached (its genetic history) based on “Og” eating the K rich organs and fat of the mastodons.
Basically, instead of insulin resistance we have a form that one may call "K" resistance. Meaning that the gut is no longer producing/absorbing "K" as it once did. The ethnic studies have proven that with age we absorb less but = = = = think about it - the demand is still there.
The net result is oxidized LDL the ultimate “bad actor”!
So, if this theory or postulate is true, then if one increases "K" then LDL and HDL should increase and CAD should be stopped and reversed.
Which the author has now proven to be true! Via EBT scans and blood tests.
Think about it = = = teens don't have CAD = = = why? - - - -far more efficient at "K" absorption. Why do pregnant mothers get so tired? Because the baby is putting vitamin K demands and vitamin D demands on the mother. Cravings? Most likely the body saying we need "K" or some such gut derivative.
Baby rats die from brain hemorrhages when the mother is fed rat chow without vitamin K included.
The literature is replete with the instances of a lack of K and primate death due to CAD. Where is the research showing the vitamin K content of free-ranging beef as compared to corn- fed beef? Same with free-range chickens versus factory-raised chickens. Could it be not the meat or the fat but the lack of K found in the meat/fat itself that is the key variable?
The author has had this happen with the last three LDL checks since starting vitamin K. Reference the test result section.
Some Idle Thoughts:
Who ever said that we want HDL? Where is the literature that states that HDL is supposed to be higher than LDL? - - - if it is so, then why is it that babies and young children/teens don't have this condition when it would be considered most critical?
The Milano variant on HDL - - - never was the vitamin K level checked of this family.
Fats come into play when the “wrong” fats results in LDL particles that are not formed correctly, resulting in LDL particles that are incapable of either proper K attachment, proper K delivery, aka, small dense LDL.
There is talk of the APOE gene and its impact. Simple, the 3/4 variant and the 4/4 variant cause the liver to clear the K quicker than the 3/3 and the 2/2 and the 3/2. So, if you test for the "4" variant, keep a close watch on your K levels.
Well there you have it - - - my best guess as to what the heck is going on.