No Mevalonate = No new liver cells. Why would I make this up. Too bizarre for me to imagine out of nothingness.
Mevalonate-derived proteins in liver regeneration
The higher end of dosing for statins is ill-conceived. It doesn't do anything other than take a sledgehammer to LDL cholesterol. Lp(a) is still happily made by the liver at the same level, and along with it, Lp(a)'s cholesterol inside it.
That is not the way statins work anyways. When they do work, taken at low doses, it is through non-mevalonate pathway pleiotropic effects discussed in the literature.
The early generation "dirty" statins were so powerful at jamming cholesterol synthesis that they were studied as chemotherapeutics because cells do not divide if they are underneath a threshold of intracellular cholesterol. This body of research is older but easily found.
Tuesday, August 8, 2017
Sunday, August 6, 2017
Interleukin-6, the gambit of the crusaders of cholesterol as a plumbing gunk.
As if in possession of a powerful secret bit of information, the petty crusaders of the idea that LDL particles gum up their pathway in the human body, rather than being present at sites of chronic inflammation, will point to IL-6 and snicker as if I didn't know.
IL-6 causes LDL receptor upregulation, and fit and trim appearances.....But also a myriad of degenerative diseases when it is emitted by the immune cells or arterial cells.
One acknowledgement: Atherosclerosis occurs elsewhere besides the coronary arterial bed, the carotids, the cerebrovasculature, the renal bifurcation, and the iliac bifurcations. Because of the mechanical nature of the heart, these plaques are most often lethal there. DeBakey published in detail about this. In fact, it is NOT the heart that most commonly suffers atherosclerosis, but the split that feeds our left and right legs. Yet, this is in line with what the "backwards conspiracy theorists" claim - that atherosclerosis occurs at bifurcations and curves with hemodynamic alteration. There is nothing contrary. Yet, the iliac plaques are generally not lethal. The second most common areas is....the heart arteries.
Patterns of atherosclerosis and their surgical significance.
Yes, IL-6 like nearly all things in the body has a positive function. You need IL-6 signaling.
Inhibiting Interleukin-6 (IL-6): The Key To Health, Successful Aging and Vitality
Some would have a myopic focus on hyper IL-6 reducing plasma lipids and quietly chuckle internally while saying to themselves, "Cholesterol causes heart disease, not IL-6." Not so. Maybe for a while, but the factual mechanism is that chronic IL-6 is destructive and involved in several chronic degenerative diseases, including atherosclerosis. Nothing backwards about anything that anyone has seen. It is a matter of time scale. Short term versus long term. For example, from the link above, "In people who exercised for 3-3.5 hours (marathon exercise), IL-6 increased from 1.5 pg/ml to 94.4 pg/ml immediately post-exercise and to 22.1 pg/ml 2 hours post-exercise (half-life of 1-2 hours) (R, R2). This means blood levels should be completely normal the next day – even after running a marathon." If you had some simmering internal damage emitting the amount of IL-6 generated after a marathon everyday for many years, say a lot of widespread endothelial denudations (torn off lining of the artery), that situation is very different.
In the context of chronic diabetes mellitus, IL-6 drives higher LDL levels in the blood, not lower levels as would be seen in certain acute inflammatory episodes.
Interleukin-6 mediates hepatic hypersecretion of apolipoprotein B
You can have low LDL but high Lp(a). IL-6 is a straightforward upregulator of Lp(a) if not LDL. Lowering IL-6 lowers Lp(a), much more atherogenic than LDL will ever be.
IL-6 blockade by monoclonal antibodies inhibits apolipoprotein (a) expression and lipoprotein (a) synthesis in humans
It doesn't report "IL-6 blockade RAISES blood Lp(a) in humans." Now that would be backwards.
IL-6 causes LDL receptor upregulation, and fit and trim appearances.....But also a myriad of degenerative diseases when it is emitted by the immune cells or arterial cells.
One acknowledgement: Atherosclerosis occurs elsewhere besides the coronary arterial bed, the carotids, the cerebrovasculature, the renal bifurcation, and the iliac bifurcations. Because of the mechanical nature of the heart, these plaques are most often lethal there. DeBakey published in detail about this. In fact, it is NOT the heart that most commonly suffers atherosclerosis, but the split that feeds our left and right legs. Yet, this is in line with what the "backwards conspiracy theorists" claim - that atherosclerosis occurs at bifurcations and curves with hemodynamic alteration. There is nothing contrary. Yet, the iliac plaques are generally not lethal. The second most common areas is....the heart arteries.
Patterns of atherosclerosis and their surgical significance.
Yes, IL-6 like nearly all things in the body has a positive function. You need IL-6 signaling.
Inhibiting Interleukin-6 (IL-6): The Key To Health, Successful Aging and Vitality
Some would have a myopic focus on hyper IL-6 reducing plasma lipids and quietly chuckle internally while saying to themselves, "Cholesterol causes heart disease, not IL-6." Not so. Maybe for a while, but the factual mechanism is that chronic IL-6 is destructive and involved in several chronic degenerative diseases, including atherosclerosis. Nothing backwards about anything that anyone has seen. It is a matter of time scale. Short term versus long term. For example, from the link above, "In people who exercised for 3-3.5 hours (marathon exercise), IL-6 increased from 1.5 pg/ml to 94.4 pg/ml immediately post-exercise and to 22.1 pg/ml 2 hours post-exercise (half-life of 1-2 hours) (R, R2). This means blood levels should be completely normal the next day – even after running a marathon." If you had some simmering internal damage emitting the amount of IL-6 generated after a marathon everyday for many years, say a lot of widespread endothelial denudations (torn off lining of the artery), that situation is very different.
In the context of chronic diabetes mellitus, IL-6 drives higher LDL levels in the blood, not lower levels as would be seen in certain acute inflammatory episodes.
Interleukin-6 mediates hepatic hypersecretion of apolipoprotein B
You can have low LDL but high Lp(a). IL-6 is a straightforward upregulator of Lp(a) if not LDL. Lowering IL-6 lowers Lp(a), much more atherogenic than LDL will ever be.
IL-6 blockade by monoclonal antibodies inhibits apolipoprotein (a) expression and lipoprotein (a) synthesis in humans
It doesn't report "IL-6 blockade RAISES blood Lp(a) in humans." Now that would be backwards.
Tuesday, August 1, 2017
Cholesterol DOES or DOES NOT cause heart disease? Which is backwards?
Given that diabetes causes atherosclerosis, and that cholesterol is never found alone in food, but often with culprits of atherosclerosis, or in a toxic oxidized form, it is easy to confuse the idea that lipoprotein cholesterol DOES NOT cause atherosclerosis with the idea that ox-cholesterol is inflammatory.
If cholesterol were the cause of atherosclerosis, chimpanzees, our nearest genetic cousins in the wild, would all die of atherosclerosis. The fact in the real world is that they do not despite having what is considered extremely high blood cholesterol. Chimpanzees have high cholesterol throughout their entire lives and it gets higher in old age from menopause and andropause. LDL above 170mg/dL, and total cholesterol above 200mg/dL are routine in chimpanzees. They die of heart tissue fibrosis and/or arrythmia resulting from it, but not "clogged arteries."
So, for those who a priori subscribe to the old "cholesterol causes atherosclerosis in people" idea, here is an eye opening look at the facts as they really are.
Heart disease is common in humans and chimpanzees, but is caused by different pathological processes
"This difficulty in inducing advanced lesions in rodent and rabbit models is in stark contrast to the prevalence of severe atherosclerosis in humans, which occurs even in some individuals with mildly elevated LDL levels and no other obvious risk factors (Vasan et al. 2005). Indeed, despite statin treatment of their hypercholesterolemia 70% of such patients still have adverse cardiovascular events (Steinberg 2008)."
"While captive great apes have a relatively healthy diet from the perspective of atherosclerotic risk (low in cholesterol and saturated fat), this is not reflected in their serum lipid profiles. At the Yerkes Primate Center, a mean total cholesterol level of 211.13 ± 38.85 mg/dL was found in a population of 106 male captive chimpanzees over their 50-plus-year lifespan (Herndon and Tigges 2001). Similar ranges were noted at PFA (Howell et al. 2003), and at another center (Hainsey et al. 1993)."
"Second and most intriguingly, we see that unlike the case in humans, captive chimpanzees have high serum cholesterol levels even in the early decades of life (Fig. 2). Thus, the chimpanzee vasculature is exposed to high cholesterol levels throughout adolescence and adulthood. Indeed the levels in very young chimpanzees fall into a high enough range wherein pharmacological statin therapy would now be seriously considered in children (Daniels and Greer 2008)."
The important key fact is the carefully examined result that in humans, after lowering LDL drastically by statins, 70% of these treated patients have CVD events anyways. By simple deductive logic with empirical proof, cholesterol could NOT be the cause of atherosclerosis in these patients with therapeutically lowered cholesterol. So what is the cause? There is the vitamin C deficiency debacle which the deep white hat state knows with certainty to be a major culprit. There are dozens of MOA's for vitamin C in the human cardiovascular and coagulation/hemostasis system. The simple solution is just take lots of vitamin C (and K2, B-complex, and magnesium) for this group and be on with their great noble lives. For the evil hats, it is all about stubborn denial, and mass murdering people around the world indirectly for profit and weird, petty, ulterior motives.
Atherosclerosis happens a lot in people. It is associated with higher LDL levels, but it is NOT cholesterol causing the atherosclerosis. It is there with the atherosclerosis. Hypertension, arterial and blood inflammation, and accidental immune system attacks on the artery wall, mechanical damage, and....insulin resistance and/or diabetes mellitus are increasingly being revealed as the underlying reason FOR high blood cholesterol. We are not chimpanzees, there is a major difference in the aspects of our cardiovascular diseases. The 1% genetic difference is a vast one. Diet in chimpanzees is unrelated to cholesterol which is always high in them regardless of an immaculate vegetarian diet. Diet may however, actually account for their lack of atherosclerosis. The human diet, westernized with globs of trans-fatty acids, rancid oxidized toxic lipids, tons of excess sugar, salt, and hydrogenated oil (alkanes aka gasoline), and void of ascorbate, b-vitamins, magnesium, and vitamin k2 probably is the key to solving this particular mystery. A wild zoo diet will probably put humans back on track to avoiding atherosclerosis too.
If cholesterol were the cause of atherosclerosis, chimpanzees, our nearest genetic cousins in the wild, would all die of atherosclerosis. The fact in the real world is that they do not despite having what is considered extremely high blood cholesterol. Chimpanzees have high cholesterol throughout their entire lives and it gets higher in old age from menopause and andropause. LDL above 170mg/dL, and total cholesterol above 200mg/dL are routine in chimpanzees. They die of heart tissue fibrosis and/or arrythmia resulting from it, but not "clogged arteries."
So, for those who a priori subscribe to the old "cholesterol causes atherosclerosis in people" idea, here is an eye opening look at the facts as they really are.
Heart disease is common in humans and chimpanzees, but is caused by different pathological processes
"This difficulty in inducing advanced lesions in rodent and rabbit models is in stark contrast to the prevalence of severe atherosclerosis in humans, which occurs even in some individuals with mildly elevated LDL levels and no other obvious risk factors (Vasan et al. 2005). Indeed, despite statin treatment of their hypercholesterolemia 70% of such patients still have adverse cardiovascular events (Steinberg 2008)."
"While captive great apes have a relatively healthy diet from the perspective of atherosclerotic risk (low in cholesterol and saturated fat), this is not reflected in their serum lipid profiles. At the Yerkes Primate Center, a mean total cholesterol level of 211.13 ± 38.85 mg/dL was found in a population of 106 male captive chimpanzees over their 50-plus-year lifespan (Herndon and Tigges 2001). Similar ranges were noted at PFA (Howell et al. 2003), and at another center (Hainsey et al. 1993)."
"Second and most intriguingly, we see that unlike the case in humans, captive chimpanzees have high serum cholesterol levels even in the early decades of life (Fig. 2). Thus, the chimpanzee vasculature is exposed to high cholesterol levels throughout adolescence and adulthood. Indeed the levels in very young chimpanzees fall into a high enough range wherein pharmacological statin therapy would now be seriously considered in children (Daniels and Greer 2008)."
The important key fact is the carefully examined result that in humans, after lowering LDL drastically by statins, 70% of these treated patients have CVD events anyways. By simple deductive logic with empirical proof, cholesterol could NOT be the cause of atherosclerosis in these patients with therapeutically lowered cholesterol. So what is the cause? There is the vitamin C deficiency debacle which the deep white hat state knows with certainty to be a major culprit. There are dozens of MOA's for vitamin C in the human cardiovascular and coagulation/hemostasis system. The simple solution is just take lots of vitamin C (and K2, B-complex, and magnesium) for this group and be on with their great noble lives. For the evil hats, it is all about stubborn denial, and mass murdering people around the world indirectly for profit and weird, petty, ulterior motives.
Atherosclerosis happens a lot in people. It is associated with higher LDL levels, but it is NOT cholesterol causing the atherosclerosis. It is there with the atherosclerosis. Hypertension, arterial and blood inflammation, and accidental immune system attacks on the artery wall, mechanical damage, and....insulin resistance and/or diabetes mellitus are increasingly being revealed as the underlying reason FOR high blood cholesterol. We are not chimpanzees, there is a major difference in the aspects of our cardiovascular diseases. The 1% genetic difference is a vast one. Diet in chimpanzees is unrelated to cholesterol which is always high in them regardless of an immaculate vegetarian diet. Diet may however, actually account for their lack of atherosclerosis. The human diet, westernized with globs of trans-fatty acids, rancid oxidized toxic lipids, tons of excess sugar, salt, and hydrogenated oil (alkanes aka gasoline), and void of ascorbate, b-vitamins, magnesium, and vitamin k2 probably is the key to solving this particular mystery. A wild zoo diet will probably put humans back on track to avoiding atherosclerosis too.
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