Cholesterol and triglyceride levels and age?

[Doogles31731]

Cholesterol is the main precursor ingredient of all the steroid hormones formed in animals (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757135/). It is essential for the production of corticosteroids, and sex hormones. This article supports Arya Stark in the statement that “Cholesterol does go up but think about this... why would your body do that? Does it want to commit suicide?
No, if your body wants cholesterol to go up... maybe there is a reason (likely protective).”

As guidoLaMoto pointed out, the evidence for role of statins in the prevention of coronary heart disease and other manifestations of blocking arteries is not good. The pharmaceutical companies called them ‘statins’ because they don’t reverse cholesterol-associated problems, they just slow them down or at very best have been shown to reduce atheroclerosis by 1 or 2% (See see Nissen et al; 2006; http://jama.jamanetwork.com/article....ticleid=202629) and Nicholls et al (2006; https://jamanetwork.com/journals/jam...?redirect=true). The first paper was the result of a commendable world-wide experiment performed by many workers, but although it demonstrated a 53% reduction in LDLPChol, it showed only a 1% reduction in atherosclerosis of heart arteries (The cause of coronary heart disease).GuidoLaMoto also affirmed that “You're right, but the real problem is that there's precious little data on cause & effect of chol vs artery disease. It's all "correlation."”

Here are some studies suggesting that vitamin K2 deficiencies are associated with coronary heart disease.

Geleijnse et al (2004; https://www.ncbi.nlm.nih.gov/pubmed/15514282), after studying the daily vitamin K intakes of 4807 people in the Rotterdam study concluded that the high tertile of menaquinone, but not phylloquinone, was associated with lower risk of coronary heart disease.

Beulens et al (2009; https://www.sciencedirect.com/scienc...21915008005078) found that menaquinone intake was associated with a decreased risk of coronary calcification with an RR of 0.80 (95%-CI: 0.65–0.98; ptrend = 0.03) in a group of 564 postmenapausal women of whom 62% had coronary calcification.

Gast et al (2009; https://www.sciencedirect.com/scienc...39475308002093) found an inverse association between vitamin K2 and the risk of CHD. This association was mainly due to vitamin K2 subtypes MK-7, MK-8 and MK-9. Vitamin K1 intake was not significantly related to CHD.

Ueland et al (2011; https://www.ncbi.nlm.nih.gov/pubmed/21294711) matched 178 patients suffering chronic heart failure with healthy patients. They found that the level of proteins necessary for artery health (and which had not been activated because of low vitamin K) were higher in patients who died.

Van den Heuvel et al (2014; https://www.maturitas.org/article/S0...319-8/abstract) also found dp-ucMGP (proteins that had not been activated because of a deficiency of vitamin K) a useful biomarker for cardiovascular disease.

I had a heart attack associated with angina in 2004, had a stent inserted in an artery, and began to get recurrences of anginas in 2013. In 2014, after researching the literature, I began to take 10 times the recommended daily allowance of vitamin K1 and K2. My anginas disappeared within a month or so and I can push myself to a physical limit now without heart pain.

Whilst the above cited research suggests that vitamin K deficiency is intimately involved with cardio-vascular diseases, to date NO satisfactory therapeutic trials have been conducted. Nobody has ensured that all subjects in trials have sufficient vitamin D status to produce the primary proteins responsible for artery health, and nobody appears to have used high enough doses of both vitamin K1 and K2 in their trials. Vitamin K is essential for the activation of the raw proteins produced by vitamin D.

[kell490]

Originally Posted by Doogles31731

Cholesterol is the main precursor ingredient of all the steroid hormones formed in animals (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757135/). It is essential for the production of corticosteroids, and sex hormones. This article supports Arya Stark in the statement that “Cholesterol does go up but think about this... why would your body do that? Does it want to commit suicide?
No, if your body wants cholesterol to go up... maybe there is a reason (likely protective).”

As guidoLaMoto pointed out, the evidence for role of statins in the prevention of coronary heart disease and other manifestations of blocking arteries is not good. The pharmaceutical companies called them ‘statins’ because they don’t reverse cholesterol-associated problems, they just slow them down or at very best have been shown to reduce atheroclerosis by 1 or 2% (See see Nissen et al; 2006; http://jama.jamanetwork.com/article....ticleid=202629) and Nicholls et al (2006; https://jamanetwork.com/journals/jam...?redirect=true). The first paper was the result of a commendable world-wide experiment performed by many workers, but although it demonstrated a 53% reduction in LDLPChol, it showed only a 1% reduction in atherosclerosis of heart arteries (The cause of coronary heart disease).GuidoLaMoto also affirmed that “You're right, but the real problem is that there's precious little data on cause & effect of chol vs artery disease. It's all "correlation."”

Here are some studies suggesting that vitamin K2 deficiencies are associated with coronary heart disease.

Geleijnse et al (2004; https://www.ncbi.nlm.nih.gov/pubmed/15514282), after studying the daily vitamin K intakes of 4807 people in the Rotterdam study concluded that the high tertile of menaquinone, but not phylloquinone, was associated with lower risk of coronary heart disease.

Beulens et al (2009; https://www.sciencedirect.com/scienc...21915008005078) found that menaquinone intake was associated with a decreased risk of coronary calcification with an RR of 0.80 (95%-CI: 0.65–0.98; ptrend = 0.03) in a group of 564 postmenapausal women of whom 62% had coronary calcification.

Gast et al (2009; https://www.sciencedirect.com/scienc...39475308002093) found an inverse association between vitamin K2 and the risk of CHD. This association was mainly due to vitamin K2 subtypes MK-7, MK-8 and MK-9. Vitamin K1 intake was not significantly related to CHD.

Ueland et al (2011; https://www.ncbi.nlm.nih.gov/pubmed/21294711) matched 178 patients suffering chronic heart failure with healthy patients. They found that the level of proteins necessary for artery health (and which had not been activated because of low vitamin K) were higher in patients who died.

Van den Heuvel et al (2014; https://www.maturitas.org/article/S0...319-8/abstract) also found dp-ucMGP (proteins that had not been activated because of a deficiency of vitamin K) a useful biomarker for cardiovascular disease.

I had a heart attack associated with angina in 2004, had a stent inserted in an artery, and began to get recurrences of anginas in 2013. In 2014, after researching the literature, I began to take 10 times the recommended daily allowance of vitamin K1 and K2. My anginas disappeared within a month or so and I can push myself to a physical limit now without heart pain.

Whilst the above cited research suggests that vitamin K deficiency is intimately involved with cardio-vascular diseases, to date NO satisfactory therapeutic trials have been conducted. Nobody has ensured that all subjects in trials have sufficient vitamin D status to produce the primary proteins responsible for artery health, and nobody appears to have used high enough doses of both vitamin K1 and K2 in their trials. Vitamin K is essential for the activation of the raw proteins produced by vitamin D.

You said you got a stent in put in in 2004 but you started to get angina's in 2013. Did they do a stress test is the stent still keeping the artery open? Did your cholesterol numbers change after taking the Vitamin K1 and K2?

[LongevitySeeker]

Originally Posted by guidoLaMoto

The choiesterol in your blood steeam is not the cholesterol you ate-- It's the stuff your liver manufactured out of the basic building blocks utlimatley obtained thru your diet. That's why dietary measures, including use of fiber, has an insignificant effect on blood levels (lowering your chol from, say, 200 to 180 (10%) still keeps your numbers in the same risk category)...Besides, it's the HDL that really counts, and that's almost all genetic.

The stuff about omega 6 vs omega 3 is also built on some pretty flimsy evidence that is probably not significanrt for the individual.

People like to obsess about diet because it's one of the few things they can control themselves, but it really doesn't make much difference. The only good advice about diet is "Eat a balanced diet, everything in moderation." Further micro-management is fruitless.

Dr. Dean Ornish, in one of his books, stated that not everyone has the same number of cholesterol receptors in their body. Those who have many receptors can process and eliminate lots of cholesterol so as to prevent a buildup in the blood. Those who have only a few receptors will need to consume less cholesterol so as to maintain a normal blood level.