[quote]kakno wrote:
[quote]LoRez wrote:
My very naive theory… [/quote]
Dietary cholesterol has almost no effect on serum cholesterol, so eating more cholesterol will not lead to any of the effects you desire. The concentration of cholesterol in your blood is not what limits test synthesis. The concentrations of test, GnRH and LH are.
If you want significantly more test in your blood, inject test. And since you’re still a beginner, don’t.[/quote]
Med school endocrinology classes ftw
[quote]OzyNut wrote:
The two most common transgenics are the LDL receptor knockout and ApoE knockout. [/quote]
Apo E is for liver uptake right? (just jog my memory here)
[quote]rehanb_bl wrote:
all the statin lovers on here will just skip over this video or think you’re just not educated enough in medicine
btw- thanks for sharing, fantastic and quite scary. While everyone is worried over piddly shit these days, this is something that is on a scale almost like nothing else.
[quote]jehovasfitness wrote:
all the statin lovers on here will just skip over this video or think you’re just not educated enough in medicine
btw- thanks for sharing, fantastic and quite scary. While everyone is worried over piddly shit these days, this is something that is on a scale almost like nothing else.[/quote]
Any medical student and therefore any doctor is very aware of publication bias, submission bias, industry funded data, the role follow up times play and weighing risk to benefit. But go ahead, pretend you know better. And while you’re at it, read this: Dunning–Kruger effect - Wikipedia
My medical school spends a lot of time teaching us statistics and how to review literature properly. In fact, we are assessed on it.
[quote]kakno wrote:
[quote]jehovasfitness wrote:
all the statin lovers on here will just skip over this video or think you’re just not educated enough in medicine
btw- thanks for sharing, fantastic and quite scary. While everyone is worried over piddly shit these days, this is something that is on a scale almost like nothing else.[/quote]
Any medical student and therefore any doctor is very aware of publication bias, submission bias, industry funded data, the role follow up times play and weighing risk to benefit. But go ahead, pretend you know better. And while you’re at it, read this: http://en.wikipedia.org/wiki/Dunning–Kruger_effect[/quote]
Well, unlike you I clicked your link, it lost me in the first sentence 
j/k
did you happen to read the article I linked maybe last page?
What’s with all the messed up quotes lately, I don’t seem to be typing in the wrong area
On a serious note, decent wiki page and makes a lot of sense.
I for one hope I don’t come across as in this thread example that statins ARE NOT effective, as the evidence does seem to support they are.
My issues are:
[quote]rehanb_bl wrote:
[quote]OzyNut wrote:
The two most common transgenics are the LDL receptor knockout and ApoE knockout. [/quote]
Apo E is for liver uptake right? (just jog my memory here)
[/quote]
Apo E is a ligand for any LDL(and like/related) receptor. It is principally responsible for the uptake of IDL and chylomicron remnants by any tissue.
It also important for the effective hydrolysis of triglycerides.
[quote]kakno wrote:
[quote]LoRez wrote:
[quote]kakno wrote:
[quote]LoRez wrote:
My very naive theory… [/quote]
Dietary cholesterol has almost no effect on serum cholesterol, so eating more cholesterol will not lead to any of the effects you desire. The concentration of cholesterol in your blood is not what limits test synthesis. The concentrations of test, GnRH and LH are.
If you want significantly more test in your blood, inject test. And since you’re still a beginner, don’t.[/quote]
Hey, you’ve got to give me some credit for admitting it
Obviously (?) injecting test is the best route if that’s what I’m after… I was really just trying to hedge my bets by approaching it from a diet standpoint. Either way, eggs and liver is a good protein and B-vitamin source.
But serious question: If dietary cholesterol has almost no effect on serum cholesterol, what happens to it? Where does it go? Really only three things can happen to it: it’s broken down, stored somewhere, or excreted… right?
If dietary cholesterol was quickly transformed into pregnenalone after absorption, I wouldn’t expect there to be much effect on serum cholesterol, since it has no need to hang out in the bloodstream.[/quote]
Some goes straight through, some goes to the liver. If a lot goes to the liver, the liver doesn’t have to produce as much on its own. If nothing goes to the liver, it will have to produce more. Some is metabolized to bile or roidz.[/quote]
This is correct, however I would like to note that dietary cholesterol, once absorbed, is packaged into chylomicrons, by the intestinal epithelial, and secreted into lymph. It then enters the blood stream and follows the typical path of lipoproteins - apolipoprotein exchange, hydrolysis of triglycerides and clearance (albeit with a few distinct differences).
So, infact, dietary cholesterol does impact blood cholesterol levels. To reach the liver, it must first be travel through the blood. That is one reason why fasting cholesterol measures are taken, to remove dietary cholesterol as a confounder.
This forms the crux of one of the theories of atherosclerosis, that dietary cholesterol and chylomicrons/remnants are key players.
[quote]OzyNut wrote:
[quote]kakno wrote:
[quote]LoRez wrote:
[quote]kakno wrote:
[quote]LoRez wrote:
My very naive theory… [/quote]
Dietary cholesterol has almost no effect on serum cholesterol, so eating more cholesterol will not lead to any of the effects you desire. The concentration of cholesterol in your blood is not what limits test synthesis. The concentrations of test, GnRH and LH are.
If you want significantly more test in your blood, inject test. And since you’re still a beginner, don’t.[/quote]
Hey, you’ve got to give me some credit for admitting it
Obviously (?) injecting test is the best route if that’s what I’m after… I was really just trying to hedge my bets by approaching it from a diet standpoint. Either way, eggs and liver is a good protein and B-vitamin source.
But serious question: If dietary cholesterol has almost no effect on serum cholesterol, what happens to it? Where does it go? Really only three things can happen to it: it’s broken down, stored somewhere, or excreted… right?
If dietary cholesterol was quickly transformed into pregnenalone after absorption, I wouldn’t expect there to be much effect on serum cholesterol, since it has no need to hang out in the bloodstream.[/quote]
Some goes straight through, some goes to the liver. If a lot goes to the liver, the liver doesn’t have to produce as much on its own. If nothing goes to the liver, it will have to produce more. Some is metabolized to bile or roidz.[/quote]
This is correct, however I would like to note that dietary cholesterol, once absorbed, is packaged into chylomicrons, by the intestinal epithelial, and secreted into lymph. It then enters the blood stream and follows the typical path of lipoproteins - apolipoprotein exchange, hydrolysis of triglycerides and clearance (albeit with a few distinct differences).
So, infact, dietary cholesterol does impact blood cholesterol levels. To reach the liver, it must first be travel through the blood. That is one reason why fasting cholesterol measures are taken, to remove dietary cholesterol as a confounder.
This forms the crux of one of the theories of atherosclerosis, that dietary cholesterol and chylomicrons/remnants are key players.[/quote]
I’ve been told by a doctor and testing place two different things. The doctor told me on an NMR fasting was not required, the testing place said yes.
The net seems mixed on it.
[quote]jehovasfitness wrote:
[quote]OzyNut wrote:
[quote]kakno wrote:
[quote]LoRez wrote:
[quote]kakno wrote:
[quote]LoRez wrote:
My very naive theory… [/quote]
Dietary cholesterol has almost no effect on serum cholesterol, so eating more cholesterol will not lead to any of the effects you desire. The concentration of cholesterol in your blood is not what limits test synthesis. The concentrations of test, GnRH and LH are.
If you want significantly more test in your blood, inject test. And since you’re still a beginner, don’t.[/quote]
Hey, you’ve got to give me some credit for admitting it
Obviously (?) injecting test is the best route if that’s what I’m after… I was really just trying to hedge my bets by approaching it from a diet standpoint. Either way, eggs and liver is a good protein and B-vitamin source.
But serious question: If dietary cholesterol has almost no effect on serum cholesterol, what happens to it? Where does it go? Really only three things can happen to it: it’s broken down, stored somewhere, or excreted… right?
If dietary cholesterol was quickly transformed into pregnenalone after absorption, I wouldn’t expect there to be much effect on serum cholesterol, since it has no need to hang out in the bloodstream.[/quote]
Some goes straight through, some goes to the liver. If a lot goes to the liver, the liver doesn’t have to produce as much on its own. If nothing goes to the liver, it will have to produce more. Some is metabolized to bile or roidz.[/quote]
This is correct, however I would like to note that dietary cholesterol, once absorbed, is packaged into chylomicrons, by the intestinal epithelial, and secreted into lymph. It then enters the blood stream and follows the typical path of lipoproteins - apolipoprotein exchange, hydrolysis of triglycerides and clearance (albeit with a few distinct differences).
So, infact, dietary cholesterol does impact blood cholesterol levels. To reach the liver, it must first be travel through the blood. That is one reason why fasting cholesterol measures are taken, to remove dietary cholesterol as a confounder.
This forms the crux of one of the theories of atherosclerosis, that dietary cholesterol and chylomicrons/remnants are key players.[/quote]
I’ve been told by a doctor and testing place two different things. The doctor told me on an NMR fasting was not required, the testing place said yes.
The net seems mixed on it.
[/quote]
Whenever in doubt, trust the people actually doing the test.
The NMR cholesterol test measures the number of LDL particles separated by size. Having chylomicrons or chylomicron remnants shouldn’t interfere with detection because they are MUCH larger than LDL. However, chylomicron remnants competitively compete with apoB100 lipoproteins for uptake. The uptake of a chylomicron remnant by the LDL receptor requires 4 receptors, in comparison to just 1 for LDL.
In my opinion, fasting would be better (but not strictly necessary for a healthy person).
Interestingly, chylomicrons are secreted continuously by the intestines even without you actually eating anything. This rhythm can be upregulated in conditions like insulin resistance and may never return to a normal slower pace. The liver, on the other hand, will only secrete VLDL once a complete particle is formed.
Since particle size has come up: It has been known for a long time that lipoproteins are actively transported through the endothelium and could be entrapped in the subendothelial matrix (cause for macrophage infiltration). A mathematician calculated the number of particles that would theoretically get trapped and concluded that it wouldn’t be possible for people to live past 20, if that were true. So researchers started to look for other theories. Some proposed that size was a limiting factor for transport, but this turned out to be false. They realised that entrappment was the important factor and not cholesterol flux. It is now known that chylomicron remnants are trapped much more than LDL.
A small dense LDL indicates a problem with lipoprotein uptake (therefore they have a higher blood residency time). It isn’t the small size that causes them to be a problem, but rather what their small size represents.
Interesting, I’ve read the same on how LDLb in and of itself may not be the problem, thanks for the break down.
[quote]jehovasfitness wrote:
On a serious note, decent wiki page and makes a lot of sense.
I for one hope I don’t come across as in this thread example that statins ARE NOT effective, as the evidence does seem to support they are.
My issues are:
[quote]kakno wrote:
[quote]jehovasfitness wrote:
On a serious note, decent wiki page and makes a lot of sense.
I for one hope I don’t come across as in this thread example that statins ARE NOT effective, as the evidence does seem to support they are.
My issues are:
Does any of it really matter at this point? You’re set in your beliefs, I in mine.
[quote]jehovasfitness wrote:
[quote]kakno wrote:
[quote]jehovasfitness wrote:
On a serious note, decent wiki page and makes a lot of sense.
I for one hope I don’t come across as in this thread example that statins ARE NOT effective, as the evidence does seem to support they are.
My issues are:
Does any of it really matter at this point? You’re set in your beliefs, I in mine.[/quote]
I asked if you could back up your statement. That means I’m not set in my beliefs.
[quote]kakno wrote:
[quote]jehovasfitness wrote:
[quote]kakno wrote:
[quote]jehovasfitness wrote:
On a serious note, decent wiki page and makes a lot of sense.
I for one hope I don’t come across as in this thread example that statins ARE NOT effective, as the evidence does seem to support they are.
My issues are:
Does any of it really matter at this point? You’re set in your beliefs, I in mine.[/quote]
I asked if you could back up your statement. That means I’m not set in my beliefs.[/quote]
From the current research it seems people under the age of 80 with history of CVD benefit.
They have never been shown to be effective for women (this is a huge % of users).
It has never been shown to be effective for males w/o a history of CVD, this is a big chunk of users.
What is being debated here?
Statin trials where they used a low dose vs higher dose, which resulted in 20% TC drop (may be off a little here) compared to a 50% drop in TC, showed no significant improvement on reduction in heart attacks. Top this with the fact we know high cholesterol does not cause HD, it should be evident that if a high dose statin reduces TC more than a low-dose we should expect a bigger reduction in incidences, but we do not.
Dr. Dwight Lundell and others have stated that statins are anti-inflammatory, as I’m sure you know that this is a major player in the disease.
Let’s not forget the wide range of side effects from statins and that large % of the population just blindly being put on them for the war on cholesterol that is as you know way misguided.
I’m not sure why you still feel that these drugs are not often overprescribed, but on the other hand I will admit can have their place (though for myself I would make lifestyle changes first if it were me, though many people are iwlling to do so).
Just ran across this today
So, the consensus is that if my LDL is 431 I should… ?
lol
[quote]DoubleDuce wrote:
So, the consensus is that if my LDL is 431 I should… ?
lol[/quote]
lol, get a new liver and genetics?