Discussion of dietary cholesterol and cardiovascular disease


They used to be called life assurance companies…maybe they still are?

After today’s episode I couldn’t care less what they call themselves, :slight_smile:


Oh, here, Google has cleared that up :slight_smile:

Both are forms of protection designed to pay out after the policyholder passes away – but they don’t work the same way. The key difference is that life insurance is designed to cover the policyholder for a specific term, while life assurance usually covers the policyholder for their entire life .

I was going for insurance, but they wanted to assure my 5.5 years old beautiful pup she could inherit my estate upon my death, 53 years from now. Great deal.

Yeah, I just wanted my house to go to someone in my family…I didn’t want a big payout.
I’ll have paid up soon anyway.

They tried to sell me everything…funeral cr*p (already covered), critical illness (I have long service in work and get full sick pay, and then the Union pays me). Then they got annoyed that I wasn’t playing ball.

(B Creighton) #83

There are large data bases on all of us. They probably bought a database, and you are just one of millions in it. They probably pay less than a dime for data on each person in the database. Here in the U.S. the gubbermint agencies can buy these databases as well…


At the risk of sounding an idiot…what are gubbermint agencies?

Insurance? Financial vultures? Wolves of Wall Street?

(B Creighton) #85

Gubbermint is just my tongue in cheek name for our wasteful federal agencies of the U.S. government - like the IRS, the DOJ, the FBI and now the DHS - all the three lettered monstrosities. I recently heard I think it was the FBI bought personal data.


Does the federal reserve have an acronym these days?

What’s the third word…

(B Creighton) #87

The federal reserve is actually I believe somewhat inaptly named. It is actually a private bank, and is supposed to operate independently from our government. It is not supposed to operate off of tax dollars, but makes its money to operate from charging banks for money. So it is not a governmental agency. As of late our government has been doing lots of borrowing from it - it is at an unsustainable clip, and of course no one has the political will power to stop it. The democrats seem to believe that Keynes only preached spend to stimulate the economy, and ignore his teaching to pull back spending to bring back down the deficit in non-recessionary years. So, the spending continues bordering on the level of banana republics, and all the democrats ever do is talk about spending more.


I won’t go political mate, even though I may have an opinion on what you say.

I’ve enough nonsense happening in my own part of the world :wink:

But hey, sorry folks, that may have been partly my fault for the brief diversion from topic- but I had to tell you what happened earlier to me, in relation to life expectancy. (True Story!)

Please carry on with longevity/CVD topic as previously.

(I’ll be tired tomoorrow at the parades lol.)

(Bacon enough and time) #89

That’s wise. We don’t appreciate politics on this site; it’s too contentious. I don’t know what it’s like elsewhere, but n the U.S., the caricatures the main parties have of each other are wildly inaccurate, and the potential for actually listening to one another is very low.


I’ve read the rules a couple of times now :smiley:


XXXX them. I won’t talk to nosy strangers on the phone - at all.

(Jenna Ericson) #92

So Statins lower LDL because LDL is linked to atherosclerosis. My guess is that Statins can cause muscle aches as a result of a lack of LDL as a fuel source.

When it comes to diet, saturated fat has been demonized because it correlates with higher LDL and higher incidents of atherosclerosis. If anyone’s familiar with the ROS theory of obesity, part of the theory says that saturated fat, as opposed to glucose or other fatty acids, causes insulin resistance at the level of the cell. Basically cells that have saturated fat for fuel create more ROS in their mitochondria, which signal to turn off auto-phosphorylation of insulin receptors in cells (that’s just from memory so I’d like to double check as some point).

I think there is an argument that insulin resistance starts at muscle cells, which would be the main sink for glucose. So if muscles are not able to accept glucose there are downstream effects. There would be a backup at the liver and fat cells would become too full because they would have to accept excess fat and glucose.

This might indicate the correlation between high LDL and insulin resistance. LDL is fat that is transported from the liver to peripheral cells. What type of fat does the liver make? It makes saturated fat, like other organs.

Saturated fat on it’s own is not bad, as with anything, but if metabolic dysfunction starts to occur where there is excess glucose and fat being exported from the liver, to be taken up by muscles, it would cause a cascade effect resulting in chronic insulin resistance. Strangely, this would seem to be the opposite hypothesis to that proposed by the ROS theory of obesity, but based on the same mechanics. I think that it still actually fits with the ROS theory in that high omega 6 fats may be the tipping point for dysfunction. Under other circumstances the body can compensate properly, I would argue.

(Bacon enough and time) #93

It’s actually glucose metabolism that causes more oxidative damage, along with advanced-glycation end-products. The advantage of a low-carb, high-fat diet is that the body enters fat-metabolising mode, and the ketones produced in the liver when insulin is low have epigenetic effects. One of those is to restore our endogenous anti-oxidants, which had been inhibited by high insulin.

Too much glucose metabolism leads to mitochondrial damage from glycation and excess oxidation. This is why there is a fat-adaptation period when we start keto: the mitochondria need time to heal and to make new mitochondria.

According to Robert Lustig, even more important than muscular insulin resistance is the visceral fat that fills up our internal organs, especially the liver and pancreas, causing them to become insulin-resistant. Sub-cutaneous fat, which is believed to be the problem, is actually benign in terms of metabolic health, as witnessed by the 20% of obese people who are metabolically healthy (MHO–metabolically healthy obese). Visceral fat, on the other hand, can affect thin people and give them all the same metabolic diseases commonly associated with obesity and diabetes (TOFI–thin on the outside, fat on the inside). Fortunately, visceral fat clears up pretty quickly, once fructose is removed from the diet (both where it is found separately, and where it is found as part of a sucrose molecule).

The adipocytes in our fat tissue actually remain sensitive to insulin longer than other cells. (“Exquisitely sensitive” is the phrase used by Berson and Yalow in their famous paper.) The excess glucose that the skeletal muscles cannot handle gets sent to the liver, where it is made into triglycerides and sent to adipocytes in the form of VLDL. This is why a high-carb, low-fat diet raises triglycerides and lowers HDL, and why a low-carb, high-fat ketogenic diet lowers triglycerides and raises HDL (the latter especially when we eat saturated fat).

This is new to me. I wasn’t aware of such a correlation. In fact, about half of people with familial hypercholesterolaemia, along with Dave Feldman’s lean-mass hyper-responders, all have greatly elevated LDL with no concomitant insulin resistance. If there really is such a correlation, I’d suspect that causality would be explained by a confounder, and that elevated LDL (in some cases, at least) and insulin-resistance are both caused by hyperinsulinaemia, for example.

Again, this is something I’ve never heard before. The liver does make fatty-acid droplets when a particular metabolic pathway is overloaded with fructose and/or alcohol, but I’ve not heard that that is all saturated fat. I think that would depend on the point in the cycle at which the fat droplet is thrown off. The problem is that most of this fat never escapes the liver, which is the cause of fatty liver disease. The mechanism that exports triglycerides in VLDL to the fat tissue is a different beast, so far as I know, but I’ve never heard that it creates saturated fat only. Dietary fat is sent to peripheral cells in chylomicrons, and that would be any type of fatty acid that we happened to eat in the course of that meal. (Chylomicrons do not show up in a fasting lipid panel, since by the time of the blood draw they will have done their job and returned to the liver for processing.)

So far as I know, ω-6 fatty acids are not absorbed by the liver in any greater quantity than by any other cell in the body. The main problem is that while certain ω-6 fatty acids are essential to our diet, the quantity needed is exceedingly small. In larger quantities, ω-6 fatty acids cause systemic inflammation. The other problem, of course, is that ω-6 fatty acids compete with ω-3 fatty acids for the same cell receptors. If there is too much ω-6, then the ω-3 stands little chance of getting absorbed. The best ratio of ω-6 to ω-3 is around 1.0-1.25. Given the vast quantities of ω-6 fatty acids in seed oils and highly processed foods, there is no way to consume enough ω-3 fatty acids to bring the ratio into the correct range. The better strategy is to greatly reduce the consumption of ω-6.

(Jenna Ericson) #94

While I agree that glucose metabolism causes more oxidative damage, I was talking about a specific mechanism whereby ROS are used as signalling molecules in cells. below is a link to the fire in a bottle blog by Brad Marshall. If you click “next post” at the bottom it says on that page “Mitochondrially produced ROS (superoxide and hydrogen peroxide) are a signal to the organism that fat is being oxidized rather than carbohydrate. This has been conserved in evolution for perhaps a billion years, as we saw with C elegans worms. The signal to the body that fat is being oxidized is the production of ROS. ROS is the signal. Unsaturated fat eliminates the signal.”

(B Creighton) #95

I don’t believe that is quite accurate. I may be wrong, but I don’t think statins lower LDL per se. They lower the amount of cholesterol ester made by the liver for transport in LDL. So, if it is lowered enough, I imagine the number of LDL might be lowered.

Technically, LDL is not fat. It is a lipoprotein container which carries the fat. Often this fat is not made by the liver, but is simply triglycerides consumed, and then packaged by the liver into LDL for transport. But, I believe if these fats are oxidized, they end up getting packaged into the LDL, and lend their oxidated state to the whole particle. You are right that the liver does make fat, and it seems to usually do this with excess fructose, which it makes into palmitate or palmitic acid which is a saturated fat. Usually at this point the person is eating too much sugar which is already causing a triglyceride buildup, which is apparently why the liver ends up storing this palmitic acid locally - and one ends up with fatty liver disease. Someone can correct me if I’m wrong.

There could be a correlation between the number of LDL and insulin resistance, but it is probably a loose one. I don’t believe there is much correlation between fat intake and insulin resistance. Eskimos and certain Polynesians have historically had remarkably high fat diets with no insulin resistance until modern processed foods made their appearance. I have little doubt that excess sugar and simple carb intake is the primary or sole driver of insulin resistance.

(Bacon enough and time) #96

Here is a talk Nick Mailer gave at Ketofest in 2018, on precisely the topic of how statins work:

(Robin) #97

I would like this guy to come to my house and speak to me.
Preferably slowly and loudly.
While I take notes.
I hear this stuff repeatedly and don’t seem to retain it.

(Peter - Don't Fear the Fat ) #98

Funny, I immediately hate him. And will loudly shout, ‘Back Off’ …damn sweet talker, I’ll give him chemical attraction :joy:

(Bacon enough and time) #99

I have to say that the first couple of times I listened to this lecture, I found it hard to absorb, but this last time, it really made sense. I don’t know whether that’s because I was in different frame of mind while listening this time, or because I’ve learned more over the intervening years since Nick gave this talk. Perhaps both.

(Robin) #100

Oh, I didn’t listen or watch him! No reason, as I truly don’t retain info from videos.
But there is usually enough feedback from everyone that I get the gist of it.