Journey 2 Remission/Reversal II (Don't call it a comeback).

[JITR]

I read what Davis wrote in the book and then searched for current research and opinion such as the paper I quoted. At the next opportunity, I'll ask for a small LDL test.

 

[CliffH]

I've tried looking for the studies myself, but SEO being what it is, all roads seem to lead back to Davis.

In that case, how about giving up and sticking to Groucho Marx quotes instead? Here's my favourite: "I'll dance with you until the cows come home. On second thoughts, I'll dance with the cows until you come home!".

 

[beating_my_betes]

I read what Davis wrote in the book and then searched for current research and opinion such as the paper I quoted. At the next opportunity, I'll ask for a small LDL test.

Can you point to where the paper you linked to demonstrates that wheat is either causally-linked to heart disease, or is particularly problematic for large amounts of small ldl particles, with those then going on to cause heart disease. I'm finding it difficult to get hold of such data.

Having squinted at the photoyou sent me, I cant see anything like that either. However, there seems to be a lot of the aforementioned problematic dogma.

In the meantime, this would be worth perusing. Of course, this is referring to whole grains. However, I've not seen anything to suggest Davis is only talking about whole wheat:

Whole grain consumption and risk of cardiovascular disease, cancer, and all cause and cause specific mortality: systematic review and dose-response meta-analysis of prospective studies - PMC

Objective To quantify the dose-response relation between consumption of whole grain and specific types of grains and the risk of cardiovascular disease, total cancer, and all cause and cause specific mortality. Data sources PubMed and Embase ...

pmc.ncbi.nlm.nih.gov

 

[everydayupsanddowns]

Perhaps you could just link me to the links that convinced you of his case?

I would suspect it would be a combination of aspects of multiple studies? It usually seems to be. Some for background/context. Others for specific results that show similarity (or difference) with what the researcher is attempting to investigate.

I think you’d have to pick your way through the references yourself really if you are curious?

 

[beating_my_betes]

In that case, how about giving up and sticking to Groucho Marx quotes instead? Here's my favourite: "I'll dance with you until the cows come home. On second thoughts, I'll dance with the cows until you come home!".

Why would I give up? A claim has been made, with what seems like scant supporting evidence, and from an author who has a track record of getting a lot of things wrong. I don't think everyone should be expected to read all the linked studies etc. But if people are going to share info, posited as fact, then I think it's important they check the sources...

...and if they'e checked the sources, it'd be much easier for everyone to pass the relevant info on.

If you want to mak fun of that process, fair enough...I guess

 

[beating_my_betes]

I would suspect it would be a combination of aspects of multiple studies? It usually seems to be. Some for background/context. Others for specific results that show similarity (or difference) with what the researcher is attempting to investigate.

I think you’d have to pick your way through the references yourself really if you are curious?

F'sure...If the author were hypothesising about a suggestion...of a possibility, then that chase would be worthwhile. But Davis is making a sweeping and damning case about a causal association between wheat consumption and heart disease. I cant find that data, but that doesn't mean it does not exist. I'm just assuming that someone who uses this book to validate a position has made sure that the rhetoric in the book is backed up by the sources linked.

Believe me, if the staff-of-life truly is broken, then I'd like to know about it.

 

[Drummer]

I read what Davis wrote in the book and then searched for current research and opinion such as the paper I quoted. At the next opportunity, I'll ask for a small LDL test.

I asked what type my LDL was - the NHS don't test for it, or at least they didn't back in the twenteens

 

[CliffH]

Why would I give up? A claim has been made, with what seems like scant supporting evidence, and from an author who has a track record of getting a lot of things wrong. I don't think everyone should be expected to read all the linked studies etc. But if people are going to share info, posited as fact, then I think it's important they check the sources...

...and if they'e checked the sources, it'd be much easier for everyone to pass the relevant info on.

If you want to mak fun of that process, fair enough...I guess

The saying, "Don't sweat the small stuff" comes to my mind.

 

[everydayupsanddowns]

I asked what type my LDL was - the NHS don't test for it, or at least they didn't back in the twenteens

I gather your Trigs component can be used as a reasonable proxy measure? Though I don’t think mainstream expert opinion puts much store in ratios / particles. It’s mostly about totals, or possibly LDL and TC-HDL these days I think?

 

[JITR]

@beating_my_betes

Here is a link to a high-res image of the references: https://mega.nz/file/n1NEmIhI#5PVAbvI7aiqw7QN8RpelCZGZl_Kyy61X3r0SAxCRXMQ

For starters I'd have a look at Chapter 10: 1-2, 6-11, 24-25.

The Abstract in #2 (1999) begins:
More than decade ago, several cross-sectional studies have reported differences in LDL particle size, density and composition between coronary heart disease (CHD) patients and healthy controls. Three recent prospective, nested case-control studies have since confirmed that the presence of small, dense LDL particles was associated with more than a three-fold increase in the risk of CHD. The small, dense LDL phenotype rarely occurs as an isolated disorder. It is most frequently accompanied by hypertriglyceridemia, reduced HDL cholesterol levels, abdominal obesity, insulin resistance and by a series of other metabolic alterations predictive of an impaired endothelial function and increased susceptibility to thrombosis.

 

[beating_my_betes]

The saying, "Don't sweat the small stuff" comes to my mind.

Of course I just dont think unsubstantiated claims, misinformation and bad messaging around health is small stuff.

 

[beating_my_betes]

@beating_my_betes

Here is a link to a high-res image of the references: https://mega.nz/file/n1NEmIhI#5PVAbvI7aiqw7QN8RpelCZGZl_Kyy61X3r0SAxCRXMQ

For starters I'd have a look at Chapter 10: 1-2, 6-11, 24-25.

The Abstract in #2 (1999) begins:
More than decade ago, several cross-sectional studies have reported differences in LDL particle size, density and composition between coronary heart disease (CHD) patients and healthy controls. Three recent prospective, nested case-control studies have since confirmed that the presence of small, dense LDL particles was associated with more than a three-fold increase in the risk of CHD. The small, dense LDL phenotype rarely occurs as an isolated disorder. It is most frequently accompanied by hypertriglyceridemia, reduced HDL cholesterol levels, abdominal obesity, insulin resistance and by a series of other metabolic alterations predictive of an impaired endothelial function and increased susceptibility to thrombosis.

I've already addressed this. I've asked for the evidence that heat is uniquely causal. I've also given you evidence showing reverse association between whole-grans, including wheat, to heart disease.

 

[beating_my_betes]

I read what Davis wrote in the book and then searched for current research and opinion such as the paper I quoted. At the next opportunity, I'll ask for a small LDL test.

Also, in the context of this conversation, what would you be looking to solve via a test?

 

[JITR]

Also, in the context of this conversation, what would you be looking to solve via a test?

I do not eat much wheat or other whole grains, I'd like to know if my small dense LDL particle level is low.

 

[beating_my_betes]

I do not eat much wheat or other whole grains, I'd like to know if my small dense LDL particle level is low.

How are you expecting to isolate any results from given stimuli? Are you suggesting that only wheat/grains would be responsible for the density of your particles?

 

[JITR]

How are you expecting to isolate any results from given stimuli? Are you suggesting that only wheat/grains would be responsible for the density of your particles?

How are you expecting to isolate any results from given stimuli?
All I'd like to know is the result of a test to measure my small LDL particle level (mmol/l).

Are you suggesting that only wheat/grains would be responsible for the density of your particles?
No. I'll accept what William Davis wrote until a better model* presents itself, 'Think of it this way: anything that provokes an increase in blood sugar will also provoke small LDL particles. Anything that keeps blood sugar from increasing, such as proteins, fats, and reduction in carbohydrates such as wheat, reduces small LDL particles....' (see one of my previous posts, above)
* such as ApoB?

 

[Eddy Edson]

It's not completely unambiguous, but the weight of evidence these days tends to the view that the *number* of LDL particles is at any rate more important than their *size*.

Simon Hill has a good brief overview with references: https://theproof.com/does-ldl-particle-size-matter/

The process of atherosclerosis begins when LDL particles circulating in the bloodstream are absorbed into the wall of the artery. (3) A special protein called apolipoprotein B (ApoB) is present on every LDL particle, regardless of size, and it interacts with an LDL receptor to essentially activate a shuttle allowing it inside the artery wall.

Once LDL is inside the artery wall, its size may determine whether it is retained or removed. And here is where the grain of truth in the claim about total LDL versus the size of LDL comes into play.

It is true that small dense LDL particles are more easily retained in the artery wall. However, because of their small size, they deposit less cholesterol per particle. In contrast, the large fluffy LDL particles, while less easily retained in the artery wall, deposit more cholesterol per particle.

And it’s that last part that people are overlooking. Yes, large fluffy LDL particles are less likely to get stuck in the artery wall, but each time they do, compared to a small particle, they deposit a lot more cholesterol.

The net result is the same for both types of particles. Whether you deposit a lot all at once or a little at a time, you’ll still end up with atherosclerosis.

It doesn’t matter if your LDL particles are small and dense or large and fluffy. What matters is the total number of LDL particles and, more specifically, the total number of ApoB-containing lipoproteins, which includes all forms of LDL. The higher the concentration of ApoB-containing lipoproteins in the bloodstream, the more that will get moved into the artery wall, and ultimately, the more small AND large particles will be retained. (4)

Anyway, not sure what this has to do with wheat in particular. Any kind of refined carb can screw up lipids, but generally not eg wholegrains, which are protective.

 

[Eddy Edson]

It's not completely unambiguous, but the weight of evidence these days tends to the view that the *number* of LDL particles is at any rate more important than their *size*.

Simon Hill has a good brief overview with references: https://theproof.com/does-ldl-particle-size-matter/

The process of atherosclerosis begins when LDL particles circulating in the bloodstream are absorbed into the wall of the artery. (3) A special protein called apolipoprotein B (ApoB) is present on every LDL particle, regardless of size, and it interacts with an LDL receptor to essentially activate a shuttle allowing it inside the artery wall.

Once LDL is inside the artery wall, its size may determine whether it is retained or removed. And here is where the grain of truth in the claim about total LDL versus the size of LDL comes into play.

It is true that small dense LDL particles are more easily retained in the artery wall. However, because of their small size, they deposit less cholesterol per particle. In contrast, the large fluffy LDL particles, while less easily retained in the artery wall, deposit more cholesterol per particle.

And it’s that last part that people are overlooking. Yes, large fluffy LDL particles are less likely to get stuck in the artery wall, but each time they do, compared to a small particle, they deposit a lot more cholesterol.

The net result is the same for both types of particles. Whether you deposit a lot all at once or a little at a time, you’ll still end up with atherosclerosis.

It doesn’t matter if your LDL particles are small and dense or large and fluffy. What matters is the total number of LDL particles and, more specifically, the total number of ApoB-containing lipoproteins, which includes all forms of LDL. The higher the concentration of ApoB-containing lipoproteins in the bloodstream, the more that will get moved into the artery wall, and ultimately, the more small AND large particles will be retained. (4)

Anyway, not sure what this has to do with wheat in particular. Any kind of refined carb can screw up lipids, but generally not eg wholegrains, which are protective.

For further references & what I think is the common current view on LDL size, see this standard endicronology text (2023 update): https://www.ncbi.nlm.nih.gov/books/NBK355893/#lipid_testing.LDL_SIZE


The size of LDL particles is heterogeneous and there are a number of different methods to determine LDL size (ultracentrifugation, gradient gel electrophoresis, ion mobility, NMR) (55). As noted above, the different methods of LDL subclass analysis may produce different results and significant variations are possible even within one method (48). Studies have shown that small dense LDL is more pro-atherogenic than large LDL particles. Small dense LDL are thought to be more atherogenic because they are better able to penetrate the endothelial cell barrier and enter the intima, are more susceptible to oxidation, bind to proteoglycans in the arterial wall, and have a longer half time in the circulation than large LDL particles (56). It should be noted though that large LDL particles are also pro-atherogenic (57-61). For example, patients with familial hypercholesterolemia tend to have large LDL particles and these patients are at high risk to develop ASCVD (60). Small LDL particles are typically seen in patients with elevated triglyceride levels and decreased HDL-C levels (i.e. patients with the metabolic syndrome, obese patients, patients with diabetes) (62). Numerous studies have documented a link between small dense LDL particles and an increased risk of ASCVD (63,64). However, the association of small dense LDL with ASCVD is markedly reduced or entirely eliminated when the analyses are adjusted for other factors that affect the risk of ASCVD (63,64). The National Lipid Association expert panel was unable to identify any patient subgroups in which measuring LDL size is necessary (65). The author concurs with that viewpoint.

 

[JITR]

@Eddy Edson
Thank you for those references.
While the headlines may be clear it will take me some time to digest the detail.

 

[Docb]

@Eddy Edson
Thank you for those references.
While the headlines may be clear it will take me some time to digest the detail.

Quite agree with your last sentiment....the headlines might be clear especially when they are constructed to attract attention rather than inform. The detail is not a place for amateurs, something neatly illustrated by @Eddy Edson 's cut and paste above.