• Please Remember: Members are only permitted to share their own experiences. Members are not qualified to give medical advice. Additionally, everyone manages their health differently. Please be respectful of other people's opinions about their own diabetes management.
  • Diabetes UK staff will be logging into the forum at various times throughout this Bank Holiday weekend, however, if you require emergency medical assistance or advice please call 999, or if it is less urgent then please call the 24 hour NHS 111 service on 111. Alternatively, please speak to your GP or healthcare team.
  • We seem to be having technical difficulties with new user accounts. If you are trying to register please check your Spam or Junk folder for your confirmation email. If you still haven't received a confirmation email, please reach out to our support inbox: support.forum@diabetes.org.uk

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

@Eddy Edson
Thank you for those references.
While the headlines may be clear it will take me some time to digest the detail.
This might be useful also: Gil Cavalhao interviewing a National Lipid Association etc leader, setting out the current nuanced mainstream view:

With a bunch of references.
 
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.
As far as I am aware the NHS don't test for LDL, let alone small LDL
 
This might be useful also: Gil Cavalhao interviewing a National Lipid Association etc leader, setting out the current nuanced mainstream view:

With a bunch of references.
I already posted that earlier. Of course, such important info bears repeating.
 
As far as I am aware the NHS don't test for LDL, let alone small LDL
No, they use an equation - something like total cholesterol - HDL-(trigs/2.2).
I think the trigs bit is an attempt to eliminate VLDL.

Total = LDL-C+HDL+VLDL
 
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?
But you've yet to demonstrate that what Davis is saying holds water. So why would you accept what he has written, at all?

There're so many things that causes blood-sugar to increase (Try a CGM if you're unsure), and were blood-sugar rises to be inherently bad it would be unlkely any of us would've made it into double-digit years, if we managed to make it past weaning (Human milk is relatively carb rich compared to cow's milk, which human chidren are made to drink anyway).

As I've said, even if wheat were uniquely problematic (the raison d'être of his book), why would he be advising a low-carb diet? The answer may be that low-carb was his starting point, and everything was reverse-engineered from there. And it's in these non-wheat-specific claims where the bread absolutely falls out of the basket. Not only does he seem to not be making a causal association between wheat, but he also seems to have fallen for all the anti-grain/carb nonsense.

At this point, I've given you a link to a meta-analysis, discussing the health effects of grains. Seems like a much stronger hook upon which to hang your coat than the one in Davis' cloakroom.
 
Last edited:
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.

It's interesting to see the summary of #64 (2010) concludes, ' ... recent studies suggest that more refined analyses of lipoprotein subspecies may lead to further improvements ... particularly in identification of appropriate targets for therapeutic intervention in individual patients.' (https://pubmed.ncbi.nlm.nih.gov/20531184/)

In other words, diagnostics like the level of small LDL particles could help people avoid becoming CVD patients. Clinicians' needs may differ from mine. In much the same way as my HbA1c result led my GP to prescribe Metformin and me to prioritise weight loss without medication.
 
It's interesting to see the summary of #64 (2010) concludes, ' ... recent studies suggest that more refined analyses of lipoprotein subspecies may lead to further improvements ... particularly in identification of appropriate targets for therapeutic intervention in individual patients.' (https://pubmed.ncbi.nlm.nih.gov/20531184/)

In other words, diagnostics like the level of small LDL particles could help people avoid becoming CVD patients. Clinicians' needs may differ from mine. In much the same way as my HbA1c result led my GP to prescribe Metformin and me to prioritise weight loss without medication.
This is still emerging science, and nothing is set in stone. What is clear is that all factors need to be considered. If it is the case that sdLDL is indeed the huge antagonist that people like Davis claim, then we need to cast a wider net when it comes to the causes. Within such an appraisal, its important to look at hard outcome human data e.g. the reverse association between ALL whole grains and various types of disease, despite Davis et al's claims and contrary to ALL expectations by those who feel emboldened, for whatever reason, to blame everything on BG rises via carbs.

Anyway, as far as interesting, I'll 'see' your advice to reduce grains to reduce sdLDL, and raise you 'the advice to reduce saturated-fat, and eat more fibre via fruits & vegetables'...for the same outcomes:


Screenshot 2025-04-14 at 19.51.48.png
 
Back
Top